Lectures in ICU . . . . .

Lectures in
Critical Care Medicine

Clinical notes on
common topics in ICU
May 2023

Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital

Lectures in Critical Care Medicine
Title Page
1) Advanced Cardiac Life Support Treatment Algorithm 3
2) Assessment of the seriously ill patient & ICU admission criteria 55
3) Monitoring in ICU 111
4) Basic Airway Management 139
5) Oxygen therapy 191
6) Acute respiratory failure & Ventilatory Management of ARDS and Asthma 227
7) Mechanical Ventilation 276
8) Noninvasive ventilation (NIV) for acute respiratory failure 348
9) Circulatory Shock 376
10) Fluid management in ICU 432
11) Blood products & transfusion 472
12) Disorders of consciousness & TBI 544
13) Sedation in ICU & Pain, Agitation and Delirium Care 584
14) Sepsis Management and Antimicrobials use in ICU 656
15) Renal & Electrolyte Emergencies 712
16) ICU Management of the Burn Patient 791
17) Nutrition in ICU 839
18) Diabetic Emergencies 879
19) Critical Care Management of Obstetric Emergency 935
20) General management of poisoning & Snake bite 1011

1)Advanced Cardiac Life Support
Treatment Algorithm
Critical Care 3

Introduction
•Resuscitationistheprocessofcorrectingphysiologicaldisorders
(suchaslackofbreathingorpulse)inanacutelyillpatient.
•Itisanimportantpartofintensivecaremedicine,trauma
surgeryandemergencymedicine.
•Wellknownexamplesarecardiopulmonaryresuscitation4

Systemic Approach
Initial
approach
Conscious
patient
Primary survey
Secondary survey
Unconscious
patient
BLS approach5

BLS Approach
1.Safety
2.Checkresponsiveness
3.Activateemergencyresponse
4.Checkpulseandbreath
5.StartCPR6

Primary survey
Exposure
Disability
GCS AVPU Eye pupil
Circulation
Vital signsAbdominal examination Pelvic examination FAST
Breathing
Ventilation Oxygenation
Airway
Basic management Advance management7

Secondary survey
Event
Last meal
Past medical history
Medications
Allergy
Sings & Symptoms8

The unresponsive patient
Take 5 to no more than 10
seconds for:
•Pulse check
•Normal breathing check
Open Airway
Look for signs of life9

CPR 30:2
Until defibrillator /
monitor attached
Open Airway
Look for signs of life
Call
Resuscitation
Team
Cardiac or respiratory arrest confirmed10

High Quality CPR(Chest compression)
1.Push hardand fast
•Achieving a rate of 100–120 compressions per minute
•Compressing the chest to a depth of 2–2.4 inches (5–6 cm) in
adult (1/3 depth of chest in children & infants).
2.Allow chest recoil
3.Avoid hyperventilation
4.Minimized interruption11

12

Airway and ventilation techniques during CPR
•Bag-maskventilation(BMV)withsupplementaloxygenisthemost
commoninitialapproachandcanbeaidedwithanoropharyngealor
nasopharyngealairway.
•Twopositivepressurebreathsafterevery30chestcompressions.
Thesebreathsshouldbeofaninspiratorytimeof1secondandproduce
avisiblechestwallrise.13

Airway and ventilation techniques during CPR
•Ifthereisanadvancedairwayinplace,deliveronebreathover1second
every6-8seconds(rate8-10/min)regardlessofchestcompression(rate
100-120/min).
•Ifthereisapulseandnospontaneousbreathing,giveonebreathover1
secondevery6seconds(every2-3secondsinchildren)andreassessthe
pulseafter2minutes.14

15

CPR 30:2
Until
defibrillator/monitor
attached
Assess
Rhythm
Open Airway
Look for signs of life
Call
Resuscitation
Team
Adult ALS
Algorithm16

CPR 30:2
Until
defibrillator/monitor
attached
Assess
Rhythm
Shockable
(VF/Pulseless VT)
Non-shockable
(PEA/Asystole)
Open Airway
Look for signs of life
Call
Resuscitation
Team
Adult ALS
Algorithm17

Shockable
(VF)
•Bizarre irregular waveform
•No recognizable QRS complexes
•Random frequency & amplitude
•Uncoordinated electrical activity
•Coarse / fine
•Exclude artifact
–Movement
–Electrical interference18

Shockable
(VT)
•Monomorphic VT (without pulse)
–Broad complex rhythm
–Rapid rate
–Constant QRS morphology19

1
st
shock
•150 -200 J biphasic
•360 J monophasic
Assess
Rhythm
Shockable
(VF/Pulseless VT)
1 Shock
150-200 J biphasic
or 360 J monophasic
Immediately resume
CPR 30:2
for 2 min20

Defibrillation energies
•Vary with manufacturer
•Check local equipment
•If unsure, deliver maximum Joules (do not delay shock)21

If VF/VT persists
–200 J biphasic or
–360 J monophasic
After 2
nd
shock give Adrenaline
(1mg IV)
After 3
rd
shock, give Amiodarone
(300mg IV push) or
Lidocaine(70-100mg)
After 4
th
shock, give adrenaline
After 5
th
shock, give Amiodarone(150mg)
Or Lidocaine(35-50mg)
Deliver 2
nd
shock
CPR for 2 min
Deliver 3
rd
shock
Deliver 4
th
shock
If VF/VT persists
If VF/VT persists
CPR for 2 min22

After delivery of shock
•Continue CPR for another 2 min
–Stop CPR only if patient there is pulse23

After 2 min, assess rhythm
•If organised electrical activity, check for pulse:
–If present start post resuscitation care
–If not present go to non-shockable algorithm
•If asystole, go to non-shockable algorithm24

Asystole
Pulseless electrical
activity (PEA)
Assess
Rhythm
Non-shockable
(PEA/Asystole)
Immediately resume
CPR 30:2
for 2 min25

Non-shockable
Asystole
•Absent ventricular (QRS) activity
•Atrial activity (P waves) may persist
•Rarely a straight line trace26

Asystole
•During CPR:
–Check leads are attached
–Adrenaline 1 mg IV every 3 –5 min27

Non-shockable
(PEA)
Any ECG activity (excluding ventricular tachycardia and fibrillation),
even organized, withoutclinical evidence of a palpable pulse or
myocardial contractions28

Pulseless electrical activity
•Exclude / treat reversible causes
•Adrenaline 1 mg IV every 3-5 min29

30

31

Role of waveform capnography during CPR
1.Ensuring tracheal tube in trachea
2.Monitoring ventilation rate during CPR & avoiding
hyperventilation
3.Monitoring quality of chest compressions during CPR
–Greater depth of chest compression →↑EtCO
232

Role of waveform capnography during CPR
4.Identifying ROSC during CPR
–↑EtCO
2during CPR may indicate ROSC & prevent unnecessary &
potentially harmful dosing of adrenaline in patient with ROSC33

Role of waveform capnography during CPR
5.Prognostication during CPR
–Low EtCO
2values during CPR associated with lower ROSC rates &
increased mortality
–Failure to achieve EtCO
2> 10 mmHg after 20 min of CPR associated
with poor outcome34

Waveform capnography 35

36

ROSC
1.Advanceairway(ifnotalreadyinserted)
2.Fluidsresuscitation
3.ECG12leads
4.Targetedtemperaturemanagement(TTM)37

38

Tachyarrhythmia39

Cardiac Arrest Algorithm 40

Cardiac ArrestAlgorithm 41

SupraventricularTachycardia
Atrial Flutter
Atrial Fibrillation42

Ventricular Tachycardia (VT)
Polymorphic Ventricular Tachycardia (VT)
(Torsade de pointes)43

Bradyarrhythmia44

Cardiac ArrestAlgorithm Bradycardia45

Sinus Bradycardia
2nd degree AV Block:, Mobitz I (WenckebachPhenomenon)
2nd degree AV Block:, Mobitz II
Third-degree AV block(completeheart block)46

Compromised
Pacing
Arrhythmia
Tachycardia Bradycardia
Not Compromised
Medications
Compromised
Cardioversion
No response
Not Compromised
Monitor & observeMedications
No response47

Summary48

49

50

Pulseless electrical activity51

Supraventricular tachycardia52

Ventricular tachycardia53

Ventricular fibrillation54

2)Assessment of
the seriously ill patient
& ICU admission criteria
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care 55

The aim of assessment
of seriously ill patient
1)Identifythephysiologicalabnormalities.
2)Identifythemostappropriatewaytocorrect
thoseabnormalities.
3)Diagnosetheunderlyingproblem.56

Cont.
•Theprocessinvolvestakingafullhistoryandthoroughly
examiningandinvestigatingthepatientoccursisdifferent
mannerintheseriouslyillpatient.Thedifferenceisdueto
theurgencywithwhichtreatmentneedstobestarted.
•Thereisrarelytimetotakeafullhistoryorcarryoutavery
detailedexaminationbeforeinitiatingtreatment.
•Tasksthataretypicallycarriedoutsequentiallyoftenhaveto
becarriedoutinparallelwithhistorytaking,examinationand
initialresuscitationoftenoccurringsimultaneously.57

Cont.
•Oftenitisnecessarytorestrictoneselftoonlythe
informationrequiredtoguidethenexttreatment
decisionandtofillinmissingcomponentsofhistory,
examinationandinvestigationaftertreatmenthasbeen
Initiatedona"bestguess"basis.
•Theworkingdiagnosisneedstoberepeatedlyreassessed
asmoreinformationbecomesavailableandonthebasis
ofresponsetotreatment.58

1)Initial assessment
•Thefirststepinassessingaseriouslyillpatientisto
estimatehowillthepatientisandhowmuchtimeis
availableforassessmentandinvestigationbefore
initiatingtreatment.59

Warning signs of a severely ill patient
Apatientwithanyofthesefeaturesshouldbeassessed
urgentlyby an experiencedphysician
ValuesParameter
Systolic <90 or mean <70 mmHgBlood pressure
>150 or < 50 bpmHeart rate
>30 or <8 breaths/minRespiratory rate
GCS <12Conscious level
<0.5 ml/kg/hOliguria
<120 mmol/l or > 150 mmol/lSodium
<2.5 mmol/l or >6 mmol/lPotassium
<7.2pH
<18 mmol/l Bicarbonate
Concerned experienced nurse Worried nurse 60

Components of the initial assessment
•KeycomponentsoftheInitialassessmentare
assessmentofairwaypatency,breathingand
circulation.
•Absenceofanyoftheseshouldpromptimmediate
resuscitation.61

Cont.
•Theseverityofillnessisoftenjudgedbyassessingthe
compensatoryresponsetotheprimaryabnormality.Inmost
casesthiscompensationinvolvesactivationofthe
sympatheticnervoussystem,andthemagnitudeofthe
sympatheticresponsegivesanindicationoftheseverityof
illness.
•Itshould,however,benotedthatinthepre-terminalpatient
thecompensatoryresponseisexhaustedandthepatientmay
bebradycardiacandbradypnic.62

Cont.
•Ifthepatientisalreadyreceivingsupportivetherapyitis
importanttonotetheintensityofsuchtherapy.
•Forexampleapatientwithanarterialoxygensaturation
of92%on2L/minofoxygenthroughanasalcannulais
muchlessillthanasimilarpatientwithasaturationof
92%on15L/minofoxygen.63

Assess intensity of support
•Inspiredoxygenfractionneededtomaintainsaturationabove
90%
•Intensityofventilatorysupport—positiveend-expiratory
pressure,minuteventilation
•Doseofvasopressor&inotropeneededtomaintainmeanarterial
pressureabove60mmHg
•Needforvolumesupporttokeepadequateurineoutput
•Needforbloodtransfusiontokeephemoglobinabove8g/dL
•Needforsedationinagitatedpatients
•NeedfordialysissupportorWorseningbiochemistry64

Seek help for specific problems
•Cardiologist—completeheartblock,acutecoronarysyndrome,
cardiogenicshock,intra-aorticballoonpumpinsertion,pericardial
tamponade,massivepulmonaryembolism
•Nephrologist—dialysis
•Neurologist—acutestrokeorundiagnoseddepressedconsciouslevel
•Neurosurgeon—intracranialhemorrhage,headinjury,severe
cerebraledema
•Traumasurgeon—polytrauma,abdominaltrauma,thoracictrauma,
compartmentsyndrome
•Obstetrician—rupturedectopicpregnancy,postpartumhemorrhage65

Construct a working diagnosis and plan for
further management
•Afterinitialresuscitation,assessment,investigation,
andresponse,adifferentialdiagnosisshouldbe
arrivedat.
•Reassessthepatientfrequentlytomodifyinitialplan
ifneeded.66

Brief relatives
•Afterinitialresuscitation,assessment,investigation,and
response,thefamilyshouldbebriefedaboutthe:
✓likelydiagnosis,
✓treatmentplan,
✓approximateprognostication,
✓approximatedurationofstayand
✓consentshouldbetakenforanyinvasiveprocedures.
•Familybriefingshouldbedocumentedinclinicalnotes.67

Airway
•Assessmentofairwaypatencyisvital.Look,listenandfeel
forevidenceofairwayobstruction.
•Lookfortachycardia,tachypnea,sweating,useofaccessory
muscles,drooling(epiglottitis),see-sawthoracoabdominal
(paradoxicalchestwall)movementandrecession.
•Rememberthatchestmovementcanoccureveninthe
presenceofcompleteairwayobstruction.68

Airway
•Listenforgurglingorstrider(notethatstridormaybe
absent,particularlyinseverecasesandthepresenceofa
normaloxygensaturationdoesnotexcludea
compromisedairway).
•Hypercarbiaandaresultingdecreaseinconsciouslevel
indicatethatthecompensatorymechanismsare
exhausted.Bradycardiaindicatesimpending
cardiorespiratoryarrest.69

Airway
➢Inspiratorystridorisaraspingsoundheardduring
inspirationandisaresultofobstructionaboveorinvolving
thelarynx
➢Wheezeisusuallyheardonexpirationasaresultofthe
lowerairwayscollapsing
➢Gurglingoccurwhensecretionorliquidispresentinthe
upperairways
➢Snoringoccursduringpartialocclusionoftheoropharynx
duetorelaxationoftheoropharyngealmusclesandtongue70

Breathing
✓EffectivenessofBreathing
✓WorkofBreathing71

Breathing
•Cyanosis,hypoxia?
•Rate,depth,symmetryofchestmovement?Useof
accessorymuscles?
•Palpatechestwallforstructuralintegrity
•Chestinjury/flail/pneumothoraces
•O2therapy/Assistedventilation
•Manageinjury/pnuemothoraces72

Breathing
•Notethatmarkedtachypneaisausefulmarkerofaseverelyill
patient,regardlessofwhetherthepatienthasrespiratory
failure.
•Detectionofcyanosisisoftendifficultandtachypneais
usuallyamoreobvious,althoughnon-specificsignofa
problem.
•Aswithairwayproblemstheseverityoftheproblemisoften
bestjudgedfromthemagnitudeofthecompensatory
response.73

Breathing
•Pulseoximetryisausefulbedsidetestinvestigation,but
itshouldbenotedthatsignificantdesaturationisoftena
latefeatureofventilatoryabnormalities.
•Absenceofadefectinoxygenationinabreathless
patientshouldalsopromptasearchfornon-respiratory
causessuchasmetabolicacidosisandsepsis.74

Circulation
•Quickheadtotoesurveytonoteandcontrolbleeding
•Skincolor,moisture,temperature
•Pulsequality,rate,regularity,volume
•Bloodpressure
•Capillaryrefill(shouldbe<2seconds)
•ChestCompressions/Positioningetc.75

Circulation
•Rapidinitialassessmentofcirculatorystatusshould
concentrateontissueperfusionandnotjustbloodpressure.
•Asaresultofcompensatorymechanisms,hypotensionisa
latefeatureofcardiovasculardysfunction.
•Evidenceofinadequatetissueperfusion(decreasedconscious
level,skinmottling,coldperipheries,poorcapillaryrefill,
oliguriaandmetabolicacidosis)indicatesaseverelyillpatient,
evenintheabsenceofhypotension.76

Circulation
•Anindicationofthetypeofshock(cardiogenic,
distributiveetc.)canbeobtainedbyfeelingthepulse
andtheperipheriesandexaminingthejugular
venouspressure.77

Conscious state
•Amarkedreductioninconsciouslevelindicateseither
thatcompensatoryhomeostaticmechanismshavebeen
overwhelmedorsevereneurologicaldisease.
•Ineithercase,thepatientisseverelyillandrequires
urgentsupportivetherapy.
•Thepupillaryresponseshouldbecheckedfrequently.78

Investigations
•Theseshouldnotdelayinitialresuscitationbutcanbe
carriedoutwhilethepatientisbeingresuscitated.
•Usefulscreeninginvestigationsincludepulseoximetry,
arterialbloodgases,electrolytes,renalfunctiontests,
completebloodcountandclotting.79

2)Subsequent assessment
Part or all of this assessment may be carried out before
initiating any treatment in less severely ill patients.80

History
•Oftenitisnotpossibletotakeafullhistoryfromthepatient
andthereforeothersourcesofinformationbecamemore
important.
•Theseincludemedical,nursingandambulancestaff,relatives,
andnotesandcharts.Aswellasrevealingthehistorythe
notesandchartsmaygiveusefulinformationontherateof
deterioration.Inpost-operativepatientstheoperationnote
maybeparticularlyhelpful.81

History
•Thehistorywillrevealwhetherthepatientfallsintoa
groupthatisdifficulttoassess.
•Theseinclude:
–Youngadults
–Elderlyorimmunocompromised.
–Traumapatients82

Groups of patients who are difficult to assess
DifficultyGroup
Compensatorymechanismsinyoungpatientstendto
masksignsofsevereillnessuntiltheillnessisvery
advanced.Significantphysiologicalabnormalitiesin
thesepatientsthereforeindicateverysevereillness.
Young adults
Theinflammatoryresponsemaybedamped,again
hidingsignsofsevereillness.Inadditionthe
physiologicalreserveofthesepatientsisoftenseverely
compromised
Elderly or
immuncompromised
patients
Notoriouslydifficulttoassessduethemultitudeof
possibleInjuriesandtheeffectofdistractingpain
makinginjuriesdifficulttolocalizeInthesepatientsa
detailedhistoryofthemechanismofInjuryprovides
vitalcluestolikelyinjuries.
Trauma patients 83

History
•Thehistoryisinvaluableintheassessmentof
physiologicalreserve.
•Anassessmentofcardiopulmonaryreservecanbe
obtainedfromthepatientexercisetolerance.
•InassessingexercisetoleranceitisImportanttoenquire
aboutbothdistancecoveredandspeed.Forexample
thereisaconsiderabledifferenceinexercisetolerance
betweenthepatientwhocanwalkuponeflightofstairs
atanormalpaceandthepatientwhotakes5minutesto
walkuponeflightofstairs.84

Examination
•Whiletheaimoftheinitialexaminationistodetectlife
threateningphysiologicalabnormalitiesandtodetermine
appropriatesupportivetherapy,thefocusofsubsequent
examinationistodeterminetheunderlyingcause,inorderto
determinetheappropriatedefinitivetherapy.
•Examinationshouldberepeatedfrequentlytodeterminethe
responsetotherapyandbecausetheclinicalsignsmay
change.85

Investigations
•InadditiontotheInvestigationscarriedoutduringtheinitial
assessment,liverfunctiontests,calcium,phosphate,
magnesiumestimationandachestX-rayareusefulscreening
tests.Otherinvestigationsshouldbeorderedonthebasisof
thehistoryandclinicalfindings.
•Ifadvancedradiologicalimagingisindicated,consideration
shouldbegiventoultrasoundscanningbecauseofthelow
riskofadverseeffectsandbecauseitmayobviatetheneedto
transportthepatienttotheradiologydepartment.86

Clinical and laboratory features suggestive of
severe illness
FeatureSystem
Tachycardia,hypotension,coldperipheries,skinmottling.
Bradycardiamayindicateapre-terminalstate.
Cardiovascular
Tachypnea,recession,useofaccessorymusclesof
respiration,lowoxygensaturation.Lowrespiratoryrate
mayindicateimpendingrespiratoryarrest.
Respiratory
OliguriaRenal
Decreasedconsciousness,confusionagitation,aggressive
behavior
Nervoussystem
Acidosis,severeelectrolyteabnormalities(particularly
severehyperkalemiaandseverehyponatremia),severe
anemia,thrombocytopenia,coagulopathy,elevated
lactate.
Metabolic
SweatingMiscellaneous87

Review
•Followingtheprimaryassessment,initiationofemergency
treatmentandfullassessment,aworkingdiagnosisand
planforthesubsequentmanagementshouldbedeveloped.
•Thisplanshouldincludeanongoingreviewoftheresponse
totreatment,andaconsiderationoftheappropriate
placementofthepatient,possiblyinIntensiveCareor
anotherhighcarearea.88

89

ICU admission criteria
•Lifesupporttechnologyisintendedtoprovide
temporarysupportforpatientswithpotentially
reversibleorganfailureandisnotameasureto
conquer(defeat)death(advancedorterminallyill
cases).90

System approach
•Airway: compromise or impending compromise (e.g. burn).
•Respiratory failure: (not responding to conservative treatment).
–Type IRespiratory failure (hypoxia).
–Type IIRespiratory failure (hypercapnia).
•Circulatory failure:
–Hypovolemic shock:
–Distributive shock: (e.g. septic, most common type in ICU).
–Cardiogenic shock: (usually treated in CCU).
–Obstructive shock: 91

System approach
•CNS emergency:
–Severe traumatic brain injury.
–Encephalitis.
–Refractory status epilepticus.
–Brain tumor (post operative).
–Stroke (post operative or post tPA).
–Altered LOC (poisoning or toxicity).
•Endocrine emergency:
–Diabetic: (severe DKA, HHS, recurrent hypoglycemia).
–Adrenal: (adrenal crisis).
–Thyroid: (thyrotoxicosisand myxedema coma).92

System approach
•Visceral and metabolic:
–Acute liver failure or acute on chronic liver failure.
–Acute kidney injury (complicating sepsis or rhabdomyolysis).
–Severe electrolyte imbalance (requiring close monitoring).
•Obstetric emergency: (e.g. eclampsia & its complications).
•Postoperative cases:
–Major general surgery (e.g. large fluid shift).
–Major vascular surgery.
–Neurosurgery (brain tumor).
•Massive blood transfusion.93

ICU Discharge Criteria
•Stablerespiratorystatus.
•Noorminimaloxygensupport.
•Stablehemodynamicparameters.
•Inotropicsupport,vasodilatorsandantiarrhythmicdrugs,
andintracranialpressuremonitoringarenolongerrequired.
•NeurologicstabilitywithcontrolofSeizures.
•Closemonitoringisnolongerrequired.94

Question 1
A19-year-oldmanisejectedthroughthefrontwindowofacarduring
ahighspeedimpactandisbroughtintohospitalbytheparamedics.
TheprimarysurveyshouldincludethefollowingpointsEXCEPT:
A. Use of airway adjuncts if indicated.
B. Control of external hemorrhage.
C. Cervical spine assessment.
D. Pupillary light reflex determination.
E. Percussion of the chest.95

Answer 1
A19-year-oldmanisejectedthroughthefrontwindowofacarduring
ahighspeedimpactandisbroughtintohospitalbytheparamedics.
TheprimarysurveyshouldincludethefollowingpointsEXCEPT:
A. Use of airway adjuncts if indicated.
B. Control of external hemorrhage.
C. Cervical spine assessment.
D. Pupillary light reflex determination.
E. Percussion of the chest.96

Answer 1
•Theprimarysurveyisdesignedtodetectandaddresslife-
threateningpathology.
•Airwayadjunctsortrachealintubationmayberequireddueto
airwayobstruction,adepressedconsciouslevelaffectingventilation
orchestinjuriesreducingthemechanicalefficiencyofbreathing.
•Pressureshouldbeappliedtocontrolexternalhemorrhagewhilea
surgicalopinionissought.
•Percussionisakeycomponentofchestexaminationandmayreveal
signsofhemothoraxortensionpneumothorax.97

Answer 1
•Abnormalpupillarylightreflexesinconjunctionwithlateralizing
signsandadepressedconsciouslevelsuggesttentorialherniation
duetodiffuseaxonalinjuryorintracerebralhematoma,andshould
prompttemporizingmeasuressuchasmechanicalventilation,
sedationandmannitolwhileobtainingneurosurgicaladvice.
•Althoughthecervicalspineshouldbemaintainedinneutral
alignmentthroughouttheprimarysurvey,acervicalspinefracture
isnotimmediatelylife-threateningandshouldbeassessed
radiographicallyandclinicallyaspartofthesecondarysurvey.98

Question 2
Themosturgentmaneuverintheinitialmanagementofa
patientwithapossibleheadinjuryis:
A.PerformaCTscanandtransfertoaneurosurgicalunit.
B.Intravenousmannitolandhyperventilation.
C.Emergencyexploratoryburrholes.
D.Airwaymanagement.
E.Spinestabilization99

Answer 2
Themosturgentmaneuverintheinitialmanagementofa
patientwithapossibleheadinjuryis:
A.PerformaCTscanandtransfertoaneurosurgicalunit.
B.Intravenousmannitolandhyperventilation.
C.Emergencyexploratoryburrholes.
D.Airwaymanagement.
E.Spinestabilization100

Answer 2
•Themostimportantimmediateprotectivemaneuversforany
CNSinjuryaresecuringandpreservingtheairway,
maintainingandsupportingbreathing,andmaintaining
effectivecirculation.
•Protectingthespine(especially,butnotexclusively,the
cervicalspine)shouldalsobeamongthefirstprioritiesofthe
personprovidingcare.
•Mannitol,anosmoticdiuretic,canbeusefulinthe
managementofcerebraledemaandincreasedICPassociated
withheadtrauma,butshouldnotbefirst-linetherapy.101

Question 3
Theinitialmanagementofapatientinhemorrhagicshockshould
consistof:
A.Rapidinfusionofisotoniccrystalloidfluids
B.Ensuringadequateoxygenationandventilation.
C.Pharmacologicsupporttomaintainstablehemodynamics.
D.Stabilizationofalllongbonefractures.
E.Immediatetransfusionofuncrossmatchedblood.102

Answer 3
Theinitialmanagementofapatientinhemorrhagicshockshould
consistof:
A.Rapidinfusionofisotoniccrystalloidfluids
B.Ensuringadequateoxygenationandventilation.
C.Pharmacologicsupporttomaintainstablehemodynamics.
D.Stabilizationofalllongbonefractures.
E.Immediatetransfusionofuncrossmatchedblood.103

Answer 3
•Asinmostpatients,theinitialmanagementrevolvesaround
evaluatingandensuringthatthepatienthasadequateoxygenation
andventilation.
•Therapidinfusionofisotoniccrystalloidsispartofthestandard
managementaftertheairwayismanaged.
•Pharmacologicagentstosupporthemodynamicsmayplay
secondaryroleinthefaceofhemorrhagicshock.
•Stabilizationofalllongbonesfracturesisasecondarypriority.
•Thetransfusionofuncrossmatchedbloodisoftenusedinthe
scenarioofrefractoryhypotensionaftercrystalloidresuscitation.104

Question 4
Thephysicalfindingmostlikelytodifferentiatecardiac
tamponadefromtensionpneumothoraxis:
A.Absentbreathsounds.
B.Agitation.
C.Distendedneckveins.
D.Hypotension.
E.Cyanosis.105

Answer 4
Thephysicalfindingmostlikelytodifferentiatecardiac
tamponadefromtensionpneumothoraxis:
A.Absentbreathsounds.
B.Agitation.
C.Distendedneckveins.
D.Hypotension.
E.Cyanosis.106

Answer 4
•Bothconditions(cardiactamponadeandtension
pneumothorax)cancauseshock.Thephysicalfindingscan
includedyspnea,agitation,restlessness,cyanosis,tachycardia,
hypotension,anddecreasingmentalactivity.
•Beck’striadforpericardialtamponadeishypotension,distended
neckveins,and,rarely,distantormuffledhearttones.
•Thecardinalsignsoftensionpneumothoraxaretachycardia,
jugularvenousdistention,andabsentbreathsoundsonthe
ipsilateralside.
•Absentbreathsoundsarethekeytoclinicallydifferentiating
thesetwoconditions.107

Question 5
Neurologicevaluationofatraumapatientrevealseyeopeningonlyto
pain,noverbalresponse,anddecorticaterigidity.TheGlasgowComa
Scoreis:
A.5.
B.6.
C.7.
D.8.
E.9.108

Answer 5
Neurologicevaluationofatraumapatientrevealseyeopeningonlyto
pain,noverbalresponse,anddecorticaterigidity.TheGlasgowComa
Scoreis:
A.5.
B.6.
C.7.
D.8.
E.9.109

Answer 5
ThispatientwouldreceivethefollowingGlasgowComa
Score:
•Eyeopeningtopain,2points.
•Noverbalresponse,1point.
•Abnormalflexion,3points.
Totalscore:6110

3)Patient Monitoring in ICU
Critical Care 111

Outlines
•Definition
•Goals
•Whattomonitor?
•Howtomonitor?
•Clinicaltips112

Monitoring, definition
Interpreting available clinical data to help
recognize present or future mishaps or
unfavorable system conditions113

Monitoring, goals
•Enhances(butnotreplaces)thevigilanceofthe
intensivist.
•Providesmeanstoassessphysiologicalfunction.
•Providesinformationthatimprovesthesafetyof
patient.114

Monitoring guidelines
•QualifiedpersonnelshouldbepresentintheICU
•Physicalexamination,Assessment&Diagnosis
remainthemostimportanttoolsavailabletothe
intensivist115

Basic Monitoring
1)Oxygenation
2)Ventilation
3)Circulation
4)Temperature
should be continually evaluated.116

1)Oxygenation
Objective:Toensureadequateoxygen
concentrationinthedeliveredgasandinthe
blood.117

Methods
1)Clinical:color,respiratorypattern(rate,rhythm,depth,
etc.),equalairentry,wheezing,crackles.
2)Deliveredgas:theconcentrationofoxygeninthepatient
breathingsystemshallbemeasuredbyanoxygenanalyzer.
3)Bloodoxygenation:aquantitativemethodofassessing
oxygenationsuchaspulseoximetryshallbeemployedand
ABGsshowPaO2.118

2)Ventilation
A.Every patient should have the adequacy of ventilation
continually evaluated.
1)Qualitative : * Clinical signs such as chest movement and
auscultationof breath sounds are useful.
2)Quantitative: * ABGs show PaCO2
* Continual end-tidal carbon dioxide analysis
* Monitoring of the volume of expired gas is
strongly encouraged in mechanically
ventilated patients.119

B.Whenventilationiscontrolledbyamechanical
ventilator,thereshallbeincontinuoususea
devicethatiscapableofdetecting
disconnectionofcomponentsofthebreathing
system.Thedevicemustgiveanaudiblesignal.120

3)Circulation
•EverypatientshallhavetheECGcontinuously.
•EverypatientshallhaveBPandHRdeterminedand
evaluatedatcloseintervals.
•OtherclinicalevaluationmethodslikePalpationofa
pulse,Auscultationofheartsounds&Oximetry121

Other used monitors
•Temperature[pharyngeal,axillary,esophageal]
•Urineoutput
•Central venous line: measuring CVP
•Arterial line:
–Continuous BP monitoring,
–Easy access allowing for frequent ABGs122

•Swan-Ganz catheter, PCWP: pulmonary artery
pressures, cardiac output
•ICP monitoring
•EEG
•Transesophageal echocardiography (TEE)
Less frequently used monitors123

Airway / Respiratory Axis
•Oxygenation
•Ventilation
•CorrectETTplacement
•ETTcuffpressure(keepbetween20-30cmH2O)
•Airwaypressure124

Respiratory Monitoring
Various alarms by the ventilator:
–Low airway pressure: leakage, disconnection.
–High airway pressure: kink, biting of the tube,
blocked tube, bronchospasm.
–Low expired tidal volume: leakage.
–Apneaalarm: disconnection.
–O2 sensor failure: (unfortunately common in many
of our ventilators).
–Flow sensor failure: (unfortunately common in
many of our ventilators).
NEVER ignore an alarm by the ventilator!125

PEAK INSPIRATORY PRESSURE (PIP)
•Dependson:Airwayresistance(R
aw)&lung
compliance(Cl).
•Duringcontrolledventilationlookforincrease
airwayresistance(e.g.,bronchospasm,kinkedETT)
ordecreaseinpulmonarycompliance(e.g.,
pulmonarycongestion).126

Oxygenation and ventilation
•Pulse oximetry (vital sign for Oxygenation)
–Measures O2saturation in blood
–Slow to indicate change in ventilation
•Capnography (vital sign for ventilation &perfusion)
–Measures CO2in the airway
–Provides a breath-to-breath
status of ventilation127

Cardiovascular Axis
•Arterial Blood Pressure
•Electrocardiography
•Central Venous Catheterization
•Pulmonary Artery Catheterization
•Cardiac Output
•Thermodilution
•Dye Dilution
•Pulse Contour Devices
•Esophageal Doppler
•Fick Principle
•Echocardiography
•Thoracic Bioimpedance128

Electrolyte / Metabolic Axis
•Fluid balance
•Sugar
•Electrolytes
•Acid-base balance
•Nutritional status129

Visual Monitoring
•Respiratory: patient color,respiratory pattern
(accessory muscle use etc.)
•Patient monitor numbers and waveforms
•Bleeding/coagulation
•Diaphoresis / movements
•Line quality (is my IV reliable?)
•Positioning safety review130

Detecting Mishaps Using Monitors
1. Disconnection
2. Hypoventilation
3. Esophageal intubation
4. Bronchial intubation
5. Hypoxia
6. Hypocarbia or hypercarbia
7. Hypovolemia
8. Pneumothorax
9. Air Embolism
10. Hyperthermia
11. Aspiration
12. Acid-base imbalance
13. Cardiac dysrhythmias
14. IV drug overdose131

•Rate.
•Rhythm.
•Axis.
•Intervals.
•Waveforms.
Ona12-leadelectrocardiogram,whichfeatures
shouldbeanalyzedbytheinterpretingclinician?132

What is the differential diagnosis for low voltage?
•AIR: Chronic obstructive pulmonary disease.
•FLUID:Pericardial effusion.
•FAT: Obesity. 133

Does a normal ECG exclude the possibility of
severe coronary artery disease?
No,althoughanECGdoneduringischemicchestpain
isusuallyabnormal.Itiscommonforpatientswith
severecoronaryarterydiseasetohaveanECGwith
onlynonspecificabnormalities.134

High Tech Patient Monitoring
Examples of Multiparameter Patient Monitors 135

Clinical Tips
•ALWAYSrememberthatyourclinicalsense&
judgementissuperiortoanymonitor.
•Youareaclinician,notatechnician.
•Themonitorispresenttohelpyou,nottobe
ignoredandnottocancelyourbrain.136

Clinical Tips
•NeverpanicParticularlywhenthepatientisgoingto
dieandyouhavenoideawhy.
•Ifamonitorgivesanabnormalvalue,suchaslow
oxygensaturation,Checkthepatientfirstthenthe
equipment.
•Knowwherethedefibrillatoriskeptintheunitand
howitworks.137

Clinical Tips
•All1mlampouleslookthesame
(check very carefully)
•Alwayslabelallsyringes
•Atropineandadrenaline
are often stored next to each other138

4)Basic Airway Management
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care 139

Components of the initial assessment
•Keycomponentsoftheinitialassessmentofaseriouslyill
patientareassessmentofairway,breathingandcirculation.
•AirwaymanagementisthemostessentialskillinEmergency
Medicine.
•Establishingorprotectinganairwayisfrequentlytheessential
maneuverforsavingaperson’slife.
•Conversely,failuretodosoisthefastestwaytoassurea
patient’sdemise.140

The goal of Airway Management
•Airway Patency(airflow integrity).
•Airway Clearance(e.g. secretion, blood, FB).
•Airway Protection(e.g. against aspiration).141

Airway
•Assessmentofairwaypatencyisvital.Look,listenandfeel
forevidenceofairwayobstruction.
•Lookfortachycardia,tachypnea,sweating,useofaccessory
muscles,drooling(epiglottitis),see-sawthoracoabdominal
(paradoxicalchestwall)movementandrecession.
•Rememberthatchestmovementcanoccureveninthe
presenceofcompleteairwayobstruction.142

Airway
➢Inspiratorystridorisaraspingsoundheardduringinspiration
andisaresultofobstructionaboveorinvolvingthelarynx
➢Wheezeisusuallyheardonexpirationasaresultofthelower
airwayscollapsing
➢Gurglingoccurwhensecretionorliquidispresentintheupper
airways
➢Snoringoccursduringpartialocclusionoftheoropharynxdueto
relaxationoftheoropharyngealmusclesandtongue
➢Hoarseness(laryngealedema/vocalcordparalysis)143

Airway
•Listenforgurglingorstrider(notethatstridormaybe
absent,particularlyinseverecasesandthepresenceofa
normaloxygensaturationdoesnotexcludea
compromisedairway).
•Hypercarbiaandaresultingdecreaseinconsciouslevel
indicatethatthecompensatorymechanismsare
exhausted.Bradycardiaindicatesimpending
cardiorespiratoryarrest.144

Airway anatomy145

Anatomic considerations in children
•Prominent occiput
•Small mouth opening
•Large tongue, tonsils and adenoids
•Superior laryngeal position
•Weaker hyoepiglottic ligament
•Large, floppy epiglottis
•Shorter trachea
•Anatomic subglottic narrowing146

Cont.147

Potentially life-threatening causes
•Foreign body
•Epiglottitis
•Croup
•Bacterial tracheitis
•Retropharyngeal abscess
•Peritonsillar abscess
•Blunt or penetrating injury
•Upper airway burns
•Anaphylaxis
•Laryngotracheomalacia
•Hereditary angioedema
•Vocal cord dysfunction
•Laryngospasm148

Mild Airway Obstruction
Ability to speak
Hoarse cry
Forceful cough
Good air entry
Inspiratory stridor
Snoring
Minimal or no
retractions
No nasal flaring or
grunting
Encourage continuing
coughing
Stay and monitor
Take steps if progress
to severe obstruction
Symptoms Action149

Severe Airway Obstruction
Universal Choking sign
Unable to speak or cry
Poor or no air entry
Retractions
nasal flaring
Prolonged inspiratory
time
Tachypnea
Audible inspiratory
stridor
loss of consciousness
Take steps to relive
obstruction: Abdominal
thrusts/ Chest thrusts/
Back thrusts
No Blind finger-sweeps
CPR when unconscious
Symptoms Action150

Management
•History and Examination
•Radiological images and Endoscopy
•Positioning Manoeuvres
•Airway Adjuncts
•Patient position
•Breathing Techniques151

Basic Airway
management
Inadequate
Ventilation
Decrease
Respiratory
Effort
Airway
obstruction
Cardiopulmonary
Resuscitation152

Basic Airway Management
•Head tilt-chin lift
•Jaw thrust
•Oropharyngeal airways
•Nasopharyngeal airways
•Positioning153

Head tilt-Chin lift154

Jaw-Thrust Maneuver155

Oropharyngeal Airway by Arthur Guedel
•AGuedelisarigidplastictubewhichsits
alongtopofmouthandendsatbaseof
tongue(anadjuncttohelpkeepairway
open).
•Toosmalladeviceisineffective
•Toolargeadevicecanobstructthelarynx
•Cantraumatizesofttissue
•Caninducevomitingifintactairway
reflexes.156

Oropharyngeal Airway157

Inserting anOPA
STEP1:Clearthemouthofbloodandsecretionswith
suctionifpossible.
STEP2:Selectanairwaydevicethatisthecorrectsizefor
theperson.
•Too large of an airway device can damage the throat.
•Too small of an airway device can press the tongue into the
airway.
STEP3:Placethedeviceatthesideoftheperson’sface.
Choosethedevicethatextendsfromthecornerofthe
mouthtotheearlobe.158

Cont.
STEP4:Insertthedeviceintothemouthsothepointis
towardtheroofofthemouthorparalleltotheteeth.
•Donotpressthetonguebackintothethroat.
STEP5:Oncethedeviceisalmostfullyinserted,turnit
untilthetongueiscuppedbytheinteriorcurveofthe
device.159

160

Nasopharyngeal Airway
Used when
➢OPA insertion is difficult
➢Oral trauma
➢Clenched Jaw
➢Arousable patient
➢Intact airway reflexes
•Select NPAs based on length
•nostril to the earlobe or the
angle of the jaw
•long NPA may enter
oesophagus
•Injury to the nasal mucosa
Aflexiblerubbertubewhichgoesthroughthenoseendsat
baseoftongue(anadjuncttohelpkeepairwayopen)161

Nasopharyngeal Airway162

InsertinganNPA
STEP1:Selectanairwaydevicethatisthecorrectsizefor
theperson.
STEP2:Placethedeviceatthesideoftheperson’sface.
Choosethedevicethatextendsfromthetipofthenoseto
theearlobe.Usethelargestdiameterdevicethatwillfit.163

Cont.
STEP3:Lubricatetheairwaywithawater-solublelubricant
oranestheticjelly.
STEP4:Insertthedeviceslowly,movingstraightintothe
face(nottowardthebrain(.
STEP5:Itshouldfeelsmooth,donotforcethedeviceinto
thenostril.Ifitfeelsstuck,removeitandtrytheother
nostril.164

165

•OPAstoo large or too small mayobstruct the airway.
•NPAs sized incorrectly may enter the esophagus.
•Always check for spontaneousrespirations after
insertion of either device.166

Sniffing Position167

Sniffing Position168

Positioning169

Breathing Techniques: Bag Valve Mask
•DevelopedbyHolgerHesse&HenningRuberin1953
•AMBUcompany:ArtificialManualBreathingUnit
•ManualResuscitatororSelfInflatingBag
•ProvidesPPVinemergencyorTemporaryVentilation
•DisposableorReusable
•Sizes:Infant,childrenandadult170

Components171

Technique 172

173

Predicting difficulty with bag-maskventilation
Mnemonic “MOANS
•Mask seal (e.g beard)
•Obesity or Obstruction (at or lower than glottis)
•Age > 55 yrs
•No teeth
•Stiffness of the lungs174

Complications
•Stomach Inflation
•Hyperventilation
How to avoid:
•Tidal volumes 6 to 8
mL/kg
•10 breaths each minute
•Each breath over 1
second 175

Advanced Airway Management
•ExtraglotticTechniques(Supraglotticairwaydevices
e.g.laryngealmaskairways(LMAs)orRetroglottic
airwaydevicese.g.Combitube).
•TrachealIntubationTechniques(endotrachealintubation
withcuffedtubeisthedefinitiveairway).
•Surgicalairway:
–Needlecricothyrotomy
–Surgicalcricothyrotomy176

Question 1
Themainpurposeofthejaw-thrustmaneuveris
to:
a.Openthemouthwithonlyonehand
b.Opentheairwaywithoutmovingtheheadorneck
c.Createanairwayforthemedicalpatient
d.Createanairwaywhenitisnotpossibletojutthe
jaw177

Answer 1
Themainpurposeofthejaw-thrustmaneuveris
to:
a.Openthemouthwithonlyonehand
b.Opentheairwaywithoutmovingtheheadorneck
c.Createanairwayforthemedicalpatient
d.Createanairwaywhenitisnotpossibletojutthe
jaw178

Question 2
Uponassessmentofthepatient'sairway,younote
significantgurglingwitheachbreath.Whatwouldbe
thenextappropriateairwayinterventionyoushould
performtoeliminatethisfinding?
a.Head-tilt,chin-liftmaneuver
b.Modifiedjaw-thrustmaneuver
c.Oropharyngealsuctioning
d.Insertionofanasopharyngealairway179

Answer 2
Uponassessmentofthepatient'sairway,younote
significantgurglingwitheachbreath.Whatwouldbe
thenextappropriateairwayinterventionyoushould
performtoeliminatethisfinding?
a.Head-tilt,chin-liftmaneuver
b.Modifiedjaw-thrustmaneuver
c.Oropharyngealsuctioning
d.Insertionofanasopharyngealairway180

Question 3
Uponinsertionofanoropharyngealairway(OPA),the
tipofthedeviceshouldbepositionedinwhat
anatomicalspace?
a.Oropharynx
b.Nasopharynx
c.Hyperpharynx
d.Laryngopharynx181

Answer 3
Uponinsertionofanoropharyngealairway(OPA),the
tipofthedeviceshouldbepositionedinwhat
anatomicalspace?
a.Oropharynx
b.Nasopharynx
c.Hyperpharynx
d.Laryngopharynx182

Answer 3
TheOPAworksbyliftingthebaseofthetongueoffthe
posteriorpharynx.Withproperinsertion,thetipshould
restinthelaryngopharynxsoitcanfullysupportthe
tongue.183

Question 4
Apatientisfoundwitharespiratoryrateof8
perminute,absentbasalbreathsounds,apulse
oxreadingof83%,andcyanoticlipsand
fingernails.Thispatientisinimmediateneedof
whatintervention?
a.Ventilation
b.Oxygenation
c.Airwaysuctioning
d.Semi-Fowler'spositioning184

Answer 4
Apatientisfoundwitharespiratoryrateof8
perminute,absentbasalbreathsounds,apulse
oxreadingof83%,andcyanoticlipsand
fingernails.Thispatientisinimmediateneedof
whatintervention?
a.Ventilation
b.Oxygenation
c.Airwaysuctioning
d.Semi-Fowler'spositioning185

Answer 4
Thepatientinthisscenarioisinimmediateneedof
ventilation.Althoughhehasaspontaneous
respiratoryrateof8/minute,ifthedepthof
breathingisnotsufficienttocreatealveolarbreath
soundsthentheratereallydoesn'tmatter;the
patientisstillbreathinginadequately.Thereisno
indicationinthescenariothatthepatientneeds
suctioning,andchangingthebodypositionmay
helpwithbreathingbutdoesnotinherentlyimply
thatbreathingwillbecomeadequate.186

Question 5
Whichofthefollowingclinicalindicationswouldfirst
appeartoindicatethatthepatientisbeingadequately
ventilatedwithaBVM?
a.Thechestwallmoveswitheachbreath
b.Theventilationsareatarateof12/minute
c.Thepatienthasbreathsoundsinalllungfields
d.Thevitalsignsandpulseoximeterreadingsstartto
normalize187

Answer 5
Whichofthefollowingclinicalindicationswouldfirst
appeartoindicatethatthepatientisbeingadequately
ventilatedwithaBVM?
a.Thechestwallmoveswitheachbreath
b.Theventilationsareatarateof12/minute
c.Thepatienthasbreathsoundsinalllungfields
d.Thevitalsignsandpulseoximeterreadingsstartto
normalize188

Answer 5
•Whenapatientisbeingadequatelyventilated,one
ofthefirstthingstoensureisthatthepatientis
beingventilateddeepenoughtocreatebreath
soundsbilaterally.
•Althoughchestwallmotionisanindication,youmay
stillseesomechestwallmotioneventhoughthe
patientisnotbeingventilateddeepenough(i.e.just
deadspaceventilationisbeingdone).189

Answer 5
•Therateofventilationisnotakeyfindingsince
ventilatingattherightratebutinsufficientdepthis
ofnousetothepatient.
•Finally,changesinthevitalsignsandpulseoximeter
readingswilloccuronlyaftergoodventilationsare
beingperformed;theirpresenceisagoodfindingbut
notasreliableorasearlyasthepresenceofbilateral
breathsoundsinalllungfields.190

5)Oxygen therapy
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care 191

Oxygen
–Oxygen(O
2)isthemostessentialelementforlife.
–Itisessentialbecauseitisusedincellular
metabolism.
–Thereisaconstantsupplyof21%colorless,tasteless,
andodorlessoxygenintheinspiredatmosphericair.192

Determinants of oxygen delivery to tissues193

Hypoxia
•Inadequate oxygen delivery to tissues.
•Hypoxia level:
–PaO
2< 80 mmHg or
–O
2saturation < 95%194

Severity of hypoxemia 195

O
2is considered a drug that has
•Indications.
•Modes of administration.
•Dose.
•Monitoring.
•Complications.196

Important points to consider
about oxygen therapy
•Oxygenisalifesavingdrugforhypoxemicpatients.
•Oxygenmustbeprescribedinallsituationsexceptfor
theimmediatemanagementofcriticalillness
•Givingtoomuchoxygenisunnecessaryasoxygen
cannotbestoredinthebody.197

Important points to consider
about oxygen therapy
•COPDpatients(andsomeotherpatients)maybe
harmedbytoomuchoxygenasthiscanleadto
increasedcarbondioxide(CO2)levels.
•Otherpatients(e.g.myocardialinfarction)mayalsobe
harmedbytoomuchoxygen.
•Onlygiveasmuchasneeded–noneedforextra!198

Indications for Oxygen Therapy
•Hypoxemia
–Inadequate amount of oxygen in the blood
–S
PO
2< 90%
–PaO
2< 60 mmHg
•Excessive work of breathing
•Excessive myocardial workload199

Initially target saturation
•94-98%Most patients (Those not at risk of CO
2retention)
•88-92%COPD or CO2 retaining patients: Chronic hypoxic lung
disease, COPD, Severe Chronic Asthma, Bronchiectasis, Chest
wall disease (Kypho-scoliosis), Neuromuscular disease, Obesity
hypoventilation.
•Other : Some patients may require a different lower target
range such as 85-90%
•Target saturations should be reviewed and changed if required.200

Oxygen Sources
1.Wall oxygen: piped in through the wall in hospitals
2.Oxygen cylinders: color-coded with a green label
3)Oxygenconcentrators:
(oxygengenerators)
convertsroomairtooxygen
anddeliversittothepatient
deliveroxygenflowsupto
5L/min(newerones10L)
Oxygen cylinder
Oxygen concentrator 201

Oxygen Delivery Devices
1.Low-flow devices (Variable-Performance)
–Do not provide exact oxygen concentrations.
–The patient’s breathing pattern influences the
concentration of oxygen obtained.
2)High-flow devices (Fixed-Performance)
–The oxygen percentage is constant.202

1.Low-flow devices
•Nasal cannula
•Simple facemask
•Facemask with gas reservoirs:
–Partial rebreathing mask
–Non-rebreathing mask203

Suitable for all ages.
▪Thisdevicedeliversanunpredictableamountofoxygen
rangingfrom25-45%at1-6L/mindependingonhow
muchthepatientinhalesthroughthemouth
▪Higherflowratesareuncomfortableforthepatient
▪Ahighflowratecanquicklydryoutthenasalmucosaand
becomerapidlyuncomfortable
Nasal cannula
1 liter O2give extra O24% → 21%+4% = FiO20.25
6 liter O2give extra O224% → 21%+24% = FiO2 0.45204

Simple facemask (Hudson mask)
Suitableforallages.
▪It seals poorly and its large ventilation holes allow the oxygen flow
to be diluted with air
▪The simple facemask at an oxygen flow of 5 L/min delivers
approximately 40 % oxygen
▪Increasing the flow to 10 L/min may increase oxygen concentration
to about 60 %
▪Iftheflowrateislessthan5L/minthepatientmayre-breathe
muchofhisownexhalationandthus,theconcentrationofoxygen
deliveredwillbelow.205

Partial Rebreathing Mask with reservoir
❑Simplefacemaskplusareservoirbag.
❑Suitable for all ages.
❑Part of the patient’s expired VT refills the bag.
❑Typicalminimumflowofoxygenare10–15L/min.
❑Supplies:60%-80%oxygen.
Reservoir206

Non-Rebreathing Mask with reservoir
❑Partialrebreathingmaskplustwovalves(oneway)
betweenthebagandmaskandoverexhalationportsto
prevent:
–Entrainmentof room air during inspiration
–Entry of exhaled gases into the reservoir bag during expiration
❑Supplies80%-100%oxygenat10-15L/min
❑Suitableforallages.
Valves207

2.High-flow devices
•Venturi mask
•Oxygen Hood
•Incubators
•Ambu-Bag
•Mechanical ventilator208

•Airentrainmentmask:Suitableforbigchildrenandadults.
-Suppliespreciseoxygenconcentration:
(24%-28%-31%-35%-40%-60%).
-Indicatedforchronicobstructive
pulmonarydisease(COPD).
Venturimask
•Increasingflowdoesnotincrease
oxygenconcentration,itisafixeddose
device
•Gooddeviceforpatientswithraised
CO2(patientswithatargetof88-92%)209

24%Venturi-2L/min-
Use3l/minifRR>30
31%Venturi-6L/min-
Use9l/minifRR>30
35%Venturi-8L/min-
Use12l/minifRR>30
40%Venturi-10L/min–
Use15l/minifRR>30
60%Venturi-15L/min–
ChangetoNRMif60%Venturiis
notsufficient
28%Venturi-4L/min-
Use6l/minifRR>30210

Oxygen Hood
▪Clear plastic shell encompasses the baby's head
▪Well tolerated by infants
▪Size of hood limits use to younger than age 1 year
▪Allows easy access to chest, trunk, and extremities
▪Allows control of Oxygen Delivery:
▪Oxygen concentration
▪Inspired oxygen temperature and humidity
▪Delivers 80-90%oxygen at 10-15 liter per minute211

Incubators
-Suitablefor:neonatesandyounginfants.
-Supplies:40%-50%oxygenat10-15literperminute212

•Suitableforallages
•Supplies21-100%oxygen
•Fitandflowdependent
Bag mask ventilationBag tube ventilation
•Suitableforallages
•Supplies100%oxygen213

Mechanical ventilator
▪Suitableforallages.
▪Supplies21%-100%oxygen214

Simple humidifiers
•Don’tprovideameansofheating.
•Capableofachieving100%relativehumidityatroom
temperature.
•Usedwithdeliverysystemsthosedonotbypassnormal
upperairways(mask).215

Heated humidifiers
•Incorporateelementsformonitoredheating.
•Usedwithdeliverysystemsthatbypassnormalupper
airways.
•Generallyusedforintubatedpatients.216

Oxygen dosage
▪Do not forget that:
➢High FIO
2
causes complications, but hypoxemia kills.
➢Once oxygen is indicated, it should be given:
➢continuously,
➢with least possible FiO
2
,
➢for the least possible time.
▪In urgent situations,
➢use 100% oxygen (bag –mask, bag –endotracheal tube).
▪In less urgent situations:
➢use 40% –60% oxygen (face mask, nasal cannula–etc.).217

Monitoring & starting oxygen therapy
Iftargetsaturationis94-98%
•Choosemaskand/orflowratetoachievetargetsaturation
•Repeatbloodgasesarenotneededforthesepatientsifwithintarget
range
Iftargetsaturationis88-92%
•Startwithnasalcannulaat1-2l/minuteor28%Venturimaskthen
titrateuptoachievethetargetsaturation
•Bloodgasesareneededafter30-60mins
AlwaysmonitorSpO
2for5minafteranychangeinoxygen
therapytoensuretargetsaturationisachieved218

Three general methods:
➢Clinical monitoring
➢Bed-side monitoring
➢Laboratory monitoring
Methods for monitoring O
2therapy219

Clinical monitoring
➢Heartrate,
➢respiratoryrate,
➢peripheralperfusion,
➢bloodpressure,
➢consciouslevel,
➢skinandmucousmembranescolor(Cyanosis).220

Bed-side monitoring
Oxygen analyzer
-AninstrumentthatisusedformeasuringFIO
2
nearthe
patientairways.
-Usefulwithheadbox,incubators.
-Limitedusewithfacemaskandnasalcannula.221

Bed-side monitoring
Pulse oximeter
-AninstrumentthatisusedformeasuringO
2
saturation.
-Worksbytheprinciplethatoxygenatedhemoglobin
allowsmoretransmissionofredlightthandoesreduced
hemoglobin.
-Theprobemaybeplacedonthefoot,palm,fingers,orear
lobule.222

What is the error margin with pulse oximeter use??
Measures with high accuracy O
2
saturation above 70%
(error margin +/-2%).
➢Patient movement
➢Poor peripheral perfusion
➢Hypothermia
➢Presence of abnormal hemoglobin
➢Nail polish/false nails
➢Excessive illumination
What are the limitations for pulse oximeter use?? 223

Hazards of Oxygen Therapy
•AbsorptionAtelectasis:Highconcentrationsofoxygencancause
pulmonaryatelectasisinareasoflowV/Qratios.Asnitrogenis
“washedout”ofthelungs,theloweredgastensioninpulmonary
capillarybloodresultsinincreaseduptakeofalveolargasand
absorptionatelectasis.
•RetinopathyofPrematurity:vascularproliferationandfibrosisand
mayleadtoretinaldetachmentandblindness.Therecommended
arterialconcentrationsforprematureinfantsreceivingoxygenare
50–80mm.224

Hazards of Oxygen Therapy, cont.
•Hypoventilation: patients with COPD (altered respiratory drive) they
are partly dependent on the maintenance of relative hypoxemia.
•Pulmonary Toxicity: Oxygen toxicity is thought to be due to
intracellular generation of highly reactive O2 metabolites (free
radicals) which are cytotoxic and cause injury of the alveolar–capillary
membrane like ARDS.225

Factors affecting toxicity of O2therapy
-FiO
2:
(Increased risk with FiO
2
> 40%).
-Periodofadministration:(100%O
2
istoxicin12hours,
70%istoxicin4days,40%issafeforonemonth).
-Age of the patient: (PaO
2> 100 mmHg is toxic to the
premature).226

6)Acute respiratory failure
& Ventilatory Management
of ARDS and Asthma
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care 227

Alveolar-arterial gradient (A-a Gradient)
➢Itmeasuresthedifferencebetweentheoxygenconcentration
inthealveoliandarterialsystem(A-aGradient=PAO2–PaO2),
normal5-15(atageof40year)or([ageyear/4]+4).
➢GradientincreasesbyincreasingageandFiO2.
➢A-agradientincreases7forevery10%increaseinFiO2.
➢PAO2=PiO2–PaCO2/0.8
➢PiO2=(BarometricPressure–PH2O)XFiO2
➢BarometricPressure(760mmHgatsealevel),PH2O47mmHg.
➢Example:PAO2=(760-47)0.21-40/0.8=99.7mmHg.
➢PaO2normally80-100mmHg(givenfromABGs).228

A-a Gradient
•Causedbyanatomicalright-to-leftshunting(bloodsupplyingthe
lungtissuesviathebronchialveinsisbeingreturnedviathe
pulmonaryveinswithoutundergoinggasexchange)andV/Q
mismatchcausedbygravity-dependentdifferencesinperfusionto
variouszonesofthelungs.
•(A-a)oxygengradientcanaidinnarrowingthecauseofhypoxemia.
Approximationequation:
•PAO2FiO2X6(e.g.21%X6≈120)
•PaO2FiO2X5(e.g.21%X5≈100)
A-agradient=120-100=20229

Increased A-a Gradient
•Right to Left Shunt:
✓Intrapulmonary shunt (due to fluid filled alveoli).
✓Intracardiac shunt.
•V/Q Mismatch (most common):
✓Pulmonary Embolism
✓Atelectasis
✓Pneumonia
✓Obstructive Lung Disease (e.g. Asthma, COPD)
✓Pneumothorax
•Low mixed venous oxygen tension
✓Decreased cardiac output
✓Decreased hemoglobin concentration
✓Increased oxygen consumption
•Diffusion defect (rare, e.g. emphysema & ILD)
CLASSIFICATION OF HYPOXIA BASED ON A-a GRADIENT230

Normal A-a Gradient
•Hypoventilation
✓Neuromuscular disorders
✓Central nervous system disorder
•Low inspired FIO2:
✓High altitude.
✓Leak in the breathing circuit.
✓Improper installation of oxygen
✓Supply lines failure.
CLASSIFICATION OF HYPOXIA BASED ON A-a GRADIENT231

Acute respiratory failure
•Failure in one and/or both gas exchange functions:
Oxygenation & Ventilation (CO
2elimination)
•In practice:
–Hypoxemic respiratory failure: PaO
2< 60 mmHg
–Hypercapnic:PaCO
2> 50 mmHg232

Type I Respiratory Failure
(Oxygenation failure)
V/Q mismatch
•Pneumonia
•Pulmonary edema
•Asthma
•Pulmonary embolism
•Acute respiratory distress syndrome (ARDS)233

Type II Respiratory Failure
(Ventilation failure)
•DecreasedCNSdrive(Thepatientisunabletosensethe
increasedPaCO2,thepatientwillnotbreathe).
•Neuromusculo-skeletaldisease(Thepatientisunableto
neurologicallysignalthemusclesofrespirationorhas
significantintrinsicrespiratorymuscleweaknessorhas
limitationofventilation,Thepatientcan'tbreathe).
•Abnormalitiesinlungparenchyma:(Thepatienthaspoor
capacitytoexchangegases).234

Type II Respiratory Failure
(Ventilation failure)
•DecreasedCNSdrive:CNSlesion,overdose,anesthesia.
•Neuromusculo-skeletaldisease:MyastheniaGravis,
Guillian-Barre,Residualparalysis“musclerelaxants”,
spinalcorddisease,myopathies,flailchest,
kyphoscoliosis,etc.
•Abnormalitiesinlungparenchyma:COPD,Pulmonary
fibrosis.235

•Pneumonia
•Pulmonary edema
•Asthma
•Pulmonary embolism
•Aspiration Pneumonia
•Acute respiratory distress syndrome (ARDS)
Type I Respiratory Failure
(Oxygenation failure)236

Acute Respiratory Distress Syndrome (ARDS)
•ARDSisanacuteinjuryofapreviouslyhealthylung
(ARDSisnotaprimarydisorder).
•Non-hydrostaticpulmonaryedemaandhypoxemia.
•Refractoryhypoxemiaduetoreductioninfunctional
residualcapacity(FRC)andlungcompliancearethe
hallmarksofARDS.
•ARDSisusuallyassociatedwithahighmortalityrate
rangeswidelyfrom30%to58%accordingtothe
underlyingcause.237

Major Categories of ARDS Risk
DIRECT (Respiratory)
•Pneumonia
•Aspiration
•Pulmonary contusion
•Fat emboli
•Near-drowning
•Inhalational injury
INDIRECT (non Respiratory)
•Sepsis
•Severe trauma
•Multiple transfusions
•Major burn
•Acute pancreatitis
•Cardiopulmonary bypass 238

ARDS diagnostic criteria (Berlin 2012)239

Itisimportanttoconsiderhowmuch
oxygenapatientrequiresto
achievetheirPaO
2onanABG.The
P/Fratioisaveryusefultoolto
monitoryourpatient’soxygenation
status.
Calculating PaO
2 / FiO
2ratio
PaO
2
FiO
2
= P/F ratio
PaO
2/FiO
2=P/FRatio
HealthyadultPaO
2=80-100mmHg
Roomair=FiO2is0.21oxygen
100/0.21=P/Fratio476forahealthyadult240

Pathophysiology of ARDS
•Increased permeability
•Surfactant destruction
•Thelungresponsetoinjurycanbedividedintoan
exudativephase,aproliferativephase,andafibrotic
phase.
•Theseverehypoxemiaassociatedwiththissyndromeis
causedbyintrapulmonaryshuntingthatoccurswith
interstitialedema,andalveolarfloodingandcollapse.241

Phases of ARDS
Pathophysiology
•Reduced blood flow to lungs
•Inflammatory mediator release
•Increased capillary permeability
•Intrapulmonary shunting begins
Symptoms
•Refractory hypoxemia
•Increased respiratory rate
•Decreased tidal volume
•Respiratory alkalosis
•CXR infiltrates
Phase no. 1 –Exudative
1-7 days post-injury,
50 percent of cases within 24 hours of event242

Phase no. 2 –Proliferative
1-2 weeks after initial injury
Pathophysiology
•Increased capillary permeability
•Protein and fluid leakage
•Pulmonary edema
•Alveolar collapse
Symptoms
•Decreased lung compliance
•Worsened hypoxia
•CXR “white out”
Phases of ARDS243

Phase no. 3 –Fibrotic
2-3weeks after injury
Pathophysiology
•Fibrous tissue throughout lung
•Diffuse scarring
Symptoms
•Severe acidosis on ABG
•Overwhelming hypoxemia
•Multi-organ dysfunction (MODS)
•Hypotension
•Low urine output
Phases of ARDS
Normal Human Lung
Capillaries
Lung Capillaries –
14 day ARDS
Early ARDS
Fibrotic ARDS244

ARDS epidemiology
Severe ARDS survivors
•Ventilator LOS 11 days
•ICU LOS 14 days
•Hospital LOS 26 days
Analysis of ARDS worldwide, 459 ICUs, 50 countries
over 4 weeks in Winter 2014 (3022 patients studied)245

–Tachypnea.
–Tachycardia.
–Cyanosis.
–Active accessory muscles.
–Agitation ,lethargy.
–Severe hypoxemia refractory to oxygen therapy.
Clinical Findings of ARDS246

Management of ARDS
•Correct the underlying cause
•Fluid restriction and diuretics (keep low normal CVP) ,while
perfusion is carefully supported
•Bronchodilators
•Antibiotics
•Gastrointestinal-prophylaxis (Famotidine)
•Deep venous thrombosis (DVT) prophylaxis (heparin)
•Early enteral nutrition247

–KeepPaO255-80mmHgorSpO288-95%withtheleast
possibleFiO2(<0.6wheneverpossible).
–UseahighPEEP(minimumof5cmH2O).
–Lowtidalvolume4-8ml/kgIBW(Permissivehypercapnia
ifnecessary).
–PlateauPressure≤30cmH2O.
–Patientventilatorsynchronization(musclerelaxantmay
beused).
–Inverseratioventilation(I:Eratio1:1or2:1)
Ventilator management in ARDS248

•Calculatepredictedbodyweight(PBW)*
•Selectanyventilatormode
•AchieveaTVof6mL/kg/PBW
•Setrespiratoryrate(RR)tomaintainoptimalminute
ventilation(RR<35/min)
•AimforSpO288-95%orPaO255-80mmHg
•IncreasePEEPwithincreasingFiO2(5-24cmH2O)
accordingtoaslidingscale(seetablebelow)
Ventilator Setup and Adjustment
(ARDSnet ventilation strategy)
* male PBW = 50 + 0.91 x (height in cm –152.4)
* female PBW = 45 + 0.91 x (height in cm –152.4)249

•Aimforplateaupressure(Pplat)<30cmH2O
•ifnecessarydecreaseTVstepwiseby1mL/kgPBWtoa
minimumof4mL/kgPBW
•IfPplat<25cmH20,increaseTVstepwiseby1mL/kgPBW
untilPplat>25cmH20orTVof6mL/kgPBW
•Pplat>30cmH20allowedifTV4mL/kgIBWandpH<7.15
•TVcouldbeincreasedupto8mL/kgPBWforpatientswith
severedyspneaifPplatmaintained<30cmH20
•pHgoal=7.30-7.45
•ifpH<7.15increaseTV,giveNaHCO3
Ventilator Setup and Adjustment
(ARDSnet ventilation strategy)250

Arterial oxygenation and PEEP
Oxygenationgoal:
PaO2:55-80mmHgorSpO2:88-95%
UsetheseFiO2/PEEPcombinationstoachieveoxygenationgoal:
1.00.90.80.70.60.50.40.3FiO2
18-2414-181410-14108-105-85PEEP
PEEP should be applied starting with the minimum value for a given FiO2251

Advantages of PEEP
•Preventionofairwayandalveolarcollapse(increases
functionalresidualcapacity(FRC)):
–Icreasescapillary-alveoliinterfaceforgasexchange.
–Decreasesshuntfraction,themostcommonmechanismof
hypoxia(improvesventilation/perfusionratio).
•Improvesalveolarrecruitment(thusimproveslung
compliance).252

Ventilator graphics of an ARDS patient from ICU253

Ventilator graphics of an ARDS patient from ICU254

Treatment modalities for ARDS255

Prone positioning
Ventilation benefitsCardiovascular benefitsOxygenation benefits
•Shape of the lungs
Dependent fluid
accumulation
•Alveolar recruitment
Mobilization of secretions
•PleuralPressure
distributedmore
evenlyintheprone
position.
•Reliefofpressureon
diaphragmandlungs
fromabdomen.
•Reliefofpressureof
heartonlungs
-Improved tidal volume
-Reduced pressure on
right ventricle256

Contraindications
Patient conditions for which the application of prone
therapy is contraindicated include:
•Unstable cervical, thoracic, lumbar, pelvic, skull or
facial fractures
•Cervical and/or skeletal traction
•Uncontrolled intracranial pressure (ICP)257

Manualproning
•Typicallyinvolves5-7nursesorcaregivers.
•Unsafeinemergencysituations.
•Suboptimalwithobesepatients.
•Highercomplications.258

Prone position evidence based practice
Lowtidalvolumeventilationisessential
Earlyinterventionofpronepositioningcansignificantlyimpact
mortality
•P/Fratio<150
•FiO
2>60percent
•PEEP>5
•IntubationforARDSfor<36hours
Extendedperiodsofpronepositioning
•Average17hoursinproneposition–
Discontinuationoftherapy
•P/Fratio>150ANDPEEP<10ANDFiO
2<60percentforatleastfour
hoursinsupine259

260

At enrollment
ARDS lung and effect of proning
After 2 days of proning261

Bronchial asthma
Staging and ventilatory support262

Staging of asthma
Chronicasthmaisusuallyclassifiedasfollows:
•Intermittent
•Mildpersistent
•Moderatepersistent
•Severepersistent
40263

Staging of asthma
Acuteasthmaisclassifiedasbelow:
•Acutesevereasthma
•Life-threateningasthma
•Near-fatalasthma
41264

•Acutesevereasthma:theremaybeafine
tremorinthehandsduetosalbutamoluse,and
mildtachycardia.Patientswillshowsome
respiratorydistress,oftensittingforwardto
splintopentheirairways.Onauscultation,a
bilateral,expiratorywheezewillbeheard.
42265

•Life-threateningasthma:thechestmaybesilent,as
aircannotenterorleavethelungs,andtheremaybe
signsofsystemichypoxia.
•Near-fatalasthma:imminentarrestmayappear
drowsy,unresponsive,cyanotic,andconfused.
Wheezingmaybeabsent,andbradycardiamayoccur,
indicatingsevererespiratorymusclefatigue.
43266

Whenconservativetreatmentsfail,andthe
patientremainsinsevererespiratorydistress,
decisionsmustbemadeaboutwhetherto
initiateventilatorysupport.
Thiscanbeaccomplishedbyeither
noninvasiveorinvasivetechniques.
Management267

Noninvasive ventilation
•Mayoffershort-termsupportforsomesubjects
withhypercapnicrespiratoryfailurewhocan
cooperatewiththeircareandareabletoprotect
theirairways,butitsapplicationislimitedbypoor
patientacceptance.
45268

Endotracheal intubation
Absolute indications
◦cardiac or respiratory arrest.
◦severe hypoxia.
◦rapid deterioration of conscious state.
Relative indications
◦progressive deterioration.
◦hypercapnia with increasing distress.
◦physical exhaustion.
46269

Thedecisiontointubateisbasedprimarilyon
thedegreeofrespiratorydistressasassessed
byanexperiencedclinicianandthepatient
themselves.
47270

Intubationperformed/supervisedbyexperienced
anesthetistsorintensivists.
Use larger endotracheal tube:
◦to facilitate the suctioning of secretions.
◦to decrease resistance to airflow.
◦to reduce the work of breathing.
48271

Oncetheendotrachealtubeisinplace,slow
handventilation(8–10breaths/minute)
shouldmaintainoxygenationuntilthe
ventilatorcanbeconnected.FiO2=1.0
(initially)
49272

Theprinciplesofinitialmechanicalventilationareavoid
excessivedynamichyperinflationandtoavoidexcessive
hypoventilationbycommencingwithaminuteventilation<115
ml/kg/min(<8L/minina70kgpatient)bestachievedwith:
•Tidalvolumeof5–7mL/kg.
•Respiratoryrateof10–12breaths/min.
•Shortinspiratorytime.
•Increaseflowrate(80-100L/min)(toachievea
shortinspiratorytime).
•Longexpiratorytime(I:Eratio>1:2)ensurean
expiratorytime≥4seconds
50273

•PEEP<5cmH2OandPEEPtotal<10
•Setinspiratorypressure30–35cmH2Oonpressure
controlventilationorlimitpeakinspiratorypressure
to<40cmH2O.
•Pplat<25mmHg
Theuseofvolume-controlledventilationismost
establishedforthisventilatorypattern.However
Pressure-controlledorassistedmodeshavebeenused
withoutadverseconsequences.
51274

•Permissivehypercapnia
•Sedation/paralyzejudiciously(keepthepatient
relaxedandbreathinginsynchronywiththe
ventilator).
•Ifhypotension:
–Disconnectfromventilator
–Volumeloading.
–Considertensionpneumothorax
52275

7)Mechanical Ventilation
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care
1276

•Negative-pressure ventilators (“iron lungs”)
•Non-invasive ventilation first used in Boston Children’s
Hospital in 1928
•Used extensively during polio outbreaks in 1940s –1950s
•Positive-pressure ventilators
•Invasive ventilation first used at Massachusetts General
Hospital in 1955
•Now the modern standard of mechanical ventilation
The era of intensive care medicine
began with positive-pressure ventilation
2277

Mechanical Ventilation
•Asupportivemeasurenotatherapeutictool.
•Useventilatortosupportorrestpatientuntil
underlyingdisorderimproved.
•UsuallyperformedviaETTbutnotalways
(non-invasiveventilationwithoutETT).
3278

Goals of MV
1)To improve oxygenation
2)To improve ventilation
3)To decrease work of breathing
4279

Indications for MV
1)Respiratory Failure
–Apnea / Respiratory Arrest
–Inadequate ventilation (acute vs. chronic)
–Inadequate oxygenation
2)Cardiac Insufficiency
–Eliminate work of breathing
–Reduce oxygen consumption
3)Neurologic impairment :
•Prevention or management of increased ICP
•GCS <8
4)Airway protection or Airway obstruction
5)Need for surgery (esp. on cavities e.g. thoracic or abdominal)
5280

Any of these criteria despite conservative treatment:
–Tachypnea:RR > 30-40 /minute (according to age)
–Hypoxia:PaO
2< 60 mmHg
–Hypercapnia:PaCO
2> 50 mmHg
–PH< 7.2 (respiratory acidosis)
6
Respiratory Failure281

Definitions
•Tidal Volume (T
V): Volume of air inspired & expired in each quiet breath.
•Rate:Breaths per minute.
•Minute Ventilation (MV): Total ventilation per minute, (MV = T
Vx Rate).
•Flow:Volume of gas per time.
•Inspiratory time (T
I):Amount of time delegated to inspiration.
•Expiratory time (T
E):Amount of time delegated to expiration.
•Inspiratory/expiratory ratio (I:E ratio): ratio between inspiratory and
expiratory time (usually I:E ratio is 1:2)
•Peak inspiratory pressure (PIP):Maximum pressure measured by the
ventilator during inspiration.
•Positive end expiratory pressure (PEEP):Pressure present in the airways
at the end of expiration.
7282

Breathing Circuit
•Thesetupofthecircuitisthesameforadults,childrenor
neonate.Thedifferenceismarkedbythediameterofthetubes:
22mmforadults,15mmforpediatric,and10mmforneonates
patients.
•Thebreathingcircuitiscomposedof:
–Inspiratory limb
–Expiratory limb
8283

The inspiratory limb includes
1.Oxygen sensor:
2.Heater humidifier:
3.Water trap: (to trap excessive
moisture if overheating)
9
1
2
3284

The expiratory limb includes
1.Expiratory Valve:
2.Expiratory flow sensor:
–Ittransmitstheairway
pressure,expiratory
volumeandflow
integration.
3.Water trap: (to trap the
condensed water vapor
from expiration to go
to ventilator)
10
1
2
3285

Modes of Mechanical Ventilation
YoushouldputinyourmindwhenspeakaboutMODE
thefollowingterms:
•Trigger: who/what starts a breath (patient/ventilator)
•Targetor control : what the ventilator is trying to
achieve (volume or pressure)
•Cycle:what causes the inspiration to end and the
expiration to start (volume, time, flow or pressure)
11286

Modes of Mechanical Ventilation
A-Volume Modes
B-Pressure Modes
12287

•The volume ventilator is commonly usedin critical care units.
•The basic principle of this ventilator is that a selected volume
of air is delivered with each breath.
•The amount of pressurerequired to deliver the set volume
depends on :-
-Patient’s lung compliance.
-Patient–ventilator resistance factors.
1-Volume Ventilators
13288

•Therefore, peak inspiratory pressure (PIP)must be
monitoredin volume modes because it varies from
breath to breath.
•With volume mode of ventilation, we select:
–Tidal volume (for the mechanical breaths).
–Respiratory rate.
–Inspiratory time.
14289

•Theuseofpressureventilatorsisincreasingincriticalcare
units.
•Atypicalpressuremodedeliversaselectedgaspressureto
thepatientearlyininspiration,andsustainsthepressure
levelthroughouttheinspiratoryphase.
2-Pressure Ventilators
15
•Itusuallyusedifcomplianceis
decreasedandtheriskof
barotraumaishigh(e.g.ARDS).
Time (second)
Pressure (cm water)290

•Volumewillchangewithchangesinairwayresistanceor
lungcompliance.
•Althoughpressureisconstantwiththesemodes,volume
isnot(sovolumemustbemonitoredbecauseitvaries
frombreathtobreath).
•Withpressuremodes,weselect:
–Thepressureleveltobedelivered.
–Respiratoryrate
–Inspiratorytime(withsomemodeoptions(i.e.,
pressurecontrolled).
16291

Common applicable Modes
1.Controlled Mechanical Ventilation (CMV)
(volume or pressure)
2.Assist-control (A/C) (volume or pressure)
3.Synchronized intermittent mandatory ventilation
(SIMV) (volume or pressure)
4.Pressure-support ventilation (PSV)
(pressure mode ventilation)
5.Continuous positive airway pressure (CPAP)
17292

1-Controlled Mechanical Ventilation (CMV)
•Ventilationiscompletelyprovidedbythemechanical
ventilatorwithapresettidalvolume(orpressureinPC
mode),respiratoryrateandoxygenconcentration.
•Ventilatortotallycontrolsthepatient’sventilation(the
ventilatorinitiatesandcontrolsboththevolume
deliveredandthefrequencyofbreath).
•Patientdoesnotbreathespontaneously.
•Patientcannotinitiatebreathe
18293

CMV-VC
•Trigger –Machine initiates allbreaths
Patient can notinitiate
•Target–Volume
•Cycle : –Reaching the pre-set volume
e.g. Ventilator gives 10 bpm at 500 ml each
(Minute ventilation is fixed at 5L/min)
Patient gets zero extra breaths (even he tries)
19294

CMV-PC
•Trigger –Machine initiates allbreaths
Patient can notinitiate
•Target–Pressure
•Cycle : –Time has been elapsed
e.g. Ventilator gives 10 bpm at pressure 30 cmH2O each
Total breaths 10 at fixed pressure & variable volume
Patient gets zero extra breaths (even he tries)
20295

CMV
21296

2-Assist Control Mode A/C
•Theventilatorprovidesthepatientwithapre-settidal
volume(orpressureinPCmode)atapre-setrate.
•Thepatientmayinitiateextrabreathonhisown,butthe
ventilatordeliveredthepresettidalvolume(inVC)orpre-
setpressurein(PCmode)tothepatient.
•Sothepatientcanbreatheatahigherratethanthepreset
numberofbreaths/minute.
22297

•Thetotalrespiratoryrateisdeterminedbythenumber
ofspontaneousinspirationinitiatedbythepatientplus
thenumberofbreathssetontheventilator.
•InA/Cmode,amandatoryrateisselected.
•Ifthepatientwishestobreathefaster,heorshecan
triggertheventilatorandreceiveafull-volumebreath.
Assist Control Mode A/C
23298

•Often used as initial mode of ventilation:
–Traumatic brain injury (TBI)
–Severe poly trauma.
–Post cardiopulmonary resuscitation (CPR)
Disadvantages:
-Hyperventilation (if the patient triggers too many breaths)
Assist Control Mode A/C
24299

25
Assist Control Mode A/C300

AC-VC
•Trigger–ventilator and patient
•Target –volume
•Cycle–reaching the preset volume
Settings–Mode: AC-VC
Rate 10; TV 500cc
e.g. ventilator gives 10 bpm at 500 ml each
patient initiates 6 bpm –ventilator provides 500 ml
Total: (10 ×500) + (6 ×500) = 8000 ml
26301

AC-PC
•Trigger–Ventilator and patient
•Target –Pressure (above PEEP)
•Cycle–Time has been elapsed.
Settings–Mode: AC-PC
Rate 10; Pressure 30 cm H2O
e.g. ventilator gives 10 bpm to a peak Paw = 30
patient initiates 6 bpm, ventilator provides peak Paw =30
Total breaths 16 at fixed pressure (30) & variable volume
27302

3-Synchronized Intermittent Mandatory Ventilation
(SIMV)
•Theventilatorprovidesthepatientwithapre-setnumber
ofbreaths/minuteataspecifiedtidalvolume(orpressure
inPCmode).
•Inbetweentheventilator-deliveredbreaths,thepatientis
abletobreathespontaneouslyathisowntidalvolumeand
ratewithnoassistancefromtheventilator.
•Ventilatorsbreathsaresynchronizedwiththepatient
spontaneouseffort(nofighting).
28303

•However,unliketheA/Cmode,anybreathstakenabovethe
setratearespontaneousbreaths,thetidalvolumeofthese
breathsvariesfromthetidalvolumesetontheventilator,
becausethetidalvolumeisdeterminedbythepatient’s
spontaneouseffort.
•Addingpressuresupport(5-10cmH2O)duringspontaneous
breathscanaugmentthetidalvolumeandminimizetherisk
ofincreasedworkofbreathing(overcometheresistanceof
breathingcircuitandendotrachealtubeandthedemandvalve
oftheventilator)themodebecomes(SIMV+PS).
29
SIMV304

•Usedtostartweaningthepatientfromthe
mechanicalventilator(e.g.afterA/Cmode).
•Weaningisaccomplishedbygraduallyloweringthe
setrateandallowingthepatienttoassumemore
work
30
SIMV uses305

SIMV-VC
•Trigger–Ventilator and patient
•Target–Volume
•Cycle –Reaching the pre-set volume
Settings–Mode: SIMV -VC
Rate 10; Vt 500ml
e.g. Ventilator gives 10 bpm at 500 ml each
patient takes 6 bpm at 150 ml each
Total MV = (10 ×500) + (6 ×150) = 5900 cc
31306

SIMV-PC
•Trigger–Ventilator and patient
•Target–Pressure
•Cycle –Timehas been elapsed
Settings-Mode: SIMV-PC
Rate 10; Pressure 30 cmH2O
e.g. ventilator gives 10 bpm at Pressure 30cmH2O each
& variable volume
patient takes 6 bpm at his own pressure
32307

The effect of patient triggering in different parts of the SIMV cycle
IftheventilatoristriggeredduringtheSIMVperioditdeliversasynchronized
mandatorybreath.Ifitistriggeredduringthespontaneousperioditdeliversa
pressuresupportbreath(spontaneousbreath).
(Spontaneous breath)308

Comparisons between SIMV and AC
•Theyarethemostfrequentlyusedformsofvolume-controlled
mechanicalventilation.
•ACisbettersuitedforcriticallyillpatientswhorequirea
constanttidalvolumeorfullornear-maximalventilatory
support.
•SIMVhasbetterpatient-ventilatorsynchrony,better
preservationofrespiratorymusclefunction,lowermean
airwaypressures,andgreatercontroloverthelevelof
support.309

Revision: Modes of Ventilation
35310

4-Pressure Support Ventilation (PSV)
•Thepatientbreathesspontaneouslywhiletheventilator
appliesapre-determinedamountofpositivepressuretothe
airwaysuponinspiration.
•Pressuresupportventilationaugmentspatient’s
spontaneousbreathswithpositivepressureboostduring
inspirationi.e.assistingeachspontaneousinspiration.
•Helpstoovercomeairwayresistanceandreducingthework
ofbreathing.
36311

•Indicatedforpatientswithsmallspontaneoustidal
volumeanddifficulttoweanpatients.
•Patientmustinitiateallpressuresupportbreaths.
•Itisamodeusedprimarilyforweaningfrommechanical
ventilation.
•Pressuresupportventilationmaybecombinedwithother
modessuchasSIMV(SIMV+PS)orusedalonefora
spontaneouslybreathingpatient.
37
PSV312

Pressure Support Ventilation (PSV)
•Trigger–patientonly
•Target –pressure
•Cycle–patient flowdecreases to certain level
(usually 25% of peak flow)
Settings–Mode: PSV = 10 cm H2O
FiO2 0.4; PEEP 5
e.g. patient takes 18 bpm at variable Vt (e.g. 400-500cc)
machine gives zero breaths
Trigger
Pressure (cmH
2
O) Target (pressure)
Flow cycled)313

•Constant positive airway pressureduring spontaneous
breathing (throughout the entire respiratory cycle).
•CPAP allows to observe the ability of the patient to breathe
spontaneously while still on the ventilator.
•CPAP can be used for intubated and non-intubated patients.
•It may be used as advanced weaning mode
•Can be used for nocturnal ventilation(nasal or mask CPAP)
5-Continuous Positive Airway Pressure (CPAP)
39314

CPAP
•Trigger –patient only
•Cycle –patient effort ceases
•Settings: PEEP 5; FiO2 0.4
•e.g. patient takes 24 bpm at variable Vt (e.g. 250-350
ml each)
40
Trigger
5
0
Time (sec)
Pressure (cmH
2
O)315

Modes of mechanical ventilation
Mode
Target
Trigger Cycle Types of breaths*
VentilatorPatient MandatoryAssistedSpont.
CMV
Volume Yes NoVolume Yes No No
PressureYes No Time Yes No No
AC
Volume Yes YesVolume Yes Yes No
PressureYes YesTime Yes Yes No
SIMV
Volume Yes YesVolume Yes No** Yes
PressureYes YesTime Yes No** Yes
PSV
PressureNo YesFlow No SupportedYes
CPAP
No No Flow No No Yes
*Mandatory:Breathsareinitiated&controlledbytheventilator
*Assisted:Breathsareinitiatedbythepatientandcontrolledbytheventilator
*Spontaneous:Breathsareinitiated&performedbythepatient
** Unless PS is added, it becomes supported 316

Positive end expiratory pressure (PEEP)
•PEEP:anelevationinalveolarpressureabove
atmosphericpressureattheendofexhalation
•ItdiffersfromCPAPinthat:
–PEEPisonlyappliedduringexpiration,whereasCPAP
isappliedthroughouttheentirerespiratorycycle.
–PEEPisnotamodebutaparameter.CPAPisamode.
–PEEPisusedinamandatoryventilatorbreath,CPAP
isusedduringspontaneousbreath.
42317

Positive End-Expiratory Pressure
–Physiologic:(3-5cmH20)
–Improvesgasexchangebyopeningsmallairwaysinthe
dependentlungzonesanddistributinginspiredgas
homogeneously(maximizingtheFRC).
–Decreasesoxygenconsumption
•AdverseeffectsofPEEP
–Hypotension(decreasedvenousreturn)
–Barotraumaandpneumothorax
–IncreasedICP(when>10)
43318

Gas trapping (Auto-PEEP)
44
Progressive rise in end-expiratory pressure (intrinsic PEEP)
(hyperinflation of alveoli)
Predisposing factors:
–Long inspiratory time (expiratory time short)
–High respiratory rate (absolute expiratory time short)
–Large tidal volume
–Expiratory flow limitation or increased expiratory resistance
(Asthma or COPD)
Adverse effects
1.Barotrauma & possible pneumothorax. 2. Cardiovascular compromise.319

High-Frequency Ventilators
•High-frequencyventilatorsusesmalltidal
volumes(1to3mL/kg)atfrequenciesgreater
than100breaths/minute.
•Thehigh-frequencyventilatoraccomplishes
oxygenationbythediffusionofoxygenand
carbondioxidefromhightolowgradientsof
concentration.
45320

•Ahigh-frequencyventilatorwouldbeusedtoachieve
lowerpeakventilatorpressures,therebyloweringtherisk
ofbarotrauma(e.g.ARDS).
•3differentmodes:high-frequencypositive-pressure
ventilation(HFPPV),high-frequencyjetventilation(HFJV),
andhigh-frequencyoscillatoryventilation(HFOV).
46
High-Frequency Ventilators321

Non-invasive ventilation (NIV)
•Itistheapplicationofrespiratorysupportviaasealedface-
maskornasalmaskwithouttheneedforintubation.
•PositivepressureventilatorysupportmaybewithCPAPor
bi-levelmodesanddeliveredbyarangeofventilatorsfrom
specificallydesigneddevicestofull-serviceICUventilators.
•NIVdecreasesresourceutilizationandavoidsthe
associatedcomplicationscomparedwithinvasive
ventilation.
47322

Main determinants
Oxygenation(Oxygen in):
•FiO2
•PEEP (Re-open
alveoli and shunt)
•↑Inspiratory time
Ventilation(Carbon
dioxide out):
•RR
•tidal volume
•Expiratory time
48323

What mode to be used?
•Largely apneic patient:
–Control of minute ventilation important
•Assist control-volume control (AC-VC)
–Control of peak pressure important
•Assist control-Pressure control (AC-PC)
•Intermittent spontaneous breaths
–SIMV
•Regular spontaneous breaths, improving condition
–Pressure support
49324

50
•Mode:(e.g.Fullventilatorysupport:ACventilation)
•Respiratoryrate:startat10-14(adjustaccordingtoPaCO2).
•Tidalvolume:6-8ml/kg(IBW)(adjustaccordingtoPaCO2).
•FiO2:initial1.0thenadjusttomaintainPaO280-100mmHg
•I:Eratio:1:2(InverseI:EinARDS,1:3inAsthma&COPD)
•Variousalarmlimits(e.g.inspiratorypressure10-15cmH2O
below&aboveexpected)
Initial ventilator setting325

•Is it working ?
–Look at the patient !!
–Listen to the patient !!
–Vital signs!!
–Look at the ventilator/ the alarms
–Pulse oximeter, ABG
–Chest X-ray
•When in doubt, DISCONNECT THE PATIENT FROM THE
VENTILATOR, AND BEGIN BAG VENTILATION
•Ensure you are bagging with 100% O
2
•This eliminates the ventilator circuit as the source of the problem
•Bagging by hand can also help you gauge patient’s compliance
Troubleshooting
51326

Implementation of the ventilator Bundle
52
Ventilator associated pneumonia prevention bundle327

328

Parameters Indicating Readiness to Wean
1.Underlying cause for mechanical ventilation resolved
–Improved chest x-ray
–Minimal secretions
–Normal breath sound
2.Mental readiness (conscious & can protect his A/W)
3.Hemodynamic stability:
–Adequate cardiac output
–Absence of hypotension
–Minimal vasopressor therapy
•L/min
54329

Parameters Indicating Readiness to Wean
4.Adequate oxygenation & ventilation:
–Adequate respiratory muscle strength
–PaO2 >60 mmHg with FiO2 < 0.6
–PCO2 <50 mmHg
–RR<30 /min
–Spontaneous TV > 5 ml /kg
–Vital capacity > 10 ml /kg
–Minute ventilation < 10 L/min
–PEEP < 8 cm H2O
–Pressure support < 8 cm H2O
55330

Parameters Indicating Readiness to Wean
5.Absence of factors that impair weaning
–Infection
–Anemia
–Hypokalemia
–Sleep deprivation
–Pain
–Abdominal distention
56331

Complications of intubation
During laryngoscopy and intubation
•Malpositioning
–Esophageal intubation
–Bronchial intubation
•Airway trauma
–Dental damage
–Lip, tongue, or mucosal laceration
–Sore throat
57332

Complications of intubation
During laryngoscopy and intubation
•Physiological reflexes
–Hypoxia, hypercapnia
–Hypertension, tachycardia
–Intracranial hypertension
–Intraocular hypertension
–Laryngospasm
58333

Complications of intubation
Following extubation
–Edema and stenosis (glottic, subglottic, or tracheal)
–Hoarseness (vocal cord granuloma or paralysis)
–Laryngeal malfunction and aspiration
–Laryngospasm
–Negative-pressure pulmonary edema
59334

Adverse Effects of Mechanical Ventilation
•Pulmonary:
–Barotrauma(and possible pneumothorax): induced by
excessive pressure
–Volutrauma: induced by excessive volume
–Ventilator-associated pneumonia
–Air trapping (auto-PEEP)
–Increase work of breathing (Improper mode or setting)
•Cardiovascular:
–Decrease preload & decrease afterload
–Decrease cardiac output in patients with normal contractility
& increase cardiac output in patients with low contractility
60335

Factors that increase airway resistance
(increased peak airway pressure “PIP”)
• Biting down on tube
• ETT obstructed, narrowed,
• Cough
• Secretions
• Bronchospasm
• Fast respiratory rate
61
↑ PIP
Normal336

Factors that decrease lung compliance
(increase plateau pressure “PP”)
•Pulmonary edema
•Pneumonia
•Atelectasis
•Pneumothorax
•Increased abdominal pressure against diaphragm
(ascites, gas distention)
62
↑ PP337

Which Ventilator Mode am I describing?
1-Acompositemodeinwhichtheventilator
deliversasetvolumeatasetfrequencyand
allowsthepatienttotakeadditional
spontaneousbreaths
63338

64
SIMV339

Which Ventilator Mode am I describing?
2-Aspontaneousmodeinwhichthepatient
triggersandcycleseverybreathandthe
ventilatoraugmentthepressureduringthe
inspiration
Pressure Support ventilation
65340

Which Ventilator Mode am I describing?
3-Amodeinwhichtheventilatordeliversaset
volumeataminimumsetfrequency(itallows
thepatienttoinitiateadditionalmandatory
breathsofthesetvolume)
66341

67
Assist Control-Volume Control342

What variables affect ventilation?
A.PEEP
B.Tidal volume
C.Minute ventilation
D.FiO2
E.Respiratory rate
68343

What variables affect ventilation?
A.PEEP
B.Tidal volume
C.Minute ventilation
D.FiO2
E.Respiratory rate
minute ventilation = tidal volume x respiratory rate
69344

What variables affect oxygenation?
•PEEP
•Tidal volume
•Minute ventilation
•FiO2
•Respiratory rate
70345

What variables affect oxygenation?
•PEEP
•Tidal volume
•Minute ventilation
•FiO2
•Respiratory rate
V/Q matching allows the optimal diffusion of
oxygen between the alveoli and the capillaries
71346

Which of the following is not
a criteria for extubation?
A.FiO2 < 50%
B.PEEP < 8 cm H2O
C.PaO2 > 75 mm Hg
D.Minute ventilation > 15 L/min
E.pH = 7.30 –7.50
72347

8)Noninvasive ventilation (NIV)
Hani Sammour, MD, PB
Anesthesia and IC, Shifahospital
Critical Care 348

High-flow nasal cannula (HFNC)
•High-flownasalcannula(HFNC)oxygentherapy,also
referredtoasheated,humidified,high-flownasal
cannula(HHHFNC),involvesthedeliveryofanadjustable
mixtureofheatedandhumidifiedairandoxygenatrates
thatexceedspontaneousinspiratoryflow.
•FlowRatewillvarybytheageandweightofthepatient,
witharangeof2to60L/min&FiO2rangesfrom0.21-1.349

High-flow nasal cannula oxygen delivery circuits350

Benefits of HFNC
HFNCoffersdistinctadvantagesoverothermodesof
oxygendeliveryandrespiratorysupportincluding:
•Betteroxygendeliverythanlow-flownasalcannula&
facemask.
•CangeneratePEEP(1cmH2Oforeach10L/minofflow).
•Bettercomfortandeaseofinitiationthannoninvasive
ventilation.351

Indications & Contraindications of HFNC
•Indications–HFNCmaybetrialedinanypatientwhocanmaintain
theirairway(alertandabletoswallow),whodoesnothave
contraindicationstoitsuseasdescribedbelow,andwhohas
respiratorydistressorhypoxemia.
•Contraindications–HFNCshouldnotdelayadvancedairway
managementinapatientdeemedtorequireimmediate
endotrachealintubation.Thismayincludepatientswithacutely
impairedmentalstatus,riskofaspiration,orotherneedfor
airwayprotection.352

High-flownasalcannula(HFNC)oxygentherapyis
beingusedmorecommonlythanNIPPVtoavoid
endotrachealintubationinpatientswith
hypoxemiaspeciallyininfants.353

Noninvasive ventilation (NIV)
•Noninvasiveventilation(NIV)describesthedeliveryof
mechanicalrespiratorysupportwithouttheneedfor
endotrachealintubationthroughaninterface(e.g.nasal
mask,facemask,orhelmet)thatdeliverscontinuous
positiveairwaypressure(CPAP)orbilevelpositiveairway
support(BPAP).354

Benefits of NIV
ThebenefitsofNIVincludereducedcomplicationsrelated
toinvasiveairwaymanagement,includingavoidanceof:
1)Laryngealortrachealinjurypotentiallyresultingfromthe
intubationprocedureorlongstandingmucosalpressure
fromanendotrachealtube/cuff.
2)Ventilator-associatedpneumoniapotentiallyresulting
frominterruptionofthenaturalairwayclearance
mechanisms.
3)Potentialadverseeffectsrelatedtosedationwithor
withoutneuromuscularblockade.355

MECHANICS
Interface:Anumberofpatient-ventilatorinterfaces
areavailableforuseduringNIVinpatients
including:
•Nasalmask.
•Facemask(oro-nasal).
•Helmet.356

Facemaskprovidesareliablemeansfordeliveringnoninvasiveventilation
(eitherCPAPorBiPAP,howeversomepatientmaybecomeanxiousor
agitatedwhenthemaskisappliedandmaydobetterwithnasalmask.
Face mask for noninvasive ventilation 357

INDICATIONS
•WesuggestatrialofNIVformosthemodynamicallystable
patientswithhypoxemic(e.g.cardiogenicpulmonary
edema)orhypercapnicrespiratoryfailure(e.g.
exacerbationofCOPD),whodonotrequireemergency
endotrachealintubationonceitisconfirmedthattheylack
contraindicationstoNIV.
•HypoxemicrespiratoryfailurebenefitsmorefromCPAP.
•HypercapnicrespiratoryfailurebenefitsmorefromBiPAP.358

CONTRAINDICATIONS
Theneedforimmediateendotrachealintubationbaseduponclinical
assessmentisanabsolutecontraindicationtoinitiatingNIV.Specific
examplesofsituationswhereNIVshouldnotbeusedinclude:
•Cardiopulmonaryarrest
•Acutelyimpairedmentalstatus
•Highaspirationrisk
•Needforairwayprotection
•Hemodynamicinstability
•Uppergastrointestinalbleed
•Facialinjuries
•Untreatedpneumothorax359

•Carefulpatientselection,thepatient'sabilityto
toleratetheselectedinterface.
•Properinterfacesizing:
–Maximalcomforttopromotecompliance
–Appropriatefitwithminimalleaktomaximizeefficacy
•Interfaceleastlikelytoresultinadverseevents(eg,
skinbreakdownorocularinjury)
For successful use of NIV360

•Useofwarmedandhumidifiedgasdeliveryhelpavoid
thecomplicationsnasalmucosaltrauma.
•Frequentmonitoringbykeymembersofthecare
team,suchasnursesandrespiratorytherapistswith
frequenttitrationtooptimizesupport(Clinical
responseshouldoccurwithinthefirstonetotwo
hoursafterinitiation).
For successful use of NIV361

Ifthereisnoimprovementinrespiratoryrate,heartrate,
workofbreathing,pulseoximetry,and/orbloodgasindices:
•Escalateinthecurrentlevelofsupportor
•Changeintheventilatorsupportstrategy(eg,progression
fromcontinuouspositiveairwaypressureCPAPtobilevel
positiveairwaypressureBiPAP)or
•Endotrachealintubationandmechanicalventilation.
Failure to see improvement 362

Complications of NIV
•Claustrophobia/anxiety/agitation
•Pressureulcers/necrosis(nasalbridge)
•Facialorocularabrasions
•Oronasalmucosaldryness
•Airswallowingwithabdominaldistension,potentiallyleading
tovomitingandaspiration
•Hypotension(ifhypovolemicoroversedatedorhigherPEEP)
•Pneumothorax(ifairtrappingorhigherlevelofPEEP>10)363

Affixing a noninvasive ventilation interface
(A)Firstthenoninvasive
ventilationinterfaceisheld
in placemanually.
(B)Afterthepatienthas
becomecomfortable,the
strapscanbesecured.
(C)The noninvasive
ventilationinterfaceisheld
inplaceuntilthestrapsare
inplace.364

•Keepingpatientscalm,withappropriatesedationas
needed.
•Adjustingsettingsaslowaspossibletoachieve
physiologicimprovementwiththeleastamountof
positiveairwaypressure.
To lower the risk of adverse events365

Conclusion
Atrialofnoninvasiveventilationisindicatedinthe
presenceofacutehypoxemicorhypercapnic
respiratoryfailureandintheabsenceof
contraindications,andappearstobesafewithless
complicationsthaninvasiveventilationwhen
appropriatelyusedandcarefullymonitored.366

Case 1:Immunosuppressed hypoxemic
respiratory failure
59year-oldmanwithAMLhasrecentundergonechemotherapy.
Hehasa2-dayhistoryofdrycoughandgraduallyworsening
breathlessness.
•BP120/70;HR100;sO
288%on15L/minviafacemask,RR30/min;
Temp39.2C;WBC1.4;
•CXRshowsinfiltratesinleftlowerzoneandrightmiddlezone.
•ABG:pH7.40,pCO
239mmHg,pO
257mmHg,HCO
3
-
24.2mmol/l,
BE-0.6mmol/l367

Case 1
WouldyouuseHFNC?
ThisisanacceptableindicationforHFNCuse(hypoxemic
respiratoryfailure,startFiO20.8-1andflow30-40L/min).
WouldyouuseNIV?
•NIVcanbebeneficialinimmunosuppressedpatientswith
moderaterespiratoryfailure,pyrexiaandinfiltrationsonCXR.
•Inadditionthepatientappearstobehaemodynamically
stableandnotacidemic.368

Case 1
•WherewouldyouperformNIV?
•Thisdependsonthepatient’sconditionandthelocalsetup.Ifthe
patientisrelativelystablethenNIVmaybesafelycommencedona
respiratorywardwithexperiencedstaff.
•ACriticalCareenvironmentshouldbechosenifapatientthatis
likelytofailNIVandrequireintubationorifnootherdepartment
canprovideNIVsafely.NIVcanbecommencedandcontinueden
routetoCriticalCareifrequired.Emphasisethatapatientthathas
failedNIVandisinextremisonsupport(NIV)isahigh-risk
intubation.369

Case 1
Whatmodewouldyouuse?
•CPAPmayhelprecruitalveoli,increasetheFRCandimprovehis
oxygenation.Itmayalsoimprovethecomplianceandreducehis
workofbreathing.
PleasesetuptheNIV.
•Checkforsizeofleak–thereshouldbesomeleakbutitshouldnot
exceedtheleakcompensationcapabilityoftheventilator.
•StartatCPAP4-6cmH
2O.Thismaybegraduallyincreasedtoamax
10-15cmH
2O.F
IO
21.0.370

Case 1
RepeatABGonCPAP5cmH
2O,F
IO
20.7after45
minutes:pH7.38pCO
240mmHgpO
265mmHg
HCO
3
-
23.7mmol/lBE-1.4mmol/l
•Whatwouldyoudo?
•Increase CPAP to 7 or 8 cmH
2O. Aim to reduce F
IO
2.371

Case 2
71year-oldmanwithinfectiveexacerbationofCOPD.On
optimalmedicaltreatment,drowsy,,chestmildwheezes.
•F
IO
20.28,SpO289%,RR27/minBP180/95,HR83,
•CXR:hyperinflated,nofocalchanges
•ABG:pH7.23,pCO
272mmHg,pO
257mmHg,HCO
3
-
29.2
mmol/l,BE2.4mmol/l372

Case 2
•WouldyoustartthispatientonNIV?
•ThereisgoodevidenceforthebenefitofNIVinpatientswith
hypercapnicrespiratoryfailureduetoinfectiveandnon-
infectiveexacerbationofCOPD.Itmayreducetheworkof
breathing,increasetidalvolumes,normalisepCO
2andpHand
helpavoidintubation.
•However,ifthepatient’soverallconditiondidn’tresponseto
conventionaltreatmentandtheusualcontraindicationstoNIV
needtobeconsidered.373

Case 2
Whatmodewouldyouchoose?
•BiphasicVentilation(BiPAP).Thisisaventilationproblemnot
anoxygenationproblem.
Pleasesettheventilator.
•Emphasizetheimportanceofcorrectmasksizeandfit.
•WecanstartwithIPAP10&EPAP5(PressuresupportisIPAP-
EPAP=5)andgraduallyincreaseofpressuresupportif
needed.374

Case 2
RepeatABGafter1hour(F
IO
20.35):Drowsy
pH7.15
pCO
288mmHg,
pO
263mmHg
RR28/min,
Whatwouldyoudonow?
•ThepatientisnotrespondingtoNIV,consultseniorabout
intubationandventilation375

9)Circulatory Shock
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care 376

Objectives
•Physiology of circulation.
•Definition of shock.
•Understand the pathophysiology of shock.
•Categorize types & management of shock.377

The Circulatory System
Components:
–Heart (pump)
–Blood Vessels
–Blood378

Hemodynamic Formulas
•BP = CO x SVR
(Cardiac Output x System Vascular Resistance)
•CO = SV x HR
(Stroke volume x Heart rate)379

Oxygen delivery-consumption relationship
•Globaloxygendelivery(DO2)isthetotalamountofoxygendelivered
tothetissuesperminute.
•Oxygenconsumption(VO2)isthetotalamountofoxygenremoved
fromthebloodduetotissueoxidativemetabolismperminute.
•Underrestingconditionswithnormaldistributionofcardiacoutput,
DO2ismorethanadequatetomeetVO2andensurethataerobic
metabolismismaintained.
•Oxygenthatisnotextractedreturnstothemixedvenouscirculation.
5380

Determinants of oxygen delivery to tissues
6
Oxygen delivery (DO2)
CaO2: arterial oxygen content ml/dl 381

Determinants of oxygen delivery to tissues
7
CaO2: assuming Hb concentration 15 g/100 dl and SaO2 of 98% and PaO2 100 mmHg
Hb O2 = 1.34 x Hb x SaO
2 =1.34 x 15 x 0.98 = 19.7 ml/dL
Dissolved O2 = PaO2 x 0.003 = 100 x 0.003 = 0.3 ml/dL
= 20 ml/dL
CO= SV x HR = 70 x 70 = 4900 ≈ 5000 ml/min (50 dl/min)
Oxygen Delivery (DO2) = CaO2 x CO DO2 = 20 x 50 = 1000 ml/min382

In shock state
8
Oxygen consumption VO2exceedsOxygen delivery DO2
VO2 approximately 250 ml/min (200-270 ml/min)
DO2 approximately 1000 ml/min (900-1100ml/min)383

Oxygen Extraction Ratio (ERO2)
•Ratioofoxygenuptake(consumption)todelivery
•ERO2=VO2/DO2x100=(250ml/min/1000ml/minx100)
•O2ER=(SaO2-SvO2)/SaO2Orevenmoresimply,
•O2ER=100%-SvO2%(assumingthattheSaO2iscloseto100%).
•Normalratiois20-30%,whichcorrespondstoanScVO2of70-80%.
•Uptakeiskeptconstantbyincreasingextractionwhendeliverydrops.
•TheO2ERcanbeusedtocalculatecardiacoutputfromcentralvenous
saturationmeasurements.
•TheO2ERcanbeusedtoassess"flowinsufficiency"incriticallyill
patients,(someevidencethathighO2ERisassociatedwithlacticacidosis.
9384

The critical DO
2
10
Itisthepointat
whichcellswill
begintoproduce
lactate.
Atthispoint(cDO2)
themaximumO2ERis
reached
BeyondcDO2any
furtherincreasein
VO2,ordeclinein
DO2,mustleadto
tissuehypoxiaand
anaerobicmetabolism385

Pathologic changes in critical DO2
11386

Objectives of shock treatment
1.Increase DO
2
2.Decrease VO
2
3.Treat the underlying cause
12387

Stoke Volume determinants
–Preload
•Stroke volumeis directlyproportional toPreload.
–Afterload
•Stroke volumeis indirectlyproportional toAfterload.
–Pump (Contractility)
•Stroke volumeis directlyproportional toContractility.388

Preload determinants
–Blood volume
–Venous tone
–Intrathoracic pressure
–Rhythm (atrial contraction)
–Heart rate389

Proportion of blood volume throughout the
Cardiovascular system390

Definition of Shock
•Shockisdefinedasastateofcellularandtissuehypoxiadue
toeitherreducedoxygendelivery,increasedoxygen
consumption,inadequateoxygenutilization,ora
combinationoftheseprocesses.
•It’sanacuteclinicalsyndromeultimatelyleadingtoorgan
dysfunctionandfailureifuntreated.
•It’sasyndromeassignsandsymptomsfollowsseriesof
pathophysiologicevents
•Itsclinicalpresentationvarieswidelybasedontheunderlying
etiology,thedegreeoforganperfusion,andpriororgan
dysfunction.391

Definition of Shock
•Inadequateoxygendeliverytomeetmetabolicdemand.
Shock is not a synonym to hypotension!
Shock can occur without hypotension
and hypotension can occur without shock.
•Shockisnotafinaldiagnosis,youshoulddiagnosethecause.
Itmaybehypovolemic(improvewithfluid)orcardiogenic(die
fromfluid)orothertype(distributiveorobstructive)392

Pathophysiology
•Hypoperfusionleadstodiminishedbloodflowthroughthe
capillaries.Thebodyshiftsfromaerobictoanaerobicmetabolism,
causingabuildupinthecellsoflacticacidandothertoxicwaste
productsaswellasacidosis.
•Ifleftuncorrected,thecellswilldie,tissuedeath,organfailure,
and,eventually,patientdeathcanresultwhenapatientcontinues
tolackadequateperfusion.
•Tomaintainhomeostasis,thebodycompensatesbyshuntingblood
tothevitalorgansfromtheperipheralvascularsystem.393

Stages of shock
•Compensatedshock:Thebodyrespondstotheinsultbyexcess
releaseofcatecholaminescausingtachycardia,andpoor
peripheralperfusion.
•Decompensatedshock:thecompensatorymechanismsfail.
Clinicallythepatienthastachycardia,poorperipheral
perfusion,andhypotension
•Irreversibleshock:permanentcellulardamage,andsignsof
multipleorgandysfunctionsyndrome(MODS).394

Pathophysiologic changes at
each stage of shock
IrreversibleDecompensatedCompensated
UnresponsiveAlteredNo changeMental status
BradycardiaIncreasedIncreasedHeart rate
DecreasedLabored or irregularIncreasedRespirations
Profound
hypotension
Hypotensionnarrows
pulse pressure
No changeBlood pressure
ColdDiaphoresisClammy, pale,
and cool
Skin395

Tips
•Notethatthebody’scompensatorymechanismcanmask
shockinitially.Thisisespeciallytrueinchildrenandpregnant
women,whocanlose20%to30%oftheirbloodbefore
showingsignsofshock,andthenrapidlydeteriorate.
•Childrendescendveryrapidlyintoirreversibleshock.Timeis
oftheessence.Diligentlymonitortheirvitalsignsand
appearance.Provideprompttreatmentandrapidtransport.396

Tips
•Normalvitalsignsdonotequatetocirculatoryadequacy.
•Monitorthemeanarterialpressure(MAP),NOTthesystolic
bloodpressure.
•Tachycardiaindicatesalossof15–30%ofbloodvolume,but
canbebluntedintheelderly,theathlete,pregnantwomen,
andpatientsmedicatedwithbeta-blockers.
•Automatedbloodpressuredeviceslackaccuracywhenthe
systolicbloodpressureisbelow110mmHg;useofamanual
deviceinthesesettingsisrecommended.
22397

Symptoms & Signs of shock
Related to decreased tissue perfusion
–Pale, cool, clammy skin
–Slow capillary refill over finger or toe nail (>3 seconds),
(pressing over the nail for 5 seconds and releasing pressure).
–Decrease urine output.
–Altered mental status.
–Cold extremities.
–Skin mottling.
–Peripheral cyanosis.
–398

Shock red flags
Thereisnosinglediagnostictestforshock,butratherthis
diagnosisismadeatthebedsideonthebasisofclinical
judgment.Patientspresentdifferently,butthisdiagnosiswill
generallybesuggestedbythepresenceofmorethanoneofthe
followingfeatures:
•Hemodynamics(trendswillusuallybemorehelpfulthana
singleabnormalvalue)
•Lowurineoutput
•Skinperfusion:
•Delirium:New-onsetdeliriumcanbeasignofshock.
24399

•Diagnosticalgorithmsforshock(likeanydiagnostic
algorithms)workbestamongpatientswithasingledisease
processwho were previouslynormal.
•Unfortunately,manypatientshavemultifactorialshockonan
abnormalbaseline(e.g.chronicallyreducedejectionfraction),
sosimplealgorithmswillfailthesepatients.
25400

•Themostcommoncauseofshockofunclearetiologyis
septicshock.
•However,othercausesshouldbecarefullyexcludedprior
toreachinganempiricdiagnosisofsepticshock(e.g.
echocardiographytoevaluateforcontractility,massive
pulmonaryembolismorpericardialtamponade).
26401

Point-of-care ultrasound (POCUS)
•Evaluationofshockisbasedonstep-wiseimagingofthe
Heart(inthesubxiphoidorparasternallongaxisviewsallow
forassessmentofventricularfillingandfunction).
•EvaluationoftheIVC(collapseinvolumedepletedpatients).
•EvaluationoftheIntraperitonealcavity(freefluidand
abdominalhemorrhage).
•EvaluationoftheLung/Pleura(allowsforidentificationof
pneumothorax,pulmonaryedema,pneumoniaandpleural
effusions).
27402

403

“Undifferentiated shock” refers to the
situation where shock is recognized but the
cause is unclear
29404

Hemodynamic parameters in
various types of shock405

Classification of Shock
Weil and Shubinclassified shock as (based on
cardiovascular parameters):
•Hypovolemic.
•Cardiogenic.
•Obstructive.
•Distributive. 406

1)Hypovolemic shock
➢Primary defect is a decrease in intravascular volume
causes include:
•Bleeding
•GI losses
•Urinary
•Third spacelosses407

Hypovolemic shock
•Hemorrhagic
Trauma, gastrointestinal, retroperitoneal.
•Nonhemorrhagic
Dehydration, emesis, diarrhea, fistulae, burns,
polyuria, “third spacing,” malnutrition, large open
wounds.408

34409

Hemodynamic response to shock
hemorrhage model
35410

Treatment of hypovolemic shock
•Initial therapy including, airway and breathing support, fluid
therapy, inotropic drugs, correction of acid base and other
metabolic defects.
•Replacement of fluid deficit
•Bolus therapy: 20 cc/kg (Adults-2 liters)
•Monitor Effect.
•Repeat if necessary.
36411

Treatment of hemorrhagic shock
–Controlofexternalhemorrhagebydirectwoundpressure,
pressureoverthesupplyingartery,andelevationofthe
part
–Mayneedbloodtransfusionafter2ndbolusoffluids.
–Controlofinternalhemorrhagebyexploration
–Replacementofbloodlossbyrapidlycrossmatched
blood,uncrossmatchedbloodofthesamegroupasthe
patientoruncrossmatchedOnegativeblood
–Titratetherapyaccordingtoheartrate,capillaryrefilling
time,bloodpressureandurineoutput
37412

End Points of Resuscitation
•Restoration of normal vital signs
•Adequate Urine output (0.5 -1.0 cc/kg/hr)
•Tissue oxygenation measurement
•Normal serum lactate levels413

2)Cardiogenic Shock
➢Primarydefectisdecreasedmyocardialcontractilitywith
elevatedcardiacchamberfillingpressures(CVP,PAWP)
causesinclude:
•Ischemia/infarction
•Cardiomyopathy
•Myocarditis
•Arrhythmias
•Severe valve lesions 414

Treatment of Cardiogenic Shock
–Initialtherapyincluding,airwayandbreathingsupport,inotropic
drugs,correctionofacidbaseandothermetabolicdefects
–IVdiuretic(furosemide1-2mg/kg/dose)Ifthereisvascular
congestionasshownbycrepitationonchestauscultation,or
radiologicallybychestX-ray,orasustainedriseofCVP>10mmHg
–Inotropicagents(norepinephrine,dopamineordobutamine)
–Vasodilators:(Nitroglycerine)ifSBP>90todecreasepreload415

3.Distributive Shock
➢Primary defect is a decrease in SVR, a relative
hypovolemiamay exist,causes include:
•Septic shock
•Anaphylactic
•Neurogenic
•Pharmacologic
•Endocrinologic. 416

Septicshock(aformofdistributiveshock)isthe
mostcommonformofshockamongpatients
admittedtotheintensivecareunit,followedby
cardiogenicandhypovolemicshock;obstructive
shockisrare.
A.Septic Shock417

Pathophysiological changes in septic shock
–Distributive:maldistributionofintravascularvolumedueto
peripheralvasodilation
–Hypovolemic:deficientintravascularvolumeduetocapillary
leak
–Cardiogenic:impairedmyocardialcontractilityduetoeffect
ofendotoxinonthemyocardium
–Alloftheseabnormalitiesoccuratdifferenttimesduring
thecourseofsepticshock
43418

Stages of Septic Shock
–Thecompensatedsepticshock:Characterizedbydecreased
vascularresistance(distributiveshock)withresultant
hypovolemia,increasedcardiacoutput,tachycardia,andwarm
extremities(hotshock)
–Theuncompensatedsepticshock:Characterizedbycapillary
leak(hypovolemicshock),myocardialdepression(cardiogenic
shock).Thepatientisnowcold,oliguric,andinrespiratory
distress
44419

Treatment of Septic Shock
•Management:
–Initialtherapyincluding,airwayandbreathingsupport,fluidtherapy,
vasopressor,correctionofacidbaseandothermetabolicdefects,
sourceidentificationandcontrol&empiricalbroadspectrumantibiotics
•Algorithmforsepticshockmanagement:
–Initialfluidtherapy(aimMAP>65mmHg)
–Forfluidrefractoryshock:Startnorepinephrine2-20µg/min
–Forfluid-norepinephrineresistantshock:
*Giveepinephrine2-20µg/minorvasopressin0.03U/min
*Giveivhydrocortisoneduetoadrenalinsufficiency(stress
replacementdose200mg/day)
45420

B.Anaphylactic Shock
•Definition:Severe allergic reaction with cardiovascular collapse due to acute
vasodilation,and fluid loss by increased capillary permeability,and
respiratory insufficiency due to upper (laryngospasm) and lower
(bronchospasm) respiratory obstruction
•Common causes:
–Allergy to drugs(antibiotics, aspirin, etc), radiographic contrast media,
certain foods, insect bite.
•Presentation:May present with mild prodromal symptomsof flushing,
itching, facial swelling, urticaria, abdominal pain, wheezes, or stridor, or with
life threatening shockand airway obstruction
46421

Anaphylacticshock
•Anaphylaxisisanacutereactiontoaforeignsubstanceto
whichthepatienthasalreadybeensensitized.Thisleadstoan
IgE-triggeredrapiddegranulationofmastcellsandbasophils.
•Anaphylactoidreactionshaveanidenticalclinical
presentationbutarenottriggeredbyIgEanddonot
necessarilyrequirepreviousexposure.Furthermore,theymay
notproduceareactioneverytime.422

Treatment of Anaphylactic Shock
–Initialtherapyincluding,airwayandbreathingsupport,fluid
therapy,vasopressor,correctionofacidbaseandother
metabolicdefects
–Initialfluidtherapy(20ml/kg)
–Epinephrine:IM0.5mgor1:10.0001ml(100mic)IVslowly
every3-5minupto5mlaccordingtoresponse
–Diphenhydramine:antihistamine
–Hydrocortisone:antiinflamatory
48423

C.Neurogenic Shock
•Pathophysiologicalchanges:Ablationofthesympatheticstimulationdue
tosympatheticchaindisruptionleadstotheunopposedparasympathetic
effect,leadingtothelossofvasomotortone
•Causes:
–Trauma to the spinal cord above the level of T1
–Spinal cord surgery
–Head trauma
•Management:
–Initialtherapyincluding,airwayandbreathingsupport,fluidtherapy,
vasporessor,correctionofacidbaseandothermetabolicdefects
–Fluidsasneeded-Typically0.9%NaCl,ratedependsuponneed
–EphedrineorAtropineforbradycardia
–Ephedrineorphenylelphrineforhypotension
49424

4)Obstructive Shock
➢Caused by mechanical obstruction of blood flow to
or from the heart, causes include:
•Cardiac tamponade
•Tension pneumothorax
•Massive pulmonary embolism
•Constrictive pericarditis (late stage)
•Severe aortic stenosis425

Obstructive shock
•Impairmentofdiastolicfilling:Intrathoracicobstructivetumors,
tensionpneumothorax,positive-pressuremechanicalventilation,
constrictivepericarditis,pericardialtamponade.
•Impairmentofsystoliccontraction:Pulmonaryembolism,acute
pulmonaryhypertension,airembolism,tumors,aorticcoarctation.426

Obstructive Shock
–The major cause is pericardial tamponade(Beck's triad) :
•Hypotension (with narrow pulse pressure)
•Muffled heart sound
•Jugular vein distension
•Management:
–Initial therapy including,airway and breathing support, fluid therapy,
vasopressor, correction of acid base and other metabolic defects
–Correction of the cause
52427

Question 1
Whichofthefollowingisnotamechanismfordecrease
oxygendeliverytotissues?
A. Inadequate blood volume
B. Inadequate cardiac performance
C. Inadequate vascular tone
D. Increased coronary perfusion
53428

Answer 1
Whichofthefollowingisnotamechanismfordecrease
oxygendeliverytotissues?
A. Inadequate blood volume
B. Inadequate cardiac performance
C. Inadequate vascular tone
D. Increased coronary perfusion
54429

Question 2
Inshock,whichofthefollowingstatementsistruerelativeto
oxygenconsumption(VO2)
A.Oxygendemandexceedsoxygendelivery
B.Oxygendeliveryandoxygendemandaredeterminedbystroke
volume
C.BecauseDO2isgreaterthanVO2inshocksituations,anaerobic
metabolismresultsinformationoflactate
D.AslongasVO2isgreaterthanDO2,anaerobicmetabolismwillbe
minimalandbloodlactatelevelswillremainnormal
55430

Answer 2
Inshock,whichofthefollowingstatementsistruerelativeto
oxygenconsumption(VO2)
A.Oxygendemandexceedsoxygendelivery
B.Oxygendeliveryandoxygendemandaredeterminedbystroke
volume
C.BecauseDO2isgreaterthanVO2inshocksituations,anaerobic
metabolismresultsinformationoflactate
D.AslongasVO2isgreaterthanDO2,anaerobicmetabolismwillbe
minimalandbloodlactatelevelswillremainnormal
56431

10)Fluid management in ICU
Hani Sammour, MD, PB
Anesthesia and IC, Shifahospital
Critical Care 432

Fluid compartment & distribution
Fluidcompartmentoftotalbodyweight:
•Neonate:75-80%
•Infant:70-75%,
•Adultmale:55-60%
•Adultfemale50-55%
•Elderly45-50%
Fluiddistribution433

Introduction
•Intravenousfluidadministrationshouldbeconsideredas
anyotherpharmacologicalprescription.
•Therearethreemainindications:Resuscitation,
ReplacementandMaintenance.
•Formaximizingbenefitsandminimizingharms
intravenousfluidadministrationshouldfollowthe
fourDs:Drug,Dosing,Duration,De-escalation.434

Concept of ‘four Ds’ when prescribing fluids
•Drug–considertheindicationforthefluidandwhat
effectisbeingsought.
•Durationoftherapy–considerwhentostartandwhen
tostoptherapy.
•Dosing–considerhowmuchfluidtogive.
•De-escalation–considerwhenthefluidtherapyisno
longereffectiveorrequired.435

Osmolarity and Tonicity of a solution
•Theosmolarityofasolutionisequaltothenumberof
osmolesperliterofsolution.
•Tonicity,atermthatisoftenusedinterchangeablywith
osmolarity,referstotheeffectasolutionhasoncellvolume.
•Anisotonicsolutionhasnoeffectoncellvolume.
•Hypotonicsolutionsincreasecellvolume.
•Hypertonicsolutionsdecreasecellvolume.
•Tonicitydescribestheeffectiveosmolalityofafluid.436

Fluids classification
•IVfluidsareclassifiedasCrystalloidsorColloidsbased
ontheirabilitytodiffusethroughbarriersseparating
bodyfluidcompartments,i.eintravascularand
extravascular(interstitial)fluidcompartments.
•Crystalloidspassedreadilythroughthemembrane,
whereascolloidsdidnot(Greekword-glue).437

Crystalloids and Colloids
•ACrystalloidsolutionisanaqueoussolutioncomposed
ofwaterandsmallsolutessuchaselectrolytesand
glucose.
•Crystalloidsolutionscanbefurthercategorizedas
hypotonic,isotonic,orhypertonic.
•AColloidsolutioncontainslargemolecularweight
particlessuchasproteinsorhydroxyethylstarches(HES)
suspendedinacrystalloidsolution.438

Theintravascularhalf-lifeofacrystalloid
solutionis20–30min,mostcolloidsolutions
haveintravascularhalf-livesbetween3and6h.439

Crystalloids when given in sufficient amounts
1.Arejustaseffectiveascolloidsinrestoringintravascular
volume.
2.Replacinganintravascularvolumedeficitwiththreeto
fourtimesthevolumeneededwhenusingcolloid
3.Severeintravascularfluiddeficitscanbemorerapidly
correctedusingcolloidsolutions.
4.Therapidadministrationoflargeamountsofcrystalloids
(>4-5L)ismorefrequentlyassociatedwithtissueedema.
Someevidencesuggeststhatmarkedtissueedemacanimpair
oxygentransport,tissuehealing,andreturnofbowelfunction
followingmajorsurgery.440

Comparison of Plasma and Crystalloid
Resuscitation Fluids441

Infusion of common fluids
Infusionof1Lof0.9%NACL
adds275mLtotheplasma
volumeand825mLtothe
interstitialvolume
Note:thetotalvolume
expansion(1100mL)slightly
greaterthantheinfused
volume.
Thisistheresultofafluid
shiftfromtheICFto
extracellularspace,because
isotonicsalineisslightly
hypertonictothePlasma
Volume Effects442

0.9% Sodium Chloride (Normal Saline)
Indicationsfortheuseofnormalsalineinfusionthathavebeen
approvedbytheFDA:
•Extracellularfluidreplacement(e.g.,dehydration,
hypovolemia,hemorrhage,sepsis).
•Treatmentofmetabolicalkalosisinthepresenceoffluidloss.
•Mildsodiumdepletion.
Additionally:diluentsfortheinfusionofcompatibledrugadditives.443

Other indications
•Usedalsointraumaticbraininjuryoranybrainedema.
•Replacementfluidinhyperkalemia.
•Itisthepreferredsolutionfordilutingpackedredblood
cellspriortotransfusion.
•ItisusedinDKAwhenthereisseverehypovolemiaand
whenserumsodiumlessthan140meq/L.444

Hypertonic saline
•Hypertonic3%salineisemployedintherapyof
severesymptomatichyponatremia.
•Hypertonic3%,7.5%or23.4%salinecanbeusedin
caseofseverebrainedema.445

0.45%Sodium Chloride
•Ahypotonicconcentrationofsodiumchloride.
•Hypotonicconcentrationsofsodiumchloride(0.45%)
arebestforparenteralmaintenancefluidsrather
thanaggressiveintravascularvolumerepletion.446

Lactated Ringer's
•Ringer'ssolution:introducedin1880bySydneyRinger(UK)
whostudiedmechanismsofcardiaccontraction.
•Thesolutionwasdesignedtopromotethecontractionof
isolatedfroghearts,andcontainedCa+andK+inasodium
chloridediluent.
•Inthe1930sAlexisHartmann(Americanpediatrician)proposed
theadditionofsodiumlactatebuffertoRinger'ssolutionforthe
treatmentofmetabolicacidosis.
•ThelactatedRinger'ssolutionisalsoknownasHartmann'ssolution447

Lactated Ringer's uses
•Havesodium,potassiumandchloridecontents
similartoextracellularfluidhavefewer
adverseeffectsonacid-basebalance(incaseof
hyperchloremicmetabolicacidosis).
•Itisusedasareplacementfluidinburnpatients
whenBSA>20%(Parklandformula).448

Lactated Ringer's disadvantages
•ThecalciuminlactatedRinger'scanbindtocertaindrugsand
reducetheirbioavailabilityandefficacye.g.Amphoterecin,
Ampicillin,Thiopentoneetc.
•Calciumbindingtothecitratedanticoagulantinblood
productscaninactivatetheanticoagulantandpromotethe
formationofclotsindonorblood.
•Forthisreason,lactatedRinger'ssolutioniscontraindicatedas
adiluentforbloodtransfusions.449

Dextrose solutions
•D5%isusedtopreventproteinbreakdowninanNPOpatients
afterconsumptionofendogenousglycogen(24-48hr).
•D5%(D5W)isusedforreplacementofpurewaterdeficitsand
asamaintenancefluidforpatientswithhypernatremia.
•D10%,D20%orD50%areusedinhypoglycemia.
•D20%,D25%orD50%areusedinTPN(Theuseof5%
dextrosesolutionstoprovidecaloriesisobsolete).450

Dextrose solutions
Whenglucosegetsutilized,onlywaterremains,Distribution:
•<10%remainsinIntravascularspace
•<30%inInterstitium
•>50%inIntracellularspace
➢ThiscauseCellularswelling
•5%dextrose-in-watersolutionisnotaneffectivevolume
expander.451

Dextrose solutions disadvantages
LactateProduction:Theproportionofaglucoseloadthat
contributestolactateformation
•5%inhealthysubjects
•85%incriticallyillpatients
Thus,inpatientswithcirculatorycompromise,abnormal
glucosemetabolismcantransformglucosefromasourceof
usefulenergytoasourceoftoxinproduction.452

Disadvantages of Glucose infusions
•EnhancedCO2production(whichcanbeaburdenin
ventilator-dependentorCOPDpatients).
•Hyperglycemia.
•Increasedriskofinfection,Neuropathy.
•Aggravationofischemicbraininjury.
•Increasedmortalityinsepticshock.453

Colloids
Donotpassacrossdiffusionalbarriersasreadilyascrystalloids.
Natural (plasma-derived) colloids:
•Human albumin.
Synthetic colloids:
•Dextran(e.g. dextran 40 and dextran 70).
•Gelatin (e.g. gelofusineand hemaccel).
•Starch(e.g.hydroxyethylstarch (HES)).454

Albumin solution
•Responsiblefor75%oftheoncoticpressureofplasma.
•Actsasbuffer,antioxidantandtransportprotein.
•Commerciallyisavailableas5%solutionor20%solutioninan
isotonicsalinediluent.
•5%solutionhascolloidoncoticpressure(COP)20mmHg(similarin
oncoticactivitytoplasma).
•Approximatelyhalfoftheinfusedvolumeof5%albuminstaysin
thevascularspace.
•Theoncoticeffectsofalbuminlast12-16hours455

Albumin solution 20%
•COPof70mmHg
•Expandstheplasmavolumeby4to5timesthevolumeinfused.
•Infusionof100mLof20%albumincanincreasetheplasma
volume400to500mL.
•Itisintendedforshiftingfluidfromtheinterstitialspacetothe
vascularspaceinhypoproteinemicconditions,
•Shouldnotbeusedforvolumeresuscitationinhypovolemia.456

Gelatins
•COP27-34mmHg
•Thecheapestcolloidavailable.
•Unlimitedvolumeforresuscitation.
•Unimpairedrenalfunctionandhemostasis.
•Rapidlyexcretedbythekidneys(shorterduration3-4hr).
•Anaphylactoidreactions:directhistaminerelease.
•Gelofusineiscompatiblewithbloodbuthemaccelcontainsca+2.
•Hemaccelandgelofusinehavethesameconcentrationofsodium
(154meq/L)butgelofusinecontainlesschloride(120meq/L).457

Hydroxyethylstarches
•COP28mmHg
•Longeliminationhalf-life(17days)butTheoncoticeffectsof
hetastarchdisappearwithin24hours
•TheearlierHESfluidswereassociatedwithcoagulation
dysfunctionandpruritis,butthetetrastarchesusedthese
dayshavenoeffectonbleedingtimes.Renalimpairmentin
criticallyillpatientsisassociatedwithosmoticnephrosislike
lesionsintheproximalanddistaltubules.458

Dextrans
•COP40mmHg(greaterincreaseinplasmavolume).
•Notusedforvolumeexpansionbecauseofahigh
incidenceofanaphylacticreactionsandnegativeeffects
oncoagulation.
•Decreaseinbloodviscosityandinhibitionoferythrocyte
aggregation.
•Interferewithcross-matching.459

Comparison between Colloid460

The ideal colloid has yet to be found461

Indications for colloids
1)Fluidresuscitationinpatientswithsevereintravascularfluid
deficits(e.g.hemorrhagicshock)priortothearrivalofblood
fortransfusion(inconjunctionwithcrystalloids).
2)Fluidresuscitationinthepresenceofsevere
hypoalbuminemiaorconditionsassociatedwithlarge
proteinlossessuchasburns.
•Itshouldbenotedthatcolloidsolutionsarepreparedin
normalsaline(Cl−145–154mEq/L)andthuscanalsocause
hyperchloremicmetabolicacidosis462

What option for fluid resuscitation
would you choose463

Crystalloids and Colloids
DisadvantagesAdvantages
Only25%remainsincirculationCheapCrystalloid
MostgoesinterstitialAvailable
Largerresuscitationvolume(X3)Lesssideeffects
MoreresuscitationtimeResuscitatetheECFspace
Shorterhalf-life
Pulmonary&peripheraledema
Expensive
Doesn'trestoreinterstitialvolume
Entersinterstitialspaceifleaky
(sepsis)
Sparespulmonary+peripheral
interstitialspace
Colloid
Moresideeffects
Immunereactions
Interferencewithhemostasis
X-matchingproblems
Useofstarchesmaybeassociated
withworseoutcome
50-100%remainsinintravascular
space(dependingontype)
Shorterresuscitationtime
Longerhalf-life464

Calculation of maintenance fluid
Ruleof4:2:1(infusionperhour)
4mL/kg/hrforkg1-10
+2mL/kg/hrforkg10-20
+1mL/kg/hrabove20kg
•Apatientwhoweighs40kilogramswouldrequire:
40mL/hr+20mL/hr+20mL=80mL/hr
•Shortcutformula:bodyweight+40(=80mL/hrinthisexample)
(Workingifbodyweight>20kg)465

Further consideration
Oncethemaintenancerequirementshavebeencalculated,
additionalpotentiallossesneedtobeconsideredtoavoidunderor
overhydration,thefollowingsourcesoffluidlossandthe
electrolytecompositionofthesefluidsneedtobeappreciated:
•Nasogastricaspirates
•Vomit
•Diarrhea
•Stoma,drains,fistulaetc.
•Polyuria466

Adequacy of resuscitation
•Ithowever,remainscontroversialastotheprecise
volumeadministered,rateofadministrationorindeed
thetypeoffluidutilized.
•Inassessingtheadequacyoffluidresuscitation
theclinicianneedstoconsiderarangeofphysiological
variablesandthetrendsratherthanisolatedparameters.467

Survival Benefit ?
•EDEMA:crystalloidsdistributeprimarilyintheinterstitialspace
causeedema,edemaisalsoariskwithcolloidfluidresuscitation
speciallywhencapillarypermeabilityisdisruptede.g.Sepsis.
•Despitethesuperiorityforexpandingplasmavolume,colloid
fluidresuscitationdoesnotconferahighersurvivalratein
patientswithhypovolemicshock.
•There is no single resuscitation fluid that is optimal for all cases
of hypovolemia.468

MCQ
A16-year-oldboypresentstohishealthcareproviderwith
dizziness,vomiting,anddiarrhea.Onphysicalexamination,
heisalert,andhisvitalsareabloodpressureof80/55
mmHg,aheartrateof120/bpm,arespiratoryrateof22
breaths/minute,andanoxygensaturationof92%onroom
air.Whichofthefollowingisthemostappropriatefirst
choiceoffluidforabolus?
A.Normalsaline
B.Normalsalinewith5%dextrose
C.Normalsalinewith10%dextrose
D.LactatedRinger'ssolution469

Answer is A
•Thispatienthashypovolemicshockduetogastroenteritis.
Normalsaline(0.9%saline)isthemostcommonlyusedinitial
resuscitationsolutionforhypovolemicshocknotdueto
bleeding.
•Normalsalineisinexpensive,andothersolutionshavenot
consistentlybeenproventobesuperior,especiallywhen
smallervolumes(eg,around2L)areadministered.
•Normalsalinemayleadtometabolicacidosis.
•Hyperchloremicacidosisisduetohighconcentrationsof
chloriderelativetothatinplasmaandmayberesolvedbythe
administrationofbufferedcrystalloid,providedcontinued
fluidresuscitationisrequired.470

Cont.
•Normalsalinemayleadtoperipheraledemaduetothesignificant
extravasculardistribution.
•Complicationsoccurwhenlargevolumesoffluidsareadministered
(e.g.>2L).
•Evidencesuggestsapotentialbenefitfrombufferedcrystalloidsin
thosecases.Suchfluidsaretermedbuffered,balanced,orchloride-
restrictivecrystalloidsandincludelactatedRinger'ssolutionor
0.45%salinesolutionwith75mmol/Lofsodiumbicarbonate.
•Dextrosesolutionsareconsideredincaseofhypoglycemia.471

11)Blood Products & Transfusion
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care 472

Objectives
•Definitionandpreparationofbloodcomponents.
•Indicationsforbloodcomponentstransfusion.
•Dosesofbloodcomponents.
•Complicationsofbloodtransfusion.473

Average blood volume in the body 474

Useofatransfusionalgorithmguidedby
appropriatelaboratorytesting,willreduce
unnecessarytransfusionofprecious(and
dangerous)bloodcomponents.475

•Thereisatrendinmajortraumacaretowardstransfusing
bloodproductsinequalratiosearlyinresuscitationin
ordertopreventorcorrecttrauma-induced
coagulopathy.
•Thisbalancedapproachtotransfusionofbloodproducts,
1:1:1(oneunitofFFPandoneunitofplateletswitheach
unitofPRBCs)istermeddamagecontrolresuscitation.476

Blood Groups
•Amongatleast20bloodgroupantigensystemsinhuman
redcellmembranes,onlytheABOandtheRhsystemsare
importantinthemajorityofbloodtransfusions.
•Individuals often produce antibodies
(alloantibodies)totheallelestheylackwithineachsystem.
Suchantibodiesareresponsibleforthemostserious
reactionstotransfusions.477

The ABO System
•ABObloodgrouptypingisdeterminedbythepresence
orabsenceofAorBredbloodcell(RBC)surface
antigens:
–TypeAbloodhasARBCantigen.
–TypeBbloodhasBRBCantigen.
–TypeABbloodhasbothAandBRBCantigens.
–TypeObloodhasneitherAnorBRBCantigenpresent.478

The Rh System
•PatientswiththeDRhesusantigenareconsideredRh-positive
andindividualslackingthisantigenarecalledRh-negative.
Approximately85%ofthewhitepopulationand92%ofthe
blackpopulationhastheDantigen.
•Rh-negativepatientsusuallydevelopantibodiesagainsttheD
antigenonlyafteranRh-positivetransfusionorwithpregnancy,
inthesituationofanRh-negativemotherdeliveringanRh-
positivebaby.479

Other Red Blood Cell Antigen Systems
•OtherredcellantigensystemsincludeLewis,P,Ii,MNS,
Kidd,Kell,Duffy,Lutheran,Xg,Sid,Car-tright,YK,andChido
Rodgers.
•Fortunately,withsomeexceptions(Kell,Kidd,Duffy,and
Ss),alloantibodiesagainsttheseantigensrarelycause
serioushemolyticreactions.480

Compatibility testing
•Thepurposeofcompatibilitytestingistopredictandto
preventantigen–antibodyreactionsasaresultofredcell
transfusions.481

ABO–Rh Testing
•Themostseveretransfusionreactionsaredueto
ABOincompatibility;naturallyacquiredantibodies
canreactagainstthetransfused(foreign)antigens,
activatecomplement,andresultinintra-vascular
hemolysis.482

Crossmatch
•A crossmatch mimics the transfusion: donor red cells are
mixed with recipient serum.
•Crossmatching serves three functions:
(1) It confirms ABO and Rh typing.
(2) It detects antibodies to the other blood group systems.
(3) It detects antibodies in low titers or those that do not
agglutinate easily. 483

Emergency Transfusions
•Whenapatientisexsanguinating,theurgentneedto
transfusemayarisepriortocompletionofacrossmatch,
screen,orevenbloodtyping.Ifthepatient’sbloodtypeis
known,anabbreviatedcross-match,requiringlessthan5
min,willconfirmABOcompatibility.
•Iftherecipient’sbloodtypeandRhstatusisnotknown
withcertaintyandtransfusionmustbestartedbefore
determination,typeORh-negative(universaldonor)red
cellsmaybeused.484

Definitions
•Bloodproduct:anytherapeuticsubstanceprepared
fromhumanblood.
•Wholeblood:Unseparatedbloodcollectedintoan
approvedcontainercontainingananticoagulant-
preservativesolution.485

Blood component
–A constituent of blood, separated from whole blood,
such as:
•Red cell concentrate
•Plasma
•Platelet concentrates
–Cryoprecipitate, prepared from fresh frozen plasma.486

Plasma derivative
Human plasmaproteinspreparedunder
pharmaceuticalmanufacturingconditions,suchas:
–Albumin.
–Coagulation factor concentrates.
–Immunoglobulins.487

1)Whole Blood
•Therehavebeenfewwidelyacceptedindicationsforwholeblood
inmoderntransfusionpractice.
•WholebloodisnotavailablefrommostbloodbanksintheUnited
States.
•Dose:6ml/kgofWBraiseHemoglobinlevel1g/dl.
•Oneunitof WBwillraisethehemoglobinof
an average-sizeadultby~1g/dl488

Whole Blood
•Duringdonation,bloodiscollectedintoasterile,
disposable,plasticpackwhichcontainsananticoagulant-
preservativesolution.Thissolutionusuallycontains
citrate,phosphate,dextroseandoftenadenine(CPDA).
•Therearevariationsinthevolumeofbloodcollectedand
inthetypeofanticoagulant-preservativesolutionusedin
differentregionsoftheworld.
•Duringstorage,metabolismcontinuesintheredcellsand
platelets,whilesomeplasmaproteinslosetheir
biologicalactivity.489

Functions of anticoagulant-preservative solution in
blood collection pack
FunctionsSolutions
Binds with calcium ions in blood in
exchange for the sodium salt so the
blood does not clot
C Sodium citrate
Supports metabolism of the red cells
during storage to ensure they release
oxygen readily at tissue level
P Phosphate
Maintains the red cell membrane to
increase storage life
D Dextrose
Provides energy sourceA Adenine 490

Effects of storage on whole blood
•ReductioninthepH(bloodbecomesmoreacidic).
•Riseinplasmapotassiumconcentration(extracellularK+).
•Progressivereductionintheredcellcontentof2,3
diphosphoglycerate(2,3DPG).
•Lossofallplateletfunctioninwholebloodwithin48hoursof
donation.
•ReductioninFactorVIIIto10–20%ofnormalwithin48hours
ofdonation.491

2)Red Blood Cells
PackedRBCsarethecommonlyutilizedbloodproduct,
providingoxygen-carryingcapacityincasesmostofacute
orchronicbloodloss.492

Cont.
Advantages
•Simpleandinexpensivetoprepare.
Disadvantages
•Ithasahighratioofredcellstoplasma(highviscosity)
therebyincreasingthetimerequiredfortransfusion
throughasmallgaugeneedleorcannula.
•Thewhitecellsareacauseoffebrilenon-haemolytic
transfusionreactionsinsomepatients.493

Leukocyte-depleted red cells
•Specialleukocytefilterscanbeusedtoremove
virtuallyallthewhitecells.
•Themajorityofredcellsandplatelettransfusionsin
theUnitedStates&UKarecurrentlyleukocyte
reduced.494

Cont.
Advantages
•Reduces acute transfusion reactions.
•Reduces cytomegalovirus infection (CMV).
Disadvantages
•Cost: special blood packs and equipment are required
•More skill and operator training is needed.495

PRBCs transfusion guidelines
•Hemodynamicinstability:Ongoingbleedingwithunresponsive
(orincompletelyresponsive)toinfusionof2-3Literscrystalloid
•HemodynamicallyStable:
•ICUPatients:Hemoglobin<7g/dL
•Post-Operative:Hgb≤8g/dL
•CardiovascularDisease:Hgb≤8g/dL496

Cont.
•Dose:4ml/kgofRBCincreaseHemoglobinlevel1g/dl.
•Oneunitof RBCwillraisethehemoglobin
of an average-sizeadultby~1g/dl
•Transfuseslowlyforfirst15 minutes.
•Completetransfusionwithin4hours.497

3)Whitecells (leukocytes)
•Whitecelltransfusionshavenoprovenclinical
uses.
•Maybeindicatedinneutropenicpatientswith
bacterialinfectionsnotrespondingtoantibiotics.
•Transfusedgranulocyteshaveaveryshortcirculatory
lifespan,sothatdailytransfusionsof1010
granulocytesareusuallyrequired.498

4)Plasma
•Thisisseparatedfromwholebloodandfrozenat–25°Cor
colderwithin6–8hoursofdonationinordertopreserveits
labilecoagulationfactors(FactorsVandVIII).
•Freshfrozenplasmacanbestoredforatleastoneyearor
longeriflowtemperaturescanbemaintained.
•Whenplasmaisstoredatatemperatureof2–6°C,the
labileclottingactivityofFactorsVandVIIIwilldeclineto
10–20%within48hours.
•Dosage:Initialdoseof15ml/kg499

Indications for transfusion of plasma
Coagulopathy(INR)>1.5with:
1.Activebleeding.
2.Bleedingtendency:
•Anticipatedinvasiveprocedureorsurgery.
•Thecorrectionofcoagulopathyassociatedwithliverdisease.
•Emergentreversalofanticoagulant(warfarin)therapy.
•Treatmentofisolatedfactordeficiencies.500

5)Platelet
•Theplateletcountat1hourposttransfusionofaunitof
plateletsshouldincreaseby5,000to10,000platelets/µL.
•Plateletsseparatedfromplasmaobtainedfrom4–6
donationsofwholebloodareoftenpooledtoproducea
therapeuticdoseofplateletsforanadultplatelet
apheresisunit,by30,000–60,000×109/L.
•Dosage:1unitofplateletconcentrate/10kgbodyweight501

Indications for transfusion of platelets
ThrombocytopeniaorDysfunctionalplateletswith:
1.Activebleeding
2.Bleedingtendency
•Neurosurgicalprocedures:100,000platelets/µL
•Vaginaldeliveryandminorsurgicalprocedures:<50,000/µL
•Massivetransfusion:<50,000platelets/µL
•Disseminatedintravascularcoagulation:20,000–50,000/µL502

6.Cryoprecipitate
•CryoprecipitateisobtainedfromasingledonationofFFP
atabout4°CandisrichinfactorVIII,vonWillebrandfactor
(VWF),factorXIII,andfibrinogen.
•Each5-to15-mLunitcontainsover80unitsoffactorVIII
andabout200mgoffibrinogen.
•Cryoprecipitateisusuallyadministeredasatransfusionof
10singleunits.503

Indications for transfusion of cryoprecipitate
•Hemophilia A
•von Willebranddisease
•Hypofibrinogemia
•Uremic bleeding 504

Component separation by apheresis
•Apheresisisanalternativemethodofproducingblood
components.Itisasterileprocessinwhichadonoris
connectedtoaspecializeddevicebywhichbloodis
withdrawn,mixedwithanticoagulantandcentrifuged
andaspecificcomponent,usuallyplasmaorplatelets,
ismechanicallyseparatedandcollected.
•Theredcellsandothercomponentsofthebloodthat
arenotrequiredarethenreinfusedbackintothe
donor.505

Cont.
•Theadvantageofapheresisisthatrelativelylarge
amountsofplasmaorplateletscanbecollectedfrom
adonor.
•Sincetheredcellsarereturnedtothedonor’s
circulation,thisavoidsmakingthedonoranemicand
theprocesscanberepeatedatfrequentintervals.506

Blood Component Characteristic
Red Cells Platelet ConcentrateFresh Frozen
Plasma
Cryoprecipita
te
Storage
Temperature
2-6°C 20-24°C -30°C -30°C
Shelf Life
Volume
35 day
200-350
5 day
30-50 ml/unit
1 yr(frozen)
150-200ml/unit
1 yr(frozen)
10-15 ml/unit
Transfusion
Interval
Transfuse within 30
min of removal
from blood
refrigerator.
Transfuse unit over
maximum of 4 hr
Start transfusion as soon as
received from blood bank.
Transfuse unit within 30
min
Once thawed,
should be
transfused
within 4 hr
884 hr
Compatibility
Testing
Requirement
Must be compatible
with recipient ABO
and Rh D type
Preferably ABO identical
with patient.
Rh negative females under
the age of 45 yrshould be
given Rh negative platelets
FFP and cryoprecipitate
should be ABO compatible
to avoid risk of hemolysis
caused by donor anti-A or
anti-B
AdministrationInfuse through a blood administration set—platelet concentrates should not
be infused through blood sets that have been used for blood.507

Complications of Blood Transfusion
1)IMMUNEComplications.
2)INFECTIOUSComplications.
3)MASSIVEBLOODTRANSFUSIONComplications.508

Complications of Blood Transfusion
1)IMMUNEComplications
A.Hemolyticreactions
•Acutehemolyticreaction.
•Delayedhemolyticreaction.
B.Nonhemolyticreactions
•Febrilereactions •Urticarialreactions
•Anaphylacticreactions•Post-transfusionpurpura
•Transfusion-RelatedAcuteLungInjury
•Graft-versus-hostdisease509

Complications of Blood Transfusion
2)Infectious (all products)510

Complications of Blood Transfusion
3)Complicationsofmassivebloodtransfusion
–Coagulopathy
–Hypothermia
–Citrate Toxicity
–Hypervolemia
–Acid–Base Balance
–Serum Potassium Concentration511

1)Immune complications
•Acute hemolytic transfusion reaction: ABO incompatibility.
•Delayed HTR: incompatible red cell antigen.
•Febrile non-HTR: anti-WBC antibodies in recipient.
•Urticarial reactions: antibody to donor plasma proteins.
•Anaphylactic: antibody to donor plasma proteins (IgA).
•Transfusion-related acute lung injury (TRALI): neutrophil
antibodiesin donorproduct.
Sensitization of the recipient to donor red cells, white cells,
platelets, or plasma proteins. 512

A.Hemolytic Reactions
•Hemolyticreactionsusuallyinvolvespecificdestruction
ofthetransfusedredcellsbytherecipient’santibodies.
Lesscommonly,hemolysisofarecipient’sredcells
occursasaresultoftransfusionofredcellantibodies.
•Hemolyticreactionsarecommonlyclassifiedaseither
acute(intravascular)ordelayed(extravascular).513

AcuteHemolytic Reactions
•AcuteintravascularhemolysisisusuallyduetoABO
bloodincompatibility,andthereportedfrequencyis
approximately1:38,000transfusions.
•Themostcommoncauseismisidentificationofapatient,
bloodspecimen,ortransfusionunit.
•Thesereactionsareoftensevere,andmayoccurafter
infusionofaslittleas10–15mLofABO-incompatible
blood.
•Theriskofafatalhemolyticreactionisabout1in
100,000transfusions.
•Inawakepatients,symptomsincludechills,fever,nausea,
andchestandflankpain.514

Cont.
•Inanesthetizedpatients,anacutehemolytic
reactionmaybemanifestedbyariseintemperature,
unexplainedtachycardia,hypotension,hemoglobinuria,
anddiffuseoozinginthesurgicalfield.Disseminated
intravascularcoagulation,shock,andkidneyfailurecan
developrapidly.
•Theseverityofareactionoftendependsuponthevolume
ofincompatiblebloodthathasbeenadministered.515

Management of hemolytic reactions
1.Ifahemolyticreactionissuspected,thetransfusionshould
bestoppedimmediatelyandthebloodbankshouldbe
notified.
2.Theunitshouldberecheckedagainstthebloodslipandthe
patient’sidentitybracelet.
3.Bloodshouldbedrawntoidentifyhemoglobininplasma,
torepeatcompatibilitytesting,andtoobtaincoagulation
studies and a platelet count.
4.Aurinarycathetershouldbeinserted,andtheurine
should be checked for hemoglobin.
5.Osmoticdiuresisshouldbeinitiatedwithmannitoland
intravenousfluids.516

DelayedHemolytic Reactions
Alsocalledextravascularhemolysis,isgenerallymildandis
causedbyantibodiestonon-DantigensoftheRhsystemorto
foreignallelesinothersystemssuchastheKell,Duffy,orKidd
antigens.
FollowinganABOandRhD-compatibletransfusion,patients
havea1–1.6%chanceofformingantibodiesdirectedagainst
foreignantigensintheseothersystems.517

Cont.
•Thehemolyticreactionisthereforetypicallydelayed2–21days
aftertransfusion,andsymptomsaregenerallymild,consisting
ofmalaise,jaundice,andfever.
•Thepatient’shematocrittypicallyfailstorise,orrisesonly
transiently,inspiteofthetransfusionandtheabsenceof
bleeding.
•Theserumunconjugatedbilirubinincreasesasaresultof
hemoglobinbreakdown.518

Cont.
•Diagnosisofdelayedantibody-mediatedhemolyticreactions
maybefacilitatedbytheantiglobulin(Coombs)test.Thedirect
Coombstestdetectsthepresenceofantibodiesonthe
membraneofredcells.
•Pregnancy(exposuretofetalredcells)canalsoberesponsible
fortheformationofalloantibodiestoredcells.
•Thefrequencyofdelayedhemolytictransfusionreactionsis
estimatedtobeapproximately1:12,000transfusions.
•Thetreatmentofdelayedhemolyticreactionsisprimarily
supportive.519

B.Nonhemolytic Immune Reactions
•Nonhemolyticimmunereactionsaredueto
sensitizationoftherecipienttothedonor’swhite
cells,platelets,orplasmaproteins.
•Theriskofthesereactionsmaybeminimizedbythe
useofleukoreducedbloodproducts.520

B.Nonhemolytic Immune Reactions
1.Febrile Reactions:
•Whitecellorplateletsensitizationistypically
manifestedasafebrilereaction.
•Suchreactionsarerelativelycommon(1–3%oftransfusion
episodes)andarecharacterizedbyanincreaseintemperature
withoutevidenceofhemolysis.
•Patientswithahistoryofrepeatedfebrilereactionsshould
receiveleukoreducedtransfusionsonly.521

Cont.
2.Urticarial Reactions:
•Urticarialreactionsareusuallycharacterizedbyerythema,
hives,anditchingwithoutfever.
•Theyarerelativelycommon(1%oftransfusions)andare
thoughttobeduetosensitizationofthepatientto
transfusedplasmaproteins.
•Urticarialreactionscanbetreatedwithantihistaminic
drugs(H1andperhapsH2-blockers)andsteroids.522

Cont.
3.AnaphylacticReactions:
•Anaphylacticreactionsarerare(approximately1:150,000
transfusions).
•Theseseverereactionsmayoccurafteronlyafewmillilitersof
bloodhasbeengiven,typicallyinIgA-deficientpatientswith
anti-IgAantibodieswhoreceiveIgA-containingblood
transfusions.
•The prevalenceof IgA deficiencyis
estimatedtobe1:600-800inthegeneralpopulation.
•Suchreactionsrequiretreatmentwithepinephrine,fluids,
corticosteroids,andH1andH2blockers.523

Cont.
4.Transfusion-RelatedAcuteLungInjury(TRALI):
•(TRALI)presentsasacutehypoxiaandnoncardiacpulmonary
edemaoccurringwithin6hofbloodproducttransfusion.
•Itmayoccurasfrequentlyas1:5000transfusedunits,and
withtransfusionofanybloodcomponent,butespecially
plateletsandFFP.
•Itisthoughtthattransfusionofantileukocyticoranti-HLA
antibodiesresultsindamagetothealveolar–capillary
membrane.
•Treatmentissimilartothatforacuterespiratorydistress
syndromewiththeimportantdifferencethatTRALImay
resolvewithinafewdayswithsupportivetherapy.524

Cont.
5.Graft-Versus-HostDisease:
•Thistypeofreactionmaybeseeninimmunocompromised
patients.Cellularbloodproductscontainlymphocytescapable
ofmountinganimmuneresponseagainstthecompromised
(recipient)host.
•Useofspecialleukocytefiltersalonedoesnotreliably
preventgraft-versus-hostdisease;irradiation(1500–3000
cGy)ofredcell,granulocyte,andplatelettransfusions
effectivelyeliminateslymphocyteswithoutalteringthe
efficacyofsuchtransfusions.525

Cont.
6.Post-TransfusionPurpura:
•Rarely,profoundthrombocytopeniamayoccurfollowing
bloodtransfusions.
•Thispost-transfusionpurpuraresultsfromthedevelopment
ofplateletalloantibodies.
•Forunknownreasons,theseantibodiesalsodestroythe
patient’sownplatelets.
•Theplateletcounttypicallydropsprecipitously5–10days
followingtransfusion.
•TreatmentincludesintravenousIgGandplasmapheresis.526

Cont.
7.Transfusion-RelatedImmunomodulation:
•Allogeneictransfusionofbloodproductsmaydiminish
immunoresponsivenessandpromoteinflammation.
•Post-transfusionimmunosuppressionisclearlyevidentin
renaltransplantrecipients,inwhompreoperativeblood
transfusionimprovesgraftsurvival.527

2)INFECTIOUS COMPLICATIONS
A-ViralInfections:
Hepatitis:
•Theincidenceofpost-transfusionviralhepatitisvariesgreatly,from
approximately1:200,000transfusions(forhepatitisB)toapproximately
1:1,900,000(forhepatitisC).
AcquiredImmunodeficiencySyndrome(AIDS):
•TherequirementfornucleicacidtestingbytheFDAhasdecreasedthe
riskoftransfusion-transmittedHIVtoapproximately1:1,900,000
transfusions.528

Cont.
OtherViralInfections:
•Cytomegalovirus(CMV)andEpstein–Barrvirususuallycause
asymptomaticormildsystemicillness.
•Someindividualsinfectedwiththesevirusesbecome
asymptomaticinfectiouscarriers;thewhitecellsinbloodunitsfrom
suchdonorsarecapableoftransmittingeithervirus.
•Immunocompromisedpatients(eg,prematureinfants,organ
transplantrecipients,andcancerpatients)areparticularly
susceptibletoseveretransfusion-relatedCMVinfections.529

Cont.
B-BacterialInfections:
•Bacterialcontaminationofbloodproductsisthesecondleading
causeoftransfusion-associatedmortality.
•Theprevalenceofsepsisduetobloodtransfusionrangesfrom
1:25,000forplateletsto1:250,000forPRBCs.
•Toavoidthepossibilityofsignificantbacterialcontamination,blood
productsshouldbeadministeredoveraperiodshorterthan4h.
C-ParasiticInfections:
•Parasiticdiseasesthatcanbetransmittedbytransfusioninclude
malaria,toxoplasmosis,andChagas’diseasealthoughveryrare.530

531

Massive Blood Transfusion
Variousdefinitionsofmassivebloodtransfusion(MBT)have
beenpublishedinthemedicalliteraturesuchas:
•Replacementofoneentirebloodvolumewithin24h
•Transfusionof>10unitsofpackedredbloodcells(PRBCs)
in24h
•Transfusionof>20unitsofPRBCsin24h
•Transfusionof>4unitsofPRBCsin1hwhenon-goingneed
isprobable
•Replacementof50%oftotalbloodvolume(TBV)within3h.532

3)Complications of massive blood transfusion
•Coagulopathy
•Hypothermia
•Citrate Toxicity
•Hypervolemia
•Acid–Base Balance
•Serum Potassium Concentration533

Complications of massive blood transfusion
•Coagulopathy
Themostcommoncauseofnonsurgicalbleeding
followingmassivebloodtransfusionisdilutional
thrombocytopenia,althoughclinicallysignificantdilution
ofcoagulationfactorsmayalsooccur.
Coagulationstudiesandplateletcounts,ifreadily
available,shouldguideplateletandFFPtransfusion.534

BJA: British Journal of Anaesthesia, Volume 111, Issue suppl_1, December 2013, Pages i71–i82, https://doi.org/10.1093/bja/aet376
The content of this slide may be subject to copyright: please see the slide notes for details.
Pathogenesis of haemostasisabnormality in MT.
Dilutionalcoagulopathy, activation of inflammatory mediators.535

Cont.
Hypothermia
•Massivebloodtransfusionisanabsoluteindicationfor
warmingallbloodproductsandintravenousfluidsto
normalbodytemperature.
•Ventriculararrhythmiasprogressingtofibrillationoften
occurattemperaturescloseto30°C,andhypothermiacan
hampercardiacresuscitation.
•Theuseofrapidinfusiondeviceswithefficientheat
transfercapabilityhasdecreasedtheincidenceof
transfusion-relatedhypothermia.536

Cont.
Citrate Toxicity
•Becausecitratemetabolismisprimarilyhepatic,patientswith
hepaticdiseaseordysfunction(andpossiblyhypothermic
patients)maydemonstratehypocalcemiaandrequirecalcium
infusionduringmassivetransfusion,asmaysmallchildrenand
otherswithrelativelyimpairedparathyroid–vitaminD
function.
•Clinicallyimportanthypocalcemia,causingcardiacdepression,
willnotoccurinmostnormalpatientsunlessthetransfusion
rateexceeds1unitevery5min,andintravenouscalciumsalts
shouldrarelyberequiredintheabsenceofmeasured
hypocalcemia.537

Cont.
Acid–BaseBalance:
•Althoughstoredbloodisacidicduetothecitricacid
anticoagulantandaccumulationofredcellmetabolites(carbon
dioxideandlacticacid),metabolicacidosisduetotransfusionis
uncommonbecausecitricacidandlacticacidarerapidly
metabolizedtobicarbonatebythenormalliver.
•Inthesituationofmassivebloodtransfusion,acid-basestatusis
largelydependentupontissueperfusion,rateofblood
transfusion,andcitratemetabolism.
•Oncenormaltissueperfusionisrestored,anymetabolicacidosis
typicallyresolves,andmetabolicalkalosiscommonlyoccursas
citrateandlactatecontainedintransfusionsandresuscitation
fluidsareconvertedtobicarbonatebytheliver.538

Cont.
SerumPotassiumConcentration:
•Theextracellularconcentrationofpotassiuminstoredblood
steadilyincreaseswithtime.Theamountofextracellular
potassiumtransfusedwitheachunitistypicallylessthan4
mEqperunit.
•Hyperkalemiacandevelopregardlessoftheageofthe
bloodwhentransfusionratesexceed100mL/min.
•Hypokalemia is commonly encountered
postoperatively,particularlyinassociationwithmetabolic
alkalosis.539

540

Compatible fluids and medications
•Nomedicationsorsolutionsshouldbeaddedtoorinfused
throughthesametubingasbloodproductsexceptfor0.9%
SodiumChloride,ABOcompatibleplasmaor4%Albumin.
•Ithasbeenshowntobesafetoco-administermorphine
(1mg/mL),pethidine(10mg/mL)andketamine(1mg/mL)if
dilutedin0.9%SodiumChloridewithredcells.Inthese
situations,thebloodproductshouldbeadministeredviathe
closesttothepatient(distallumen).541

Cont.
•Ifothermedicationsarerequiredduringabloodtransfusion,the
transfusionmustbestoppedandthelineflushedwith0.9%
SodiumChloridebeforeandafteradministrationofthe
medication.Thebloodtransfusioncanthenrecommence.
•Fluidscontainingglucosearenotcompatiblewithredblood
cells,theycauseclumpingoftheredbloodcells.
•Crystalloidorcolloidsolutionsthatcontaincalciumshouldnever
beadministeredconcurrentlywithanybloodproduct.Calcium
reversestheanticoagulantcitratecausingredbloodcellstoclot.542

References
•MorganandMikhail'sClinicalAnesthesiology,6th
edition
•TheClinicalUseofBlood-WorldHealthOrganization
•Uptodate.com2019543

12)Disorders of consciousness
& Traumatic Brain Injury
Critical Care
Hani Sammour, MD, PB
Anesthesia and IC, Shifahospital544

Definitions
•Mentality:interactionwithenvironment.
•MentalityconsistsofConsciousness&Cognition
•Mentalfunctionisconsiderednormalwhen
Consciousness&Cognitionstateareintact.545

Definitions
•Consciousness:Awarenessofselfandsurroundings,ithas
twocomponents:arousal(wakefulness)andawareness
(responsiveness).
•Cognitionconsistsof:
A.SensoryinputandOrientation:abilitytoaccuratelyperceive
whatisexperienced.
B.Memory:abilitytostoreandretrieveinformation.
C.JudgmentandReasoning:abilitytoprocessinputdatato
generatemoremeaningfulinformation.546

Other Definitions
•Vegetativestate:arousal(eyesopen)withnoawareness,
Spontaneousmovementscanoccurbutarepurposeless.
•Coma:absenceofarousalandawareness,itisastateof
unarousableunawareness.
•Braindeathissimilartocomainthatitisastateof
unarousableunawarenessbutisirreversible,andis
accompaniedbycessationofallfunctionsofthebrain,
includingthebrainstem.547

Levels of Consciousness
Conscious
–Awake:arousedandaware
–Somnolent:easilyarousedandaware
–Stuporous:arousedwithdifficulty,impairedawareness
Unconscious
–Comatose:unarousableandunaware
–Vegetativestate:arousedbutunaware548

Delirium
•Deliriumisacognitivedisordercharacterizedby
attentiondeficits,andeitherdisorderedthinkingor
analteredlevelofconsciousness.
•Thehallmarkofdelirium(andthefeaturethat
distinguishesitfromdementia)isitsacuteonsetor
fluctuatingclinicalcourse.549

Brain death
•Perquisites for brain death test:
–Core body temperatureis greater than 34°C
–Drug intoxicationmust be excluded
–No any residual neuromuscular block or sedation.
–No metabolic or endocrine disturbances.
–No improvementoccursin neurological examination over
24 hours550

Brain death
The criteria for determining brain death:
1)IrreversibleComa,unresponsiveabovetheforamenmagnum
tostimuli.Peripheralspinalreflexesmaystillbepresent.
2)Apneaoffventilatorforaperiodsufficienttoproduce
hypercarbicrespiratorydrive(usuallydefinedasaPaCO
2of50-
60mmHg).
3)Absentbrainstemreflexes,includingpupillary,corneal,
oculocephalic(Doll’seyes),oculovestibular(Calorictest),gag
andsucking551

Brain death
•Confirmatory diagnostic tests may be performed to
determine brain death:
–EEG
–Cerebral perfusion studies by MRI, CT.
–Transcranialdoppler
–Brain stem-evoked potentials552

Causesof altered consciousness
•Traumatic: head injury
•Vascular:
–Cerebral thrombosis
–Cerebral hemorrhage (ICH, SAH)
–Hypertensive encephalopathy
•Brain tumor or space occupying lesion (SOL)
•CNS infection: encephalitis, abscess
•Epilepsy & postictal state553

Causes of altered consciousness
•Organ failure:
–Hepatic coma
–Renal (Uremic) coma
–Respiratory coma (CO2 narcosis)
•Metabolic:
–Hyperglycemia, Hypoglycemia
–Hypernatremia, Hyponatremia
–Hyperthermia, Hypothermia
–Myxedema coma
•Intoxication: drugs, sedatives, alcohol, etc. 554

Sources of altered consciousness in ICU patients555

Coma scoring guides
Examining sensory response, motor response
–AVPU score: rapid rough assessment of response of patient:
▪Alertresponsivepatient
▪Voiceresponsivepatient
▪Painresponsivepatient
▪Unresponsivepatient
–Glasgow Coma Score (GCS)556

Glasgow coma score (GCS)
1-6Motor response
6Spontaneous, followscommands
5Localizespain
4Withdrawaltopain
3Decortication,abnormalflexion
2Decerbration,abnormalextension
1None
•Puts the patient coma score between 3 & 15.
•Score < 8 indicates severe neurological dysfunction.
•Score < 8 is an indication for intubation.
•Intubation abolishes the verbal response.
•Sedation is a limitation to the use of GCS.
•Does not examine the brainstem reflexes.557

1-5Verbal response
5Oriented,coosandbabbles
4Confused,irritablecry
3Inappropriatewords,Criestopain
2Inappropriatesounds,moanstopain
1None
· 1-4Eye response
4Spontaneous
3Tospeech
2Topain
1None558

Take Care
Unconsciousness = Immediate Life Threat
•Loss of airway
•Aspiration
Treatment may be needed before diagnosis
•Airway
•Breathing
•circulation559

Care of the unconscious patient
Airway and cervical spine
•Whateverthecauseofcoma,apatientmaydieor
sufferbraindamageduetoairwayobstruction,
respiratorydepression,orcirculatoryfailure.
•Clearandprotecttheairwayimmediately.
•Movetheneckaslittleaspossible.560

Care of the unconscious patient
Breathing
•Look, listen, feel
•If breathing inadequate ventilate with O2 using ambu-bag
•Intubation may be needed
•Record respiratory rate
Circulation
•Measure pulse and BP
•Observe and feel the skin for color, sweating and temperature.
•Obtain venous access
•Attach ECG monitor561

Care of the unconscious patient
Conscious level
•Assess level of consciousness using GCS
•Check the blood glucose
•Treat hypoglycemia immediately
•Record pupil size562

History
How was the patient found
•When was he/she last seen.
•Is there any suggestion of trauma.
•Is there any history of fits.
•Recent foreign travel.
•Previous medical history.
•Note any drug available.
•Check previous electrolytes. 563

Examination (airway &breathing)
•Ifrespiratoryrateincreasedconsiderairwayobstruction,
aspiration,pneumonia,DKA,hepatic/renalfailure,
poisoningbysalicylatesormethanol.
•Respiratorydepressionmaybeduetopoisoning(opioids,
barbiturates).
•Rapidorirregularbreathingmaybeduetobrainstem
compressionordamagebystroke.564

Examination (circulation)
•Ifbradycardiaconsiderhypoxia,completeheartblock,
increasedICP,digoxinorbeta-blockerspoisoning.
•Iftachycardiaconsiderairwayobstruction,hypoxia,
hypovolemia,SVT,VToranticholinergicoverdose.
•Hypotension:suggestshypoxia,shockorpoisoning.
•Hypertension:maybeduetoincreasedICP.
•Skin:lookforpallor,cyanosis,jaundice,rash,injection
marks,signsoftrauma.565

Examination (neurological)
•Measurecoretemperature(Comaiscommonat<30C)
•Neurologicalexamination:includeGCS,muscletone,
reflexes,neckstiffness,pupilsandlateralizingsigns
(stroke,intracerebralhemorrhage).
•Hypoglycemiamaycauseweaknessandcoma.
•Comawithoutlateralizingsignsmaybecausedby
poisoning,brainstemstroke.566

Examination (neurological)
•Comawithdilatedpupils,increasedmuscletone,severe
muscleflaccidityandrespiratorydepressionmaybe
causedbyTricyclicantidepressant.
•Comawithsmallpupilsandrespiratorydepression
suggestsOpioidspoisoning.
•Inunexplainedcoma,consideratherapeutictrialof
naloxone(0,4mgiv).567

Investigations
•Bloodglucoseineveryunconsciouspatient
•ABGs
•Electrolytes
•ECG
•CXR
•CTtodiagnosesubarachnoidhemorrhage,strokeorhead
injury
•Checkparacetamolandsalicylatelevelsifpoisoning
suspected568

Management of coma
•Keeppatentairway.Give100%oxygenforcyanosed
respiratorydistressedpatient.
•Mechanicalventilationforhypoventilatingorapneic
patient.
•Fluidtherapyandinotropicdrugsforshockedpatient.
•Bloodtransfusionforbleedingpatient.
•Glucoseforsuspectedhypoglycemia.
•Antidotesandothermeasures forsuspected
poisoning.569

Management of coma
•Cooling measures for hyperthermic patient.
•Rewarming measures for hypothermic patient.
•Correction of acid base status.
•Correction of metabolic abnormalities.
•Anticonvulsive agents for convulsions.
•Antihypertensive agents for hypertension.
•Measures to control elevated intracranial pressure.
•Surgical consultation for suspected trauma.570

Secondary coma care
–Eyedrops,ointments,orshieldstopreventcorneal
dryness,ulcerationorinfections.
–Oralantifungaldropstopreventoralcandidiasis.
–Nasogastrictubetodeflatestomach,toprevent
aspiration,toputmedicationsortofeed.
–Antacidstopreventstressulcer.
–HeparintopreventthrombosisifcontraindicatedputPLC.
–Foley'scathetertopreventurinaryretention.
–Laxativestopreventfecalimpaction.571

Status epilepticus
•Statusepilepticusisasevereformofseizureactivity
lastingmorethan30minutes(orsustainedtonic
clonicconvulsionmorethan5minutes)orrecurrent
seizureswithfailuretorecoverconsciousness
betweenrepeatedattacks.572

Goals of treatment
–Initial stabilization.
–Terminate seizure activity.
–Prevent seizure recurrence.
–Establish a diagnosis and initiate therapy for
treatable causes.573

Initial stabilization
•Establish airway, apply oxygen and ventilation.
•Establish IV access and take samples for initial
studies:
•Electrolytes
•Random blood sugar574

Termination of seizure
•First line (benzodiazepines):
–Diazepam, Lorazepam or Midazolam
–Benzodiazepines dose may be repeated every 10 minutes
up to 2 doses
* Monitor respiration
•Second line (phenytoin & phenobarbitone):
–Phenytoin: loading 15-20 mg/kg over 20 min :
* Monitor HR and BP, (repeat half loading if needed).
–Phenobarbitone: loading 15 -20mg/kg over 20 min
* Monitor HR, BP and respiration
•Third line: (ICU)For refractory status epilepticus:
–Propofol1-4mg/kg/hr, if no response:
–Pentothal infusion: 1-3 mg/kg/hr
* Monitor HR, BP and keep on MV575

Traumatic Brain Injury (TBI) management
•Securingtheairway(maintainingcervicalspineprecautions),achieving
adequateoxygenationandventilation,andavoidingorrapidlytreating
hypotension.
•InsevereTBI,Orotrachealintubationallowsairwayprotectionin
patientswhoareseverelyobtundedandallowsbettercontrolof
oxygenationandventilation.
•Vitalsignsincludingheartrate,BP,respiratorystatus(pulseoximetry,
capnography),andtemperaturerequireongoingmonitoring.
•Hypoxiahypoventilation,hyperventilation,andhypotensionare
aggressivelyavoided.
•Minimizethecerebralmetabolicrateofoxygenconsumption.576

TBI management
•Headofbed(HOB)elevationto30°topermitadequatevenous
drainagefromthebrainwhilenotcompromisingcerebralperfusion.
•Keepingtheneckinneutralpositiontooptimizevenousdrainage.
•Inmechanicallyventilatedpatients:fullsedationandanalgesia±
paralysisifrequired.
•Aimlungprotectiveventilation.
•TargetPaCO235-40mmHg
•Avoidroutinehyperventilation,exceptincriticalsituationswhenit
maybeneededto“buytime”(e.g.priortotheatreorCTscan).577

TBI management
•Fluidandhemodynamicmanagement:usenormalsalinerather
thanotherfluidsorcolloidsolutionstomaintaineuvolemia.
•Fever(>38°C)andhyperglycemia(>180mg/dl)shouldbeavoided
fortheirpotentialtoexacerbatesecondaryneurologicinjury.
•Coagulopathyshouldbecorrectedtomaintainaninternational
normalizedratio(INR)<1.4andaplateletcount>75,000/mm3.
•Nutritionalsupporttocaloricgoalsshouldbeachievedbyday5from
injuryusingenteralnutrition.578

TBI management
•Seizurepreventionandtreatment:werecommendone-weekuseof
antiseizuremedicationstopreventearlyseizures.
•Patientswithseizuresshouldbetreatedtopreventrecurrence.Inthe
absenceofseizurerecurrence,antiseizuremedicationsaregenerally
continuedthroughoutthehospitalstay.
•Levetiracetamcanbeusedforpreventionandtreatmentofseizures,
phenytoin(4-7mg/kg/daydividedinto2doses)canbeprovided
parenterallyasareasonablealternative(itdoesn’tcausesignificant
sedationandcanbeloadedintravenously).579

TBI management, hyperosmolar therapy
•InpatientswithelevatedICP,useaninfusionof3%NaClto
achieveasodiumgoalof145to155mEq/L.
•TotreatacuteICPelevation,canusesupplemental30mL
bolusdosesof23.4%NaCl,administeredover10minutes
•Mannitol(0.25-1g/kg/6hrasneeded)isanacceptable
alternative(speciallyinimpendingcerebralherniationor
progressiveneurologicaldeterioration).
•Hypertonicsalinemayhaveanadvantageovermannitolin
hypovolemicpatientsandiftheblood-brainbarrierisdamaged.580

TBI management
•Venousthromboembolism(VTE)prophylaxis,we
recommend mechanicalthromboprophylaxiswith
intermittentpneumaticcompressionforthepreventionof
VTE.
•Theuseandtimingofantithromboticagentsis
individualizedbaseduponanassessmentofthecompeting
risksofvenousthrombosisandintracranialhemorrhage
expansion.581

Stepwise management of elevated ICP in patients with
severe TBI (GCS<9)
Tier Zero: Standard measures
Endotracheal intubation and mechanical ventilation
Head-of-bed elevation >30 to 45 degrees
Temperature <38°C
pO2>65 to 70 mmHg
pCO2 35 to 40 mmHg
Serum sodium >135 to 140 mEq/L
TierOne:InitialtreatmentofelevatedICP
Analgesia-based sedation (fentanyl bolus and infusion) to
RASS goal 0 to -2
AddpropofolinfusiontoRASSgoal0to-2ifsedationorICPgoalnotmetwithopioidinfusion
alone
DrainCSFfromexternalventriculardrain;avoidoverdrainage
Hyperosmolartherapywithhypertonicsaline(goalsodium145to150mEq/L)ormannitol
Goals:
ICP <22mmHg
CPP >60mmHg
PbtO2>20mmHg582

Stepwise management of elevated ICP in patients with
severe TBI (GCS<9)
Tier Two: Persistent elevated ICP despite initial therapy
Repeat CT brain to identify surgically correctable pathology
Increase treatment with hypertonic saline to sodium goal 150 to 160 mEq/L
Deep sedation with propofol to goal RASS-5
Increase CPP to >70 mmHg if autoregulation is preserved
Increase FiO2 if required for Pbt02 goal
Tier Three: Refractory elevated ICP
Repeat CT brain to identify surgically correctable pathology
Decompressive craniectomy
Alternatives to decompressive craniectomy
•Barbiturate coma
•Therapeutic hypothermia to 32 to 34°C583

13)Sedation in ICU &
Pain, Agitation, and Delirium
(PAD) Care
Hani Sammour, MD, PB
Anesthesia and IC, Shifahospital
Critical Care 584

ICU Liberation Bundle (ABCDEF Bundle)585

Benefits of the ABCDEF Protocol586

The ICU Liberation Bundle
•Decreasethelikelihoodofhospitaldeathwithin
sevendaysby68%
•Reducedeliriumandcomadaysby25%-50%
•Reducephysicalrestraintusebymorethan60%
•CutICUreadmissionsinhalf
•Reducedischargestonursinghomeand
rehabilitationfacilitiesby40%587

Majorityofcriticallyillpatientsexperiencesignificantdistress,
anxiety,andagitationduringtheirintensivecareunitstays.
Numerousfactors,includingsleepdeprivation,unfamiliar
environment,delirium,adversemedicationeffect,pain,and
extremeanxietycancontributetoICUpatientdistress.
Introduction 588

IntensivistsoftenemployvarioussedativeagentstorelieveICU
associateddistressandpreventsecondarycomplicationsof
suchdistress.
Thereareavarietyofpharmacologicagentsusedforthis
purpose,includingbenzodiazepines,propofol,antipsychotic
agents,andalphaagonists.589

Importantpathophysiologicmechanismsassociatedistress
includesignificantincreasesincatecholamines,cortisol,growth
hormone,vasopressin,prolactin,glucagon,fattyacids,and
proteincatabolism.
Clinicallysignificantsequelaeofthisphysiologicdysregulation
includefluidandelectrolyteimbalances,alteredwoundhealing,
anddisturbancesofthesleepwakecycles.590

Complexity of PAD591

Pain
“An unpleasant sensory and emotional experience
associated with actual or potential tissue damage”
Disease
Invasive
Devices
Immobility
Routine
Care
Complications
Chronic pain Stress
Sleep-loss
Hyper-
metabolism
Impaired
wound healing
Impaired
immune
function
Feelings of
Helplessness
Post-traumatic
stress disorder
Causes592

Assessment of Pain
Question:Can pain be accurately assessed in the ICU?
Obstacles:
•Subjective, differs between individuals
•Self-reporting = GOLD standard
Behavioral Pain Scale (BPS)
Critical Care Pain Observation
Tool (CPOT)593

11
Options for Pain
•Acute painIV Opioids
•Neuropathic pain
Gabapentin
Carbamazepine
•Non-neuropathic pain
NSAIDS
Acetaminophen
Ketamine594

12
Pain -Summary
➢Guideline Statement:“We suggest that pain be
routinely monitored in all adult ICU patients.”
➢Guideline Statement: “We recommend that IV opioids
be considered as the first-line drug class of choice to
treat non-neuropathic pain…”
➢Guideline Statement: “Analgesia-first sedation should
be used in mechanically ventilated adult ICU patients…”595

Review Question -1
1. Among those listed, which medication is the preferred
option for acute pain in the ICU?
A.Ketamine
B.Acetaminophen
C.Morphine
D.Ketorolac596

14
Agitation
“A syndrome of excessive motor activity, usually non-
purposeful and associated with internal tension”
Pain Hypoxia
WithdrawalHypoglycemia
Delirium Hypotension
Causes597

Correctable Causes of Agitation
•Full bladder
•Uncomfortable bed position
•Inadequate ventilator flow rates
•Mental illness
•Uremia
•Drug side effects
•Disorientation
•Sleep deprivation
•Noise
•Inability to communicate598

Medications Associated With Agitation in ICU Patients
Antibiotics
Acyclovir Amphotericin B
Cephalosporins Ciprofloxacin
Imipenem–cilastatin Ketoconazole
Metronidazole Penicillin
Rifampin Trimethoprim –Sulfamethoxazole
Anticonvulsants
Phenobarbital Phenytoin
Cardiac Drugs
Captopril Clonidine
Digoxin Dopamine
Labetalol Lidocaine
Nifedipine Nitroprusside
Propranolol Quinidine Sulfate
Corticosteroids
Dexamethasone Methylprednisolone
OpioldAnalgesics
Codeine Meperidine
Morphine Sulfate
Miscellaneous Drugs
Anticholinergics Benzodiazepines
Hydroxyzine Ketamine
Metoclopramide Nonsteroidalanti –inflammatory drugs
Theophylline599

Drugs for Sedation
Benzodiazepines
Propofol
Dexmedetomidine600

18
Options for Sedation
MidazolamPropofolDexmedetomidine
Amnesia X X
Analgesia X
Anticonvulsion X X
Antiemesis X
Anxiolysis X X
Hypnosis X X
Sedation X X X
Bradycardia X
Hypotension X X X
Respiratory
Depression
X X601

19
Agitation -Summary
➢GuidelineStatement:“Maintaininglightlevelsofsedationin
adultICUpatientsisassociatedwithimprovedclinical
outcomes.”
➢GuidelineStatement:“Werecommendeitherdailysedation
interruptionoralighttargetlevelofsedationberoutinely
usedinmechanicallyventilatedadultICUpatients.”
➢GuidelineStatement:“Theuseofsedationscales,sedation
protocolsdesignedtominimizesedativeuse,andtheuseof
nonbenzodiazepinemedicationsareassociatedwith
improvedICUpatientoutcomes.”602

Review Question -2
2. Deep sedation in the ICU is associated with which of the
following outcomes?
A.Increased ICU length of stay
B.Increased mortality
C.Both A and B
D.None of the above603

21
Delirium
Acute Change or
Fluctuation in Mental
Status
Inattention
Disorganized Thinking
Altered Level of
Consciousness
Delirium
OR
“Sudden,severe
confusionand
rapidchangesin
brainfunction
thatoccurwith
physicalormental
illness.”
&
&604

Delirium
Complications
Increased LOSIncreased cost
Increased time
on ventilator
Agitation
Long term
cognitive deficits
Mortality605

Significance of ICU Delirium
❑Seenin>50%ofICUpatients
❑Threetimeshigherriskofdeathbysixmonths
❑Fourtimesgreaterfrequencyofmedicaldeviceremoval
❑Fivetimesmoreventilatordays
❑Ninetimeshigherincidenceofcognitiveimpairmentat
hospitaldischarge606

Delirium
Assessedvia:
•ConfusionAssessmentMethod(CAM-ICU)
•IntensiveCareDeliriumScreeningChecklist
(ICDSC)607

Delirium –Risk Factors
At Baseline
(Non-Modifiable)
During Stay
(Modifiable)
Dementia or CNS diseases Pain
Hypertension Benzodiazepines
Metabolic derangement
or Alcoholism
Narcotics
Higherseverity of illness Immobility
Age Sleep deprivation
Substances (withdrawal as well as
direct effect)
Infection608

Delirium Treatment
➢Correctincitingfactor
➢NotreatmentFDAapproved
➢GuidelineStatement:“Thereisnopublishedevidence
thattreatmentwithhaloperidolreducestheduration
ofdelirium.”
➢GuidelineStatement:“Atypicalantipsychoticsmay
reducethedurationofdelirium.”(LevelC)609

Delirium Prevention
➢GuidelineStatement:“Benzodiazepineusemaybe
ariskfactorforthedevelopmentofdelirium”
➢GuidelineStatement:“We recommend
performingearlymobilizationtoreducethe
incidenceanddurationofdelirium”
➢GuidelineStatement:“Weprovideno
recommendationforapharmacologicdelirium
preventionprotocol”610

Review Question -3
3.The2013PADguidelinesrecommendwhichofthe
followingagentsforpreventionofdelirium?
A.Haloperidol
B.Lorazepam
C.Ziprasidone
D.Noneoftheabove611

2018 SCCMPADIS guidelines612

613

Spontaneous Awakening Trial
SAT reduced ventilator time by = 2 days614

Spontaneous Breathing Trial
SBT reduced weaning time by = 2 days615

Parameters Indicating Readiness to Wean
1.Underlying cause for mechanical ventilation resolved
Improved chest x-ray
Minimal secretions
Normal breath sound
2.Mental readiness (conscious & can protect his A/W)
3.Hemodynamic stability:
Adequate cardiac output
Absence of hypotension
Minimal vasopressor therapy616

Parameters Indicating Readiness to Wean
4.Adequate oxygenation & ventilation:
Adequate resp. muscle strength
PaO2 >60 mmHg with FiO2 < 0.5
PCO2 <50 mmHg
RR<30 /min
Spontaneous TV > 5ml /kg
Minute ventilation < 10 L/min
PEEP < 8 cm H2O
Pressure support < 8 cm H2O617

Parameters Indicating Readiness to Wean
5.Absence of factors that impair weaning
Infection
Anemia
Hypokalemia
Sleep deprivation
Pain
Abdominal distention618

Sedation in ICU619

Goals of Sedation in ICU
•Patientcomfort
•Controlofpain
•Anxiolysisandamnesia
•Bluntingadverseautonomicandhemodynamicresponses
•Facilitatenursingmanagement
•Facilitatemechanicalventilation
•Avoidself-extubation
•Reduceoxygenconsumption
•TreatmentorDiagnosticprocedures620

Characteristics of an ideal sedation
agents for the ICU
•Lack of respiratory depression
•Analgesia, especially for surgical patients
•Rapid onset, titratable, with a short elimination half-time
•Sedation with ease of orientation and arousability
•Anxiolytic
•Hemodynamic stability621

The Challenges of ICU Sedation
•Assessment of sedation
•Altered pharmacology
•Tolerance
•Delayed emergence
•Withdrawal
•Drug interaction622

Sedation
SedativesCauses for Agitation623

Incidence of Inadequate Sedation624

Complications of Under/Over Sedation
Undersedation
Sedatives
Causes for Agitation
Agitation & anxiety
Pain and discomfort
Catheter displacement
Inadequate ventilation
Hypertension
Tachycardia
Arrhythmias
Myocardial ischemia
Wound disruption
Patient injury
Patient recall (PTSD)625

AGITATED PATIENT626

Complications of Under/Over Sedation
Oversedation
Sedatives
Causes for Agitation
Prolonged sedation
Delayed emergence
Respiratory depression
Hypotension
Bradycardia
Increased protein breakdown
Muscle atrophy
Pressure injury
Loss of patient-staff interaction
Increased LOS
Increased risk of complications
(VAP & VTE)627

Strategies for Patient Comfort
•Set treatment goal
•Quantitate sedation and pain
•Choose the right medication
•Use combined infusion
•Reevaluate need
•Treat withdrawal628

Daily Goal is Arousable, Comfortable Sedation
Sedation needs to be protocolizedand
titrated to goal:
•Lighten sedation to appropriate wakefulness daily.
Effect of this strategy on outcomes:
•One-to seven-day reduction in length of sedation and
mechanical ventilation needs
•50% reduction in tracheostomies
•Three-fold reduction in the need for diagnostic evaluation of
CNS629

Protocols and Assessment Tools
Titration of sedativesand analgesicsguided by
assessment tools:
•Validated Sedation assessment tools:
•Ramsay Sedation Scale [RSS].
•Richmond Agitation Sedation Scale [RASS].
•Sedation-Agitation Scale [SAS] etc.).
No evidence that one is preferred over another
•None validated in ICU Pain assessment tools:
•Numeric Rating Scale [NRS],
•Visual Analogue Scale [VAS], etc.)630

Sedation Scales
Very useful, very underused631

What Sedation Scales Do
•Provide a semiquantitative“score”
•Standardize treatment endpoints
•Facilitate sedation studies
•Help to avoid oversedation632

What Sedation Scales Don’t Do
•Assess anxiety
•Assess pain
•Assess sedation in paralyzed patients
•Predict outcome633

1)Ramsay Sedation Scale 634

SedationshouldbetargetedtoaRamsay
scoreof2to3.
Manylevelsofsedationandnolevelsof
agitation635

2)Richmond Agitation Sedation Scale636

Level Behaviors
7 Dangerous agitation pulls at endotracheal tube, tries to remove catheter
climbs over bed rail , strikes at staff, thrashes side -to –side.
6 Very agitated . Does not calm , despite frequent verbal reminders;
requires verbal reminding of limits, physical restraints; bites
endotracheal tube.
5 Agitated , Anxious or mildly agitated , attempts to sit up, calms down to
verbal instructions.
4 Calm and cooperative. Calm , awakens easily, follow commands
3 Sedated. Difficult to arouse, awakens to verbal stimuli or gentle shaking
but drifts off again, follows simple commands
2 Very sedated. Arouses to physical stimuli but does not communicate or
follow commands, may move spontaneously
1 Unarousable. Minimal or no response to noxious stimuli, does not
communicate or follow commands.
3)Sedation –Agitation Scale (SAS)
The SAS is scored from 1 (unarousable) to 7 (dangerous agitation)637

Choose the Right Drug
Sedation Analgesia
Amnesia AnxiolysisHypnosis638

Sedation Options:
Benzodiazepines (Midazolam and Lorazepam)
Pharmacokinetics/dynamics
•Lorazepam: onset 5 -10 minutes, half-life 10 hours,
•Midazolam: onset 1 -2 minutes, half-life 3 hours, active metabolite
•Accumulates in renal disease
Benefits
•Anxiolytic
•Amnestic
•Sedating
Risks
•Delirium
•NO analgesia
•Excessive sedation: especially after long-term sustained use
•Respiratory failure (especially with concurrent opiate use)
•Withdrawal639

Benzodiazepines
PeaksDurationOnset
5-30 min>20 hr2-5 minDiazepam
5-10 min30-120 min2-3 minMidazolam
30 min10-20 hr5-20 minLorazepam640

Sedation Options: Propofol
Pharmacokinetics/dynamics: onset 1 -2 minutes, terminal
half-life 6 hours, duration 10 minutes, hepatic metabolism
Benefits
•Rapid onset and offset and easily titrated
•Hypnotic and antiemetic
•Can be used for intractable seizures and elevated intracranial
pressure
Risks
•Not reliably amnestic, especially at low doses
•NO analgesia!
•Hypotension
•Hypertriglyceridemia; lipid source (1.1 kcal/ml)
•Respiratory depression
•PropofolInfusion Syndrome
-Cardiac failure, rhabdomyolysis, severe metabolic acidosis, and renal
failure
-Caution should be exercised at doses > 5mg/kg for more than 48 hours
-Particularly problematic when used simultaneously in patient receiving
catecholaminesand/or steroids641

Propofol
Onset PeaksDuration
Propofol 30-60
sec
2-5 min short642

PropofolDosing
•Antiemetic:0.2-0.3mg/kg/hr
•Anxiolytic:0.25-1mg/kg/hr
•Sedative,hypnotic:20-50g/kg/min
(Commonpractice1-4mg/kg/hr)
•Anesthetic:>6mg/kg/hr643

Opiate and Benzodiazepine Withdrawal
Frequencyrelatedtodoseandduration
•32%ifreceivinghighdosesforlongerthanaweek
Onsetdependsonthehalf-livesoftheparentdruganditsactive
metabolites
Clinicalsignsandsymptomsarecommonamongagents
•CNSactivation:seizures,hallucinations,
•GIdisturbances:nausea,vomiting,diarrhea
•Sympathetichyperactivity:tachycardia,hypertension,tachypnea,sweating,
fever
Noprospectivelyevaluatedweaningprotocolsavailable
•10-20%dailydecreaseindose
•20-40%initialdecreaseindosewithadditionaldailyreductionsof10-20%644

Treat Withdrawal
•Acute management
•Resume sedation
•Beta-blockade, dexmedetomidine
•Prolonged management
•Methadone 5-10 mg Tab bid
•Clonidine 0.1-0.2 mg Tab q8h
•Lorazepam1-2 mg IV q8h645

Sedation Options: Dexmedetomidine
Alpha-2-adrenergic agonist like clonidine
Has been shown to decrease the need for other sedation in postoperative
ICU patients
Potentially useful while decreasing other sedatives to prevent withdrawal
Benefits
•Does not cause respiratory depression
•Short-acting
•Produces sympatholysiswhich may be advantageous in certain patients
Risks
•No amnesia
•Bradycardiaand hypotension can be excessive646

Indications
•Intensive Care Unit Sedation
•Sedation of initially intubated and mechanically ventilated,
postsurgicalpatients during treatment in an intensive care
setting by continuous intravenous infusion.
•It has been continuously infused in mechanically ventilated
patients prior to extubation, during extubation, and post-
extubation. It is not necessary to discontinue the drug prior to
extubation.
•Conscious Sedation
•Sedation of non-intubated patients prior to and/or during
surgical and other proceduresby continuous intravenous
infusion.647

Dosage
IntensiveCareUnitSedation
•Initiation-Loadinginfusionofupto1mcg/kgover10to20minutes.
•Maintenance-Adultsgenerallyrequireamaintenanceinfusionof0.2-0.7
mcg/kg/hr.
ConsciousSedation
•Clinicallyeffectiveonsetofsedation10to15minutesafterstartofinfusion
•Initiation-Loadinginfusionof1mcg/kgover10minutes.Forpatientsover65
yearsofageorthoseundergoinglessinvasiveprocedures,aloadinginfusion
of0.5mcg/kgover10minutesmaybesuitable
•Maintenance-Generallyinitiatedat0.6mcg/kg/hrandtitratedfrom0.2to1
mcg/kg/hr648

Case Scenario: 1
22-year-old male with isolated closed head injury who was intubated
for GCS of 7
He received 5 mg of morphine, 40 mg of etomidate, and 100 mg of
succinylcholine for his intubation.
He is covered in blood spurting from an arterial catheter that was
just removed, and he appears to be reaching for his endotracheal
tube.
What sedative would you use and why?
What are the particular advantages in this situation?
How could you avoid the disadvantages of this drug?649

Case Scenario:1 -Answer
Propofolwill rapidly calm a patient who is displaying dangerous
behavior without need for paralysis.
Titratableand can be weaned quickly to allow for neurologic exam
Can treat seizures and elevated ICP which may be present in a head
trauma with GCS of eight or less
Minimizing dose and duration will avoid side effects.650

Case Scenario: 2
62-year-old, 65-kg woman with ARDS from aspiration pneumonia
Her ventilator settings are VC 400, RR 18, PEEP 8, and FIO
2100%. She is
dyssynchronouswith the ventilator and her plateau pressure is 37 mm
Hg.
She is on propofolat 3 mg/kg/hr, which has been ongoing since admit
four days ago.
She is also on norepinephrine 0.1 mcg/kg/min and she was just started
on steroids.
What do you want to do next?
Do you want to continue the propofol?
Why or why not?
What two iatrogenic problems is she likely at risk for?651

Case Scenario: 2 -Answer
Thispatientneedsoptimizationofhersedatives,andpotentially
chemicalparalysistoavoidcomplicationsofventilatordyssynchrony
andhighairwaypressures.
Ifyoucontinuetousepropofol,higherdosesarerequiredandthe
patientisalreadyonnorepinephrine.Inaddition,ifparalysisisused,
youdonothavereliableamnesia.652

ICUsedationisaimedatkeepingthepatientcomfortablebut
easilyarousable.
Deepsedationwithorwithoutmusclerelaxantsisrarely
indicatedandisassociatedwithahigherincidenceofdelirium
anddeath.
Analgo–sedation(analgesiafirst,andaddingsedation)is
administeredtorelievepain,anxietyanddiscomfortandto
facilitatetreatmentandnursing.
Summary653

ICU Agitation/Discomfort
Prevalence
•50% incidence in those with length of stay > 24 hours
Primary causes: unrelieved pain, delirium, anxiety, sleep
deprivation, etc.
Immediate sequelae:
•Patient-ventilator dyssynchrony
•Increased oxygen consumption
•Self (and health care provider) injury
•Family anxiety
Long-term sequelae: chronic anxiety disorders and post-
traumatic stress disorder (PTSD)654

Patient Focused Sedation: Key Points
Non-pharmacological measures
•Minimize:
•Blood draws, X-rays
•Blood pressure measurements, Blood glucose measurements
•Dimming lights at night (sleep-wake cycle)
Selection of Sedatives
•Benzodiazepines-Diazepam, Lorazepam, Midazolam
•Propofol
•Dexmedetomidine
•Haloperidol, other neuroleptics655

14)Sepsis Management and
Antimicrobials Use in ICU
Hani Sammour, MD, PB
Anesthesia and IC, Shifahospital
Critical Care 656

Infections & Sepsis
•Thesystemicinflammatoryresponsetoinfection
withorgandysfunctiontermedsepsis,whichdoes
notnecessarilyindicatethepresenceofbacteremia.
•Moreover,theinflammatoryresponseisnotunique
tosevereinfectionssimilarmanifestationsmaybe
encounteredwithnoninfectiousillnesses.657

Infections & Sepsis
The relationship among infection, sepsis, and the systemic
inflammatory response syndrome (SIRS)
Sepsis
(Organ
dysfun-
ction)658

Definition
•Sepsisshouldbedefinedaslife-threateningorgan
dysfunctioncausedbyadysregulatedhostresponseto
infection(SuspectedorConfirmed)
•Septicshockdefinedaspersistinghypotensionrequiring
vasopressorstomaintainMAP[meanarterialpressure]>65
mmHgandhavingaserumlactatelevel>2mmol/L(18
mg/dL)despiteadequatevolumeresuscitation.659

Common organ dysfunction in Sepsis 660

Infections in the ICU
•InfectionsarealeadingcauseofdeathinICUs.
•Seriousinfectionsmaybe“communityacquired”or
subsequenttohospitaladmissionforanunrelatedillness.
•Thetermnosocomialinfectiondescribeshospitalacquired
infectionsthatdevelopatleast48hfollowingadmission.
•ThereportedincidenceofnosocomialinfectionsinICU
patientshasrangedbetween10%and50%.661

Cont.
•Therecentattentiontoasepticplacementofcentral
venouscathetersandearlierremovalofbladder
catheters,theincidenceofbloodstreaminfectionshas
markedlydeclined.
•Nearlyuniversalelevationoftheheadofbedandusing
ventilatorbundlehavealsoledtoamarkedreductionin
ventilator-associatedpneumonia.662

Cont.
•Criticallyillpatientsfrequentlyhaveabnormalhostdefenses
fromadvancedage,malnutrition,drugtherapy,lossof
integrityofmucosalandskinbarriers,andunderlying
diseases.
•Thus,agegreaterthan70years,corticosteroidtherapy,
chemotherapyofmalignancy,prolongeduseofinvasive
devices,respiratoryfailure,kidneyfailure,headtrauma,and
burnsareestablishedriskfactorsfornosocomialinfections.663

Types of nosocomial infection
•Community-acquiredandventilatorassociatedpneumoniasare
majorproblemsintheICU.
•Infectionsoftheurinarytractaccountformanynosocomial
infections.Urinaryinfectionsareusuallyduetogram-negative
organismsandaretypicallyassociatedwiththeindwellingcatheters
orurinaryobstruction.
•Intravascularcatheter-relatedinfectionsarenowrelativelyrare
causesofICUinfections.
•Surgicalsiteandotherwoundinfectionsarehoweverseen.664

Nosocomial pneumonias
•Nosocomialpneumoniasareusuallycausedbygram-negative
organisms.Gastrointestinalbacterialovergrowthwith
translocationintotheportalcirculationandretrograde
colonizationoftheupperairwayfromthegastrointestinal
tractasaresultofaspirationarepossiblemechanismsof
entryforthesebacteria.
•Preservationofgastricacidityinhibitsovergrowthofgram-
negativeorganismsinthestomachandtheirsubsequent
migrationintotheoropharynx.665

Nosocomial pneumonias
•Trachealintubationdoesnotprovideeffectiveprotection
becausepatientscommonlyaspirategastricfluidcontaining
bacteriadespiteaproperlyfunctioningcuff;nebulizersand
humidifierscanalsobesourcesofinfection.
•Elevatingtheheadofthebedmorethan30oreducesthe
likelihoodofventilator-associatedpneumonia.
•Enteralnutritionreducesbacterialtranslocationacrossthe
gutandreducesthelikelihoodofsepsis666

Ventilator bundle667

The Four Moments of Antibiotic Decision Making
1.Doesmypatienthaveaninfection
thatrequiresantibiotics?
2.HaveIorderedappropriatecultures
beforestartingantibiotics?What
empirictherapyshouldIinitiate?
3.Adayormorehaspassed.CanIstop
antibiotics?CanInarrowtherapyor
changefromIVtooraltherapy?
4.Whatdurationofantibiotictherapy
isneededformypatient'sdiagnosis?
13668

The Surviving Sepsis Campaign Bundle 2018 Update
Hour-1 Bundle669

670

Antimicrobial therapy
•Appropriateroutinemicrobiologicculturesbefore
startingantimicrobialtherapyandwithinonehour.
•Empiriccoverageforalllikelypathogens
•Combinationtherapyforinitialmanagementof
septicshock
•Procalcitoninlevelstosupportshorteningdurationof
therapy.671

Source control
•Sourcecontrolinterventionbeimplementedassoonas
medicallyandlogisticallypractical.
•Emergentsourcecontrol(e.g.,necrotizingsofttissue
infection,peritonitiscomplicatedwithintra-abdominal
infection,cholangitis,intestinalinfarction)tobesoughtand
diagnosedorexcludedasrapidlyaspossible,andIfneeded,
surgicaldrainageshouldbeundertakenforsourcecontrolas
earlyaspossibleafterthediagnosisismade,iffeasible.672

Fluid therapy
•Fluidchallengetechniquewithcontinuedfluid
administrationaslongashemodynamicsfactors
continuetoimprove.673

Vasopressors
•Norepinephrineasthefirst-choosevasopressor
•Addingvasopressin0.03U/minorepinephrine
ifnoresponsetonorepinephrine.674

Hydrocortisone
•RecommendagainstIVhydrocortisoneif
adequatefluidresuscitationandvasopressorare
abletorestorehemodynamicsstability.
•Ifnoresponsetovasopressors,itis
recommendedtoaddsmalldose(stressdose)of
hydrocortisone(e.g.50mg/6hr).675

Transfusion
•Transfusiononlywhenhemoglobinconcentration
decreasestolessthan7g/dLintheabsenceof
acutebleedingormyocardialischemia,etc.676

Mechanical Ventilation
•MechanicalVentilationusingtargettidalvolume
of6mL/Kgpredictedbodyweight.
•Maintainplateaupressureslessthan30cmH20677

Glucose control
•Glucose control: Maintain glucose < 180 mg/dL678

4 Phases of Septic Shock
•Rescue
–Recommended goal of 30 mL/Kg of IV crystalloid
•Optimization phase
–Ischemia and reperfusion phase
–Repeated assessments of intravascular fluid status and
determination for further fluid administration
•Stabilization
–Maintain intravascular volume, replace ongoing fluid
losses, support organs dysfunction, avoid iatrogenic harm
with unnecessary fluid administration
•De-escalation679

Fluid Responsiveness
•Fluidresponsivenessdefinedasameasurementofsustained
reversalofhypotensionwithresultantsystolicbloodpressure
>90mmHgorMAP>65mmHgafterinitialfluidresuscitation
withouttheuseofvasopressors.
•36.2%refractorytofluidbolus.
•Fluidrefractorypatientshadhigherin-hospitalmortality,
mechanicalventilation,longerICUstays,longerhospital
lengthofstay.680

Fluid Responsiveness
•Predictors of being fluid refractory:
–delayed fluid resuscitation with time to fluid > 120 minutes,
–CHF.
–Hypothermia.
–lactate > 4.
–Coagulopathy.
–Immunocompromised.681

Predicting fluid responsiveness
Static tests:
(lesssensitive,lessspecificandlessuseful
thatdynamictests)
–Clinicalstaticendpoints(e.g.heartrate,blood
pressure,capillaryrefilltime,urineoutput)
–CVP/PCWP
–CXR682

Predicting fluid responsiveness
Dynamic tests
–Passive leg raising
–End-expiratory occlusion test
–Echocardiography
—Velocity Time Index (VTI) allows measurement of SV
—EDV approximates preload
–IVC ultrasound
—Assess size and degree of inspiratory collapse
—Correlates with CVP, but CVP is a poor indicator
–Systolic Pressure, Pulse Pressure (PPV) and Stroke Volume
(SVV)683

Fluid Responsiveness
(Static tests less sensitive than
dynamic tests)684

Liberal Fluid Administration associated with poor
outcomes685

Early Use of Norepinephrine in Septic Shock
Resuscitation
Early Norepinephrine verse standard care
•Improved shock control by 6 hours.
•Lower incidences of cardiogenic edema
•Lower incidences of new-onset arrhythmias.
•No difference 28 day mortality.686

Balanced Crystalloid Solutions687

Balanced Crystalloid Solutions688

689

690

Antimicrobial therapy691

Golden rules of Antibiotic
Stewardship in the ICU
•InfectionpreventionintheICUisanintegralpartofstewardship
policiestopreventdevelopmentandspreadofresistant
microorganisms.
•Decreasetimetodiagnosisbyadequatecollectionandtransportof
culturesandotherclinicalandmicrobiologicaldiagnostictests.
•Organizestructuredandefficientcommunicationbetween
microbiologylab,clinicalpharmacistandinfectiousdisease
physicianindirectICUpatientcare.
•Inseveresepsisorsepticshockstartbroadspectrumantibiotic
therapypromptly&Provideadequatesourcecontrol.692

Golden rules of Antibiotic
Stewardship in the ICU
•Knowyourself:beawareofresistancepatternsandantibiotic
usagedatainyourhospitalandunitprovideregularfeedback
onresistancepatternsandantibioticusagedatainICU.
•Considerde-escalationandIV-oralswitchbasedonavailable
cultureresultseveryday.
•Activelyreduceantibiotictreatmentduration.
•InICUconsiderusingprocalcitonin(PCT)levelsasguidance.693

Antibiotic selection options for community acquired,
immunocompetentpatients with severe sepsis/septic shock694

Antibiotic selection options for healthcare associated and/or
immunocompromisedpatients with severe sepsis/septic shock695

Antibiotic selection options for healthcare associated and/or
immunocompromisedpatients with severe sepsis/septic shock696

Antibiotic Prescribing in the ICU
RESPIRATORY :
•Community Acquired Pneumonia (CAP)
Recommended first Line :
Ceftriaxone/Cefotaxime + Azithromycin
+Vancomycin (if risk of MRSA “shock or requirement of MV”)697

Community Acquired Pneumonia (CAP)
Appropriate AntibioticsCommon,pathogens
Amoxicillin, Ceftriaxone,
Cefotaxime
Strep. pneumoniae
(pen-sens)
Ciprofloxacin, Vancomycin Strep. Pneumoniae
(pen-resistant)
2nd or 3rd gen. Cephalosporin Haemophilus influenzae
Macrolide or DoxycyclineMycoplasma, Chlamydophilia
Pneumoniae
Clindamycin (Metronidazole)Anaerobes
( Aspiration pneumonia )698

Hospital Acquired Pneumonia (HAP)
Recommended First line:
Anti-pseudomonal
(Ceftazidime, Ciprofloxacin, Amikacin)
+ Vancomycin (if risk of MRSA)699

HOSPITAL ACQUIRED PNEUMONIA, Cont.
Appropriate AntibioticsCommon,pathogens
(Ceftazidime, Ciprofloxacin,
Amikacin, Gentamycin)
Pseudomonas
Ceftazidime, Ciprofloxacin Klebsiella,Enterobacter
MeropenemAnaerobes,
Acinectobacter
VancomycinStaph.aureus
Erythromycin, Ciprofloxacin Legionella700

COPD EXACERBATIONS
Treat as community acquired pneumonia
Consider pseudomonas if recurrent hospitalization
Appropriate AntibioticsCommon,pathogens
Ceftriaxone, Cefotaxime Strep. pneumoniae
(pen-sens)
Vancomycin Strep. Pneumoniae
(pen-resistant)
2nd or 3rd gen. Cephalosporin Haemophilusinfluenzae
Macrolide or DoxycyclineMycoplasma, Chlamydophilia
Pneumoniae
Clindamycin (Metronidazole)Anaerobes (Aspiration pneumonia)
Ciprofloxacin, AmikacinPseudomonas701

ASPIRATION PNEUMONIA
Recommended First Line
Mild-moderate:Ceftriaxoneplusazithromycin,levofloxacin, ormoxifloxacin
Severe:Piperacillin/tazobactamorimipenem plusvancomycin
AppropriateAntibioticsCommonpathogens
Imipenem,ClindamycinAnaerobes
Imipenem,ClindamycinGram,negative,bacilli
Cephalosporin,
Vancomycin
Staphylococcus,aureus
MRSA(HAP)
Cefotaxime,CeftriaxoneStreptococcusspecies
Cefotaxime,CeftriaxoneHaemophilusinfluenza
Piperacillin/tazobactam,imipenemPseudomonasaeruginosa(HAP)
Piperacillin/tazobactam,imipenemKlebsiellapneumoniae(HAP)702

EMPYEMA
Recommended First Line
•Community-acquired empyema: third-generation
cephalosporins plus metronidazole
•Hospital-acquired empyema:Vancomycin plus
Metronidazole and an antipseudomonal agent
Or Vancomycin plus piperacillin/tazobactam703

EMPYEMA Cont.
AppropriateAntibioticsCommonpathogens
MetronidazoleAnaerobes
Cefotaxime,CeftriaxoneStrep.pneumoniae
Cephalosporin,
(MRSA)Vancomycin
Staphylococcus,aureus
Piperacillin/tazobactam
antipseudomonalcephalosporin
Pseudomonas704

GI TRACT
PERITONITIS
RecommendedFirstLine
3rdGencephalosporineorAmikacinorCiprofloxacin
+Metronidazole
•Uppertractsource(e.g.perforatedulcer)predominantly
gram-positiveinfections
•Lowertract(e.g.colon)predominantlyanaerobicand
gram-negativeaerobes705

PERITONITIS Cont.
Appropriate AntibioticsCommon,pathogens
Amikacin, CiprofloxacinKlebsiella,species
3rd Gen cephalosporine, Cipro,
Amikacin
Enterobacter.species
Penicillin + AmikacinEnterococcus
Metronidazole Anaerobes (secondary
peritonitis)
Penicillin, 3rd Gen Cefs Strep.pneumoniae706

ENDOCARDITIS
(Native & prosthetic valve)
Recommended First Line
Vancomycinplus gentamicinand eithercefepime or a
carbapenem (imipenem or meropenem).
Appropriate AntibioticsCommon,pathogens
Flucloxacillin+ Gentamycin
Vancomycin + Gentamycin
Staphylococcus aureus
MRSA
Penicillin + Gentamycin S.Viridans.,.S.bovis,Enterococcus
Vancomycin+GentamycinS.epidermidis
Cefepime 2 g IV q8h or
Ampicillin + Gentamicin
HACEK (G-veBacilli) .
Cefepime or CarbapenemPseudomonas 707

SEPSIS OF UNKNOWN CAUSE
Recommended First Line
Meropenem or (Piperacillin-Tazobactam)
Plus
Vancomycin 708

SEPSIS OF UNKNOWN CAUSE Cont,
Appropriate AntibioticsCommon,pathogens
CiprofloxacinE.coli
3rd Gen Cephalosporins or AmikacinOther.
Enterobacteriaceae
Penicillin, CiprofloxacinGram-negative bacilli
Vancomycin Staphylococcus aureus
Penicillin + AmikacinEnterococcus709

Take home message
•Septicshockisamedicalemergencythatrequires
immediateintervention.
•Treatmentisthreefold:
(1)Controlanderadicationoftheinfectionbyappropriate
andtimelyintravenousantibiotics,drainageofabscesses,
debridementofnecrotictissues,andremovalofinfected
foreignbodies.
(2)Maintenanceofadequateperfusionwithintravenous
fluidsandinotropicandvasopressoragents.
(3)SupportivetreatmentofcomplicationssuchasARDS,
kidneyfailure,gastrointestinalbleeding,andDIC.710

Take home message
•Hemodynamic support:
–Judicious and faster fluid
–No hetastarch
–Earlier Inotropes
–Use norepineprineand epinephrine over dopamine
–Lactic acid clearance
–Dynamic tests are better than CVP
•Antimicrobials:
–Fast <1 hr, consider early antifungals, use biomarkers to deescalate or stop
•ARDS:
–Lower TV
–Higher PEEP (if needed)
•Glucose control
–Not so tight (140-180 mg/dl)
•Nutrition
–Early once shock corrected. 711

Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care
15)Renal & Electrolyte
Emergencies712

Important questions in Acute Kidney Injury
1.Isthepatientindangerofimminentdeath?
Stabilizationonadmission
2.Assessneedforurgentdialysis
3.Begindiagnosticworkup
4.Isitpre-renal,renalorpostrenal?
5.Isitreallyacuteorchronicoracuteontopofchronicrenal
failure?713

1.Hypervolemia unresponsive to diuretics
2.Severe hyperkalemia
3.Severe acidosis
4.Severe uremic symptoms
Urgent issues in acute renal failure714

Anuric/oliguric ARF patient
Anuric<100 mL/day
Oliguric100-400ml/day
Nonoliguric> 500 ml/day715

Management of volume overload
in Renal Failure
IVaccess,O2,monitor,PlaceFoley
•UseescalatingdosesofLasix:
•Initialbolus20-40mg,observeonehour
•Range:20-250mg(IVbolusesareusuallydoubleduntildesired
effectisobtainedORmaximalsingledoserangereached250mg).
•Infusion(ifremainsoliguric):10-40mg/h(max1g/24hr)
•Lasixplusalbumin→noadditionalbenefit
•Hemodialysisifnoresponse716

•Ithassomediureticeffect(low'renal'dose).
•Mayhavearoleasaninotropeinsupportingblood
pressure(especiallyinsepsis),usuallyneed
>5mcg/kg/minforthis('pressor'dosenot'renal'dose).
•Norepinephrinealmostismoreeffectiveforthisgoal.
•NoevidencethatdopamineimprovesoutcomeinARF.
Dopamine in ARF717

Management of Acidosis in Renal Failure
Acidosis (pH<7.35)
•Contributestoriskofarrhythmiawithhyperkalemia.
•Canalsocontributetohyperkalemiaitself.
•Disruptsothercellularprocesses.
•Ifcauseofacidosisnotreversed,RRTwillbenecessary.
•RRTispreferredtotheadministrationofbicarbonateamong
hypervolemicpatientswithreducedurineoutputbecause
bicarbonateadministrationresultsinalargesodiumloadthatmay
worsenvolumeoverload.718

Hazards of giving Bicarbonate
1.Hypertonicsolution
volumeoverload(especiallyinrenalfailure).
2.Overshootalkalosis:ketonesandlactatecouldfurtherbe
metabolizedtobicarbonates.
3.RapidcorrectionofacidosismayshiftODCtoleftandmay
causehypoxia.
4.BicarbonatewilldecomposetoCO2whichpasseseasilytoBBB
andcauseCSFparadoxicalacidification.
5.MaycauseriseinPaCO2inpatientswhohavereduced
ventilatoryreserve.719

Hazards of Not giving Bicarbonate
•Atacertainstagewithacidosis(pH7.10-7.20)allthe
compensatorymechanismsareattheirmaximumpower
nomorecompensatorymechanismsavailable.
•Dysrhythmiasbecomemorelikelyandcardiac
contractilityandresponsivenesstocatecholamineswill
bereduced.720

•AlkalitherapyisnotuseduntilpH<7.2.(7.1bysomeauthors)
or(HCO3<8mEq/L)
•ThetargetpH>7.2andbicarbonatelevelisusually18to20
mEq/L
•Therateofbicarbonateadministrationisdependentupon
severityofacidosisanduponthevolumestatusofthepatient.
WhentogiveBicarbonates in AKI721

•HCO3 dose: (BW ×0.3 ×BD) / 2
•Correction should be slowly over 3 hours guided by hourly ABGs and HCO3
•A reasonable strategy is to administer 150 mEq NaHCO3 in 1L of D5% at a
rate that is determined by the severity of acidosis and the ability of the
patient to tolerate the volume load.
•In cardiac arrest : Bolus = 1 mEq/kg ( 50 -100 mEq), base subsequent
doses on results of arterial blood pH and PaCO2.
Usual rate of administration
NaHCO3 is a dangerous drug but may be essential after cardiac arrest
or severe acidosis for the successful action of inotropic agents.722

Potassium Emergencies
K+fluxacrossthecellmembraneisamajordeterminantofthe
membranepotential.PatientswithabnormalitiesofserumK*present
withdisordersofneuromuscularfunction
Potassium
3 Na+
2 K+
ICF
Na = 10 mmol/L
K = 140 mmol/L
ECF
Na = 150 mmol/L
K = 4 mmol/L723

Hypokalemia
•Defined as serum potassium concentration of less than 3.5 mmol/L.
•Common electrolyte abnormality in clinical practice (20% of
hospitalized patients have K < 3.5 mEq/L).724

•Decreased intake of potassium
▪Anorexia
▪Alcoholics
•Transcellularshift of potassium
▪ß-agonists
▪Insulin
•Renal potassium excretion
▪Diuretics
▪Decreased chloride delivery
▪Hyperaldosteronism
Etiologies of Hypokalemia725

ECG Findings With Hypokalemia
Hypokalemia produces ECG changes which are not
necessarily related to the K+ level
•Flattening of T waves
•Increased prominence of U waves (look at
V4, 5, 6)
•ST depression
•Increased prominence of P waves
•Inversion of T waves726

•Tochangeapotassiumfrom3to4mEq/Ltakesabout100mEqofpotassium
inanadult.
•PotassiumcanbereplacedorallyorIV.
•Slow-releasepotassiumchloridetabletsaretoleratedbutmaycause
gastrointestinalulcers.
•IVPotassiumreplacementtherapyisimmediatelyindicatedforpatientswho
areNPOorhavedangerouslylowpotassium(<2.5meq/L)orifthe
hypokalemiaiscausingmuscleparalysisormalignantcardiacarrhythmias.
Treatment of Hypokalemia727

•IVadministrationofmorethan10mEqofpotassiumperhourcauseslocal
irritation;centralIVlinesallowratesupto20to40mEqperhour.
•Suchhighratesofadministrationareusuallyreservedforemergent
treatmentofarrhythmiasandaregivenwithECGmonitoring.
•Alwaysconsiderthepossibilityofassociatedmagnesiumdeficiencyand
rememberthatthehypokalemiacannotbesuccessfullytreatedunlessthe
magnesiumdeficitisconcurrentlycorrected
•Cangivepotassium0.25mEq/kg/hrfor2hoursandreassessthepatient
•Usualmaximaldailydose=3mEq/Kg
Treatment of Hypokalemia728

Hyperkalemia
Definedasserumpotassiumconcentration
ofmore>than5.5mmol/L.729

Hyperkalemia
Plasmapotassiumover5.5mEq/L
Primaryproblemsare
Weakness&Paralysis
Duetoabnormalnerveconduction
AscendingparalysismimickingGBSdocumentedwithKof7
Arrhythmias
Bradycardia
Ventricularfibrillation730

Increased Intake Of K+
•Iatrogenic potassium administration (oral, IV)
•Increased ingestion
•Massive transfusion
Etiologies of Hyperkalemia
Transcellularshift of K+
•Acidosiseg DKA, lactic acidosis
•Drugs: Beta-blockers, heparin, ACE inhibitor,
•Extensive trauma, rhabdomyolysis haemolysis
Decrease Renal potassium excretion
•Renal failure
•Adrenal mineralocorticoid deficiency731

732

Pull&Push effectson potassiumon T wave of ECG733

Stop Intake of Potassium
▪Enteral
▪Parenteral
Induce Transcellular Shift of Potassium
▪Insulin
▪Albuterol
Enhance Potassium Excretion
▪Renal
▪Colonic
Treatment of hyperkalemia:734

735

736

Ineffective In Up To 40%737

15 -20738

•Inmetabolicacidosisonly(Noeffectinabsenceofacidosis)
•IncreaseKmovementtoICFviaNa/K/ATPase
•Mildtomoderatehyperkalaemia:
SodiumBicarbonate8.4%1mmol/mL:1mL/kgslowIVinfusionover30minutes
•Severehyperkalamia:
SodiumBicarbonate8.4%1mmol/mL:1-2ml/kgIVover5minutes
•OnsetofAction:30-60minutes
•Duration:2-3hours
•Note:DoNOTgivesimultaneouslywithCalcium
•SideEffects:ECFvolumeexpansion,fallincalcium,CO2retention
Bicarbonate use in hyperkalemia739

Furosemide(Lasix) Only in patients with working kidneys
20 x sCrIV push (Rule out urinary obstruction)
Increase the excretion of potassium 740

Remove K+ from body [Kayexalate]
•Exchangesodiumorcalciumforpotassiumincolon,increasingGITK
secretion
•Theinitialoraldoseis15to30gramswith50to100mlof20%sorbitol.
•Thesorbitolenhancesexcretionbycausingosmoticdiarrhea.
•Itmayberepeateduptofourtimesperday.
•Iforalintakeisnotpossible,50gramsofresinwith200mlof20%sorbitol
maybegivenasaretentionenema.
•OnsetofAction:1hourPR,4-6hoursoral
•Duration:variable741

Dialysis
MosteffectivemeansofK+removal(25-40mmol/L)
•Decreases1mmol/Linfirsthour
Dialysisshouldbeconsideredforpatientswithseverehyperkalemia
whohavefailedtorespondtopharmacologicattemptsatloweringthe
potassiumlevel,andforpatientswithacuteorchronicrenalfailure.742

Summary of treatment of Hyperkalemia743

Patientasymptomatic&normalECG
•StopKsupplements
•Recheckresult
•Considernotreatment
•Salbutamolnebulizer
•BicarbonateIVifmetabolicacidosis
•PolystyrenesulfonatePRororal(resonium)
Mild hyperkalemia K+ 5.5-6mEq/L 744

Patientasymptomatic&mayhavenormalECG
•Salbutamolneb
•Insulin/glucoseIV
•Resonium(Polystyrenesulfonate)PRororal
•BicarbonateIVifmetabolicacidosis
Moderate hyperkalemia K+ 6-7mEq/L745

At risk of increasing and/or Patient symptomatic and/or ECG disturbance:
•Calcium IV
•Salbutamolneb
•Insulin/glucoseIV
•BicarbonateIV if metabolic acidosis
•Dialysis
Consider hydrocortisone 1-2 mg/kg IV if suspicion ofadrenal insufficiency
Severe hyperkalaemiaK+ >7.0 mEq/L 746

Hyponatremia
Hyponatremia defines as serum sodium concentration
<135meq/L.
Most frequent electrolyte abnormality in the hospitalized patients.
Essentiallycommonincriticalcareunits.Inadditiontobeinga
potentiallylife-threateningcondition,hyponatremiaisan
independentpredictorofdeathamongintensivecareunitand
geriatricpatientsandthosewithheartfailure,andcirrhosis.747

Hyponatremia
▪Changes in serum sodium concentration results from
derangements in water balance.
Total body sodium
▪Serum sodium =
Total body water
▪Low serum sodium concentration denotes a relative
deficit of sodium and /or a relative excess of water.748

Approach to the patient with Hyponatremia
Check serum osmolality (increased or decreased)
1)Increased osmolality:
---Mannitol, Glycine (exogenously) or Hyperglycemia
2)Normal osmolality:
---Hyperproteinemia or Hyperlipidemia (Pseudohyponatremia)749

Approach to the patient with hyponatremia
3)Decreased serum osmolality
--Check volume status, it could be:
A.Hypovolemic
B.Hypervolemic
C.Euvolemic.750

Approach to the patient with Hyponatremia
A.Hypovolemic Hyponatremia (Dehydration)
Decrease Sodium
Decrease water
Causes
Diarrhea
Diuretic use
Mineralocorticoid deficiency
Osmotic diuresis like mannitol751

Approach to the patient with Hyponatremia
B.Hypervolemic Hyponatremia
Sodium content unchanged
Increase water
Causes
Heart Failure
Cirrhosis
Nephroticsyndrome752

Approach to the patient with Hyponatremia
C.Euvolemic Hyponatremia
Sodium content unchanged
Relative increase in water
•Cause
Syndrome of Inappropriate Anti Diuretic Hormone
(SIADH)753

Cerebral Salt Wasting Syndrome
•Cerebralsaltwasting(CSW)isapotentialcauseofhyponatremiainthe
settingofdiseaseofthecentralnervoussystem(CNS).
•Cerebralsaltwastingischaracterizedbyhyponatremiawithelevated
urinesodiumandhypovolemia.
•CSWistreatedwithintravenousadministrationofisotonicor
hypertonicfluids.
•Dependingontheacuityandclinicalmanifestationofthe
hyponatremia,isotonicorhypertonicsolutionswouldbeindicated.
HypovolemicHyponatremia754

Approach to the patient with Hyponatremia
ECF volume ECF volume ECF volume
decreased normal (euvolemic) increased (edema)
Renal Extrarenal SIADH CHF
Diuretics GI losses Cirrhosis
Nephrotic syndrome
Urine Na Urine Na Urine Na Urine Na
TB Na
TB water
TB Na
TB water
TB Na
TB water
Hyponatremia with decreases serum osmolality755

SIADH
•Inappropriate release of ADH causes SIADH.
•It is diagnosed by checking :
Serum sodium <135
Serum osmolality <280
Urine osmolality >100
Urine sodium >30756

Causes of SIADH
Neoplastic
Pancreatic or lung cancers
Central nervous system;
Meningitis, Brain abscess,
Stroke, Acute psychosis
Pulmonary
Pneumonia, Lung abscess,
Tuberculosis
Endocrine
Addison's disease, Hypothyroidisim,
Hypopituitarism757

Drugs induced SIADH
Increased ADH ADHpotentiation
Anti-depressant Carbamazepine
Anti-psychotics Chlopropamide
Carbamazepine Cyclophosphamide
Platinum alkaloids NSAIDS
Alkylating agents ADH like activity
DDAVP
Oxytocin758

Clinical manifestation of SIADH
Acute: (<48 hours)
Stupor/coma
Convulsions Treatment with
Respiratory arrest 3% NaCl
Chronic; (>48 hours)
Headache
Irritability Treat with medications
Nausea & vomiting like vasopressin receptor antagonists
Confusion & Disorientation Conivaptan or Tolvaptan
Gait disturbance759

Correcting hyponatremia
Traditional approach;
add to the numerator
Serum sodium =Total body sodium
Total body water760

Correcting hyponatremia
Current approach;
Serum sodium = Total body sodium
Total body water
Subtract from the denominator761

Vasopressin Receptor Antagonists
•CompetitivelyblockADHactionandincreasewaterexcretionare
calledaquaretics,
•Reduceurineosmolality,increaseelectrolyte-freewaterexcretion,
andraiseserumsodiumconcentration.
•Theyarelikelytobecomeamainstayoftreatmentofeuvolemicand
hypervolemichyponatremia.762

Treatment strategies for acute hyponatremic emergencies
•3% NaCl: 100ml bolus for severe symptoms.
•Can be repeated up to three times.
•Goal: correction by 4to6 mEq/L in first few hours.
•Monitor closely to avoid excessive correction.763

Rate of correction of hyponatremia
Acute symptomatic :
4to 6mEq/L in first few hours
Target 10-12 mEq/L in first 24 hours.
(10 mEq/L if high risk for ODS* and 12 mEq/L if low risk)
Chronic:
8-10 mEq/L in first 24 hours
Target correction18 mEq/L in first 48 hr
* ODS: osmotic demyelination syndrome764

Importance of appropriate serum sodium correction
Too-rapid correction of hyponatremia (e.g., >12 mEq/L/24 hours)
can cause osmotic demyelination syndrome (ODS) resulting in:
Dysarthria, Dysphagia,
Seizures, Coma and death
Spastic quadriparesis.
Risk factors for ODS:
Severe malnutrition, Severe hyponatremia
Advanced liver disease Older age
Alcoholism,765

Hypernatremia
•Normalplasmaosmolality:275to295mosmol/kg
•Naistheprimarydeterminantofserumosmolarity(numberofsolute
particlesinthesolution)
•Hypernatremiaisdefinedasserumsodiumlevel>145mEq/L
•Hypertonicbydefinition
•Usuallyduetolossofhypotonicfluid
•Occasionallyinfusionofhypertonicfluid
•Approximately1-4%ofhospitalizedpatients
•Tendstobeattheextremesofage766

Hypernatremia
•MechanismstoreturnthePlasmaosmolaritytonormal
•Sensedbyosmoreceptorscellsinthehypothalamus
•increasewaterintakeviathirst
•DecreasewaterexcretionviaADH
•increaseswaterreabsorptioninthecollectingtubules767

Mortality Eye Opener
•Mortalityrateacrossallagegroupsisapproximately45%.
•Mortalityrateinthegeriatricagegroupisashighas79%
•Usually occurs in infants or adults
•Particularly the elderly (impaired mental status)
•May have an intact thirst mechanism but are unable to ask for water
•Increasing age is also associated with diminished osmotic stimulation of
thirst (unknown mechanism). 768

Why hypernatremia is important in the ICU
•Hypernatremia is common in the ICU.
•Hypernatremia isnotbenign:
•Hypernatremiacausesprofoundthirst.Particularlyamong
intubatedpatients,thismaycausemiseryandagitation(which
maybeinappropriatelytreatedwithsedativesorantipsychotics).
•Hypernatremiamaycausedelirium,therebyincreasingthelength
ofventilationandICUstay.769

Hypernatremia should always be corrected promptly
•Untreatedhypernatremiaisahallmarkoflow-qualityICUcare.
•Hypernatremiausuallywon'timproveonitsown(itrequires
activemanagement).
•Evenmildhypernatremia(e.g.sodium146-148mEq/L)maycause
discomfortandshouldn'tbeignored.770

Hypernatremia
•Cellsbecomedehydrated(sodiumactstoextractwaterfrom
thecells).
•Dehydratedcellsshrinkfromwaterextraction.
•EffectsseenprincipallyintheCNS.771

Characteristics and symptoms of hypernatremia
Symptoms related to the
characteristics of hypernatremia
Characteristics of hypernatremia
Lethargy,obtundation,confusion,
abnormalspeech,irritability,seizures,
nystagmus,myoclonicjerks
Cognitivedysfunctionandsymptoms
associatedwithneuronalcellshrinkage
Orthostaticbloodpressurechanges,
tachycardia,oliguria,dryoralmucosa,
abnormalskinturgor,dryaxillae,Lethargy
Dehydrationorclinicalsignsofvolume
depletion
Weightloss,generalizedweaknessOtherclinicalfindings772

Causes of Hypervolemic Hypernatremia
•Hypertonic saline
•Sodium bicarbonate administration
•Accidental salt ingestion
•Mineralocorticoid excess (Cushing’s syndrome)
•ectopic ACTH
•pituitary adenoma
•pituitary hyperplasia
•adrenal tumor773

Causes of Hypovolemia Hypernatremia
•Water deficit > Sodium deficit
•Extrarenal losses
•diarrhea, vomiting, fistulas, significant burns
•Urine Na < 20 and U Osm >600
•Renal losses
•urine Na >20 with U Osm 300-600
•osmotic diuretics, diuretics, postobstructive diuresis, intrinsic renal
disease
•DM / DKA
•increased solute clearance per nephron, increasing free water loss774

Causes of Euvolemic Hypernatremia
•Diabetes Insipidus
•Typically mildhypernatremia with severe polyuria
•Central DI = ADH deficiency
•Infection, tumor, trauma, anorexics, hypoxia.
•U Osm less than 300
•Treatment is DDAVP775

Thegoalsofmanagementinhypernatremiaareasfollows:
1)Recognitionofthesymptoms,whenpresent.
2)Identificationoftheunderlyingcause(s).
3)Correctionofvolumedisturbances.
4)Correctionofhypertonicity.
Treatment of Hypernatremia776

Hypernatremia with hypovolemia
•Administerisotonicfluidtorestoreeuvolemiaandtotreat
hyperosmolality.
•Even0.9%normalsaline(308mOsm/kgor308mmol/kg),which
hasthehighestosmolalityoftheusualisotonicfluids,is
hypoosmolarcomparedwithsubstantiallyhyperosmolarplasma
•Afteradequatevolumeresuscitation,hypotonicfluidshouldbe
usedtoreplaceanyremainingfreewaterdeficit.777

Hypernatremia with euvolemia
•Give5%dextroseandwater&Encouragewaterdrinkingortocause
excretionofexcesssodiuminurine.
•Intranasaldesmopressin(DDAVP)asantidiureticreplacement
therapyinthemanagementofcentralcranialdiabetesinsipidusand
formanagementofthetemporarypolyuriaandpolydipsiafollowing
headtraumaorsurgery.10-40mcg(0.1-0.4mL)Daily,eitherasa
singledoseordividedinto2or3doses.778

Hypernatremia with hypervolemia
•Give5%dextroseinwatertoreducehyperosmolality,
thoughthiswillexpandvascularvolume.
•Loopdiuretics(eg,furosemide,0.5–1.0mg/kg)
intravenouslymaybeneededtoremoveexcesssodium
•Insevererenalinjury,considerhemodialysis779

Formula used in the management of hypernatremia
Change inserum Na
+
= (infusateNa
+
-serum Na
+
) ÷(TBW+1)
•Example:anobtunded80-year-oldmanisbroughttotheemergency
roomwithdrymucousmembranes,fever,tachypnea,andablood
pressureof134/75mmHg.Hisserumsodiumconcentrationis165
mmol/L.Heweighs70kg.Thismanisfoundtohavehypernatremia
duetoinsensiblewaterloss.
•Theman'sTBWiscalculatedbythefollowing:(0.5×70)=35L780

Formula used in the management of hypernatremia
•Toreducetheman'sserumsodium,D5Wwillbeused.Thus,the
retentionof1LofD5Wwillreducehisserumsodiumby:
•(0-165)÷(35+1)=-4.6mmol.
•Thegoalistoreducehisserumsodiumbynomorethan10mmol/L
ina24-hourperiod.Thus,(10÷4.6)=2.17Lofsolutionisrequired.
About1-1.5Lwillbeaddedforobligatorywaterlosstomakeatotal
ofupto3.67LofD
5Wover24hours,or153cc/h781

Contents of Na in Soluions
5% dextrose in water (D5W) 0 mEqNa
0.18% sodium chloride in
4.3% dextrose in water
(D4.3% 0.18% Nacl)
31 mmol/L
0.9% NS 154 mmol/L
0.45% NS 77 mmol/L
Lactated Ringer’s 130 mmol/L 782

Over-correction would be safe
•Ifover-correctiondidoccur(e.g.sodiumlevelsfalling>12mEq/L)
thiswouldprobablybesafe.
•Thereisnoevidencethatrapidfallsinsodiumaredangerousin
olderadults.Thisislikelytobeespeciallytrueamongtheelderly,
whooftenhavedecreasedbrainsizeandthusgreaterroomin
whichtoswell(shouldedemaoccur).783

Rate of correction of hypernatremia
•Rateofcorrectioninacutehypernatremia(lessthan48hours):theserum
sodiumshouldbeloweredrapidlytoanear-normallevelinlessthan24
hours.GiveD5%3-6ml/kg/hourtolowerNato145mEq/L.
•Rateofcorrectioninchronichypernatremia(morethan48hours):
maximumsaferateatwhichtheserumsodiumconcentrationshouldbe
loweredis12mEq/Lperday.GiveD5%1.5-3ml/kg/hour.
•Checktheserumsodiumq3-4hoursifacuteandq6-8hoursifchronic
andadjustthefreewaterintakeappropriately.784

Case scenario 1
A60yearoldhealthychronicsmokerpresentedtohisdoctorwithgeneral
malaise.Hewaseuvolemic,weight70kg,earlyclubbing,systemic
examinationwasunrevealing.
Labresults:s[Na]110,s[K]4,sOsm226mOsm/Kg,uOsm618mOsm/Kg,
u[Na]46.OtherbiochemicaltestsandFullBloodCount(FBC)indiceswere
withinthenormalrange.CXRrevealedasuspiciousshadowleftmid-zone.
Hewasadmittedundertherespiratoryphysiciansforfurtherinvestigations.
Thecauseofhyponatraemiais:A.SIADHB.Addison’sdisease
C.PsychogenicpolydipsiaD.Pseudo-hyponatraemia
E.Centraldiabetesinsipidus785

Answer 1
Statement(A),thecauseisSIADH,resultingineuvolemic
hypotonichyponatremia.TheSIADHislikelydueto
bronchogeniccarcinoma.786

Case scenario 2
•A21yearoldathletedevelopedagrandmalseizureafter
completingthemarathon.Hewasinpost-ictalstate;GCSwas6/15,
neededintubation.Othersystemsexaminationwasunrevealing.
s[Na]114,itwasnormalaweekearlierataroutinemedical:The
causeofhyponatraemiais:
A.CerebralsaltwastingsyndromeB.Hypothyroisism
C.Excessivewaterintake D.Diabeticketoacidosis
E.SIADH787

Answer 2
Statement(C),thecauseisexcessivewaterintake,
causingeuvolemichypotonichyponatraemia.788

Question 3
Whatistheimmediatetreatment?
A.0.9%Normalsalineat250mL/h
B750mLoralfluidrestriction
C.Intravenousanticonvulsantinfusion
D.3%HSSat100mlinfusionover20minutes789

Answer 3
•Statement (D), the immediate treatment is 3% HSS at
100ml infusion over 20 minutes,. 790

16)Critical Care Management
of the Burn Patient
Hani Sammour, MD, PB
Critical care unit, Shifa hospital
Critical Care 791

Organ Support
•Respiratory system (Airway & Breathing).
•Cardiovascular system.
•Renal system.
•GI system.792

Airway793

Airway Assessment
LookforWarningsignsofairwayburns,suspectairwayburnif:
•Burnoccurredinanenclosedspace
•Stridor,hoarseness,orcough
•Burnstoface,lips,mouth,pharynx,ornasalmucosa
•Sootinsputum,nose,ormouth
•Dyspnea
•Decreasedlevelofconsciousnessorconfusion
•Hypoxemiaorincreasedcarbonmonoxidelevels(˃2%)
(N.B.Onsetofsymptomsmaybedelayed)794

Airway Management
•Informintensivistoncallifyouhaveanyinhalationalinjury.
•Oxygen100%untilriskofCarbonMonoxidetoxicityis
excluded.
•Frequentlyassesstherequirementforintubation(avoid
delayedintubation).
•Controlairwaywithendotrachealintubationbefore
transportingthepatient.795

Ventilation management
•Followventilatorystrategiestoavoidlunginjury(lowtidalvolume
(VT)6-8mL/kgpredictedbodyweight(PBW)andplateaupressure
<30cmH2O).
•Ventilatorbundleapplication(concerningaboutVentilator
AssociatedPneumonia(VAP)prevention).
•Usingpropersedationtotoleratemechanicalventilationandapply
sedationscore.796

Pulmonary care
•NebulisedHeparin5000iudilutedwith3mlnormalsaline4hourly
for5-7days(iftherearesignsofinhalation).
•Nebulised20%Acetylcystinesolution,3mlsevery4hours(ifthere
arechestsecretions,stopifpatientdevelopsbronchospasm).
•Nebulisedsalbutamol2.5-5mg4hourly(ifwheezeispresent).
•Aggressivepulmonarytoilet,atleastevery4hours.797

Ventilation associated pneumonia
(VAP) care bundle
•Headofbed(HOB)elevation30-45degrees.
•Dailysedationhold(unlesscontraindicated,e.g.severeairway
edema).
•Twice-dailyoralhygienecarewith0.12%chlorhexidineinthe
formofsolutionorgelinassociationwithmanualorelectric
toothbrushing.798

Cont.
•ETT-cuffpressuremonitoring(continuouslyoratleast4hourly)
between20-30cmH
2O(<20allowspassageofsecretions
aroundthesidesofthecuff,andapressure>30cmH
2O
increasestheriskoftrachealpressuredamage).
•RegularsuctioningofsecretionspoolingonthetopoftheETT
cuff.799

Common sedation agents for mechanical ventilation
•Propofol:0.4-4mg/kg/hr(rapidonsetandoffset,cancause
hypotension).
•Fentanyl:0.5-2mic/kg/hr(cancausehypotension).
•Ketamine:0.5-2mg/kg/hr(acceptedalternativeif
hypotension).
•Midazolam:0.05-0.1mg/kg/hr(cancausehypotensionand
accumulation).800

Respiratory Monitoring
•Monitorpulseoximetrycontinuously.
•InitialchestX-ray(CXR)onadmissionandrepeatedifclinically
indicated.
•Arterialbloodgases(ABG)every8hoursuntilstabilization&
extubationtheneveryday.
•Regularchestphysiotherapy.
•Considertimelytrachealextubation(whenventilatorisno
longerrequired).
•Prophylacticantibioticsshouldnotbegiven.801

Sedation score
Sedation score (many can be used, Ramsayis an example)
(goal is 2-4)
1)Patientisanxiousandagitatedorrestless,orboth.
2)Patientiscooperative,orientedandtranquil.
3)Patientrespondstocommandsonly.
4)Patientexhibitsbriskresponsetolightglabellartaporloud
auditorystimulus.
5)Patientexhibitsasluggishresponsetolightglabellartaporloud
auditorystimulus.
6)Patientexhibitsnoresponse.802

Circulatory management
•Assesadequatefluidresuscitation(patientswithinhalationinjury
needmorefluid).
•Continuousvitalsignsandelectrocardiogram(ECG)monitoring.
•UrineoutputhourlyforallpatientinICU.
•Centralvenouspressure(CVP)monitoringinallintubatedpatients.
•Vasopressorifmeanarterialpressure(MAP)remainslowdespite
normalCVP.803

Fluid Resuscitation
Parklandformulaforburnresuscitation:
Totalfluidrequirementin24hrs(Ringer’sLactate)iscalculatedasfollows
2-4mlxbodyweight(KG)xtotalburnsurfacearea%(maximal50%)
•50%giveninfirst8hoursSINCETHETIMEOFBURN.
•50%giveninnext16hours
•Incaseofinhalationalinjury,use4mlxTBSA%xBW.
•Inhightensionelectricalinjury,theParklandformulacalculationmay
beashighas6ml×TBSA×weight(kg).804

Fluid Resuscitation
•Childrenshouldreceivemaintenancefluidaswellwhichcontains:
Dextrosee.g.D4.3%NaCl0.18%
•Keepurineoutput0.5-1ml/kg/hrinadultsand1to2ml/kg/hrforchildren.
•Ifthereismyoglobinuria(orariskfactorforrhabdomyolysis),theexpected
urineoutputis200-300ml/hrinadultsand2-3ml/kg/hrinchildren.
•Incaseofinitialoliguria,suspicionofsignificantmusclelysisor
hyperkalemia,use0.9%salineratherthanRinger'sLactatesolution805

Kidney failure prevention
•Earlyrenalfailureafterburninjuryisusuallydueto
delayedorinadequatefluidresuscitation,butitmayalso
resultfromsubstantialmusclebreakdown
(rhabdomyolysis)orhemolysis.806

Management
•Monitorurineoutputhourly.
•Monitorureaandcreatinedaily.
•IfrhabdomyolysissuspectedcheckCPKregularly.
•EnsureAdequatefluidresuscitation.
•Ifnoresponsetofluidmanagement,patientmayneed
earlyhemodialysis.807

Gastrointestinal system
•Stressulcerprophylaxis.
•Earlyfeeding.808

Stress Ulcer Prophylaxis (SUP)
Generalprinciples:
•Adequateresuscitation.
•Earlyenteralfeeding.
•Avoidanceofulcerogenicdrugswheneverpossible(e.g.
NSAID).809

Cont.
Stressulcerprophylaxisshouldbegivenwiththe
followingconditions:
•MechanicalVentilation.
•Coagulopathy(Platelets<50.000orINR>1.5).
•Burninjury>15%TBSA.
•Episodeofsepsis/hypotension.810

SUP Agent Choice
•Famotidine(H2blocker):
•20mgIVq12hr(inpatientswithnogastric/enteralaccess)
•20mgPO/NGTq12hr(inpatientswithgastricfeeds/gastric
access)
•Pediatric:0.25-0.5mg/kgq12hr
IfCrCl<50ml/mingivethesamedosebutq24hr811

SUP Agent Choice
•Proton Pump Inhibitors (patients with overt and clinically
significant GI bleeding):
•EsomeprazoleorOmeprazole:40mgIVq12hours
•Pediatric:
•<10kg5mg q12hours
•10-20kg10mgq12hours
•>20kg10-20mgq12hours812

Cont.
•Initiation
•At the onset of risk factors.
•Duration of Treatment
•Until risk factors resolve and no longer critically ill and feeding
well established (daily review of prescription).
•Signs of GI Bleeding
•High index of suspicion.
•Hypotension, hematemasis, malena, falling hemoglobin.813

Sepsis
•Sepsishasrecentlybeendefinedas“life-threateningorgandysfunctioncaused
byadysregulatedhostresponsetoinfection”.
•Burnpatientslosetheirprimarybarriertoinfection,theskin.
•Sepsisintheburnpatientisadifferentproblemthansepsisinthegeneral
population.
•Sepsisisalsotheleadingcauseofdeathintheburnpatient.
•Watchforthesubtleearlysignsofsepsisandthenpromptinitiationof
aggressivetherapy.814

Cause of sepsis
•Burnwoundsepsis.
•Catheter-relatedinfection.
•Urinaryinfection,
•Pneumonia.
•Others(inthosewithcombinedburntraumainjury).
Physicalexaminationorisolationofapathogeninblood,urine,
orsputumculturesmaysuggestanalternativesourceforsepsis
thanwound.815

Sepsis diagnosis
Suggestive Criteria for Sepsis (two or more):
•Hyper or hypothermia (>39°C or <36.5°C).
•Progressive tachycardia (>100 beats per minute).
•Progressive tachypnea (>30 breaths per minute).
•Leukocytosis or leukocytopenia (>12.000 or <4.000 WBC/microL).
•Thrombocytopenia <100.000 platelets per microliter (3days after burn).
•Refractory hypotension816

Cont.
Andfulfilmentofoneofthefollowingthreecriteria:
1)Culturepositiveinfectionor
2)Pathologictissuesourceidentified(woundtissuebiopsy)or
3)Clinicalresponsetoantimicrobials817

Treatment
•Dependsupontheburnwoundcategoryandconsistsofa
combinationofburnwoundcare(ie,cleansing,dressings),
antimicrobialtherapy(topicalwithorwithoutsystemicagents),and
burnwoundexcisionordebridement.
•Insystemicburnsepsisorsuspectedsepsisanattemptshouldbe
madetoisolatetheorganism(takeculturesincludingblood)before
startingtreatment(thisshouldnotdelayempiricaluse).818

Suggested empirical antimicrobial therapy
•Sepsiswithoutshock:
•Vancomycin+ciprofloxacin(orceftazidime)+amikacin.
•Presenceofsepticshock:
•Vancomycin+meropenem+\-amikacin.
•Whencultureresultisavailableshiftantibioticsaccordingly.
•Adjustdosesofantibioticsifrenalimpairment(after48hrsifAKI).
•Quinoloneantibioticsarenotrecommendedinchildren<12yearsofage.819

Antimicrobial Dosing Recommendations
Agent Dosing recommendations
Piperacillin-tazobactam 4.5 g IV q6h infused over 4 h
Ceftazidime 2 g IV q8h infused over 3 h
Cefepime 2 g IV q8h infused over 4 h
Imipenem 500 mg IV q6h
Meropenem 1–2 g IV q8h
Gentamicin 7 mg/kg (actual body weight) IV q24h
Ciprofloxacin 400 mg IV q8h
Levofloxacin 750 mg IV q24h
Vancomycin 30–60 mg/kg per day
Linezolid 600 mg IV 12h820

Venous Thromboembolism Prophylaxis
•Unlessthereareclinicalsignsofableedingdisorder,active
bleedingorbleedingtendency.Thromboprophylaxis
shouldbeusedfor:
•Allpatientswithage>12yearsor
•Burn≥20%TBSAor
•Riskfactorsfordeepveinthrombosis.821

Risk assessment for Thromboembolism
•Moderateriskpreventivedose:ifburn20to50%TBSAand
largelowerextremityburnsandNODVTriskfactors.
•Highriskpreventivedose:ifburn>50%TBSAandhigh-
voltageAND/ORDVTriskfactor.822

Mechanical prophylaxis
•IntermittentPneumaticCompression(IPC)Deviceshould
beusedforhighriskpatients.
•IPCdevicemaynotbeabletobeeffectivelyplacedon
patientswithlowerextremityburnsduetopatient
discomfortorpossibleinjurytothehealingburnwounds
and/orskingrafts823

Chemoprophylaxis
LMWH:
For high risk: Clexane 0.5mg/kg/12hours
For moderate risk: Clexane 0.5mg/kg/24hours,
If clexane is not available or CrCl<30ml/min use:
Unfractionated heparin (UFH):
•If patient Weight <50kg : heparin 5000 units subcutaneous q12h
•If patient Weight <100kg: heparin 5000 units subcutaneous q8h
•If patient Weight >100kg: heparin 7500 units subcutaneous q8h824

Monitoring
•Notethatperipheraledemacanaltertheabsorptionof
subcutaneously-administereddrugs.
•Monitorforsignsofoverdose(gingivalbleeding,
spontaneousbleeding).825

Risk Factors for DVT
■Stasis
•Surgery, trauma, immobility,
paresis
•Increasing age
•Pregnancy and postpartum
•Heart or respiratory failure
•Obesity
■Vessel Injury
•Previous DVT
•Smoking
•Varicose veins
•Central venous catheterization
■Hypercoagulability
Increasing age
Malignancy
Cancer therapy
Estrogen therapy (OCP or HRT)
Acute medical illness
Inflammatory bowel disease
Nephrotic syndrome
Myeloproliferative disorders
Inherited or acquired thrombophilia826

Case
•A60-year-oldmanisrescuedfromahousefireandbroughttothe
emergencydepartment.Accordingtoparamedics,thepatientwas
foundunconsciousinanupstairsbedroomofahouse.Thepatient’s
pastmedicalproblemsareunknown.Hispulseis112beats/min,
bloodpressure150/85mmHg,andrespiratoryrate30breaths/min.
Apulseoximeterregisters92%O2saturationwithafacemask.His
faceandtheexposedportionsofhisbodyarecoveredwitha
carbonaceousdeposit.Thepatienthasblisteringandopenburn
woundsinvolvingthecircumferenceofhisleftarmandleftlegand
morethan80%ofhisbackandbuttocks.Hedoesnotrespond
verballytoquestionsandreactstopainfulstimulationwith
occasionalmoans.827

Summary
A 60-year-old man presents with an approximately 40% total body
surface area (TBSA) burn injury and inhalation injuries and was found
unconscious.828

Question 1
1.Whatisthemostappropriatenextstep?
Definitiveairwaymanagementbyintubationisappropriate
inthispatientwithpossibleinhalationinjuriesandcarbon
monoxide(CO)poisoning.829

Question 2
2.Whataretheimmediateandlatecomplications
associatedwiththermalinjuries?
•Airwaycompromiseandtissuehypoperfusionarecommon
earlycomplications,
•Sepsisandfunctionallossarepossiblelatecomplications.830

Considerations
•Giventhecircumstancessurroundingtheinjury(ahousefire),thesizeof
theburn,andtheageofpatient,allofwhichindicateahighlikelihoodof
pulmonarycomplications,immediateintubationisclearlyindicated.
•Personsatriskforupperairwaythermaldamageincludethisparticular
patientbecausehewasfoundunconsciousinaclosed-spacefire.
•FluidresuscitationwithlactatedRingersolutionshouldbeinitiatedbased
on2to4mL/kg/%burn.
•Unlessthepatientisalreadyatafacilitythatspecializesinburncare,
immediatearrangementsshouldbemadeforatransferafterinitial
stabilization.831

Burn complications
•Systemic:Burnslargerthan20%TBSAareassociatedwithsystemic
hypermetabolicresponses.
•Theseresponsesincludetheactivationofthecomplementandcoagulation
pathwaysproducingmicrovascularthromboses,capillaryleak,and
interstitialedema.
•Thesystemicactivationoftheproinflammatorycascadealsotriggers
subsequentcounter-regulatoryanti-inflammatoryreactionsthatproduce
subsequentimmunesuppressionandincreasedsusceptibilitytonosocomial
infectionsandsepsis.832

Whichofthefollowingisthemostappropriateresuscitationstrategyfora
30-year-oldmanweighing70kgwitha40%TBSAburnwound?Usethe
Parkland formula for this determination.
A.D5%0.45%NSataninitialrateof700mL/hfortheinitial8hours
followedbyarateof350mL/hforthenext16hours.
B.LactatedRingersolutionat350mL/hfortheinitial8hoursfollowedby
aninfusionrateof700mL/hforthenext16hours.
C.LactatedRingersolutionataninitialrateof700mL/hforthefirst8
hoursfollowedbyaninfusionrateof350mL/hforthenext16hours.
D.LactatedRingersolutionat500mL/hforthefirst8hoursandthen
titratetheIVinfusionratetoanhourlyurineoutputof0.5mL/kg.
E.LactatedRingersolutionat700mL/hoverthefirst8hoursandinfusion
totitratetoanhourlyurineoutputofgreaterthan0.5mL/kg/h833

Whichofthefollowingisthemostappropriateresuscitationstrategyfora
30-year-oldmanweighing70kgwitha40%TBSAburnwound?Usethe
Parkland formula for this determination.
A.D5%0.45%NSataninitialrateof700mL/hfortheinitial8hours
followedbyarateof350mL/hforthenext16hours.
B.LactatedRingersolutionat350mL/hfortheinitial8hoursfollowedby
aninfusionrateof700mL/hforthenext16hours.
C.LactatedRingersolutionataninitialrateof700mL/hforthefirst8
hoursfollowedbyaninfusionrateof350mL/hforthenext16hours.
D.LactatedRingersolutionat500mL/hforthefirst8hoursandthen
titratetheIVinfusionratetoanhourlyurineoutputof0.5mL/kg.
E.LactatedRingersolutionat700mL/hoverthefirst8hoursandinfusion
totitratetoanhourlyurineoutputofgreaterthan0.5mL/kg/h834

Answer
•Forthis70-kgmanwith40%TBSAburn,thetotalvolume=4mL×70kg×
40%=11,200mL.
•Halfoverthefirst8hourswouldbe5600mL/8h=700mL/h.
•Forthesubsequent16hours,infusionvolume=5600mL/16h=350mL/h.
•TheParklandformulaisrecommendedfluidadministration.Itisa
guidelineorstartingpointforfluidadministration835

Question 2
Whichofthefollowingisthemostappropriatenextstep,ifthepatient
describedabovehasanaveragehourlyurineoutputoflessthan15mL/h
duringthefirst4hoursofhisburnresuscitation?
A.Initiatevolumeresuscitationwith5%salt-freealbumin.
B.AdjustIVfluidratetoachieveanaverageurineoutputof3mL/kg/hforthenext
fewhours.
C.AdjustIVfluidratetoachieveaverageurineoutputof0.5to1.0mL/kg/h.
D.Initiatedopaminedripat0.3μg/kg/mintoimproverenalperfusion.836

Answer 2
Whichofthefollowingisthemostappropriatenextstep,ifthepatient
describedabovehasanaveragehourlyurineoutputoflessthan15mL/h
duringthefirst4hoursofhisburnresuscitation?
A.Initiatevolumeresuscitationwith5%salt-freealbumin.
B.AdjustIVfluidratetoachieveanaverageurineoutputof3mL/kg/hforthenext
fewhours.
C.AdjustIVfluidratetoachieveaverageurineoutputof0.5to1.0mL/kg/h.
D.Initiatedopaminedripat0.3μg/kg/mintoimproverenalperfusion.837

Answer 2
•Giventhispatient’syoungage,thepatient’slowurineoutputispossiblyrelatedto
inadequatefluidadministration;therefore,adjustmentofIVfluidinfusionrate
maybeappropriate.
•Ifthepatientcontinuestorespondinadequately,centralvenouspressure(CVP)
monitoringmaybeneededtoguidetherapy.
•Theinfusionofcolloidssuchasalbuminmaypotentiatecapillaryleakandtissue
swellingduringtheinitial8hoursofresuscitation.
•Dopaminetherapyshouldnotbeinitiateduntilintravascularvolumehasbeen
adequatelyrestored.838

17)Nutrition in ICU
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care 839

•Dietsare composed of nutrients: macronutrients (protein, fats and
carbohydrates) and micronutrients(vitamins, minerals and trace
elements).
•Malnutritionis caused by an imbalance (deficiency or excess) of
energy, protein and other nutrients.
•Malnutritionleads to adverse effects on tissue/body form, function
and clinical outcome.840

▪Preservingtissuemass.
▪Decreasingcatabolismandusageofendogenousnutrientstores.
▪Maintainingorimprovingorganfunction(immune,renal,hepatic
systems;muscle,maintaininggutbarrier).
▪Improvewoundhealing&decreaseinfectionrate.
▪Decreasingmorbidityandmortality&overalloutcomeandLOS.
Goals of nutritional support for critically ill patients 841

Consequences of malnutrition
❑Underfeeding :
-Loss of muscle mass
-Reduced respiratory function
-Reduced immune function
-Poor wound healing
-Gut mucosal atrophy
-Reduced protein synthesis842

Consequences of malnutrition
❑Overfeeding:
-Increased oxygen consumption (VO
2)
-Increased CO
2production (VCO
2)
-Hyperglycemia
-Fatty infiltration of liver843

Starvation
•++Glycogenolysis(storesdepletedwithin24hrs)
•++Lipolysis(Glycerol“glycolysis”&F.A.“ketosis”)
•++Gluconeogenesis
(a.a“glutamine,alanine,”F.A,)
•Neurons,RBCs,renalmedullautilizeglucosenormally
•Glucoseadministrationdecreasesproteincatabolism&ketosis844

Nutritional Assessment Tools
•No single standard way of assessing nutritional status.
•Various validated assessment tools developed:
•Some disease specific
•Some age specific
•Example:
Subjective Global Assessment (SGA)
Mini Nutritional Assessment (MNA)845

DIAGNOSIS OF MALNUTRITION
oAnthropometric measurements:
(e.g. skin fold thickness, mid-arm circumference). These are unreliable
due to weight gain/loss, fluid shifts and edema.
oBiochemical tests:
-Albumin falls as part of the acute phase response,
-Hemoglobin may be affected by disease process, hemorrhage,
transfusion, hemolysis, bone marrow suppression,
oBody Mass Index:
BMI = mass (kg) / height (m)2
Although low BMI is a predictor of higher mortality in ICU, acute
changes do not accurately reflect nutritional status.846

Timing of Nutritional Support
•Datasuggestthatoutcomecanbeimprovedwithearlyand
optimalnutritionalsupport.
•Currentrecommendationsincludeinitiationofnutritional
supportwithinthefirst24to48hoursafteradmissiontothe
ICU.847

•TheaverageREEisapproximately25kcal/kgIBW/day
•IBWmale=50+2.3×(HtInch-60)
•IBWfemale=45.5+2.3×(HtInch-60)
•Caloricrequirementofthecriticallyillpatientishigherastheyarehypercatbolic
accordingtothestressfactor:
•Trauma:REE×1.3
•Sepsis:REE×1.5
•Burn:REE×2(especiallyifextensiveanddeep)
Caloric requirement and composition848

•Mixtureinwhichtotaldailykilocaloriesaresplitinto20%protein,
30%lipids,and50%carbohydrates
•Mostpatientsrequire1to1.5g/kgofproteindailyor7-14gof
nitrogendaily(6.25gofproteincontains1gofnitrogen).
•Patientswithorganfailureordiseasemayhaveincreasedor
decreasedneedsandshouldbeconsideredindividually.
Caloric requirement and composition849

Quantity of nutrient
➢Calories
-Lipids provide 9 kcal/g
-Carbohydrates provide 4 kcal/g
-Proteins provide 4 kcal/g.850

851

852

Daily requirement of water and electrolytes853

Working example
Calculatethecaloricrequirementandcompositionforan80kgpatientwho
ishavingsepsisinICU.
•REE=80×25=2000Kcal/day
•Requirementinsepsis=1.5×2000=3000Kcal/day
•Composition:50%carbohydrates(1500Kcal)“1500mlD25%”
30%lipids (900Kcal)“500mlIntralipid20%”
20%protein (600Kcal)“750mlAminosol20”
Totalcalories3000Totalfluid2750ml854

855

What is the preferred feeding method
•Oralfeedingistheoptimalrouteofnutritionalsupport.
•HowevermostICUpatientsareincapableorintolerantoforaldietandare
thereforefedenterallyorparentrally
•Enteralnutritionisrequiredforoptimalgutfunction&maintenanceofgut
barrier.
•Enteralnutritionislessexpensivethanparenteralnutrition.
•Enteralnutritionisthepreferredrouteofnutritionalsupportinboth
pediatricandadultpatients.856

•Parenteral nutrition is indicated when enteral nutrition is not possible,
for example :
•Intestinal obstruction/perforation.
•Non-functioning gut, prolonged ileus
•High output gastrointestinal fistula.
•Esophageal/gastric surgery.
•TPN is not superior to enteral nutrition in patients with inflammatory
bowel disease or pancreatitis.
Enteral vs Parenteral nutrition857

Enteral nutrition
-Enteralnutritionshouldbestartedwithinthefirst24-48hoursof
admission(unlesscontraindicated).
-Routesincludenaso-gastric,naso-duodenal/jejunal,gastrostomy
andjejunostomy.
-Enteralfeedingprovidesamorecompletedietthanparenteral
nutrition,maintainsstructuralintegrityofthegut,improvesbowel
adaptationafterresectionandreducesinfectionrisk.858

Enteral nutrition859

Enteral nutrition
❑Feed composition
-Most patients tolerate iso-osmolar, non-lactose feed.
-Carbohydrates are provided as sucrose or glucose polymers.
-Protein as whole protein or oligopeptides
-Fats as medium chain (better absorbed) or long chain
triglycerides. 860

Enteral nutrition
-Feed is formulated at 1 cal/ml .
-Special feeds are available, e.g. high fiber, high protein-calorie,
restricted salt, high fat or concentrated (1.5 or 2Cal/ml) for fluid
restriction.861

-Confirmtubeposition
-Securetubewellandchecksiteregularlyforpotentialtube
dislodgment.
-Startfeedingearly.
-Aspirateregularly(4hourly)andacceptgastricresidualvolumes
of200ml.
Important steps to ensure adequate enteral nutrition862

•Patient should be head-up tilt at least 30°.
•Avoid bolus feeds.
•Use prokinetics early: metoclopramide 10mg IV 8 hourly +/-
erythromycin 75mg IV 6 hourly.
•Consider switch to post-pyloric tube feed.
Development of diarrhea associated with tube feeding needs further
evaluation.
Minimize aspiration risk 863

-Onceadecisionismadetostartenteralnutrition,30ml/hfullstrength
standardfeedmaybestartedimmediately.
-After4hat30ml/hthefeedshouldbestoppedfor30minpriorto
aspirationofthestomach.
-Itisreasonabletoacceptanaspirateof<200mLasevidenceofgastric
emptying,andthereforetoincreasetheinfusionrateto60mL/h.
-Ifthegastricaspiratevolumeis>200mltheinfusionrateisnotincreased
butthefeediscontinued
Management of enteral nutrition864

•Bolus:300to400mlrapiddeliveryviasyringeseveraltimesdaily
•Intermittent:300to400ml,20to30minutes,severaltimes/dayviagravity
driporsyringe
•Cyclic:viapumpusuallystartsatnightandends16-18hourslater
•Continuous: via gravitydrip or infusionpump
Methods of Enteral Nutrition Administration865

•Tubeplacement:tracheobronchialintubation,nasopharyngealperforation,
intracranialpenetration(basalskullfracture),esophagealperforation.
•Reflux
•Pulmonaryaspiration
•Nauseaandvomiting
•Abdominaldistension
Complications of Enteral feeding 866

•Diarrhea:largevolume,bolusfeeding,highosmolality,infection,
lactoseintolerance,antibiotictherapy,highfatcontent.
•Constipation
•Metabolic:dehydration,hyperglycemia,electrolyteimbalance.
Cont.867

Feed composition
-Carbohydrate is normally provided as concentrated glucose.
-30–40% of total calories are usually given as lipid (e.g. soya bean
emulsion).
-The nitrogen source is synthetic, crystalline L-amino acids which
should contain appropriate quantities of all essential and most non-
essential amino acids.
Parenteral nutrition868

•Carbohydrate,lipidandnitrogensourcesare
usuallymixedintoalargebaginasterile
pharmacyunit.
•Vitamins,traceelementsandappropriate
electrolyteconcentrationscanbeachievedina
singleinfusion,thusavoidingmultiple
connections.869

Formulation of TPN870

•Centralvenous
-Adedicatedcatheter(ormultilumencatheter)isplacedunder
sterileconditions
-Forlong-termfeeding,asubcutaneoustunnelisoftenused.
-Thismayreducetheriskofinfectionandclearlyidentifiesthe
specialpurposeofthecatheter.
Choice of parenteral feeding route871

-Ideally,bloodsamplesshouldnotbetakennorotherinjectionsor
infusionsgivenviathefeedinglumen.
-Thecentralvenousrouteallowsinfusionofhyperosmolar
solutions,providingadequateenergyintakeinreducedvolume.872

Peripheralvenous
•Parenteralnutritionviatheperipheralrouterequiresasolutionwith
osmolality<800mOsmol/kg.
•Eitherthevolumemustbeincreasedortheenergycontent
(particularlyfromcarbohydrate)reduced.
•Peripheralcannulasitesmustbechangedfrequently.
Peripheral PN873

Peripheral PN
•5 -10 % Glucose
•3 -4 % A.A.
•1 % Lipids
•Osmolarity :not exceeding 800 mOsm/Litre
Unfortunately,volumerestrictionusuallylimitscaloric
intaketoonly1500-1800Kcal/day.Thus,givenforshort
period874

•Catheter related: misplacement, infection, thromboembolism
•Metabolic:--/ ++ CHO, Fat, Protein, electrolytes, vitamin
•Fluid excess
•Hyperosmolar, hyperglycemic state
•Rebound hypoglycemia: (abrupt TPN withdrawal)
•Hypophosphatemia
•Pancreatitis, Cholestasis & Fat embolism
•Hypercarbia
•Metabolic acidosis: hyperchloremia, metabolism of cationic amino
acids
Complications of TPN875

Monitoring TPN
•S. Glucose/4 hrs
•S. Triglycerides 6 hrs after end of infusion (normal)
•Nitrogen balance Alb (&LFTs) weekly
•Fluid balance & KFTs daily
•Electrolytes daily
•Complete & Differential blood count876

877

878

18)Diabetic Emergencies
1
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care 879

1.Hypoglycemia
2.Diabetic Ketoacidosis
3.Hyperosmolar nonketoticcoma
2880

Hypoglycemia
•20%ofdiabetesmellitususinginsulinororal
hypoglycemicagentswillexperiencesymptomsof
hypoglycemiaintherelifetime.
•Itisdefinedasadecreaseinthebloodglucoselevelorits
tissueutilizationthatresultsindemonstrablesignsor
symptoms.
•Todiagnosehypoglycemia,theWhippletriadispresent:
oThedocumentationoflowbloodsugar.
oPresenceofsymptoms.
oReversalofthesesymptomswhenthebloodsugar
levelisrestoredtonormal.881

Investigation
•Glucosebedsidetestisessentialforseriouslyillpatient
•Hypoglycemiaisdefinedaccordingto:
<50mg/dLinadults
<40mg/dLininfantsandchildren
•Cut-offvalueofequaltoorlessthan70mg/dlforalerting
patientsandcaregiverstotheriskfordeveloping
hypoglycemia.
•Previousbloodsugarlevelscaninfluenceanindividual's
responsetoaparticularlevelofbloodsugar.882

Causes
ExplainMnemonic:
•Ex: Exogenous drugs: (insulin or oral hypoglycemics)
•Pituitary insufficiency :
•Liver failure :
•Addison's disease :
•Islet cell tumors ( insulinoma)
•Non-pancreatic neoplasms
5883

Pathophysiology
•Glucoseistheprincipalenergysubstrateforthemyocardium
andbrain,sohypoglycemiadepressesmyocardialcontractility
andaltermentalstatus(similartoshock)
•Theorgansystemsthatmanifestthesignsandsymptomsof
hypoglycemiaarethecentralandautonomicnervoussystems.
•HypoglycemiashouldbeconsideredintheDDinanypatient
withalteredmentalstatusorfocalneurologicalsigns
•Delayintreatmentcanresultinprofoundsequelae,including
death.884

Symptoms of hypoglycemia 885

ICU Admission
•Massive insulin or OHA ingestion
•Marked malnutrition
•Sepsis
•Acute hepatic failure
8886

Treatment
Glucosesupplement
•0.25-0.5g/kg(D50%,D20%orD10%),administrationwithin15
minutes.Measureabloodglucose15minutesaftertheIVbolus.
•Readministerasecondbolusofglucoseasneededtomaintainthe
bloodglucoseabove80mg/dLoruseacontinuousinfusionifneeded.
•Leakofhypertonicglucosecausescutaneousnecrosis.
Glucose-elevatingagents
Glucagonhydrochloride(insulinantagonist):1mgIM/SC(onsetof
action7-10min-slowerthandextrose),followedbycarefulglucose
monitoringandoralorintravenousglucoseadministration.887

Diabetic ketoacidosis
(DKA)
10888

Diabetic ketoacidosis
Diabeticketoacidosis(DKA)isametabolicemergency
characterizedbyInsulindeficiency&:
•Ketoacidemia(Ketonuria).
•Hyperglycemia(Glucosuria).
•Hypertonicdehydration(Osmoticdiuresis).
11889

Epidemiology
•MostpatientspresentingwithDKAhavetype1DM,but,
thosewithtype2DMcanalsodevelopDKAduringtimes
ofsignificantphysiologicstress.
•OverallmortalityfromDKAislessthan5%.
•Mortalityincreasessubstantiallywithextremesofage,
thepresenceofcoma,orthedevelopmentof
hypotension.
12890

Pathophysiology
•Seriousdysregulationofnormalglucosehomeostasis.
•Hyperglycemiaandketonebodyformation&subsequent
systemicsequelae.
•Adeficiencyininsulinproduction,combinedwithanexcess
productionofcertaininsulincounterregulatoryhormones.
•Productionofproinflammatorycytokinesduetoprotein,
lipid,andcarbohydratemetabolismdisruption.891

Cont.
•Hepaticgluconeogenesis,glycogenolysis,and
lipolysis&decreasedperipheralinsulinuptake.
•Ketosisisworseningglucosehomeostatic
decompensation.
•Thenormalbufferingsystemsarerapidly
overwhelmedbytheongoinghydrogenload,and
highaniongapacidosisdevelops.892

Cont.
•Hypertonicintravascularenvironment,cellular
dehydrationandelectrolyteshifts.
•Osmoticdiuresisofwaterandelectrolytesoccurs.
•Sodium,potassium,magnesium,calcium,chloride,and
phosphatearealllostduringthisosmoticdiuresis.
•Poororalintakeandprotractedvomiting.
•FurtherincreaseinCRH.893

Factors most often associated with the
development of DKA
Approximate
frequency (%)
Factor
35Infection
30Omission of insulin or inadequate insulin
20Initial presentation of diabetes mellitus
10Medical illness
5Unknown894

Presentation and Diagnosis
1)Thorough patient history.
2)Focused physical examination.
3)Appropriate laboratoryanalysis. 895

1)History
•Polyuria,polydipsia,weightloss,andlethargy.
Nausea,vomiting,andabdominalpainsignify
anovertDKA.
18896

2)Physical examination
•Dehydration,tachycardia,hypotension,prolonged
capillaryrefilltime,poorskinturgor,drymucous
membranes,andweightloss.
•Additionally,Kussmaulrespirations,anacetone
breathodor,depressedmentalstatus,andevenfocal
neurologicdeficitsorcoma.897

3)Laboratory analysis
•glucose,serumelectrolytes,serumosmolality,urea,
creatinine,arterialorvenousbloodgas,serum
ketones,andurinalysisshouldbeorderedinpatients
withsuspectedDKA&appropriatecultures.
•Other tests:(β-HCG), ECG, CXR, and CT may be
indicated, depending on the clinical scenario.
Total serum osmolality = (Na ×2) + (Glu /18) + (BUN /2.8)
Anion Gap = Na –( Cl + HCO3) 898

Diagnostic Criteria for DKA
HHS DKAParameter
> 600> 250Plasma glucose
> 7.30< 7.30Arterial pH
> 15< 18Serum bicarbonate (mmol/L)
< 12> 12Anion gap
>320VariableSerum osmolality (mOsm/kg)
NoneModerate to highSerum ketones
NoneModerate to highUrine ketones899

Typical deficits
Water: 6 L, or 100 mL per kg body weight
Sodium: 7 to 10 mEqper kg body weight
Potassium: 3 to 5 mEqper kg body weight
Phosphate: ~1.0 mmolper kg body weight900

Translational hyponatremia
•ECFosmolalityrisesandexceedsthatofICFresultingin
movementofwateroutofcellsintotheECF.
•SerumNaconcentrationfallsinproportiontothedilutionof
theECF,declining2mEq/Lforevery100mg/dLincrementin
theplasmaglucoselevelabovenormal.
•Corrected Sodium=
Measured sodium + {[(glucose -100)/100] x 2 {
•Example: Na 130, Glu600.
•Corrected Sodium = 130 + {2x (600-100)/100{
= 130 + 10 = 140901

Management
1)Initial resuscitation.
2)Correction of hyperglycemia and resolution
of ketosis.
3)Treatment of any precipitating causes.
4)Provide chronic therapy to prevent repeated
episodes.902

Initial resuscitation
•Airwayandrespiratorycare.
•Intravascularvolumeresuscitation.
–Correctingthehemodynamicinsults.
–Replacethefluiddeficitoverthefirst24-48hr.
–0.9percentsalinesolutionadministeredatarateof7to
14mLperkgperhouraccordingtovolumestatus.
–Oncethepatientiseuvolemic,givefluidaccordingtothecorrected
serumsodium(iflowgiveNS,ifcorrectedNa>135give0.45%NaCl).
•TheadditionInsulin&Potassiumtothefluids.903

Insulin therapy
•Initialbolusofregularinsulinof0.1U/kg(ifK>3.3)followedby
aninfusionat0.05to0.1U/kg/hour,withagoalofdecreasing
plasmaglucoselevelsbynomorethan50to75mg/dL/hour.
•Duplicationofinfusionrateiftheplasmaglucoseleveldoesnot
respondappropriatelyinthefirstfewhours.
•Ifglucoseconcentrationreaches200mg/dL,theinsulin
infusionrateshouldbedecreasedby50%,anddextroseshould
beaddedtothereplacementfluid.904

Potassium replacement
•Potassium replacement should begin once the serum
potassium concentration falls below 5.5 mEq/L, assuming
adequate urine output using the following guidelines:
–K+ level: 4 to 5 mEq/L, add 20-30 mEq KCL/liter of IV fluid.
–K+ level: 3 to 4 mEq/L, add 30-40 mEq KCL/liter of IV fluid.
–K+ level: < 3 mEq/L, add 40-60 mEq KCL/liter of IV fluid
Stop insulin infusion if K+<3.3 mEq/L & give 20meq KCL
per hour till K+ >3.3 then resume insulin. 905

Bicarbonate Therapy
Indication
•pH < 6.9
•pH < 7.0 after 1 hr of hydration
•Circulatory failure due to acidosis
•Hyperkalemia with ECG changes
*If given, dose 1-2 meq / kg and should be given as a
nearly isotonic solution and administered as slow
infusion over 1-2 hours (never bolus). 906

Bicarbonate Therapy
•TheuseofbicarbonateinapatientwithapHgreater
than7.0isnotrecommended.
–plasmabicarbonateconcentrationincreaseswithinsulin
therapy.
–bicarbonatetherapycarriesrisks,includinghypokalemia,
sodiumoverload,intracellularacidosis,paradoxicCSF
acidosis,hypoxiaandhyperosmolality907

Criteria for resolution of DKA
•Glucose <200 mg/dL.
•Serum bicarbonate ≥15 mEq/L.
•Venous pH >7.3.
•Anion gap <12 mEq/L.
•Recently, β-OHB <1 mmol/L908

Shifting to subcutaneous insulin
•AfterresolutionoftheDKAepisode.
•Thepatientisabletotolerateenteralnutrition.
•Intravenousinsulinshouldbecontinuedfor1to2
hoursfollowingthefirstdoseofsubcutaneous
insulin.909

Working example for shifting
•Calculatetherequiredinsulinintheprevious24hours(e.g.48
units).
•Take60-80%ofthoserequiredinsulin(toavoidhypoglycemia),
assume2/3forsimplicity(32unitsinourcase).
•Dividethecalculateddoseinto2/3intermediate&1/3rapid
acting(approximately20intermediate&12rapidacting).
•Intermediateinsulinisgiveninto2doses(10unitseach)&rapid
actingisgivenatmeal(4unitseach).
32910

Monitoring
•Criticalcareadmission:
–Patientswitholiguriaorhypotensionrefractoryto
initialrehydration.
–Mentalobtundation.
–Respiratoryinsufficiency.
–Pregnancy.
–Significantcomorbiditiesorprecipitatingevents,
suchasMIordecompensatedCHF.911

Monitoring
•MildtomoderateDKAmayrequireNIBPmonitoring
•Severediseasestatesandcomorbiditiesmayrequire
arterialandcentralvenouscatheterization.
•Recently,β-hydroxybutyrate(β-OHB)levelsasthe
preferredmethodofmonitoringDKA
34912

Monitoring
•Theserumglucoseshouldinitiallybemeasuredevery
houruntilstable.
•SerumelectrolytesandvenouspHshouldbemeasured
everytwotofourhours,dependingupondisease
severityandtheclinicalresponse.913

Complications
▪Hypoglycemia
▪Hyperglycemia
▪Electrolyte disturbances (hypokalemiathe most common
cause of death in adults, hyperkalemia)
▪Hyperchloremicmetabolic acidosis
▪Cerebral edema (the most common cause of death in children)
▪Intravascular volume overload
▪Thromboembolism 914

Complications
are iatrogenic and preventable
THERAPEUTIC ERROR COMPLICATION
Delay in starting IV Shock, thrombosis
Rapid / hypotonic fluidsCerebral edema
High dose insulin Hypoglycemia, hypoK+, CE
Injudicious use of HCo3 Alkalosis, hyperNa+,
hypoK+, CNS acidosis→CE
Delay in giving K+ /
Over Rx with K+
Hypokalemia /
Hyperkalemia
Excess chloride Hyperchloremicacidosis915

Hypoglycemia & Hyperglycemia
•Hypoglycemicepisodescanbedecreased:
–institutionoflow-doseinsulinprotocols.
–additionofdextrose-containingsolutionstointravenous
fluidwhenthebloodglucoseconcentrationreaches200
mg/dL.
–frequentbloodglucosemonitoringwithfrequentinsulin
infusionratetitration.
•Hyperglycemicepisodescanbedecreased:
adequateoverlapofsubcutaneousinsulintherapy.916

Hypokalemia
•Duringinsulintreatment,treatmentoftheacidemic
statewithbicarbonateandinadequatepotassium
replacementpredisposespatientstohypokalemia.
•Hypokalemiamaybeassociatedwithdysrrhythmias,
skeletalmuscleweakness,andileus.917

Cerebral edema
•Itoccursmorecommonlyinpediatricpopulations.
•Upto1%ofthepatientstreatedforDKA.
•Relatedtoarapidcorrectionofthehyperosmolarstate.
Prevention:
✓Changeinserumosmolalityshouldnotexceed3
mOsm/kg/hour.
✓Checkserumosmolalityevery4to6hours.
✓Slowlycorrectsodiumandwaterdeficits
✓Avoidrapiddecreasesinbloodglucoselevels918

41
Treatment of diabetic
ketoacidosis in adults919

Treatment of hyperosmolar
hyperglycemic state in adults920

43
Hyperosmolar NonKetotic Coma (HNKC)
Or
Hyperosmolar Hyperglycemic State (HHS)921

Hyperosmolar nonketotic coma
oAnacutemetaboliccomplicationofdiabetesmellitus
characterizedbyimpairedmentalstatusandelevated
plasmaosmolality(>320mosmol/L))inapatientwith
hyperglycemia(usually>600mg/dl).
oOccurspredominatelyinTypeIIDiabetics
oAfewreportsofcasesintypeIdiabetics.
44922

Hyperosmolar nonketotic coma
Symptoms:
oPolyuria
oPolydipsia
oFatigue, Blurred vision
oNausea, Vomiting, Abdominal Pain
oDisturbed consciousness level
45923

Hyperosmolar Nonketotic Coma
•Plasma osmolarity >320 mosm/l
•Plasma glucose >600
•Diabetic diuresis
•Lack of ketoacidosis
•Coma
•The average age is higher than DKA
•Prolonged prehospital phase > DKA
46924

Treatment
oHydration:
oEvenmoreimportantthaninDKA
oFindunderlyingcauseandtreat
oInsulindrip:
oShouldbestartedonlyonceaggressivehydration
hastakenplace.
oSwitchtosubcutaneousregimenonceglucose250-
300mg/dlandpatienteating.
47925

Treatment of HHS
oSerialElectrolytes:
oPotassiumreplacement.
oComplications:
oHighmortalityrate(40-50%)becauseof
coexistenceofseriousmedicalproblem
oCommon complications:brainedema,cerebral
hemorrhage,thromboembolization,acutetubular
necrosis,andMI
48926

Question 1
Thepathogenesisofhyperglycemiaindiabeticketoacidosis
includesallthefollowingmechanismsexceptfor:
A.Increasedglycogenolysisintheliver.
B.Increasedgluconeogenesisinthekidneys.
C.Increasedserumglucagon.
D.Increasedgluconeogenesisinadiposetissue.
E.Decreasedglucoseuptakefromthemuscles.
49927

Answer 1
Thepathogenesisofhyperglycemiaindiabeticketoacidosis
includesallthefollowingmechanismsexceptfor:
A.Increasedglycogenolysisintheliver.
B.Increasedgluconeogenesisinthekidneys.
C.Increasedserumglucagon.
D.Increasedgluconeogenesisinadiposetissue.
E.Decreasedglucoseuptakefromthemuscles.
50928

Question 2
A67year-oldpatientpresentstotheemergencyroomwith
uncontrolleddiabetes.Thefollowinglaboratoryvaluesare
found:plasmaglucose920mg/dl(51.1mmol/L),serumNa+148
mEq/L,serumK+3.9mEq/L,BUN68mg/dl(24.3mmol/L).The
effectiveserumosmolalityis:
A.355.5
B.347.1
C.371.4
D.379.8929

Answer 2
A67year-oldpatientpresentstotheemergencyroomwith
uncontrolleddiabetes.Thefollowinglaboratoryvaluesare
found:plasmaglucose920mg/dl(51.1mmol/L),serumNa+148
mEq/L,serumK+3.9mEq/L,BUN68mg/dl(24.3mmol/L).The
effectiveserumosmolalityis:
A.355.5
B.347.1
C.371.4
D.379.8
Ureaisfreelypermeablethroughthecell
membraneviaspecificureatransportersso
thereisnoeffectiveosmoticpressureelicited
byhighconcentrationsofurea.930

Question 3
Whatisthefirststepinthemanagementofdiabetic
ketoacidosis?
A.Toprovidefluidsintravenously
B.Toprovideinsulin
C.Toprovidebicarbonate
D.Toinitiateinsulinandfluidssimultaneously
53931

Answer 3
Whatisthefirststepinthemanagementofdiabetic
ketoacidosis?
A.Toprovidefluidsintravenously
B.Toprovideinsulin
C.Toprovidebicarbonate
D.Toinitiateinsulinandfluidssimultaneously
54932

Question 4
A35year-oldfemalewithdiabeticketoacidosisisadmittedto
thehospitalwiththefollowingprofile:serumglucose412mg/dl,
pH7.12,K+4.4mEq/L,Na+141mEq/L.Whichofthefollowingis
theappropriateinitialtreatment?
A.Administrationofhypotonicsodiumchloride(0.45%)
solution,potassium,andinsulin.
B.Administrationofnormalsalineandinsulin.
C.Administrationofnormalsaline,potassium,andinsulin.
D.Administrationofnormalsaline,potassium,insulin,and
bicarbonates.
55933

Answer 4
A35year-oldfemalewithdiabeticketoacidosisisadmittedto
thehospitalwiththefollowingprofile:serumglucose412mg/dl,
pH7.12,K+4.4mEq/L,Na+141mEq/L.Whichofthefollowingis
theappropriateinitialtreatment?
A.Administrationofhypotonicsodiumchloride(0.45%)
solution,potassium,andinsulin.
B.Administrationofnormalsalineandinsulin.
C.Administrationofnormalsaline,potassium,andinsulin.
D.Administrationofnormalsaline,potassium,insulin,and
bicarbonates.
56934

Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
19)Critical Care Management
of Obstetric Emergency
Critical Care 935

Obstetric Emergencies
1)CardiacArrestinPregnancy
2)Eclampsia
3)AcuteRespiratoryFailureDuringPregnancy
4)SevereObstetricHemorrhage
5)JaundiceinPregnancy936

1) Resuscitation of the Pregnant Patient in
Cardiac Arrest
Modifications of cardiopulmonary resuscitation
Patient Positioning
ImportantstrategytoimprovethequalityofCPRand
resultantcompressionforceandoutput.
Thepregnantuterusespeciallyof>20weeksgestation
orgraviduteruspalpatedabovetheumbilicus,
compressestheinferiorvenacava,impedingvenous
returnandtherebyreducingstrokevolumeandcardiac
output.937

Leftlateraltilt-30
degreesusingwedge
(hard)ofpredetermined
anglee.g.Cardiffwedge.
ManualLeftUterine
Displacement(LUD),
withthepatientin
supine,alsorelieves
aortocavalcompression.938

Leftuterinedisplacement:
withthe 2-handed
technique
Thepatient’srightsidewith
the1-handedtechnique,
depending on the
positioningof the
resuscitationteam.
Ifchestcompressions
remaininadequateafter
lateraluterinedisplacement
orleft-lateraltilt,immediate
emergencyCesareansection
shouldbeconsidered.939

Circulation
•Chestcompressionsshouldbe
performedslightlyhigheron
thesternumthannormally
recommendedtoadjustfor
theelevationofthe
diaphragmandabdominal
contentscausedbythegravid
uterus.
•Positionisslightlyabovethe
centreofthesternum.
•Currentrecommendeddrug
dosages forusein
resuscitationofadultscan
alsobeusedinresuscitation
ofthepregnantpatientin
cardiacarrest.940

Defibrillation
•Managementofventriculararrhythmiasrequire
defibrillationduringmaternalresuscitation.
•Thereshouldbenodelayifuseofdefibrillationis
indicated.
•EnergylevelsaresameasACLSprotocol.
•Beforedeliveringtheshock,REMOVEFETAL
MONITORING EQUIPMENTS toprevent
electrocutioninjurytopatientorrescuer.941

Causes of cardiac arrest
MnemonicwasdevisedbytheAmericanHeartAssociation
tohelpprovidersremembercausesofcardiacarrestthat
shouldbeconsideredinpregnantwomen:
A: Anesthetic complications, Accident/trauma
B: Bleeding
C: Cardiac
D: Drugs
E: Embolic causes
F: Fever
G: General including hypoxia, electrolyte disturbances
H: Hypertension 942

Reversible Causes
Electrolyte
abnormalities
Tamponade Hypothermia
Hypovolemia Hypoxia Hypomagnesemia
Myocardial
infarction
Pulmonary
embolism
Tension
pneumothorax943

Emergency Caesarean Section
in Cardiac Arrest
•Delivery of the fetus is a part of resuscitation process
when applicable.
•Despiteappropriatemodifications,mechanicaleffect
ofgraviduterusdecreasesvenousreturnfromIVC,
obstructsbloodflowthroughabdominalaorta,
decreasesthoraciccomplianceleadstounsuccessful
CPRwhichincreasesriskofhypoxiagoinginfor
anoxiatomotherandfetusBEYOND4MINUTES
OFARREST.944

Why Perform an Emergency Cesarean
Section in Cardiac Arrest?
RecentstudiesindicatesROSCandmaternal
hemodynamicstabilityofthemotherandnormal
neurologicaloutcomeoftheneonatepost
perimortemcesarean.
Thecriticalpointtorememberisthatbothmother
andinfantmaydieiftheprovidercannotrestore
bloodflowtothemother’sheart.945

The importance of timing with
emergency Cesarean section
Whenthematernalprognosisisgraveand
resuscitativeeffortsappearfutile,movingstraightto
anemergencyCesareansectionmaybeappropriate,
especiallyifthefetusisviable.946

Decision making for emergency
cesarean delivery
Gestational age less than 20 weeks
Need not be considered because this size gravid uterus is
unlikely to significantly compromise maternal cardiac
output
Gestational age approximately 20 to 23 weeks
Perform to enable successful resuscitation of the mother,
not the survival of the delivered infant, which is unlikely at
this gestational age
Gestational age greater than 24 weeks
Perform to save the life of both the mother & infant947

Perimortem Cesarean Section
•Prognosisforintactsurvivalofinfant
isbestifdeliveredwithin5minutesof
maternalarrest.
•Goal:toremovefetusandcontinue
resuscitationofbothmotherandfetus
•DuringtheprocedurematernalCPR
hastobecontinued.
•Verticalmidlineabdominalincision
from4-5cmbelowxiphoidprocess
topubicsymphysis
•Incisethroughthefasciaandmuscles
intotheperitoneum948

•Verticaluterineincision
•Deliveryofthefetus
•Manualremovalofplacenta
anditsmembranes.
•Closureofabdomenmaybe
delayeduntilmaternalblood
pressureandpulseisrestored.
•Diluteoxytocin10unitsin9ml
NStopreventuterineatony.
•INFORMEDCONSENTFOR
PERIMORTEM CSISNOT
NECESSARY949

Summary
Successfulresuscitationofapregnantwoman&survival
ofthefetusrequireprompt&excellentCPRwithsome
modificationsintechniques
Bythe20thweekofgestation,thegraviduteruscan
compresstheIVC&aorta,obstructingvenousreturn&
arterialbloodflow
Rescuerscanrelievethiscompressionbypositioningthe
womanonleftsideorbypullingthegraviduterustothe
side950

Defibrillation&medicationdosesusedforresuscitation
ofthepregnantwomanarethesameasthoseusedfor
otheradults.
RescuersshouldconsidertheneedforERCesarean
Deliveryassoonasthepregnantwomandevelopscardiac
arrest.
Rescuersshouldbepreparedtoproceedifthe
resuscitationisnotsuccessfulwithin4minutes.951

952

2)Eclampsia953

Management of Eclampsia
•Eclampsiaisdefinedasseizuresthatcannotbe
attributabletoothercausesinawomanwith
preeclampsia.
•Theinitialmanagementofeclampsiaincludes
Airway,Breathing,andCirculation&Disability
(neurological).954

Course of eclampticseizures
•Eclampsiamanifestsas1seizureormore,witheach
seizuregenerallylasting60-75seconds.
•Thepatient’sfaceinitiallymaybecomedistorted,
withprotrusionoftheeyes,andfoamingatthe
mouthmayoccur.Respirationceasesforthe
durationoftheseizure.955

Criteria for the diagnosis of preeclampsia
Systolicbloodpressure≥140mmHgordiastolicbloodpressure≥90mmHgon
twooccasionsatleastfourhoursapartafter20weeksofgestationina
previouslynormotensivepatientANDthenewonsetofoneormoreofthe
following:
Proteinuria≥0.3gina24-hoururinespecimen
Plateletcount<100,000/microL
Serumcreatinine>1.1mg/dL
Livertransaminasesatleasttwicetheupperlimitofthenormalconcentrations
Pulmonaryedema
Cerebralorvisualsymptoms(eg,new-onsetandpersistentheadaches;blurred
vision,scotomata.956

Key principles
•Iftheseizureiswitnessed,maintainingairwaypatencyand
preventingaspirationaretheinitialpriorities.Thewoman
shouldberolledontoherleftside.Theimmediateissues
include:
•Preventionofmaternalhypoxiaandtrauma.
•Treatmentofseverehypertension,ifpresent.
•Preventionofrecurrentseizures.
•Evaluationforpromptdelivery.957

A.Seizure control
•Theinitialbolusofmagnesium(4gdilutedin100mLover15-20
min)isfollowedbyaninfusionof1–2g/h.
•Magnesiumhasarelativelynarrowtherapeuticrange,andtarget
magnesiumserumconcentrationsare5–8mg/dL.
•Monitortoxicity—lossofdeeptendonreflexes;lossofpatellar
reflexoccurswhentheplasmamagnesiumlevelismorethan10
mg/dl.Lookforrespiratorymuscleweakness.
•Infusiondoseshouldbereducedincaseofrenaldysfunctionor
oliguria.958

•Forwomenwitheclampsia,werecommendtreatment
withmagnesiumsulfateratherthanother
anticonvulsants(Grade1A).Comparedwithphenytoin
anddiazepam,magnesiumsulfatereducestherateof
recurrentseizuresbyone-halftotwo-thirdsandreduces
therateofmaternaldeathbyone-third.959

Cont.
•Inrecurrentseizure,additional2gofmagnesiumsulfate
canbegivenconcurrentlywiththemagnesiumsulfate
infusion.
•Ifseizuresarenotcontrolledbyrepeatmagnesium
bolus,thendiazepamcanbeadministered.
•Discontinuemagnesiumsulfate24hafterdelivery.960

Clinical manifestations related to serum
concentration of Magnesium
Serum magnesium levels
(mg/dL)
Effects
5–8 Therapeutic
8–12 Loss of deep tendon reflexes
>12 Prolonged atrioventricularconduction
15–17 Muscular paralysis and respiratory
difficulties
>20 Cardiac arrest961

B.Blood pressure control
•Arterial pressure greater than 160/110 mmHg can
increase the risk of complication, and it should be
controlled.
•Aim of BP is < 150/100.962

Blood pressure control, Drugs:
•Labetalol(IV20mg)canbegiveninitiallyfollowedbydoublingthedoseevery
10mintoacumulativedoseof300mg.Thisdrugcanresultinsevere
bradycardia.Acontinuousinfusionoflabetalolatarateof1–2mg/mincan
alsobeused.IftargetBPisnotachieved,switchtoanotherclassofagent.
•Hydralazine(5–10mg)canbegivenevery20min(maximumof30mg)until
BPiscontrolled.IftargetBPisnotachieved,switchtoanotherclassofagent.
•Nifedipine(10mgcap)canbegiven,onset5minutesandpeak30min(usually
reservedonlyforwomenwithoutIVaccess,suddenprecipitousdecreaseinBP
orbradycardiacanoccur,avoidsublingualuse,monitorFHR).963

Cont.
•Intravenousnitroglycerinorsodiumnitroprussidecanbe
given.Prolongeduseofnitroglycerinmayleadto
methemoglobinemia.Cyanidetoxicityinthemotherandfetus
mayoccurwithsodiumnitroprusside,limitingitsusetoless
than4handonlyasalastresort.964

965

Oral agents post delivery
•Suggestedfirstlineantihypertensivedrugsthataresafein
breastfeedingmothersincludelabetalol,nifedipine,andenalapril.
•Insufficientevidenceonthesafetyinbabiesreceivingbreastmilkof
theARBs&amlodipine(avoiddiuretictreatment).
•Ifawomanhastakenmethyldopatotreatchronichypertension
duringpregnancy,stopwithin2daysofbirthandrestartthe
antihypertensivetreatmentthewomanwastakingbeforeshe
plannedthepregnancy.966

Watch for complications of eclampsia
•Disseminatedintravascularcoagulopathy(DIC)
•Renalinsufficiencyandacuterenalfailure
•Pulmonaryedema
•HELLPsyndrome
•Cerebralhemorrhage967

Managing acute pulmonary edema
•Managementissimilarasinnonpregnantpatients.
•Intravenousfurosemide(bolus20–40mgover2min)isused
topromotediuresis.Therepeateddosesof40–60mgare
givenafter30minorinfusionifthereisinadequatediuretic
response(maximumdose120mg/h).968

Managing HELLP syndrome
•HELLPsyndromecancomplicate4–12%ofpatientswithsevere
preeclampsia.
•Signsandsymptomsarerightupperquadrantorepigastricpain,nausea
andvomiting,malaise,andnonspecificviral-likesymptoms.Physical
examinationfindingsincluderightupperquadrantorepigastrium
tendernessandgeneralizededema.
•DeliveryisthedefinitivetreatmentforHELLPsyndrome.
•DeliveryisindicatedforwomenwithHELLPsyndromeatgreaterthan34
weeks'gestation.Duringlaborandfor24-hpostpartum,patientsshould
receiveintravenousmagnesiumsulfateforseizureprophylaxis.969

Cont.
•Ifgestationislessthan34weeks,deliverymaybedelayedfora
steroidcourseofbetamethasone(12mgintramuscularly,every24
h)intwodoses,withdelivery24hafterthelastdose.
•Plateletsaregenerallytransfusedwhentheplateletcountisless
than20,000/mm3.Forcesareandeliveryorwithanysignificant
bleeding,plateletsshouldbetransfusediftheplateletcountisless
than50,000/mm3.970

3)Acute Respiratory Failure
During Pregnancy971

Differential diagnosis of
Acute Respiratory Failure During Pregnancy
Conditions unique to
pregnancy
Conditions can be
affected by pregnancy
Conditions unaffected by
pregnancy
Peripartum cardiomyopathyAcute pulmonary edema ARDS
Amniotic fluid embolism Aspiration of gastric
contents
Fat embolism
Ovarian hyperstimulation
syndrome (OHSS)
Asthma Sepsis, trauma, burn
Tocolytic-induced pulmonary
edema
Pneumonia Pneumonia
Severe preeclampsia Pulmonary embolism Acute pancreatitis972

Make a diagnosis of respiratory failure in pregnancy
A.ARDS
ThecriteriafordiagnosisofARDSaresimilartononpregnant
women.
B.Asthmainpregnancy
Ruleofthirds—one-thirdofpatientswithasthmainpregnancy
improve,andone-thirdshowsnochange.One-thirdworsensand
canpresentinacutesevereasthma.(Thisexplainsthe
unpredictableeffectofpregnancyonasthma).973

Cont.
C.Pulmonaryembolisminpregnancy
•D-dimersmaybefalselyhighinpregnantpatients.
•Radiographicimagingremainstheprimarytestingmodalityfor
diagnosingPE,anditshouldnotbedelayedbecauseofconcerns
aboutradiationexposure.
•Multidetectorcomputedtomography(MDCT)pulmonary
angiographyiscurrentlythemostpreferredmodeforconfirming
diagnosingPEinpregnantpatients.974

Cont.
C.Pulmonaryembolisminpregnancy
•ThemainconcernswithMDCTareradiationandcontrastexposuretothe
fetusinsuspectedPE.Ithasbeenseenthattheexposureofradiationis
lesstothefetus.
•Compressionultrasonographyandtransesophagealechocardiography
(TEE)aretheinitialtestofchoicetoexcludedeepvenousthrombosis.
•Chestradiographsinvolveminimalradiation;theyrarelyshowsigns
suggestiveofPE,whichmaydetectotherdiagnosis.975

Cont.
D.Ovarian hyperstimulation syndrome (OHSS)
•Gestationof3–8weeks.
•Increasedvascularpermeability—fluidshiftfromthe
intravasculartoextravascularspace—causingpleuralor
pericardialeffusions,ascites,dyspnea,oliguria,severely
enlargedpolycysticovaries,hemoconcentration,and
hypercoagulability,electrolyteimbalancearethecommon
presentations.976

Criteria that define the severe and life-threatening
stages of OHSS
Severe OHSS Life-threatening OHSS
Variably enlarged ovary Variably enlarged ovary
Massive ascites with or without
hyrothorax
Tense ascites with or without
hyrothorax
Hematocrit > 45% Hematocrit > 55%
WBC count >15.000 WBC count >25.000
Oliguria Oliguria
Creatinine level 1.0-1.5 Creatinine level >1.6
Creatinine clearance >50ml/min Creatinine clearance <50ml/min
Liver dysfunction Renal failure
Anasarca Thromboembolic phenomena
ARDS977

Cont.
E. Peripartum cardiomyopathy (PPCM)
•Riskfactorsincludehypertension,preeclampsia,multiparity,
multiplegestations,andoldermaternalage.
•Signsandsymptomsareparoxysmalnocturnaldyspnea,chestpain,
nocturnalcough,newregurgitantmurmurs,pulmonarycrackles,
increasedjugularvenouspressure,andhepatomegaly.978

Cont.
•Identifyothercardiacandnoncardiacdisorderssuchascoronary,
rheumatic,orvalvularheartdisease;arrhythmias;andfamilyhistoryof
cardiomyopathyorsuddendeathandotherriskfactorsofcardiacdiseases
suchashypertension(chronic,gestational,preeclampsia),diabetes,
dyslipidemia,thyroiddisease,anemia,priorchemotherapyormediastinal
radiation,sleepdisorders,currentorpastalcoholordrugabuse,and
collagenvasculardisease.
•ThediagnosisofPPCMisadiagnosisofexclusionandshouldbemade
whenotherpossiblecausesofacute/subacuteheartfailurehavebeen
ruledout979

Cont.
Clinical criteria for the diagnosis of PPCM
•Developmentofcardiacfailureinthelastmonthofpregnancyor
within5monthspostpartum
•Absenceofanotheridentifiablecauseforthecardiacfailure
•Absenceofrecognizableheartdiseasebeforethelastmonthof
pregnancy
•LVsystolicdysfunctionshownbyechocardiographicdata(e.g.,
ejectionfractionlessthan45%)andanLVenddiastolic.980

Cont.
F.Amniotic Fluid Embolism
•Rare and often fatal.
•Presentation usually sudden during labor or immediately postpartum.
•Acute dyspnea, cyanosis, shock, cardiac arrest, bleeding from
disseminated intravascular coagulation (DIC) and tonic-clonicseizures
may all occur.
•Sudden change in woman’s behavior can be an early warning feature.981

Initiate assessment and resuscitation
of respiratory failure in pregnancy
Airway
•Airwayevaluationandmanagementremainsthefirstpriorityintheinitial
resuscitationasinnonpregnantpatients.
•Definitiveairway(trachealintubation)isneededinpersistenthypoxemia,airway
obstruction,impairedlaryngealreflexes,orinalteredconsciousness.
•Difficultairwayequipmentforairwaymanagementmustbethoroughlychecked
beforeproceedingtointubation,andanalternativeplanfordefinitiveairway
includingsurgicalaccessshouldbeidentified.
•Intubationshouldbeperformedbyaseniorintensivist/anesthesiologistespecially
inlaterpartofpregnancyduetoupperairwayedemaandnarrowairwaycaliber.982

Cont.
Breathing
•Supplementaloxygenmayberequiredinsomepatientsdependingontheir
oxygensaturation.
•Noninvasiveventilation(NIV)canbetriedonlyinthecontrolledICUsetting.
•SignsoffailureofNIVandrequirementofintubationshouldalsobeidentified
soonerthanlater.Thisincludesincreasedworkofbreathing,mentalstatus
deterioration,hemodynamicinstability,andinabilitytoprotecttheairwayor
managesecretions.
•AlwaystargetSpO2ofmorethan95%.Foradequatefetaloxygenation,amaternal
arterialoxygentension(PaO2)ofmorethan70mmHgisrequired,which
correspondstoanoxyhemoglobinsaturationof95%.983

Cont.
Circulation
•Twolarge-boreintravenouscannulae(14Gor16G)shouldbeplaced
toadministerfluids.
•Administratefluidjudiciouslytooptimizepreloadandatthesame
timetoavoidoverload.
•Maintainhighcardiacoutput.
•Nursingintheleftlateral(30°wedgetotherighthip)positionis
neededtopreventsupinehypotensionsyndrome.984

Treat the specific cause
•Thegeneralmanagementofrespiratoryfailurein
pregnancyissimilartothemanagementinnonpregnant
women,althoughoneshouldbecarefulaboutnormal
physiologicalterationsthatoccurintheparturientstate
andeffectofventilatorstrategies.985

A. Management of ARDS and mechanical ventilation in
pregnant patients
•Lung-protectivestrategytoavoidvolutrauma,biotrauma,
atelectrauma,leadingtolessventilatorinducedlunginjuryhas
beenfoundtoreducemortalityandimproveoutcomeinpatients
withARDS.
•Lung-protectivestrategycauseshypoventilation,whichistolerated
tomaintain(permissivehypercapnia)thepHbetween7.25and
7.35.986

A. Management of ARDS and mechanical ventilation in
pregnant patients
•Permissivehypercapniacancausefetalacidosis,anincreasein
intracranialpressure,andarightshiftinthehemoglobin
dissociationcurveandinfirst72hmayleadtoretinopathyof
prematurity,solung-protectiveventilatorstrategyinpregnant
patientsshouldbeusedwithclosemonitoringofthefetal
•statuswiththebiophysicalprofile.
•Oxygenlevelsshouldbecloselymonitoredinpregnancyandkept
higherthaninnonpregnantwomen(preferablySpO295%).987

B. Management of asthma in pregnancy
•Managementofasthmainpregnancyissimilarto
nonpregnantwomen.
•Beta-agonistsbronchodilatorsandcorticosteroidsarethe
mainstayofthetreatment.988

C. PE during pregnancy
•AcutetreatmentofPEcanbedonewithlow-molecular-
weightheparin(LMWH)orunfractionatedheparin(UFH)and
shouldbestartedwithoutdelaywheneverPEissuspectedor
confirmed.
•LMWHisfirst-linetherapyforthetreatmentofacutePEinthe
generalpopulationandinpregnancyastheriskofbleedingin
pregnantwomenisnotdifferentfromnonpregnantwomen.989

C. PE during pregnancy
•Thrombolysisincreasestheriskofobstetricandneonatalcomplications
suchaspregnancyloss,abruption,andpretermlabor.Therefore,theuse
ofthrombolyticsinpregnancyshouldbereservedforwomenwithPEwho
arehemodynamicallyunstableorwithrefractoryhypoxemia.
•TheAmericanCollegeofChestPhysiciansguidelinerecommendstheuse
ofanticoagulationfor6monthsatleastinthepostpartumperiod.
•Alwaysgiveinjectableheparinsduringtheentireperiodofpregnancy.
Startoralanticoagulantsonlyafterdelivery.990

D. OHSS
•Syndromeisself-limiting,andresolutionparallelsthedeclinein
serumHCGlevels:7daysinnonpregnantpatientsand10–20
daysinpregnantpatients.
•Monitorfrequentlyfordeteriorationwithphysicalexaminations,
dailyweights,andperiodiclaboratorymeasurementsof
completebloodcounts,electrolytes,andanalysisofrenaland
hepaticfunction.991

Cont.
•Severedisease—placementoftwolarge-boreperipheral
intravenouscathetersoracentralvenouscatheter(preferred)for
fluidmanagementmayberequired.
•UsetheFoley’scatheterforclosemonitoringoftheurineoutput.
•Normalsalinewithorwithoutglucoseisthecrystalloidofchoice,
andpotassium-containingfluidsshouldbeavoidedbecause
patientswithOHSScoulddevelophyperkalemia.992

Cont.
•Inmoreseverecaseswithsignificanthypovolemia,
hemoconcentration(hematocrit>45%),hypoalbuminemia(serum
albuminlevel<3.0g/dL),orsevereascites,albumincanbegivenas
aplasmaexpanderalongwithdiuretics(furosemide)once
hematocritis36–38%.
•Ifrespiratorysymptomsworsen,thoracentesis/paracentesisshould
beperformed.
•IfARDSdevelopsandmechanicalventilationisrequired,lung-
protectivestrategiesmustbeused.993

E. PPCM
•Diureticsareindicatedformostpatientsbecausetheycause
symptomaticreliefofpulmonaryandperipheraledemaandare
usuallyusedasadjuvanttootherdefinitivetherapies.
•Furosemideisthemostcommonlyuseddiuretic.
•Aldosteroneantagonistshavebeenshowntoimprovesurvivalin
selectedheartfailurepatients.Theseagentsarestillnotadvised
inpregnancy(lackofsafetydata);however,theycanbeadded
postpartum.994

Cont.
•Hydralazineand nitrates are the vasodilators of choice for pregnant
women, as angiotensin-converting enzyme inhibitors, the first-line agent
for nonpregnantpatients, are contraindicated for pregnant women.
•β -Blockers (sustained-release metoprololsuccinate, carvedilol, and
bisoprolol) have been shown to reduce mortality with current or prior
heart failure and reduced ejection fraction and therefore constitute the
first-line therapy for all stable patients unless contraindicated.
•Digoxinimproves symptoms, quality of life, and improves exercise
tolerance in mild-to-moderate heart failure.995

Treatment o PPCM
TherapiesavoidedInselectedpatientsDrugsorroutine
use
Nonpharmacological
measures
Angiotensin-
convertingenzyme
inhibitors
Aldesterone
antagonists
DiureticsHypertensioncontrol
Angiotensinreceptor
blockers
InotrpesB-blockers(saltrestriction)
Manyantiarrhythmic
drugs
AnticoagulationDigoxinFluidrestriction
NSAIDsImplantable
defibrillators
Vasodilators
Nondihydropyridine
calcium channel
blockers
Biventricularpacing
Cardiac
transplantation996

F. Amniotic Fluid Embolism
•If necessary, deliver immediately –ideally vaginally. If not
possible, by cesarean section under general anesthetic.
•Insert second large bore (16 G) IV cannula and prepare to
manage massive obstetric hemorrhage.
•Consider early insertion of central venous catheter and
arterial line.997

Cont.
•Discussneedforbloodproducts(includingfreshfrozen
plasmatocorrectDIC)withconsultanthematologist,
withoutwaitingforbloodresults.
•Womanwillrequirecirculatorysupport,whichcan
includeinotropes,withinvasivemonitoring.
•TransfertoCriticalCareUnit.998

4)Severe Obstetric
Hemorrhage999

Antepartum hemorrhage
•Antepartumhemorrhageisdefinedasbleedingfromthe
genitaltractafter24weeksofgestation.Thecommon
causesareplacentapreviaandplacentalabruption1000

Postpartum hemorrhage
•Postpartumhemorrhageismostcommonlyduetouterine
atonyandabnormalplacentation,withretainedtissues,
traumatothegenitaltractandcoagulopathyasothercauses.
•Inanemergency,theaortacanbecompressedagainstthe
vertebralcolumnbyafistpressedontheabdomenabovethe
umbilicus1001

Cont.
Uterine atonyis managed initially with bimanual compression, uterine
massage and drugs that include:
•oxytocin: 5 units slow intravenous injection, or infusion(40 units in 500 mL
Ringer’s lactate solution at125 mL/h)
•ergonovine(ergometrine): 0.5 mg slow intravenous or intramuscular
injection (contraindicated in patients with hypertension)
•carboprost: 250 μgintramuscular injection, repeated at intervals of not
less than 15 minutes to a maximum of 8 doses (contraindicated in patients
with asthma) or 500 μgdirect intramyometrialinjection
•misoprostol: 1000 μgrectally.1002

Cont.
•Ifbleedingpersists,tamponadetechniquesusinggauzepacksor
balloonscanbeuseful.Specificinvasivemanagementsuchas
angiographicarterialembolization,laparotomyforuterine
hemostaticsuturingtechniques,surgicalbilateraluterineartery
ligation,ordefinitivehysterectomymayberequired.
•Withmassivebleedingandtransfusion,thereshouldbenoneedto
waitforacoagulationprofilebeforegivingcoagulationfactors.1003

5)Jaundice in Pregnancy1004

Pregnancy-related liver diseases
A.Intrahepaticcholestasisofpregnancy(ICP)
B.Preeclampsiaandeclampsia
C.Hemolysis,elevatedliverenzymes,lowplatelet(HELLP)
syndrome
D.Acutefattyliverofpregnancy(AFLP)
E.Hyperemesisgravidarum1005

Management
A.Acutefattyliverofpregnancy(AFLP)
•Prompt delivery is essential (steroids if fetal maturity in doubt).
•Supportive treatment, control of hypertension and correction of coagulation
abnormalities and hypoglycemia.
•Manage complications:
–Renal failure
–Acute pulmonary edema or acute respiratory distress syndrome
–Coagulopathy/disseminated intravascular coagulation
•Rarely, liver transplantation is indicated for liver rupture with necrosis, fulminant
liver failure, hepatic encephalopathy, or worsening coagulopathy. 1006

Cont.
B. Hyperemesis gravidarum
•Treatmentissupportiveandincludesintravenousrehydrationand
antiemetics.
•Vitaminsupplementation,includingthiamine,ismandatoryto
preventWernicke’sencephalopathy.
•Thereisnoroleofsteroids.
•Relapseandrecurrenceinsubsequentpregnanciesiscommon.1007

Cont.
C. Intrahepatic cholestasis of pregnancy:
•Treatmentofchoiceisursodeoxycholicacid,whichhelpstorelieve
pruritisandimprovehepatitis.
•Mechanismofactionisunknown.
•Otherdrugsarecholestyramine,dexamethasone,andvitaminK
supplementation.
•Terminationofpregnancy—whenmedicalmeasuresfailorifthe
patient’sconditiondeteriorates.1008

Cont.
D.Severe preeclampsia–eclampsia:
E.HELLP syndrome:
See Management of Eclampsia & HELLP syndrome above.1009

References
•AHA : Circulation 2015 –cardiac arrest in pregnancy
•ICU Protocols (2012) A Stepwise Approach
•Obstetric Guidelines (2015) National Health Service
(NHS) UK
•Oh'sIntensive Care Manual (2014)
•Uptodate.com 20181010

20)General management of poisoning
& Snake bite
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
1
Critical Care1011

General management of poisoning
1)SupportiveCare
2)Preventabsorptionofpoison
3)Enhanceeliminationofpoison
4)Antidoteadministration1012

1)Supportive Care
•Oxygenation/ ventilation
•Hemodynamic support
•Treatment of arrhythmias
•Treatment of seizures
•Correction of metabolic derangement
•Correction of temperature abnormality1013

2)Prevention of further poison absorption
•Gastrointestinal decontamination
A.Gastric lavage
B.Activated charcoal
•Other sites decontamination
Eye and skin decontamination1014

3)Enhancement of poison elimination
A.Forced diuresis
B.Alternation of urine PH
C.Hemodialysis1015

4)Antidotes mechanism of action1016

Antidotes mechanism of action
1)Directactiononthetoxin:
A.Specificbindingcanbeachievedbychelation(e.g.,
heavymetals).
B.Nonspecificbindingoccurswiththeuseofactivated
charcoalorintralipidforlipophiliclocalanesthetics.
2)Actiononthetoxinbindingsite:
A.Competitiveinhibitionoftheenzyme(e.g.,ethanolor
fomepizoleformethanolandethyleneglycol
poisoning).
B.competitiveblockadeofthereceptor(e.g.,naloxone
foropioidoverdoseandflumazenilfor
benzodiazepineoverdose.
71017

Mechanisms of action of Antidotes
3)Decreasingtoxicmetabolites(N-acetylcysteinefor
paracetamoloverdose)orconversiontolesstoxic
metabolites(e.g.,sodiumthiosulphateforcyanide
poisoning).
4)Counteractingtheeffects:(atropinecounteractthe
muscariniceffectsofOPpoisoning)orDirect
antagonismoftoxinaction(warfarinandvitaminK).
81018

Organophosphate poisoning
•Organophosphatetoxicitycanresultfromhousehold
oroccupationalexposure,militaryorterroristaction,
oriatrogenicmishap.
•Exposuretoorganophosphatesisalsopossiblevia
intentionalorunintentionalcontaminationoffood
sources.
91019

Pathophysiology
•Organophosphatesinactivateacetylcholinesterase
(AChE)whichdegradestheneurotransmitter
acetylcholine(ACh)intocholineandaceticacid.
•AChaccumulatesthroughoutthenervoussystem,
resultinginoverstimulationofmuscarinicandnicotinic
receptors.
101020

Once an organophosphate binds to AChE,
the enzyme can undergo one of the following:
1)Endogenoushydrolysisofthephosphorylatedenzyme
byesterasesorparaoxonases.
2)Reactivationbyastrongnucleophilesuchas
pralidoxime(2-PAM).
3)Irreversiblebindingandpermanentenzymeinactivation
(aging).
111021

Signs and symptoms
(1)Muscariniceffects:DUMBELS(diaphoresisanddiarrhea;
urination;miosis;bradycardia,bronchospasm,bronchorrhea;
emesis;excesslacrimation;andsalivation).
(2)Nicotiniceffects:musclefasciculations,cramping,weakness,
anddiaphragmaticfailure.Autonomicnicotiniceffectsinclude
hypertension,tachycardia,mydriasis,andpallor.
(3)Centralnervoussystem(CNS)effects:anxiety,
confusion,tremors,seizuresandcoma.
121022

Diagnosis
•Organophosphatetoxicityisaclinicaldiagnosis.
Confirmationoforganophosphatepoisoningis
basedonthemeasurementofcholinesterase
activity.
131023

Treatment
•Beginswithdecontamination.
•Airwaycontrolandoxygenationareparamount.
•Activatedcharcoal(AC)canbegiventopatients
presentingwithinonehourofanorganophosphorusagent.
•ThestandarddoseofACis1g/kg(maximumdose50g).
•Themainstaysofpharmacologicaltherapyinclude
atropine,pralidoxime(2-PAM),andbenzodiazepines(eg,
diazepam).
141024

Cont.
•Immediateaggressiveuseofatropinemayeliminatethe
needforintubation.
•Intubationmaybenecessaryincasesofrespiratory
distressduetolaryngospasm,bronchospasm,
bronchorrhea,orseizures.
•Succinylcholineshouldbeavoidedbecauseitis
degradedbyplasmacholinesteraseandmayresultin
prolongedparalysis.
151025

Cont.
•Nondepolarizingneuromuscularblockingagents(eg,
rocuronium)canbeused,butmaybelesseffectiveat
standarddosesduetocompetitiveinhibitionatthe
neuromuscularjunction.
•Centralvenousaccessandarteriallinesmaybeneeded
totreatthepatientwithorganophosphatetoxicitywho
requiresmultiplemedicationsandblood-gas
measurements.
161026

Atropine
•Atropinecompeteswithacetylcholineatmuscarinic
receptors,preventingcholinergicactivation.
•Formoderatetoseverecholinergictoxicity,atropine
administeredbeginningatadoseof1-2mgIVforadults&
0.05mg/kgIVforchildren,canberepeatedifnecessary
every5-15min,ordoubledifthereisnoresponse.
•Afterdesiredresponseisachievedwithatropinebybolus,
weadminister10-20%ofthetotalcumulativebolusdoseas
anIVcontinuousinfusionperhour.
171027

Cont.
•Weadjusttheinfusionrateasneededtomaintain
adequateresponse(eg,clearlungauscultation,dry
axilla,HR>80beats/minute,SBP>80mmHg,pupilsno
longerpinpoint)withoutcausingatropinetoxicity(eg,
confusion,pyrexia,absentbowelsounds,urinary
retention)andtaperuntilrecovery.
181028

Cont.
•Tachycardiaandmydriasisarenotappropriatemarkers
fortherapeuticimprovement,astheymayindicate
continuedhypoxia,hypovolemia,orsympathetic
stimulation.
•Whenatropinetoxicityoccurs,holdtheinfusionuntil
toxicityresolvesandrestartat70-80%oftheprevious
infusionrate.
191029

Pralidoxime (an antidote for OP poisoning)
•Nucleophilicagentthatreactivatesthephosphorylated
AChEbybindingtotheOPmolecule.
•Usedasanantidotetoreversemuscleparalysis
resultingfromOPAChEpesticidepoisoningbutisnot
effectiveoncetheOPcompoundhasaged.
•Currentrecommendationisadministrationwithin48hof
OPpoisoning.
201030

Cont.
•Pralidoximeshouldnotbeadministeredwithout
concurrentatropineinordertopreventworsening
symptoms due totransientoxime-induced
acetylcholinesteraseinhibition.
•Wesuggestthatoximetherapybegiventoallpatients
withevidenceofcholinergictoxicity,patientswith
neuromusculardysfunction,orpatientswithexposuresto
organophosphorusagentsknowntocausedelayed
neurotoxicity.
211031

Management of Snake bite
–ABC.
–Calmandreassurethepatient.
–ObtainvitalsignsincludingO
2saturation.
–Tourniquetsarenotrecommended.
–Removeallwatches,rings,andjewelry(notjustfromaffectedlimb).
–Prepareforimmediatetransport.
–DonotCutandSuck.SnakebiteisanIMinjection.Thevenomisn’t
goingtobesuckedout.Cuttingincreasesdamagetoareaalready
infiltratedwithdigestiveenzymes.1032

Management of Snake bite
•Antivenomsaregenerallyindicatedwhen:
–Thereisevidenceofsystemicenvenomation(neurotoxicity,
coagulopathy,rhabdomyolysis,persistenthypotension,and/or
renalfailure)
–Thereisseverelocalenvenomation,manifestedbylocal
tissuedestruction
•Antivenomtherapy:
–Monovalentantivenom:Forknownspecificsnake
–Polyvalentantivenom:Forunknownsnake
•Antivenomshouldbeideallyadministeredwithin4hoursofthe
bite;however,itiseffectiveifgivenwithin24hours.1033

Antivenin administration
➢Dose depends on severity
* mild = 1-5 vials
* moderate = 5-10 vials
*severe = 10-20 vials
➢Each vial should be diluted (10 ml water)
➢It should be given slowly while observing for allergic or
hypotensive reactions (hydrocortisone of epinephrine
may be needed)1034

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