Physiology of shock

MBBS lecture

2. 2The Physiology of Shock
The Physiology of Shock
R.E.B, 4MedStudents.com, 2003

4. •Shock occurs when
the rate of arterial blood flow is inadequate to meet
metabolic tissue needs and is the consequence of
cardio-vascular collapse
•Essentials of diagnosis are
–Hypotension (<60 mmHG)
–Tachycardia
–Oliguria
–Altered mental status
–Peripheral hypoperfusion and hypoxia

6. y c(eiySgoyekyohe P major types of shockT
eeg yohe P
h
lllgskScsclslcSkssss
gysysscgskgsllS Sls
T
)ciegf yohe P
h
!csclsgclsSs gsglssls
ScSksscS"sSS
T
*oSisSgyohe P
h
hlgcSksscslSkls
T
fl
T
#k$ %
T
f SlskS slkls kgls&f'hf(
•Hypovolemic shock
–Decreased intravascular volume resulting form loss of
blood, plasma, or fluids and electrolytes
•Cardiogenic shock
–Pump failure due to myocardial damage or massive
obstruction of outflow tracts
•Distributive shock
–Reduction of vascular resistance form
•Sepsis
•Anaphylaxis
•Systemic inflammatory response syndrome (SIRS)

7. eeg yohe Py
eoSy eefySgyekyohe P" Hypovolemic shock
(most common type of shock)
•Loss of blood (hemorrhagic)
–External bleeding (wound to the outside or gastrointestinal)
–Internal bleeding (hematoma, hemothorax,
hemopertitoneum)
•Loss of plasma
–Burns
–Exfoliative dermatitis
•Loss of fluids and electrolytes
–External (vomiting, diarrhea, excessive sweating)
–Internal ( “third spacing” = pancreatitis, ascitis, bowl
obstruction
–Excessive sweating

8. fSlss$ ls$, Stages of hypovolemic shockT
,yeooyeky y- .yeeyesg"
h
-l"sl%Slksksksckls cksSlkSscS
T
'kllgs slsSls&sklssles+s./scls(
T
,egicSgyeooyeky- / .yeeyesg"
h
!SlkSsllsklk sk%cskgsS$ gs0.slS1ks
& S$lSslkl(
h
s cs
h
gslcls slskSklgskscklsSlkS
T
Tggigyeooyeky0y/ .yeeyesg"
h
2skss$,sls"S$s$lg kskSS
)cg1ykygfScy efksoefye sioyoycfyefesoy f cyof"
$fygiyoheiSySgykicgycyogcicSgyycfyoggigyohe Py
oSeoyShcSygc2ylhgfygkSysfSigcSg2ySeyieigoogycfy
iiggiogy gyf(siycfygcSh
•Mild (loss of < 20% blood volume)
–Few external signs in supine young patients but
•Increased capillary refill time ( longer 3 sec. = 10% volume loss)
•Moderate (loss of 20-40% blood volume)
–Patient becomes increasingly anxious and tachycardic >100 beats/min
(sympathetic response)
– oliguria
–blood pressure may be maintained in supine patient
•Severe (loss of > 40% blood volume)
–Classic signs of shock appear with hemodynamic instability
(Cave: if mental confusion occurs is an ominous clinical sign)
Only very short time frame may separate mild and severe shock
symptoms that lead, when left untreated, to progressive and
irreversible cell injury and death

9. Signs and SymptomsT
3"sPgs!lcl
h
f SsP!sscc sl"s4s5
T
!clssgskgs"l,
T
hlSkssgskgs$"s
T
f,ksslysyskgs
T
"kl
•Low Blood Pressure
–Systolic BP is usually below 90 mmHg
•Pulse is rapid and weak
•Respiration is rapid and shallow
•Skin is pale, cool, and clammy
•Drowsiness

10. eeg yThe P
T
hlcSssScsks"$$sS$llssgs

T
lllgsgsclsclssglllsks
gslcl
T
'kclkSsckSss6
T
sslksSkSlgs
Ssg sSclskgsks Hypovolemic Shock
•Results from trauma in which there is blood
loss
•Decreased blood volume causes a decrease in
blood pressure
•Insufficient amounts of O
2
is being transported
to body tissues and organs

13. Compensated ShockT
sSlss$,s"$llsS$lsg 7s
lkS sl$kslslsSs
kSkskslcks
•Early stages of shock where the body’s
compensatory mechanisms are able to
maintain normal perfusion

14. Decompensated ShockT
#gklgsSlss$,sS$Sscs"$lksS$ls
g 7slkS sl$kssSs
kSkskslck
•Advanced stage of shock that occurs when the
body’s compensatory mechanisms fail to
maintain normal perfusion

15. Irreversible ShockT
fSlss$,sS$Ss$sllgsSsS$lskSs
S$SsS$lsg skslgskSllkSkslSs
S$lsl
•Stage of shock that has progressed to the point
that the body nor medical interventions correct
the problem

22. Compensated and Decompensated
shockT
sigocPghlgsgiPgohgShe PysioPgog
cPygocPsPgePSciysesgigschSkglPPh sg
iylgeig hPss
•Usually the body is able to compensate but
when these mechanisms fail shock develops
and may progress

23. Compensation MechanismsT
TioPSchieyPsgeigPgsPSPoPlggg
yP cyPgiylgyhP yP cyP
T
!cPg"Pyy#$yoPysygssoPegilsgyg
eiyoiyyghhlg PssP
T
ylhSyPg"Ps hysPgg ooigiylgPsosg
ygsPSPohyghgiyo#lPoSgchehyPg$f%
•Catecholamines may be secreted ( I.E.
Epinephrine and norepinephrine)
•The Renin-Angitensin system aids in
maintaining blood pressure
•Endocrine Response by pituitary gland results
in secretion of anti-diuretic hormone (ADH)

24. Catecholamine ReleaseT
yP cyPgiylg&hP yP cyPgPPisPg
iPSosgocPgSilhisSigssoPe'gSisyg
ySPisPgyg%"'gySPisPgygTiliSgShyoiSoog
soPyoc'gioPhigShysoSohygcScg
PPioPsghhlg PssP
•Epinephrine and Norepinephrine release
affects the cardiovascular system, causing
increase in HR, increase in Cardiac contractility
strength, arteriolar constriction which
elevates blood pressure

25. Renin-Angiotensin systemT
"PyygsgPPisPlghegocPgklyPsgiylgiSosghyg
s PSi(Plg iseig hoPygSiPlg
$yhoPysyhPyg)gg hlSPsg$yhoPysyg
T
$yhoPysyggsgShyPoPlgohg$yhoPysyggg
Py(ePsgygocPgysgSiPlg$yhoPysyg
ThyPoygy(ePg$T
•Renin is released from the kidneys and acts on
specialized plasma protein called
Angiotensinogen & produces Angiotensin I.
•Angiotensin I is converted to Angiotensin II by
enzymes in the lungs called Angiotensin
Converting Enzyme (ACE)

26. Anti-Diuretic HormoneT
TisPsgocPgklyPsgohgPishgioPgSPioyg
iygilloPgohgocPgilhsohyP
•Causes the kidneys to reabsorb water creating
an additive to the aldostrone

27. The PysiosTligf Stages of Shock
•Initial non-progressive stage
–Baro-receptor reflexes
–Release of catecholamine
–Activation of renin-angiotensin-aldosteron system
–ADH release
results in tachycardia, peripheral vasoconstriction (cool skin) and renal fluid
conservation
•Progressive stage
–Widespread tissue hypoxia results in anaerobic glycolysis and
–Lactate acidosis (pH < 7.35)
–Vasodilation with blood pooling in microcirculation
–Declined cardiac output
–Oligouria
–Widespread tissue hypoxia
•Irreversible stage
–Widespread cell injury leading to
–Further decreased myocardial contractility
–Anuria with tubular necrosis
–Ischemic bowl may lead to leakage of bacterial flora
–Fluid in lung (ARDS)

32. S/S of Hypovolemic ShockT
$oPPlg-3T
T
8iP'gShh'gSieegsky
T
*hhlg PssPgeigPgyheigocPygi
T
8sPgeigPgyheigocPygPShePgi l'gyig
shygiylglsi Piy
T
yiohyglPSPisPs
T
TiliSglscoceisgeighSS
•Altered LOC
•Pale, cool, clammy skin
•Blood pressure may be normal then fall
•Pulse may be normal then become rapid, finally
slowing and disappearing
•Urination decreases
•Cardiac dysrhythmias may occur

33. Tx for Hypovolemic ShockT
$igShyoh
T
$leysoPgccghgh+Py
T
ThyohgsPPPgPPlyg
T
9PP g ioPyogie
T
PioPghPgP+oPeoPs
T
soiscg2giylgileysoPghsghgSsoihlg
shohyghglgP iSPePyo
•Airway control
•Administer high flow oxygen
•Control severe bleeding
•Keep patient warm
•Elevate lower extremities
•Establish IV and administer bolus of crystalloid
solution for fluid replacement

36. eki Pckgsyligf Cardiogenic shock
•Pump failure
–Secondary to myocardial infarction (most common)
–Cardio-myophathy
–Acute valvular dysfunction (regurgitations)
–Rupture of the ventricular septum
•Arrhythmia
–Tachyarrhythmia
–Bradyarrhythmia
•Obstructions
–Tension pneumothorax
–Pericardial diseases (tamponade or constrictive pericarditis)
–Pulmonary hypertension (emboli or other vascular diseases)

37. Characteristics of Cardiogenic Shock
•Low cardiac output
•Peripheral vasoconstriction
•Left sided heart failure leads to pulmonary venous
congestion and pulmonary edema
•Right sided heart failure leads to systemic venous
congestion and peripheral edema

38. ShskysPyyPchkeshiskyhkc kylsesgeki PckgsoisesliiPkgs
yligf!
*hocghesgiPgisshSioPlgocgPlSPlgSiliSghog o'giylgySPisPlg
P cPigisSigPssoiySP'gchPP: It is essential to distinguish a cardiogenic from a hypovolemic
shock!
Both forms are associated with reduced cardiac out put, and increased
peripheral vascular resistance, however:eki Pckgsyligf"
s # esPciyskyhPchkics$lk ls%&
'iiPkgsyligf" s gieyPs
geegkhecgPsPkcys$is%&
Cardiogenic shock:
jugular venous distention (high CVP)
Hypovolemic shock: collapsed
capacitance veins (low CVP)

39. Cardiogenic ShockT
kSigSihegyigSighPPgygghgy g
hegPSgyy
T
hgSigeigygigioePlheghPeig
ilyo hegyghliggyegT
T
hoghPiogPgShigoyehgyy g
eiei
•The heart loses the ability to supply all body
parts with blood
•Usually the result of left ventricular failure
secondary to acute MI or CHF
•Many patients will have normal blood
pressures

40. S/S of Cardiogenic ShockT
h!yeg PieioligiiiogySiegigygSylcg
Pgeiioligyg"yoheg# ih
T
$PPlgeihSPos
T
%Sii&i'gTehlci'g(higheigSihe ghgP g
iigPoleihi
T
"ey lPiglysSgPSgSPigyegPoc)Posi g
yhg
T
ThoyP
T
*iei giohPyo
T
+PsePhg,g ileihi gePohPyo-
•Major difference between other types of shock
is presence of Pulmonary Edema
•Difficulty breathing
•Wheezes, Crackles, Rales are heard as fluid
levels increase
•Productive cough with white or pink-tinged
foamy sputum
•Cyanosis
•Altered mentation
•Oliguria ( decreased urination)

41. TX for Cardiogenic ShockT
*eigyioghPeh
T
* Poiegy/siog
T
*PgioPhPyoghgoii i
T
0iighPioghe
T
"hlighPiogPogyPPyogyglyye
T
#hPSggPSgPoPhgP gh PoPehPyo
T
yoPyeg1Ph
T
hgoii gygh PoPieg$yhPoigyeg
$yhPoi
•Assure open airway
•Adminster oxygen
•Assist ventilations as needed
•Keep patient warm
•Place patient in position of comfort
•Establish Iv with minimal fluid administration
•Monitor Vitals
•May need to administer Dopamine or
Dobutamine

42. The Phys hiolgfSck Distributive ShockT
goehe
h
$igygsehgoishPigyegsehgyPPighliePh
T
fhel
h
$igygeiPygioPP&hPyogyghoghiesio
T
osPSohc
h
$igygehhPlgPohglye gPo!e
h
#ilgygiP ehgyegPohghoiSiPl
h
(ii/ghehhSiPlgPhPyo
•Sepsis
–Due to gram negative or gram positive bacteria
•Anaphylaxis
–Due to previous sensitization to an allergen
•Neurogenic
–Due to traumatic spinal cord injury
–Effects of epidural or spinal anesthetics
–Reflex parasymapthetic stimulation

43. kigygfSylc Types of ShockosPSohclgfSck
T
(ig igygSigyiehg PhPyogygSigyy g
iigPSPogSiglhe Pyhlhegi
T
$ileihi gyy geieig
T
oPlPioghyogyg+
2
gPgiPosgehoyei g
ygy gPigho gyesho
Neurogenic Shock
•Results due to the overall dilation of the blood
vessels within the cardiovascular system
•Decreased blood pressure
•Insufficient amounts of O
2
is being transported
to body tissues and organs

46. Neurogenic ShockT
(igeygPo!egygehPogyegPohglye g
lhPosgPoieePyogygoieigPigyg
heiePi
T
*eiePigyigyoigho g PhiglhPosg
SyyiPh
T
fhSiPlgoieigPigygSigh eiohg
sho gheigy'gSPlSgeiiogSigeiihigyg
lhilSyhPoigho gSiPeglyiohyegiil
•Results from injury to brain or spinal cord
causing interruption of nerve impulses to
arteries
•Arteries lose tone and dilate causing
hypovolemia
•Sympathetic nerve impulses to the adrenal
glands are lost, which prevents the release of
catecholamines and their compensatory effects

47. Neurogenic Shock (con’t)T
PsSgliePlhgPo!ePiglhigPoieePyogyg
PigygiePSiehgoieygiglhPosg
T
3ieysioPlgSylcgPgyglyyog igyg
iieigPo!egygPohglye gyegyhgehoilPyog
yglye g,PohgSylc-
•High cervical injuries cause interruption of
impulse to peripheral nervous system causing
•Neurogenic shock is most commonly due to
severe injury to spinal cord or total transection
of cord (spinal shock)

48. S/S of Neurogenic ShockT
%he'g$e'g(i gfcPo
T
5yg6yy g"eiei
T
fyg"i
•Warm, Dry, Red Skin
•Low Blood Pressure
•Slow Pulse

49. TX for Neurogenic ShockT
*Pehglyoey
T
hPohPogy giiehei
T
yPP&hPyogPgPo Plhi
T
TyoP iegySieglhigygSylc
T
1gho gi PlhPyogShgPoleihigiePSiehg
hlhegeiPholig,7#7g3yeiPoiSePoi'g
$yhPoi-
•Airway control
•Maintain body temperature
•Immobilization if indicated
•Consider other causes of shock
•IV and medications that increase peripheral
vascular resistance (I.E. Norepinephrine,
Dopamine)

52. Anaphylatic ShockT
fiieigPoigeiyoigygyeiPsogholi
T
f fgygyiogyllegPSPogPoigglhog
hciggygSyegygylle
T
kSighiegSigeihlPyog iiygSigyeig
iieigPgPgPcigygi
T
$ihSgPgyllegPgoygeihi gey
•Severe immune response to foreign substance
•S/S most often occur within minutes but can
take up to hours to occur
•The faster the reaction develops the more
severe it is likely to be
•Death will occur if not treated promptly

54. S/S of Anaphylactic ShockT
fcPo
)gSPos
)glSPos
)gPi
)fiPos
)ThoyP
•Skin
- Flushing
- Itching
- Hives
-Swelling
-Cyanosis

55. S/S of Anaphylactic ShockT
(iPehyegfi
)g6eihSPosg PPl
)gfoii&Pos'gTysSPos
)g%Sii&Pos'gfeP ye
)g5heosihgi ih
)g5heosyh
•Respiratory System
- Breathing difficulty
- Sneezing, Coughing
- Wheezing, Stridor
- Laryngeal edema
- Laryngospasm

56. S/S of Anaphylactic ShockT
The Pyhlhegfi
)g1hy PhPyo
)goleihi gSihegehi
)g$ileihi gyy geiei
•Cardiovascular System
- Vasodilation
- Increased heart rate
- Decreased blood pressure

57. S/S of Anaphylactic ShockT
8heyPoiPohgfi
)g3hih'gyPPos
)g* yPohglehPos
)g$PheeSih
•Gastrointestinal System
- Nausea, vomiting
- Abdominal cramping
- Diarrhea

58. TX for Anaphylactic ShockT
syofelyPkckPiegcgeofeicSe
iPkyocgoSeikokPi
T
koSgeekgecyfkoSSPePSkPi
T
goyocPSPcoSeikyikPi elilgyi!e
sikgkoi"#ioyfS$!e
%PykcPkyP"&okgoPi$!e
oPlyPy"Ploi!elilgyi$!eoie
igoSekoeoPik"oSkyPS$
•Airway protection which may include
Endotracheal Intubation
•Establish IV with crystalloid solution
•Pharmacological interventions: Epinephrine,
Antihistamines(Benadryl),
Corticosteroids(dexamethasone),
Vasopressors(dopamine, Epinephrine), and
inhaled beta agonist(albuterol)

61. Pathogenesis of Septic Shock
(vasodilatory shock)T
Sscolo ee ieoeoefkcei SookPyfeylPie
kPeoeockyoSei ckPiekgeockyoe"kgPge
SPPecSkyecoieeiok$
T
Ssssgoscolo ee iefeokPioSei'Pyoie
f ickPie"PykoSkfeyok e()'*+,$
T
Sscelkgo Pk ee ieoelekgegflPkiPie
lke SeyckokPieoieiceP eio-oke
kely Pie".+'/+,$
•Sepsis is defined as a systemic inflammatory response
to a bacterial infection with bacteriemia (though
blood cultures can be negative)
•Severe sepsis is defined by additional end-organ
dysfunction (mortality rate: 25-30%)
•Septic shock is defined as sepsis with hypotension
despite fluid resuscitation and evidence of inadequate
tissue perfusion (40-70%)

63. NEJM 2004, Vol. 351;2 pp 159-169

64. Clinical Spectrum of Infection
Infection
Sepsis
Severe Sepsis
Septic Shock
Bacteremia

66. The syndrome of septic shock is characterized
byT
fkceoPSokPie"gflPkiPi$
T
8igefPcoyoSecPikyockSkf
T
9lyoeiPkgSoSei:yfeoieockokPieSoie
kPe SeSooe"colSSoyfeSo$eySkieieocke
ylyokPyfekyefiyPe"s;8$
T
sckokPieP ekgecPoSokPiecocoe"8%$
•Systemic vasodilation (hypotension)
•Diminished myocardial contractility
•Widespread endothelial injury and activation leading
to fluid leakage (capillary leak) resulting in acute
respiratory distress syndrome (ARDS)
•Activation of the coagulation cascade (DIC)

68. Disseminated intravascular coagulation (DIC) T
ecgoyocky<efelyoeockokPieP ecPoSokPie
ySkieiekgeikyoocSoye PyokPieP e yieoieSkokSfe
kgyPPkcePccSPieP eoSSeoie<eS
T
SoekPecPlyPeP eSPPellSfekPePyoieoieofe
kgy PyecPikykekPeSklSePyoie oSy
T
-ikelSkPieP elSokSkeoiecPoSokPie ockPyecoie
ySkeieyeSieoieofeekgelyikieflkP
•is characterized by widespread activation of coagulation
resulting in the intravascular formation of fibrin and ultimately
thrombotic occlusion of small and midsize vessels
•leads to compromise of blood supply to organs and may
therefore contribute to multiple organ failure
•subsequent depletion of platelets and coagulation factors can
result in severe bleeding and may be the presenting symptom

69. Virtually all patients with sepsis have coagulation
abnormalities. The extreme form of it is called:
Acute disseminated intravascular coagulation (DIC)
Severe cutaneous bleeding as a result of fulminant Meningococcal
septicemia due to activation and consumption of all coagulation
factors (consumption coagulopathy)

71. Septic ShockT
siei ckPieikyeSPPkyoeoieecoyye
kgyPgPkePf
T
TP&ieySoePycPecPliokPyfe
cgoi
T
%oiecoef ickPieP ePiePyoiefkePye
coeSklSePyoief ickPi
•An infection enters bloodstream and is carried
throughout body
•Toxins released overcome compensatory
mechanisms
•Can cause dysfunction of one organ system or
cause multiple organ dysfunction

72. S/S of Septic ShockT
icyoekPeSPeSPPelyy
T
>ge y!eiPe y!egflPkgyc
T
ie Sg!eoS!e%foiPkc
T
8 cSkfeyokgieoieoSkyeSiePi
T
sSkye?@%
•Increased to low blood pressure
•High fever, no fever, hypothermic
•Skin flushed, Pale, Cyanotic
•Difficulty breathing and altered lung sounds
•Altered LOC

73. TX of Septic ShockT
syofecPikyPS
T
sikyeP&fi
T
eP ecyfkoSSPePSkPi
T
8Ploie PyeSPPelyyellPyk
T
2PikPyePkgyekoS
•Airway control
•Administer oxygen
•IV of crystalloid solution
•Dopamine for blood pressure support
•Monitor other vitals