Shock

EMERGENCY MANAGEMENT

1. Shock : Pathophysiology Shock : Pathophysiology
Causes & ManagementCauses & Management
Dr.Anil HaripriyaDr.Anil Haripriya
Assistant Professor SurgeryAssistant Professor Surgery
NHDC & RCNHDC & RC

2. IntroductionIntroduction
 ““Rude unhinging of machinery of life’Rude unhinging of machinery of life’
-GrossGross
 Inadequate delivery of oxygen and nutrients Inadequate delivery of oxygen and nutrients
to maintain normal tissue and cellular functionto maintain normal tissue and cellular function

 Clinically accompanied by hypotension Clinically accompanied by hypotension
MAP < 60 mmHg in a previously MAP < 60 mmHg in a previously
normotensive personnormotensive person

3. Types of ShockTypes of Shock
 HypovolemicHypovolemic
 Vasodilatory (Septic)Vasodilatory (Septic)
 NeurogenicNeurogenic
 CardiogenicCardiogenic
 Obstructive Obstructive
 TraumaticTraumatic

4. PathophysiologyPathophysiology
 Physiologic response to hypovolemia directed Physiologic response to hypovolemia directed
at preservation of perfusion to vital organsat preservation of perfusion to vital organs
- Increase cardiac contractility & peripheral - Increase cardiac contractility & peripheral
vascular tone via ANSvascular tone via ANS
- Hormonal response to preserve salt & - Hormonal response to preserve salt &
waterwater
- Change in local micro circulation to regulate - Change in local micro circulation to regulate
regional blood flow regional blood flow

5. Neuroendocrine Neuroendocrine
responseresponse
 Mediated via baro & chemo receptors which Mediated via baro & chemo receptors which
stimulates ANS & HPA axis stimulates ANS & HPA axis
 release of epinephrine & norepinephrinerelease of epinephrine & norepinephrine

6. Hormonal responseHormonal response
HypothalamusHypothalamus
HyperglycemiaLypolysisGluconeogenesis
Glycogenolysis
Cortisol
ACTH
CRH

7. Hormonal responseHormonal response
 Stimulation of renin angiotensin system Stimulation of renin angiotensin system
 Release of ADH to conserve salt & Release of ADH to conserve salt &
waterwater

8. Cellular responseCellular response
 Inadequate delivery of oxygen & substrates Inadequate delivery of oxygen & substrates
leads to in oxidative phosphorylation & ATP leads to in oxidative phosphorylation & ATP
generationgeneration
 Anaerobic respiration leads to lactic acidosisAnaerobic respiration leads to lactic acidosis

9. Cellular responseCellular response
 Na+,K+ ATP ase activity decrease leading to Na+,K+ ATP ase activity decrease leading to
accumulation of Na+ & leak of K+accumulation of Na+ & leak of K+
 Cellular gene expression for HSP,VEGF,NO Cellular gene expression for HSP,VEGF,NO
synthase & cytokines is also increasedsynthase & cytokines is also increased

10. Hypovolemic shockHypovolemic shock
 M/C form of shockM/C form of shock
 Due to loss of blood, plasma, extravascular Due to loss of blood, plasma, extravascular
sequestration sequestration
 C/f and severity depends upon amount of C/f and severity depends upon amount of
volume lost volume lost

11. Hypovolemic shockHypovolemic shock
 CausesCauses
- Trauma - Trauma
- Severe dehydration- Severe dehydration
- Burns- Burns
- Intestinal obstruction- Intestinal obstruction
- Perforation peritonitis- Perforation peritonitis

12. Hypovolemic shockHypovolemic shock
PhasesPhases
- Compenseted- Compenseted
- Decompenseted- Decompenseted
- Irreversible- Irreversible

13. Hypovolemic shockHypovolemic shock
Same +
Hypotension
Mental status
deterioration
Same +
Tachycardia
Tachypnoea
Oliguria
Postural
-hypotension
Cold
extremities
CRT
Diaphoresis
Anxiety
Severe(>40%)Moderate(20-4
0%)
Mild (<20%)

14. Cardiogenic shockCardiogenic shock
 Circulatory pump failure in setting of adequate Circulatory pump failure in setting of adequate
vascular volume vascular volume
 Sustained hypotension SBP < 90 mm Hg for at Sustained hypotension SBP < 90 mm Hg for at
least 30 minutesleast 30 minutes
– CI < 2.2 L/min/mCI < 2.2 L/min/m
22
– PAWP >15mmHgPAWP >15mmHg

Surgical importance in patients with chest Surgical importance in patients with chest
trauma fortrauma for
–TamponadeTamponade
–Tension pneumothoraxTension pneumothorax

15. Cardiogenic shock Cardiogenic shock
 Chest painChest pain
 HypotensionHypotension
 ArrhythmiasArrhythmias
 Beck’s triadBeck’s triad

16. Vasodilatory shockVasodilatory shock
 Characterised by peripheral vasodilatation with Characterised by peripheral vasodilatation with
hypotension & resistance to T/t with vasopressorshypotension & resistance to T/t with vasopressors
 CausesCauses
- Septic shock- Septic shock
- Hypoxic lactic acidosis- Hypoxic lactic acidosis
- CO poisoning- CO poisoning
- terminal stage of cardiogenic & hemorrhagic shock- terminal stage of cardiogenic & hemorrhagic shock

17. Septic shockSeptic shock
 Manifestation of excessive & inflammatory Manifestation of excessive & inflammatory
response of endogenous immune mechanismresponse of endogenous immune mechanism
 Sepsis is SIRS with established focus of
infection
 Septic shock - severe sepsis unresponsive to
continuous fluid infusion and inotropes

18. Septic shockSeptic shock
Gram –ve bacilliGram –ve bacilli
LPS+CD14
TNF
IL-1
IL-6/IL-8
NO/PAF

19. Neurogenic shockNeurogenic shock
 tissue perfusion as a result of loss of
vasomotor tone to peripheral arterial beds
 Secondary to spinal cord injury from
vertebral #
- Hypotension with bradycardia
- Warm extremities
- Motor and sensory deficit

20. ManagementManagement
 Initially empirical
 Air way secured
+ oxygenation
 Two wide bore lines
 I.V. fluids NS/BSS
 Catheterisation
 Insertion of central venous catheter
 Hb, CBC, Blood sugar, urea, creatinine, electrolytes
 ABG

21. Hypovolemic shockHypovolemic shock
 I.V. fluid NS/RL 2-3 liters over 15-30 min
 If hemodynamic instability persist then start
blood transfusion & control on going heamorrhage
 Ionotropic like
Dopamine 5-10microgms/Kg/min
Dobutamine 2-20microgms/Kg/min

22. Cardiogenic shockCardiogenic shock

Conformation of diagnosis by ECG & ECHO
 Intubation & mechanical ventilation often
required
 Avoid fluid overload
 Ionotropic support preferably Dobutamine
2-20microgms/Kg/min
 USG guided pericardiocentesis

23. Neurogenic shockNeurogenic shock

Restoration of intravascular volume by
crystalloids
 Vasoconstrictor
Dopamine > 10microgms/Kg/min
Phenylephrine 0.2-2.9microgms/Kg/min

24. Septic shockSeptic shock
 Culture of body fluids
 Infuse BSS 500 cc/15min monitor SBP/CVP
 Repeat if CVP 8-12mmHg
 Goal to have a MAP of 65 mmHg & P < 120/min
 If hemodynamic instability persists start
vasopressor preferrably Norepinephrine
0.02-0.25microgms/Kg/min
 Broad spectrum antibiotic given

25. Aims of resuscitationAims of resuscitation

CVP of 8-12 mmHg/ PCWP 8-12 mmHg
 MAP of > 65 mmHg
 Urine output of 0.5ml/Kg/hr
 Hb of 7-9 gm%
 CI of > 4.2 L/Kg/m
2
of BSA

26. End Points of End Points of
resuscitationresuscitation
 Resuscitation complete when oxygen debt repaid,tissue acidosis Resuscitation complete when oxygen debt repaid,tissue acidosis
corrected & aerobic metabolism restored corrected & aerobic metabolism restored
Systemic ParametersSystemic Parameters
 LactateLactate
 Base deficitBase deficit
Tissue ParametersTissue Parameters
 Gastric tonometeryGastric tonometery
 Near infrared spectroscopy Near infrared spectroscopy

27. ConclusionConclusion
 Early recognition of warning signs and diagnosis in the
reversible phase important for successful management of
shock
 Hypovolemia and sepsis account for majority of shock in
surgical patients
 Principles of initial resuscitation same irrespective of type
of shock
 Ultimate treatment of underlying cause forms cornerstone
of management