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Cardiogenic Shock:

Perioperative Concerns

D R . A C H YUT S H AR MA
D E PART ME NT O F A N EST HESI A , PA I N
M A N AG EMENT A N D C R I T I C A L C A R E
N E PA L M E DI C I T I H O SP I TA L

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Cardiogenic Shock
 Cardiogenic shock (CS) is a clinical condition of inadequate tissue
(end-organ) perfusion due to cardiac dysfunction.
 But, there is more to it and includes the following hemodynamic
parameters:
 Persistent hypotension (SBP <80-90 mm Hg or MAP 30 mm Hg
lower than baseline)
 Severe reduction in cardiac index (<1.8 L/min per m2 without
support or < 2.0 to 2.2 L/min per m2 with support)
 Adequate or elevated filling pressures.

 Causes: Most common STEMI with LVF, others acute MR, rupture of
ventricular septal or free walls.

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Cardiogenic Shock contd..
Requires at least 40% loss of functional myocardium (single MI or
cumulative damage) - stunned, nonfunctional, but viable myocardium
may contribute to post-MI cardiogenic shock
Usually involves left main or left anterior descending obstruction
Historically, incidence of cardiogenic shock post-Q wave MI has run 8 -
20% with mortality 70 - 90% (? reduced incidence with thrombolytics 4
- 7%)
RV infarction with cardiogenic shock seen in only 10 - 20% largest
inferior wall MIs
Isolated RV infarcts rare - almost all have some degree of LV
involvement

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Cardiogenic Shock contd..
Treatment
Revascularization with either PCI or CABG preferred to fibrinolytic
therapy.
Primary PCI is preferred to CABG for patients with one or two vessel
disease and technically suitable lesions. Immediate CABG for triple
vessel or left main disease.
Prompt administration of fibrinolysis if the delay to primary PCI is
expected to be >60 minutes or door-balloon time is expected to be
>90 minutes. (Class I recommendation, ACC/AHA)
When fibrinolysis is given, should be combined with vasopressors,
IABP (if possible)
If revascularization facility not available, immediately be referred to
such center.
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Distributive Shock
 Septic shock is defined as sepsis-induced hypotension
persisting despite adequate fluid resuscitation, which may be
defined as infusion of 30 mL/kg of crystalloids (a portion of this
may be albumin equivalent).
 Septic shock is a type of vasodilatory or distributive shock.
 Other causes of distributive shock being: anaphylactic shock
and much rare neurogenic shock.
 Clinical form of shock with greatest contribution of other shock
elements - i.e., hypovolemia, cardiac failure
 Defining feature: loss of peripheral resistance

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Distributive Shock contd..
Anaphylactic shock: immediate hypersensitivity reaction
mediated by the interaction of IgE on mast cells and basophils
with the appropriate antigen resulting in mediator cascade

Anaphylactoid reactions involve similar release of mediators via


non-immunologic mechanisms.

Primary mediators include histamine, serotonin, eosinophil


chemotactic factor, and proteolytic enzymes.

Secondary mediators include PAF, bradykinin, prostaglandins,


and leukotrienes.

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Distributive Shock contd..
Stages
1. Hyperdynamic (Warm) Shock:
Warm shock characterized by high cardiac output and low peripheral
vascular resistance occurs first.
Vasodilation from the effects of histamine, bradykinins, serotonin,
and endorphins dramatically decrease total peripheral vascular
resistance.
It also makes capillaries more permeable causing leakage and fluid
shifting into tissues and physiologic third spaces.
 Further fluid loss: due to fever, high RR.
 Other sign to look for: profound diuresis:

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Distributive Shock contd..
Stages
2. Unusually high respiratory rate:
 Body fails to keep pace with profoundly decreased intravascular
volume; inadequate tissue perfusion  loss of cellular energy,
increased lactic acid production.
 Unusually high RR may in part be d/t to fever, early stages of
metabolic acidosis. But that doesn’t explain it all.
 May result from direct effect of bacterial endotoxins on the medullay
respiratory center.
 May counterbalance the metabolic acidosis.
 ABG at this stage: Metabolic acidosis, Respiratory compensation,
PaO2 elevated; Mixed venous blood oxygen saturation >80%.

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Distributive Shock contd..
Stages
Meanwhile,
 Clotting factors are used up: d/t too excessive activation of clotting
system.
 The complement system contributes to damage the vascular
endothelium and neutrophil aggregation while Hageman factor
accelerated clotting and causes multiple fibrin clots to form.
 These clots clog up small capillaries, esp in feet creeping mottling
of the legs.
 Decreased cerebral perfusion, produces symptoms of restlessness
and confusion: May be early sign of septic shock.
 How is the patient until now: May be relatively comfortable even
after all of this, d/t release of endorphins calming the patient.
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Distributive Shock contd..
Stages
3. Hypodynamic (Cold) Shock: The ’ominous’ late stage
 Most patient swill remain in warm shock for 6 to 72 hours before entering
cold shock.
 This late and nearly irreversible phase of septic shock is usually
indistinguishable from terminal hypovolemic shock.
 Two ominous signs of could shock are: a subnormal temperature and a low
white blood cell count (with many immature cells)
 By this time, patient will have profound hypotension and hypoperfusion,
cold and mottled periphery, high RR and HR.
 CO will, however, decrease: in part d/t cardiac depressant factor from
pancreatic cells and also d/t endotoxins.
 Multi-system failure sets in.
 His ABGs will show uncompensated hypoxemia, acidemia, and
hypoventilation with shunting.

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Distributive Shock contd..
Stages
3. Hypodynamic (Cold) Shock: The ’ominous’ late stage
 Most patient swill remain in warm shock for 6 to 72 hours before entering
cold shock.
 This late and nearly irreversible phase of septic shock is usually
indistinguishable from terminal hypovolemic shock.
 Two ominous signs of could shock are: a subnormal temperature and a low
white blood cell count (with many immature cells)
 By this time, patient will have profound hypotension and hypoperfusion,
cold and mottled periphery, high RR and HR.
 CO will, however, decrease: in part d/t cardiac depressant factor from
pancreatic cells and also d/t endotoxins.
 Multi-system failure sets in.
 His ABGs will show uncompensated hypoxemia, acidemia, and
hypoventilation with shunting.

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Distributive Shock contd..
Management
Therapeutic priorities in septic Maintain Oxygen delivery:
shock: Hb > 9 g/dl
Early initiation of supportive care
Arterial saturation >92%
to correct physiologic
abnormalities, such as hypoxemia Supplemental oxygen and
and hypotension. mechanical ventilation
Distinguishing sepsis from Reversal of oxygen dysfunction:
systemic inflammatory response Decreasing lactate <2.2
syndrome (SIRS) mmol/L
Early Management: Maintain urine output
Hemodynamic support: Reversal of encephalopathy
MAP > 60 mm Hg Improving renal, liver functions
tests.
PAOP: 12-18 mm Hg
Antibiotics immediate
Cardiac Index >2.2 L/min/m2
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Distributive Shock contd..
Management
First of all:
Stabilize respiration:
Supplemental oxygen
Monitoring of oxygenation continuously with pulse oximetry
May require intubation and mechanical ventilation to support
the increased work of breathing or to protect the airway (against
aspiration because of altered sensorium)
Obtaining of CXR and ABG after stabilization of the respiration.

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Distributive Shock contd..
Management
Second:
Assess perfusion:
Hypotension is the most common indicator that perfusion is
inadequate (SBP <90 mm Hg, MAP <70 mm Hg, decrease in SBP
>40 mm Hg)
Monitor BP early and often.
Arterial catheter may be inserted early if blood pressure is
labile

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Distributive Shock contd..
Management
Second:
Assess perfusion:
Hypotension is the most common indicator that perfusion is
inadequate (SBP <90 mm Hg, MAP <70 mm Hg, decrease in SBP
>40 mm Hg)
Monitor BP early and often.
Arterial catheter may be inserted early if blood pressure is
labile
Critical hypoperfusion can also occur in the absence of
hypotension, especially during early sepsis
Special considerations
Brainstorming: A ?septic patient with no hypotension. What can
be a reliable test for hypoperfusion?
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Distributive Shock contd..
Management
Third:
Establish central venous access:
A CVC can be used to infuse intravenous fluids, infuse
medications, infuse blood products, and draw blood, and of
course as a measure of hemodynamic monitoring for fluid
administration, central venous oxygen saturation.
Pulmonary artery catheters (PACs) should not be used in the
routine management of patients with severe sepsis or septic
shock
Dynamic hemodynamic measures: Respiratory changes in
radial artery pulse pressure, aortic/radial artery blood flow peak
velocity
Static hemodynamic measures: CVP and PAOP

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Distributive Shock contd..
Management
Goals of initial resuscitation:
To be noted, there are two problems happening simultaneously
in septic shock and complementing each other for complications:
a depressed heart not able to pump blood, and dilated vessels
stagnating all the blood, end result hypotension, & hypoperfusion.
Goals of the first 6 hours of resuscitation are:
Central venous pressure 8 to 12 mmHg
Central venous (superior vena cava) or mixed venous oxygen
saturation 70 or 65 percent, respectively
Mean arterial pressure ≥65 mmHg
Urine output ≥0.5 mL/kg/hour
Lactate clearance of >10%

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Distributive Shock contd..
Management
Fluid therapy:
Volume status, tissue perfusion, blood pressure, and the
presence or absence of pulmonary edema must be assessed
before and after each bolus.
The BIG question is “Is the patient really fluid responsive?”
Crystalloid versus albumin: SAFE trial (albumin vs saline), 6S trial
(HES vs RL)
Vasopressors
Inotropes

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Questions & suggestions

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Bibliography
 Miller’s Anesthesiology, 8th Edition
 Morgan and Mikhail’s Clinical Anesthesiology, 5th Edition
 Obstructive jaundice and perioperative management, A review article,
Long Wang, Wei-Feng Yu.

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Thank You
for listening

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