Shock

 Shock is affecting about 30% patients in the ICU who were assigned to receive either dopamine or norepinephrine
 Septic shock in 62%
 Cardiogenic shock in 16%
 Hypovolemic shock in 4%
 Distributive shock in 4%
 Obstructive shock in 2%

1. Introduction
 Shock is defined as acute circulatory failure, a situation in which the circulation fails to provide cells with sufficient
oxygen to be able to perform optimally
 Diagnosis of shock is based on: Clinical, hemodynamic, biochemical signs
 Shock can be broadly be summarized into three components
o Systemic circulation hypotension (in adults)
SBP <90mmHg
MAP <70mmHg, with associated tachycardia
o Tissue hypoperfusion – the three windows of the body
Cutaneous: Skin that is cold and clammy
Renal: Urine output of <o.5mL/kg/h
Neurologic: Altered mental states includes obtundation, disorientation, confusion
o Hyperlactatemia: The level >1.5mmol/L in acute circulatory failure

2. The four pathophysiological types of shock and principle

Pathophysiological types Cause
Hemorrhage, trauma
Hypovolemic
Dehydration
Myocardial infarction
Cardiomyopathy
Cardiogenic
Valvular disease
Severe arrhythmias
Pulmonary embolism
Obstructive Tamponade
Aortic dissection
Distributive Inflammatory response (mediators)

 Distributive shock: Vasodilation

 Hypovolemic shock: Loss of plasma or blood volume
 Obstructive shock: Pericardial tamponade
 Initial stage Compensatory stage Progressive stage Refractory stage
Sympathetic nervous system Electrolyte imbalance:
stimulated: Metabolic acidosis
Body switches from Catecholamine release (+) Respiratory acidosis
aerobic to anaerobic Cardiac contractility (+) Peripheral edema:
metabolism Neurohormonal response: Irregular tachyarrhythmias Irreversible cellular
Elevated lactic acid Vasoconstriction and blood shunted Hypotension and organ damage
level to vital organs Pallor: Impending death
Subtle changes in Aldosterone release: Cool and clammy skin
clinical signs Urine output (-) Altered level of consciousness
Heart rate and blood glucose level
(+)

Class I Class II Class III Class IV

Blood loss <750 750-1500 1500-2000 >2000
% Blood Vol. <15% 15-30% 30-40% >40%
Pulse <100 >100 >120 >140
Blood Pressure Normal Normal Decreased Decreased
Pulse Pressure Normal Decreased Decreased Decreased
Resp. Rate 14-20 20-30 30-40 >40
UOP >30 20-30 5-15 Negligible
Mental Status Sl. anxious Mildly anx Confused lethargic
Fluid Crystalloid Crystalloid Blood Blood

 Role of hypoxia
o O2 extraction ratio (O2ER) = VO2(Oxygen consumption)/DO2(Oxygen delivery)
o In resting state: 1/4, 1/3
o Under the condition of either increased energy expenditure or decreased DO2
 A decreased in O2 in Septic patients
o Microcirculatory derangements: A-V shunting, maldistribution
o Defective oxygen utilization at the cellular level
o Late sepsis, traumatic shock, hemorrhage
o Early shock with inadequate volume resuscitation
o Down-regulation or oxidative metabolism
Endotoxin may cause a decrease in oxidative metabolism in skeletal muscle

3. Diagnosis & monitoring

 Conventional monitoring
o Mental status
o Skin temperature
o Pulse rate and blood pressure
o Urine output (30ml/hr)
 Special monitoring
o CVP <5, 5-10, >15, >20 cmH2O
o PCWP 6-15mmHg
o CO/CI
o Serum lactate concentration
o Arterial blood gas analysis
o DIC
4. Urgent measurement
 Resuscitation
 Treat inciting cause of shock
 Control electrolyte and acid base derangement
 Inotropic agent
 Treat DIC, improve microcirculation
 Corticosteroids
 Initial resuscitation of patients in shock
Optimize oxygen delivery
Keep SaO2>90% Optimize cardiac index Optimize Hb
Supply supplemental O2
Early hemodynamic monitoring 11-13g/dl
Ventilator, if necessary
Assess volume status (preload)
PCWP<15 Volume expansion PCWP<18 Consider volume PCWP>18 Diurese
Reassess
Keep: PCWP 15-18, MAP 60-80mmHg, delivery independent O2 consumption
Goal meet Goal not meet
Treat inciting cause of shock Inotropic support, beta agonism
Control SIRS Goal meet Goal not meet
Nutritional support Consider vasodilator, alpha agonist

 Initial resuscitation of patients in shock (modified)

Optimize oxygen delivery
Keep SaO2>90% Optimize cardiac index Optimize Hb
Supply supplemental O2
Early hemodynamic monitoring 11-13g/dl
Ventilator, if necessary
Assess volume status (preload)
CVP<6 Volume expansion CVP<12 Consider volume CVP>12 Diurese
Reassess
Keep: PCWP 15-18, MAP 60-80mmHg, delivery independent O2 consumption
Goal meet Goal not meet
Treat inciting cause of shock Inotropic support, beta angonism
Control SIRS Goal meet Goal not meet
Nutritional support Consider vasodilator, alpha agonist

5. Hypovolemic shock
 Symptom
o A decrease in pulse pressure
o Tachycardia and hypotension
o Urine output falls
o Normal skin turgor is lost
o Mental status changes – in a progressive fashion
Apprehension, anxiety, complete obtundation
 Treatment: Resuscitation & control the inciting cause of shock
 Initial end-points volume resuscitation
o Reestablishment of urinary output to a rate of 0.5-1mL/kg/h
o A normal heart rate and blood pressure
o Adequate capillary refill
o Normal sensorium
o Normal CVP and PCWP

6. Trauma triad of death (Severe blood loss)

 Low body temperature (hypothermia): Decreased coagulation
 Blood clotting problem (coagulopathy): Increased lactic acid in blood
 Acidic blood (acidosis): Decreased heart performance

7. Traumatic shock
 Type: Vasogenic shock that begins as hypovolemic shock
 Character: Refractory to fluid replacement therapy
o Larger volume losses, greater fluid sequestration
 o More intense activation of inflammatory mediators
o Development of SIRS
o Devastating soft tissue injuries
 Mechanism: Increasing microvascular permeability, excessive fluid requirement
 Frequently require
o Mechanical ventilation, pulmonary artery catheter monitoring
o Cardiovascular support
o Operation

8. Septic shock
 Type: Vasogenic shock, Refractory to fluid replacement therapy
 Definition
o Sepsis with hypotension despite adequate fluid resuscitation
o Along with the presence of manifestation of hypoperfusion
Such as lactic acidosis, oliguria, or acute alternation in mental status
 Mechanism
o Cytokines
o Vasodilation, increasing microvascular permeability, excessive fluid requirement
 Treatment
o Resuscitation
o Control infection
o Normalization of electrolytes, acid base derangement
o Inotropic agent
o Corticosteroids
o Nutritional support, deal with DIC, organ function support

9. Cardiogenic shock
 Extracorporeal membrane oxygenation

10. Integrate the concept of intensive care medicine

 Oxygen supply and consumption
 Cytokine and mediators
 Glucose, electrolytes, etc
 Utilization of nutrition
 Supportive therapy for organ dysfunction
 Prevention, early identification of Shock and MODS
 Parameter of severity
 Prevention of irreversible shock and MODS