1. Core Lecture Series: Shock
Eric M. Wilson, MD
September 22, 2009

2. Definition A physiologic state characterized by
Inadequate tissue perfusion
Clinically manifested by
Hemodynamic disturbances
Organ dysfunction

3. Pathophysiology Imbalance in oxygen supply & demand
Conversion from aerobic to anaerobic metabolism
Insult initiates neuroendocrine & inflammatory mediator reponses

4. Pathophysiology Hemodynamics maintained
Continued hypoTN-> tissue injury; reversible w/resuscitation
Cont’d volume loss / inadequate resuscitation -> hypoperfusion, cell injury-death
Compensated
Decompensation
Irreversible phase

5. Shock: Compensatory Mechanisms
Neural response
Hormonal response

6. Neural Response
- Decreased filling pressures lead to decreased output from left atrial stretch receptors to the vasomotor center of the medulla.
- Decreased frequency of impulses from the Carotid and aortic arch baroreceptors to the vasomotor center of the medulla.
- Result
- Increased sympathetic output.
- Inhibition of the vagal center

7. Neural Response: Effects on cardiovascular function
Larger arterioles constrict
Increases blood pressure
Smaller arterioles dilate
Lowers capillary hydrostatic pressure resulting in fluid shift from interstitial space into intravascular space
Vasoconstriction minimal in brain & heart & most intense in peripheral tissues

8. Pathophysiology: Neuroendocrine Response
The goal of the neuroendocrine response to hemorrhage is to maintain perfusion to the heart & the brain. Afferent signals that converge in the CNS originate from a variety of sources-chemoreceptors, baroreceptors
α1 & β1
Gluconeogenesis
Insulin resistance
Glycogenolysis
Lipolysis

9. The hormonal response to injury and shock

10. Pathophysiology Cellular physiology Resultant systemic physiology
Tissue hypoxia -> decrease generation of ATP anaerobic glycolysis
Pyruvate lactate  decrease in pH 
Intracellular metabolic acidosis
Cell membrane pump dysfunction
Na & H2O in  cellular swelling; K out
Resultant systemic physiology
Cell death & end organ dysfunction
MSOF & death
As oxygen tension within cells decreases, there is a decrease in oxidative phosphorylation and the generation of adenosine triphosphate (ATP) slows or stops. As oxidative phosphorylation slows, the cells shift to anaerobic glycolysis that allows for the production of ATP from the breakdown of cellular glycogen. Under hypoxic conditions, the mitochondrial pathways of oxidative catabolism are impaired, and pyruvate is instead converted into lactate. The accumulation of lactic acid and inorganic phosphates is accompanied by a reduction in pH, resulting in intracellular metabolic acidosis.
Decreased intracellular pH (intracellular acidosis) can alter the activity of cellular enzymes, lead to changes in cellular gene expression, impair cellular metabolic pathways, and impede cell membrane ion exchange.
As cellular ATP is depleted under hypoxic conditions, the activity of the membrane Na+,K+-ATPase slows, and thus the maintenance of cellular membrane potential and cell volume is impaired.9,11 Na+ accumulates intracellularly, while K+ leaks into the extracellular space. The net gain of intracellular sodium is accompanied by a gain in intracellular water and the development of cellular swelling.

11. Pathophysiology Shock Initial signs of organ dysfunction Tachycardia
Tachypnea
Metabolic acidosis
Oliguria
Cool & clammy skin

12. Pathophysiology End organ dysfunction
Progressive irreversible dysfunction
Oliguria, anuria
Progressive acidosis & depressed CO
Agitation, obtundation, & coma
Patient death

13. Classification Distributive Hypovolemic/Hemorrhagic Cardiogenic
Vasodilatory/Septic
Neurogenic
Distributive

14. Hypovolemic Shock Results from decreased preload Etiologic classes
Hemorrhage: trauma, GI bleed, ruptured aneurysm
Fluid loss: diarrhea, vomiting, burns

15. Hypovolemic Shock Hemorrhagic Shock
Parameter I II
III IV
Blood loss (ml)
<750
750–1500
1500–2000
>2000
Blood loss (%)
<15%
15–30%
30–40%
>40%
Pulse rate (beats/min)
<100
>100
>120
>140
Blood pressure
Normal
Decreased
Respiratory rate (bpm)
14–20
20–30
30–40
>35
Urine output (ml/hour)
>30
5–15
Negligible
CNS symptoms
Anxious
Confused
Lethargic
Elderly – blood thinners, meds masking compensatory responses to bleeding (beta-blockers)

16. Hemorrhagic Shock: Treatment
Control the source of blood loss
Intravenous volume resuscitation
Crystalloid solutions
If shock state is uncorrected after 2L, transfuse blood

17. Pump Failure Cardiogenic Shock
Inadequate blood flow to vital organs due to inadequate cardiac output despite normal intravascular volume status
Pump Failure

18. Cardiogenic Shock: CausesMI
Arrhythmias
Cardiomyopathy
Myocarditis
Mechanical
Acute mitral regurgitation
Acute aortic insufficiency
Ventricular septal defect

19. Cardiogenic Shock: Treatment
Maintain adequate oxygenation
Judicious fluid administration to avoid pulmonary edema
Correct electrolyte abnormalities
Treat dysrhythmias – reduce heart rate
Inotropic agents
Intra-aortic balloon counterpulsation

20. Cardiogenic Shock: Intra-aortic balloon pump
Improves coronary blood flow
Decreases afterload
Decreases myocardial oxygen demand

21. Vasodilatory Shock
Hypotension from failure of vascular smooth muscle to constrict
Vasodilation
Causes
Sepsis
Anaphylaxis
Systemic inflammation

22. Vasodilatory Shock

23. Vasodilatory Shock: Treatment
Treat source of infection
Maximize intravascular volume status
Intubation, if necessary
Vasopressors
Immune modulators
Activated protein C (Xigris)
Promotes fibrinolysis
Inhibits thrombosis & inflammation

24. Neurogenic Shock Usually caused by an injury to the spinal cord
Not caused by an isolated brain injury

25. Neurogenic Shock: Clinical Presentation
Hypotension
Bradycardia
Sensory loss
Motor paralysis
Warm, dry skin

26. Neurogenic Shock: Pathophysiology
Hypotension
Loss of sympathetic tone to arterial system resulting in decreased systemic vascular resistance
Loss of sympathetic tone to venous system resulting in pooling of blood in venous capacitance vessels with decreased cardiac filling and diminished cardiac output
Bradycardia
Loss of sympathetic input from spinal cord
Tonic parasympathetic input to heart unopposed leading to bradycardia

27. Neurogenic Shock: Pathophysiology
Sensory loss
Loss of efferent communication from the sensory organs to the brain
Motor paralysis
Loss of afferent communication from the brain to the voluntary muscles
Warm, dry skin
Loss of sympathetic input to sweat glands leads to failure to produce sweat
Failure of peripheral vasoconstriction maintains flow of warm blood to periphery and “warm skin”

28. Neurogenic Shock: Treatment
Fluid replacement
Pressor agents to restore vascular tone once volume status restored

29. Obstructive Shock
Reduced filling of the right side of the heart resulting in decreased cardiac output
Tension pneumothorax
Increased intrapleural pressure secondary to air accumulation
Pericardial tamponade
Increased intrapericardial pressure precluding atrial filling secondary to blood accumulation

30. Distinguishing Types of Shock
CVP/
PCWP CO
SVR
Hypovolemic
Septic
Cardiogenic
Neurogenic

31. Which of the following is an appropriate definition of the shock state?
Low blood pressure
Low cardiac output
Low circulating volumes
Inadequate tissue perfusion
Abnormal vascular resistance

32. In cases of hemorrhagic shock, what initial alteration in blood pressure is seen?
Increase in systolic pressure
Decrease in systolic pressure
Increase in diastolic pressure
Decrease in diastolic pressure
Class II shock – decrease in pulse pressure, which is generally related to increase in diastolic component, which in turn is related to elevation of catecholamines produced by neural response to shock