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Core Lecture Series: Shock

Core Lecture Series: Shock. Eric M. Wilson, MD. September 22, 2009. Definition. A physiologic state characterized by Inadequate tissue perfusion Clinically manifested by Hemodynamic disturbances Organ dysfunction. Pathophysiology. Imbalance in oxygen supply & demand

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Core Lecture Series: Shock

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  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 α1 & β1 Gluconeogenesis Insulin resistance Glycogenolysis Lipolysis

  9. The hormonal response to injury and shock

  10. Pathophysiology • Cellular 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

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

  18. Cardiogenic Shock:Causes • MI • 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

  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

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