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

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Presentation on theme: "Core Lecture Series: Shock Eric M. Wilson, MD September 22, 2009."— Presentation transcript:

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

4 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 α 1 & β 1 Gluconeogenesis Insulin resistance Glycogenolysis Lipolysis

9 The hormonal response to injury and shock

10 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 Pathophysiology

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

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

13 Hypovolemic/Hemorrhagic Cardiogenic Vasodilatory/Septic Neurogenic Classification Distributive

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

15 ParameterIIIIIIIV Blood loss (ml)<750750– –2000>2000 Blood loss (%)<15%15–30%30–40%>40% Pulse rate (beats/min)<100>100>120>140 Blood pressureNormal Decreased Respiratory rate (bpm)14–2020–3030–40>35 Urine output (ml/hour)>3020–305–15Negligible CNS symptomsNormalAnxiousConfusedLethargic 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 Shock CVP/ PCWP COSVR Hypovolemic Septic Cardiogenic Neurogenic

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

32 In cases of hemorrhagic shock, what initial alteration in blood pressure is seen? A.Increase in systolic pressure B.Decrease in systolic pressure C.Increase in diastolic pressure D.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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