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Core Lecture Series: Shock

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Presentation on theme: "Core Lecture Series: Shock"— 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 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: 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
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

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