david i driver basics of shock

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    Overview:Overview: Shock (in adults)Shock (in adults)

    By:By:David I. Driver, MS IIIDavid I. Driver, MS III

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    IntroductionIntroduction

    Shock is a physiologic state characterized by asignificant, systemic reduction in tissue perfusion,thereby resulting in decreased tissue oxygen delivery.

    Prolonged oxygen deprivation leads to generalized

    cellular hypoxia and the derangement of criticalbiochemical processes: Cell membrane ion pump dysfunction

    Intracellular edema

    Leakage of intracellular contents into the extracellular space Inadequate regulation of intracellular pH

    High Mortality Hypovolemic 35-40%

    Cardiogenic 60-90%

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    Stages of ShockStages of Shock

    The shock syndrome is characterized by a temporalcontinuum of physiologic stages beginning with an

    initial inciting event which causes a systemic circulatorydisturbance; shock may subsequently progress throughthree stages, culminating in irreversible end-organdamage and death.

    Preshock

    Shock

    End-organ dysfunction

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    Stages of Shock IIStages of Shock II

    Preshock Preshock is also known as warm shock or compensated shock. During

    this stage, the body's homeostatic mechanisms rapidly compensate fordiminished perfusion. Despite a 10 percent reduction in total effectiveblood volume, for example, a previously healthy adult may beasymptomatic.

    Shock During this stage, the regulatory mechanisms are overwhelmed and signs

    and symptoms of organ dysfunction appear, including tachycardia,tachypnea, metabolic acidosis, oliguria, and cool and clammy skin.

    End-organ dysfunction During this stage, progressive end-organ dysfunction leads to irreversible

    organ damage and death: Urine output may decline, culminating in anuria.

    Restlessness evolves into agitation, obtundation, and coma.

    Acidosis further decreases cardiac output and alters cellular metabolicprocesses.

    Multiple organ system failure proceeds to cause the demise of the patient.

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    Physiologic DeterminantsPhysiologic Determinants

    Global tissue perfusion is determined bysystemic vascular resistance (SVR) and cardiac

    output (CO) SVR is governed by vessel length, blood viscosity,

    and the inverse of vessel diameter.

    CO is the product of heart rate and stroke volume;

    in turn, stroke volume depends upon preload,myocardial contractility, and afterload (impedance toblood flow).

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    Classification of ShockClassification of Shock

    Any classification scheme simplifies the complexpathophysiology underlying the many individual causes

    of shock states. Three broad types of shock states are recognized. Each

    type is characterized by one primary physiologicderangement:

    Hypovolemic

    Cardiogenic

    Distributive or vasodilatory

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    Hypovolemic ShockHypovolemic Shock

    Hypovolemic shock results from decreased preload.

    Two broad etiology based categories:

    Hemorrhage

    trauma, upper and lower gastrointestinal bleeding, ruptured aortic orventricular aneurysm, ruptured hematoma, hemorrhagic pancreatitis,and fractures.

    Fluid loss diarrhea, vomiting, heat stroke, inadequate repletion of insensible

    losses, burns, and "third spacing"

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    Distributive (vasodilatory) ShockDistributive (vasodilatory) Shock Distributive or vasodilatory shock results from a severe decrease

    in SVR, often associated with an increased cardiac output. Septic shock

    Activation of the systemic inflammatory response

    Toxic shock syndrome Anaphylaxis and anaphylactoid reactions

    Drug or toxin reactions, including insect bites, transfusion reactions, andheavy metal poisoning

    Addisonian crisis

    Myxedema coma Neurogenic shock after a central nervous system or spinal cord injury

    Some patients after acute myocardial infarction who develop cardiogenicshock accompanied by a systemic inflammatory state

    Post-cardiopulmonary bypass

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    Cardiogenic ShockCardiogenic Shock

    Cardiogenic shock results from pump failure,manifested physiologically as decreased systolic

    function and cardiac output. Four broad categories:

    Myopathic

    Arrhythmic Mechanical

    Extracardiac (obstructive)

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    Common Features of ShockCommon Features of Shock

    The clinical presentation of shock varies both with thetype and the cause, but several features are very

    common. Assessment for each of the following fivemajor features should be done immediately in anypatient suspected of developing shock. Hypotension

    Cool, clammy skin

    Oligouria

    Change in mental status

    Metabolic acidosis

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    Initial ExamInitial Exam

    History The patient rarely provides any history; instead, historical data are usually

    obtained from relatives or available medical records. The patient's general

    condition, recent complaints, and activities prior to presentation may holdvaluable information about the primary cause of shock.

    Physical Exam The physical examination should be performed rapidly and efficiently,

    with efforts directed toward uncovering the most likely causes of shock.

    Labs laboratory tests helps to identify potential causes for shock and early signs

    of organ failure

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    Pulmonary Artery CatheterizationPulmonary Artery Catheterization

    Pulmonary artery catheterization is frequently

    used to provide hemodynamic measurements in

    shock patients, including CO, pulmonary arterywedge (pulmonary capillary wedge) pressure,and SVR. These values may help distinguish

    which type of shock is affecting a patient andcan aid in identifying a specific diagnosisamongst an extensive differential.

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    ReferencesReferences

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    3. Rodgers, KG. Cardiovascular shock. Emerg Med Clin North Am 1995; 13:793. 4. Bone, RC. Toward an epidemiology and natural history of SIRS (systemic inflammatory response syndrome). JAMA 1992; 268:3452.

    5. Moscucci, M, Bates, ER. Cardiogenic shock. Cardiol Clin 1995; 13:391. 6. Hochman, JS, et al. Current spectrum of cardiogenic shock and effect of early revascularization on mortality. Circulation 1995; 91:873.

    7. Shoemaker, WC. Temporal physiologic patterns of shock and circulatory dysfunction based on early descriptions by invasive and noninvasive monitoring.New Horiz 1996; 4:300.

    8.

    Abboud, FM. Pathophysiology of hypotension and shock. In: Hurst, JW (Ed), The Heart, New York, McGraw-Hill, 1982, p. 452.

    9. Chien, S. Role of the sympathetic nervous system in hemorrhage. Physiol Rev 1967; 47:214. 10.

    Abboud, FM. Pathophysiology of hypotension and shock, In: Hurst, JW (Ed), The Heart, New York, McGraw-Hill, 1982, p. 452. 11. Tuchschmidt, JA, Mecher, CE. Predictors of outcome from critical illness. Crit Care Clin 1994; 10:179.

    12. Casey, LC, Balk, RA, Bone, RC. Plasma cytokine and endotoxin levels correlate with survival in patients with the sepsis syndrome. Ann Intern Med1993; 119:771.

    13. Chittock, DR, Russell, JA. Oxygen delivery and consumption during sepsis. Clin Chest Med 1996; 17:263.

    14. Hinshaw, LB. Sepsis/septic shock: Participation of the microcirculation: an abbreviated review. Crit Care Med 1996; 24:1072. 15. Lederle, FA, et al. Ruptured abdominal aortic aneurysm: the internist as diagnostician. Am J Med 1994; 96:163.

    16. Kinch, JW, Ryan, TJ. Right ventricular infarction. N Engl J Med 1994; 330:1211.

    17. Hochman, JS. Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm. Circulation 2003; 107:2998. 18. Bouachour, G, et al. Hemodynamic changes in acute adrenal insufficiency. Intensive Care Med 1994; 20:138. 19. Levraut, J, Ciebiera, JP, Chave, S, et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am

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    20. Mimoz, O, et al. Pulmonary artery catheterization in critically ill patients. Crit Care Med 1994; 22:573. 21. Robin, ED. The cult of the Swan-Ganz catheter. Overuse and abuse of pulmonary flow catheters. Ann Intern Med 1985; 103:445.

    22. Connors, AF Jr, Speroff, T, Dawson, NV, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORTInvestigators. JAMA 1996; 276:889.

    23. Harvey, S, Harrison, DA, Singer, M, et al. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensivecare (PAC-Man): a randomised controlled trial. Lancet 2005; 366:472.

    24. Shah, MR, Hasselblad, V, Stevenson, LW, et al. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinicaltrials. JAMA 2005; 294:1664.