I. Definition

  1. Inadequate tissue perfusion with decreased cardiac output (SBP < 90mm Hg/cardiac Index < 2.2 L/min/m2) despite adequate LV filling pressures (pulnonary capillary wedge pressure > 15mm Hg)

I. Etiology :

  1. Acute myocardial infarction (10% of patients with acute MI develop cardiogenic shock; 89% of those developing > 6h after initial hospital presentation)
  2. Valvular Heart Disease
  3. Arrhythmias
  4. Trauma
  5. Pericardial tamponade
  6. Myocarditis
  7. Cardiomyopathy (end-stage)
  8. Myocardial weakness after prolonged cardiopulmonary bypass
  9. Myocardial contusion

II. Pathophysiology:

  1. CO is so depressed that severe vasoconstriction cannot maintain normal arterial pressure (as opposed to CHF); leads to hypotension, tachycardia, tachypnea, oliguria, acidosis, MS
  2. Severe reduction in O2 delivery due to impaired CO (<1.8) accompanied by increased LVEDP

III. Diagnosis and Clinical features

  1. See definition above.  For practical purposes, diagnosis depends on hypotension accompanied by clinical signs of tissue hypoperfusion:
    1. Cool, mottled extremities
    2. Oliguria
    3. Altered mental status
  2. Need to distinguish from other causes of Shock (see section on Shock for data on BNP levels as a diagnostic tool re: the cause of shock)
  3. Px: Tachycardia, tachypnea, jugular venous distension, rales, S3 gallop, +/- murmurs
  4. Metabolic acidosis
  5. Renal failure
  6. Pulmonary edema can occur (from pulmonary congestion due to ischemic, noncompliant myocardium), with hypoxia

V. Management

  1. Workup
    1. ECG to r/o myocardial ischemia, etc.
    2. CXR to r/o pneumothorax
    3. Consider echocardiogram to diagnose etiology of the shock
    4. Chem-7 to evaluate for renal failure & acidosis
    5. Careful monitoring of blood pressure
    6. Prompt cardiac cath if acute MI is suspected (if not available, may be candidate for thrombolytics + placement of intra-aortic balloon pump then transfer to a facility with cardiac cath capabilities)
  2. One goal of management is to improve cardiac function without increasing O2 consumption (contractility, preload, heart rate, afterload)
  3. Fluid resuscitation, if needed, to ensure adequate preload is reached (usually requires continuous hemodynamic monitoring)
  4. Supplemental O2 if hypoxic
  5. Inotropic tx (dobutamine, dopamine, isoproteronol)-Used if hypotension persists despite adequate fluid status (or fluid overload is present) to maintain mean arterial pressure > 60mm Hg
  6. Vasopressors may be needed
  7. Reduce afterload (vasodilators after increasing contractility)
  8. Mechanical intervention (intraaortic balloon 07j0)
  9. Antiarrhythmics
  10. L-NMMA (a nitric oxide synthesis inhibitor; works by vasoconstricting) may be useful in cardiogenic shock from MI (Circ. 101:1358, 2000--JW)

(Sources include Core Content Review of Family Medicine, 2012)