The patient with evolving cardiogenic shock often will exhibit a rapid progression of findings indicating poor perfusion. Clinical evaluation, diagnostic testing, and treatment are initiated simultaneously. History from the patient is often blunted by the severity of the patient's condition, so family, EMS personnel, and medical records should supplement the patient's history. Key information includes current medications, allergies, and past history of MI, CHF, diabetes mellitus, and renal failure. Although the patient may experience chest pain, ischemic equivalents include profound weakness, shortness of breath, or a feeling of impending doom.
The hallmark of shock is hypoperfusion, often, but not always, accompanied by hypotension. The systolic blood pressure is typically less than 90 mmHg, although it may be within a "normal" range, especially if the patient has preexisting hypertension. Another blood pressure parameter that may be more sensitive is a 30 mmHg decrease in mean blood pressure or a pulse pressure (systolic-diastolic) of less than 20 mmHg. Although a compensatory sinus tachycardia is common and does not require specific treatment, excessively high or low heart rates do require immediate therapy. Compensatory sympathetic stimulation leads to cool and clammy skin. Oliguria reflects development of poor renal perfusion. Diminishing cerebral perfusion and hypoxemia lead to anxiety and confusion.
Signs of acute LV failure accompanied by pulmonary edema are tachypnea, rales, wheezing, and frothy sputum. The presence of jugular venous distension in the face of hypotension without signs of pulmonary edema suggest acute RV failure, from either RV infarction, tamponade, or pulmonary embolus. Careful cardiac examination is needed to identify an S3 or S4. Mitral regurgitation due to chordae tendinae rupture will exhibit a soft holosystolic murmur at the apex radiating to the axilla, although the murmur is often obscured by rales. Mitral regurgitation due to papillary muscle dysfunction usually will not be completely holosystolic. It starts with the first heart sound but terminates before the second. Acute septal rupture (acute ventricular septal defect) initially will have a loud parasternal ejection murmur, often with a palpable thrill, that decreases in intensity as the intraventricular pressures equalize.
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