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Cardiogenic Shock
General Considerations
Although overall mortality from coronary artery disease and myocardial infarction continues to decline, mortality from cardiogenic shock—which is caused primarily by acute myocardial infarction—continues at a very high rate in medically treated patients. The initial development of coronary care units and rapid cardioversion or defibrillation of life-threatening ventricular arrhythmias, followed by risk-factor modification and such major advances as thrombolytic therapy and emergency revascularization, have contributed significantly to the successful care of the acute myocardial infarction patient. To understand the reasons for the continued high mortality rates in cardiogenic shock patients, it is important to understand the pathophysiology of cardiogenic shock and to examine the optimal treatment strategies that may improve mortality rates. In a strict sense, cardiogenic shock syndrome develops as a result of cardiac muscle failure (either right or left ventricle) that causes inadequate cardiac output. The cardiovascular system can contribute in a number of other ways to the development of shock: hypovolemia, mechanical problems, nonischemic valve lesions, arrhythmias, and abnormalities of diastolic filling. Although the primary focus of this chapter is cardiogenic shock that is due to muscle failure, there is also some discussion of other mechanical causes associated with acute myocardial infarction.
A number of definitions have been proposed; although they differ in some ways, there is general agreement that both hemodynamic and clinical parameters should be included. The hemodynamic criteria include a systolic blood pressure less than 80 mm Hg (less than 90 mm Hg if the patient is on pressors, inotropic agents, or intraaortic balloon pumping) and cardiac index less than 2.2 L/min/m2. Clinical criteria require that signs of decreased peripheral perfusion be present, including cool clammy skin, cyanosis, altered mental status, and diminished urine output (less than 30 mL/h). The common denominator of the clinical findings is that they reflect a failure of tissue perfusion. Oxygen delivery is insufficient to sustain aerobic metabolism and therefore lactic acidosis is a metabolic consequence, regardless of the cause.
Using a combination of clinical and hemodynamic measurements means that fewer patients with only some symptoms (eg, low blood pressure but no signs of diminished tissue perfusion, or normal blood pressure with altered mental status or diminished urine output) are given an inappropriate diagnosis of shock.
Etiology
The most common cause of cardiogenic shock is acute myocardial infarction and is due to the loss of a large amount of myocardium. The incidence of shock in acute myocardial infarction is between 5% and 10%, and the mortality rate is extremely high in medically treated patients, ranging between 70% and 100%, a figure unchanged over the last several decades. Cardiogenic shock may occur in a patient with a massive first infarction, or it may occur with a smaller, recurrent infarction in a patient with an already substantially infarcted myocardium.
Mechanical complications of acute myocardial infarction can cause shock; ventricular septal rupture, papillary muscle rupture or dysfunction, and myocardial rupture are all associated with cardiogenic shock. Right ventricular infarction in the absence of significant left ventricular infarction or dysfunction can cause shock. Hypovolemia or hypovolemic shock, although distinct from cardiogenic shock by definition, may be an important contributor to the development of shock in acute myocardial infarction.
Refractory tachyarrhythmias or bradyarrhythmias, usually in the setting of left ventricular dysfunction, are occasionally a cause of shock, which can occur with either ventricular or supraventricular arrhythmias.
Cardiogenic shock may occur as the end-stage, final common pathway for any progressive myocardial dysfunction, including ischemic heart disease and idiopathic, hypertrophic, and restrictive cardiomyopathies.
Pathophysiology
In cardiogenic shock resulting from acute myocardial infarction, dysfunction of a large enough quantity of myocardium (if in the left ventricle, approximately 40% must be infarcted) occurs to prevent the heart from meeting its minimum work requirements as a pump. The initial event is obstruction of a coronary artery, usually the left anterior descending coronary artery in first infarctions, but it can be any artery when previous infarctions have caused significant cumulative myocardial damage. The obstruction decreases the oxygen supply, resulting in myocardial ischemia, which in turn leads to diminished myocardial contractility and impaired left ventricular function. The ensuing drop in cardiac output and blood pressure leads to decreased coronary perfusion, resulting in further ischemia and additional deterioration in left ventricular function. This process of ischemia leading to myocardial dysfunction leading to further ischemia and so on has been appropriately termed a vicious cycle. Prolonged serum enzyme elevations, rather than the characteristic rise and fall seen in acute myocardial infarction, also suggest a protracted, stuttering course. Evidence for this vicious cycle is also found in autopsy studies that show infarct extension at the edges of an infarct in addition to discrete, remote infarctions throughout the ventricle.
The majority of patients with shock in acute myocardial infarction have extensive coronary disease. In patients dying of cardiogenic shock, more than two thirds have severe three-vessel coronary artery disease.
Early studies of acute myocardial infarction identified clinical and hemodynamic subsets that had prognostic significance. The Killip classification is based on clinical subsets, as shown in Table 6–1. The Forrester classification uses hemodynamic instead of clinical subsets (Table 6–2). Although the Killip and Forrester subsets have somewhat different definitions, they very clearly establish the point that progressive worsening of left ventricular function, whether measured by clinical or by hemodynamic parameters, is associated with a poorer prognosis. The pathophysiology of cardiogenic shock in acute infarction complicated by mechanical problems is somewhat different. Acute severe mitral regurgitation from papillary muscle or chordal rupture markedly diminishes cardiac output, leading to pulmonary edema. The sympathetic nervous system response to cardiac failure results in increased afterload and a further increase in the regurgitant fraction, another example of a disastrous vicious cycle causing cardiogenic shock.
Clinical Findings
Approximately half the patients destined to develop shock will present initially with shock; the other half will develop cardiogenic shock after admission to the hospital.
Treatment
A. GENERAL
Although some general therapeutic considerations are applicable to all patients in cardiogenic shock, treatment is most effective when the cause is identified. In many situations, this identification allows rapid correction of the underlying problem. In fact, survival in most forms of shock requires a quick, accurate diagnosis. The patient is so critically ill that only prompt, directed therapy can reverse the process. It is clear that the already high mortality rates in cardiogenic shock are even higher in patients for whom treatment is delayed. Therefore, although measures aimed at temporarily stabilizing the patient may provide enough time to start definitive therapy, potentially life-saving treatment can be carried out only when the cause is known.
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