Cardiogenic Shock


John Wiley & Sons

Copyright © 2009 American Heart Association
All right reserved.

ISBN: 978-1-4051-7926-3


Chapter One

Diagnosis, epidemiology, and risk factors

Zaza Iakobishvili, Harmony R. Reynolds, and David Hasdai

Definitions and diagnosis

Definitions

Cardiogenic shock is a state of decreased cardiac output and systemic perfusion in the presence of adequate intravascular volume, resulting in tissue hypoxia. As early as 1912, Herrick described the clinical features of cardiogenic shock in patients with severe coronary artery disease: a weak, rapid pulse; feeble cardiac tones; pulmonary rales; dyspnea; and cyanosis. The term cardiogenic shock is believed to have been originated in 1942 by Stead. He described a series of two patients who had what he called "shock of cardiac origin." Later, the expression was rephrased as "cardiogenic shock."

The severity of shock can range from mild to severe, and practical definitions use somewhat arbitrary criteria. An essential feature of cardiogenic shock is systemic hypoperfusion, typically with hypotension; however, there is great variability in the severity of hypotension that defines shock, with the most common cut-off points for systolic blood pressure being <90 mm Hg or <80 mm Hg. Patients with shock typically have signs of systemic hypoperfusion, including altered mental state, cool skin, and/or oliguria. Rales, indicating pulmonary edema, may or may not be present. Neither auscultation nor chest radiograph detects pulmonary edema in 30% of patients with cardiogenic shock. The method used to measure blood pressure may also be important. Brachial cuff pressure measurements are often inaccurate in states of shock. Arterial blood pressure is more accurately monitored using intra-arterial cannulas; thus, this method is commonly advocated to ensure precise measurement.

There is a subset of severe left ventricular (LV) failure patients who have "nonhypotensive cardiogenic shock". By definition, these patients have the clinical signs of peripheral hypoperfusion described above (with preserved systolic blood pressure measurements >90 mm Hg without vasopressor support). This occurs most often among patients with large anterior wall myocardial infarction (MI) and is associated with substantial in-hospital mortality, albeit lower than that of patients with classic cardiogenic shock. Thus, a diagnosis of cardiogenic shock may be made in patients with systemic hypoperfusion and blood pressure measurements of >90 mm Hg in several circumstances: (1) if medications and/or support devices are required to maintain normal hemodynamic parameters; (2) in the presence of systemic hypoperfusion with low cardiac output, with blood pressure maintained by marked vasoconstriction; and (3) if mean systemic pressure is [greater than or equal to] 30 mm Hg lower than baseline in cases of preexisting hypertension.

In 1967, Killip and Kimball proposed a crude clinical classification of hemodynamic status based on 250 patients with acute myocardial infarction (MI). This classification has withstood the test of time and is still in widespread use (Table 1.1). As the shock state persists, hypoperfusion of both the myocardium and peripheral tissues will induce anaerobic metabolism in these tissues and may result in lactic acidosis. Hyperlactatemia is considered a hallmark of hypoperfusion and may supplement the clinical examination and blood pressure measurement when findings are inconclusive regarding shock status. The accumulation of lactic acid may cause mitochondrial swelling and degeneration, inducing glycogen depletion, which in turn may impair myocardial function and inhibit glycolysis, leading to irreversible ischemic damage. Serum lactate level is an important prognostic factor in cardiogenic shock; in one multivariate analysis, a lactate level >6.5 mmol/L in cardiogenic shock patients was a very strong independent predictor of in-hospital mortality [odds ratio (OR) 295, P < 0.01] even after adjustment for age, sex, hypertension, and diabetes history.

Hemodynamics for diagnosis of cardiogenic shock

Along with metabolic parameters, hemodynamic data are very useful for diagnosis and prognostic assessment in cardiogenic shock patients. One of the earliest attempts to use hemodynamic evaluation to determine prognosis and to guide therapy found that all cardiogenic shock patients with LV filling pressure of >15 mm Hg and cardiac index <2.3 L/min died despite medical therapy. The measurements with greatest prognostic value in addition to demographic and clinical variables appear to be cardiac output and those measurements that incorporate cardiac output with systolic blood pressure, including stroke work or cardiac power.

There is some variability in the definition of cardiogenic shock as used in clinical trials. Most studies define shock as a state with systolic blood pressure of <90 mm Hg for at least 1 hour that is (1) not responsive to fluid administration alone; (2) secondary to cardiac dysfunction; and (3) associated with signs of hypoperfusion or a cardiac index of <2.2 L/min/[m.sup.2] and pulmonary artery wedge pressure (PAWP) >18 mm Hg. Hypotension that improves (increase in systolic blood pressure to >90 mm Hg) within 1 hour following administration of inotropic/vasopressor agents is often included in studies of cardiogenic shock, as is death within 1 hour of onset of hypotension when other criteria for cardiogenic shock are met. Some studies have specified invasive hemodynamic diagnostic criteria for cardiogenic shock, such as severely decreased cardiac output measurements derived from right heart catheterization. In most of these studies, cardiac index measurements of [less than or equal to] 2.2 L/min/[m.sup.2] were regarded as supporting the diagnosis of cardiogenic shock in the presence of other signs. Other investigators [15], however, regarded measurements of [less than or equal to] 1.8 L/min/[m.sup.2] as indicative of cardiogenic shock. An important consideration is whether the values were recorded on inotropic/vasopressor or circulatory device support; a 2.2-2.5 L/min/[m.sup.2] cut point is reasonable for those on support and 1.8-2.2 L/min/[m.sup.2] for those whose measurements are made off support.

The widespread availability of noninvasive means of assessing cardiac function, such as echocardiography, has reduced the use of right heart catheterization. Echocardiography with Doppler imaging has become a readily available modality for bedside hemodynamic assessment and for the evaluation of cardiac function, valvular status, and mechanical complications of acute coronary syndrome (ACS). Its use has steadily increased over the years, and currently it is performed frequently among ACS patients in many institutions.

In an analysis from Euro Heart Survey ACS, 68% of patients with cardiogenic shock underwent an echocardiographic evaluationn. Right heart catheterzation was performed in just 111 of 549 patients with cardiogenic shock (20.2%). Noninvasively derived hemodynamic parameters, such as left atrial pressure approximated by transmitral flow patterns and cardiac output computed by echocardiography (derived stroke volume multiplied by heart rate), can advance the timely management of cardiogenic shock patients, obviating the need for right heart catheterization. The restrictive pattern of transmitral flow, defined as E wave deceleration time <140 ms, has positive predictive value of 80% for PAWP [greater than or equal to] 20 mm Hg [19]. However, deceleration time >140 ms did not exclude an elevated PAWP. Transesophageal examination may be used in difficult cases to obtain hemodynamic information and to exclude mechanical causes of LV failure.

There are possible pitfalls in interpreting hemodynamic data. For example, cardiac output measurements may be above normal in patients for whom the underlying cause of cardiogenic shock is ventricular septal defect, and PAWP may be unexpectedly high in patients with right ventricular (RV) infarction because of leftward shift of the intraventricular septum (reversed Bernheim effect) or concomitant LV systolic dysfunction. Additionally, by the time right heart catheterization is performed, the patient with shock typically is already receiving supportive pharmacological treatment that can alter hemodynamic measurements. For example, treatment with a positive inotropic agent may improve a patient's subsequent cardiac output measurements, and treatment with diuretics may decrease subsequent PAWP measurements.

The caveats listed above illustrate the difficulty of diagnosing cardiogenic shock by means of numerical and laboratory values in isolation. Accordingly, shock is primarily diagnosed based on clinical findings supported by measured hemodynamic values (Table 1.2). Clinical evidence of a reduction in cardiac output with systemic hypoperfusion despite adequate filling pressures must be present for a diagnosis of cardiogenic shock. When right heart catheterization is performed, hemodynamics values should confirm low output and high filling pressures. If right heart catheterization is not planned, the combination of clinical examination, chest radiography, and echocardiography must clearly demonstrate systemic hypoperfusion, low cardiac output, and elevation of left atrial/pulmonary artery pressure and/or right atrial pressure. If the diagnosis is in any way unclear, right heart catheterization should be performed.

Epidemiology

Etiologies

Cardiogenic shock can occur as a result of a wide variety of cardiac disorders, including ACS, valvular disease, myocardial and/or pericardial disease, congenital lesions (in both children and adults), or mechanical injuries to the heart (Table 1.3; Chapter 8). Due to the great prevalence of coronary artery disease, cardiogenic shock as a complication of ACS is the predominant etiology.

Determining the etiology of cardiogenic shock in the individual patient may be challenging. The history and clinical examination may provide information on the etiology of cardiogenic shock in an individual patient, but there is quite a bit of overlap between syndromes; for example, chest pain is a cardinal feature of acute MI, myocarditis, and pericardial tamponade, and there may be overlap in the description of pain among these syndromes. The timing of symptoms may provide a clue to the occurrence of mechanical complications if, for example, chest pain recurs days after an initial episode and that recurrence is associated with shock. The absence of this pattern is not of diagnostic value, however, and mechanical complications may occur early in the course of MI.

The physical examination may provide diagnostic clues as well, particularly in the form of a new murmur as a herald of ventricular septal or papillary muscle rupture or acute mitral or aortic valve disease. Unfortunately, worsening of valvular heart disease may be accompanied by softening of an existing murmur, and, of course, murmurs are not a reliable indicator of valvular disease or rupture. However, the presence of a murmur in a patient with cardiogenic shock should prompt rapid echocardiographic evaluation.

Electrocardiography

The electrocardiogram (ECG) may be helpful in the diagnosis of a particular etiology of shock. When ST-segment elevation acute MI (STEMI) causes LV failure, the degree and severity of the ECG abnormality should be concordant with the severity of the clinical condition. Modest ECG abnormalities should prompt consideration of other etiologies (Table 1.3). When marked ST elevations are present in several precordial leads, anterior MI is the most likely diagnosis and LV pump failure is the most likely cause of shock. A first inferior STEMI is less likely to cause shock; if inferior STEMI were the cause of shock, marked ST elevation with reciprocal ST depression, denoting extensive injury, would be expected on the ECG. RV infarction may complicate inferior MI as well; RV leads should be placed in cases of inferior MI with hypotension to search for right-sided ST elevation. Another possible finding of RV infarction is precordial ST elevation, which is largest in degree in V1-V2 and becomes smaller as one moves across the precordium. The absence of reciprocal changes or signs of RV infarction in the case of inferior MI with shock should prompt a search for complicating factors, such as myocardial or papillary muscle rupture. It should also be noted that ST elevation is not definitive evidence of STEMI; regional ST elevation may also be seen in acute myocarditis. Diffuse and marked ST depressions, most notable in V4-V6, indicate diffuse ischemia due to left main or severe triple vessel disease. Left bundle branch block may be seen as a reflection of a large STEMI, non-STEMI (NSTEMI) with prior infarcts, or underlying conditions associated with LV hypertrophy (e.g., aortic stenosis). Finally, a normal ECG in the presence of profound shock, particularly in the setting of arrhythmias, should lead to consideration of myocarditis.

ACS as a cause of shock

Cardiogenic shock complicating ACS is not confined to the typical setting of large ST-segment elevation anterior wall infarction. Although shock occurs more frequently in the setting of ST-segment elevation (4.2-7.2% in fibrinolytic trials, 8.5-14.2% in the registries), it also occurs, albeit less commonly (2.1-2.6%), in ACS patients without ST-segment elevation, even without positive cardiac biomarkers. Shock typically results from severe LV dysfunction but may also occur when LV function is well preserved. In the international SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? (SHOCK) trial registry of 1190 patients with cardiogenic shock, the predominant cause of shock was LV failure (78.5%), whereas isolated RV shock occurred in only 2.8% of patients. Mechanical complications of acute MI were observed among the remaining patients: severe mitral regurgitation (MR; 6.9%), ventricular septal rupture (3.9%), and tamponade (1.4%).

Data on the incidence of shock are derived from large population-based analyses as well as from subset analyses of randomized clinical trials examining effects of different treatment modalities in the various forms of ACS. Due to differences in the definition of cardiogenic shock and criteria for including patients, the reported incidence of cardiogenic shock complicating ACS varies among studies. For example, an incidence of cardiogenic shock during hospitalization of 2.6% was reported among 3465 patients with acute MI in the prethrombolysis era, a low figure that reflects exclusion of patients with signs of heart failure upon presentation. In comparison, cardiogenic shock was present in 6.7% of 6676 consecutive acute MI patients managed noninvasively in the Trandolapril Cardiac Evaluation (TRACE) registry, which included STEMI and NSTEMI cases.

ST-segment-elevation ACS and cardiogenic shock

Classically, cardiogenic shock has been considered a direct consequence of STEMI, most commonly caused by LV dysfunction resulting from continued ischemia and cell death. In three large international fibrinolytic therapy trials for STEMI, the incidence of shock ranged from 4.2% to 7.2% (Fig. 1.1). However, the reported incidence of cardiogenic shock among STEMI patients receiving fibrinolytic therapy may be biased, because patients with shock are often not enrolled in multicenter, randomized trials. Zeymer and colleagues reported a 14.2% incidence of cardiogenic shock in 9422 patients in an 80-hospital primary percutaneous coronary intervention (PCI) German registry.

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