Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction

INTRODUCTION — 

Cardiogenic shock is a clinical condition of inadequate tissue (end-organ) perfusion due to the inability of the heart to pump an adequate amount of blood. The reduction in tissue perfusion results in decreased oxygen and nutrient delivery to the tissues and, if prolonged, potentially end-organ damage and multi-system failure. (See "Definition, classification, etiology, and pathophysiology of shock in adults", section on 'Introduction'.)

The clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction (MI) will be reviewed here. The prognosis and treatment are discussed separately. (See "Treatment and prognosis of cardiogenic shock complicating acute myocardial infarction".)

An overview of the types of shock in adults and the diagnostic approach to such patients is presented separately. (See "Definition, classification, etiology, and pathophysiology of shock in adults".)

PATHOPHYSIOLOGY — 

All forms of shock, including hypovolemic and distributive, are characterized by relatively low blood pressure and manifestations of insufficient end-organ hypoperfusion, such as poor mentation or low urine output. Patients with cardiogenic shock usually have a low cardiac index (<2.2 L/min/m²) and elevated ventricular filling pressures (ie, pulmonary capillary wedge pressure [PCWP] >15 mmHg and/or central venous pressure [CVP] >10 mmHg), and a decreased mixed venous oxygen saturation (table 1) [1-3]. Some patients have only modest elevation of left ventricular (LV) filling pressures despite depressed LV ejection faction. These patients more often have baseline preserved renal function and first MI [4]. The systemic vascular resistance is often high, but it may be in the normal or low range in the later stage of cardiogenic shock. Individuals with normal or low range of systemic vascular resistance represent a group of patients with more profound hypoperfusion and inflammatory response and associated worse prognosis [3].

Failure of the left or right ventricle (due to myocardial muscle dysfunction) to pump an adequate amount of blood is the primary cause of cardiogenic shock in acute MI. Hypotension, tissue hypoperfusion, and pulmonary congestion or systemic venous congestion result.

Systemic hypotension, which is present in most patients with cardiogenic shock, is defined as a persistent systolic blood pressure below 80 to 90 mmHg or a mean blood pressure 30 mmHg lower than the patient's baseline level. In cardiogenic shock, hypotension results from a decrease in stroke volume and a severe reduction in the cardiac index (<1.8 L/min/m² without support or <2.2 L/min/m² with support).

The fall in blood pressure may in part be moderated by a marked elevation in systemic vascular resistance (SVR), a response that is mediated by increased release of endogenous vasopressors such as norepinephrine and angiotensin II. However, the combination of a low cardiac output and elevated SVR contribute to marked reduction in tissue perfusion.

The associated decrease in coronary perfusion pressure can lead to myocardial ischemia and subsequent myocardial dysfunction that leads to worsening myocardial ischemia in a vicious cycle that culminates in progressive end-organ hypoperfusion and, ultimately, death [5,6].

Hypotension and elevation of SVR occur in the presence of an elevated PCWP if LV dysfunction is the primary cardiac disorder. Elevation of the right ventricular (RV) filling pressure occurs when isolated RV shock is present, such as might occur with a large RV infarction [1,7]. (See "Pathophysiology of heart failure with reduced ejection fraction: Hemodynamic alterations and remodeling", section on 'Normal LV pressure-volume relationship' and 'Etiology' below and "Right ventricular myocardial infarction".)

Acute MI due to acute occlusion of one or more coronary arteries is one of the most common clinical entities leading to cardiogenic shock (see 'Etiology' below). In this setting, myocardial ischemia or infarction leads to a fall in the stroke volume (of either the left or right ventricle or both) and cardiac output and, as mentioned above, often a compensatory increase in the systemic vascular resistance.

However, not all patients fall into this hemodynamic profile. Calculated systemic vascular resistance varied widely and, on average, was not elevated despite vasopressor use [2]. Thus, in some patients, post-MI shock is accompanied by relative vasodilation rather than vasoconstriction. (See "Definition, classification, etiology, and pathophysiology of shock in adults", section on 'Distributive'.)

The most likely explanation for vasodilation in the setting of cardiogenic shock is the presence of a systemic inflammatory state similar to that seen with sepsis [2,3] (see "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis"). In the SHOCK trial, 54 of the 302 patients (18 percent) had fever and/or leukocytosis [3]. The systemic inflammation was diagnosed two to four days after the onset of shock and these patients had a relatively lower systemic vascular resistance. Among the 54 patients, 40 were subsequently considered to be potentially infected as evidenced by a positive culture; 14 were culture negative. The lower the initial systemic vascular resistance, the greater the likelihood of developing culture positive systemic inflammation. The latter observation suggests that inappropriate vasodilation may play an important role in both the pathogenesis and persistence of shock and in the likelihood of infection.

The acute inflammatory response in MI is associated with elevated serum cytokine concentrations [8,9]. Cytokine activation leads to induction of nitric oxide (NO) synthase and increased levels of NO, which can cause inappropriate vasodilation with reduced systemic and coronary perfusion pressure [2,10]. This sequence may be similar to that seen in septic shock, which is also characterized by systemic vasodilation. (See "Definition, classification, etiology, and pathophysiology of shock in adults", section on 'Distributive'.)

Another pathophysiologic pathway involves intracellular aminopeptidase dipeptidyl peptidase 3 (DPP3), which degrades angiotensin II and inhibits angiotensin II-mediated signal transduction [11,12]. High circulating DPP3 levels after acute MI are associated with cardiogenic shock development.

EPIDEMIOLOGY — 

Cardiogenic shock is present in approximately 6 to 10 percent of patients with acute MI [13,14]. Despite evidence-based therapeutic advances for the treatment of acute MI and cardiogenic shock, the risk of mortality within 30 days for patients with acute MI and cardiogenic shock is 40 to 50 percent [15,16]. The risk of mortality may be increasing as the result of the aging and higher prevalence of comorbidities in the population [17,18].

ETIOLOGY — 

Severe dysfunction of the LV is the most common presentation of cardiogenic shock in the setting of acute MI (table 2) [5,19]. The majority of patients have an acute ST elevation MI, but cardiogenic shock also occurs in approximately 2.5 percent of patients with a non-ST elevation MI [1,20,21]. Severe dysfunction is often associated with an anterior MI, but may result from an infarct in any location, particularly in patients who have had a prior infarct.

Severe extensive ischemia due to multivessel coronary artery disease can also result in shock with an infarct of any size. Autopsy studies in patients dying with cardiogenic shock due to acute MI have revealed that ≥40 percent of the LV myocardium is infarcted (old and new) [22]. Most patients have severe three vessel coronary disease on coronary angiography. Severe right ventricular (RV) failure is a cause of, or a major contributor to, cardiogenic shock in 5 percent of cases and is typically seen with an inferior MI [1]. Such patients do not develop pulmonary congestion unless there is concurrent involvement of the LV. (See "Right ventricular myocardial infarction".)

Cardiogenic shock can also be caused by mechanical complications of MI (see "Acute myocardial infarction: Mechanical complications"). Causes include:

●Acute, severe mitral regurgitation resulting from rupture of a papillary muscle or chordae tendineae or severe papillary muscle dysfunction. This is more common in the setting of inferoposterior infarction but can occur with any infarct location. When LV failure causes shock, associated mitral regurgitation is common. The SHOCK trial, which evaluated early revascularization for cardiogenic shock after acute MI, excluded patients with mechanical causes of shock; 39 percent had echocardiographic evidence of moderate or severe mitral regurgitation, which correlated with poorer survival [23].

●Rupture of the interventricular septum after either an anterior or inferior infarction, with an acute left-to-right shunt, which is associated with the highest risk of in-hospital mortality (87 percent) [24,25].

●Cardiac tamponade due to either rupture of the LV free wall or a hemorrhagic pericardial effusion, or aortic dissection can cause these complications. Rupture of the LV free wall may spontaneously seal in approximately one-third of cases, resulting in an unstable subacute rupture state, which is at high risk of electromechanical dissociation.

The frequency of these causes of cardiogenic shock complicating an acute MI was evaluated in a review of 1190 patients from the SHOCK registry [26]. LV failure was responsible in 79 percent, severe mitral regurgitation in 7 percent, ventricular septal rupture in 4 percent, isolated RV shock in 2 percent, tamponade (including subacute LV free wall rupture) in 1.4 percent, and other causes in 7 percent (eg, prior severe valvular disease, excess beta blocker or calcium channel blocker therapy, and shock resulting from a complication of cardiac catheterization).

A rare complication of dynamic LV outflow track obstruction causing cardiogenic shock has been described in the setting of acute MI [27]. This phenomenon, though, is more commonly seen in the setting of Takotsubo syndrome or hypertrophic cardiomyopathy. (See 'Differential diagnosis' below.)

Contributing factors — As discussed above, failure of the left or right or both ventricles (with or without one of the mechanical complications discussed above) to pump an adequate amount of blood is the primary cause of cardiogenic shock. However, patients with cardiogenic shock in the setting of acute MI may have other factors that contribute to hypotension:

●Hemorrhagic shock due to treatment with fibrinolytic agents and/or anticoagulants. (See "Acute ST-elevation myocardial infarction: Management of fibrinolysis", section on 'Bleeding'.)

●Septic shock in patients with indwelling catheters or suspected infectious foci. (See "Intravascular catheter-related infection: Epidemiology, pathogenesis, and microbiology".)

●Hypovolemia from any cause including diuretic therapy. (See "Etiology, clinical manifestations, and diagnosis of volume depletion in adults", section on 'Manifestations of shock'.)

●Severe valvular heart disease with limited cardiac reserve, such as in critical aortic stenosis. These patients can present with cardiogenic shock with even a small infarction. (See "Hemodynamics of valvular disorders as measured by cardiac catheterization" and "Clinical manifestations and diagnosis of aortic stenosis in adults".)

●Severe bradycardia, due either to complete heart block or sinus bradycardia. Bradycardia can cause a low cardiac output and hypotension in the setting of an acute MI with impaired ventricular function. (See "Sinus bradycardia", section on 'Clinical presentation'.)

●Rapid atrial arrhythmias, such as atrial fibrillation with rapid ventricular response or ventricular tachycardia. (See "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm", section on 'Adverse hemodynamics in AF' and "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features".)

●The excessive use of blood pressure lowering and/or negative inotropic medications such as nitrates, angiotensin converting enzyme inhibitors, beta or calcium channel blockers, diuretics, or morphine.

RISK FACTORS — 

Older age, anterior MI, history of hypertension, diabetes mellitus, multivessel coronary artery disease, prior MI, systolic blood pressure <120 mmHg, heart rate >90 beats per minute, diagnosis of heart failure on admission, ST-elevation MI, and left bundle branch block on the electrocardiogram are predictors of cardiogenic shock complicating acute MI [1,28].

Based upon these and other variables, models have been devised for predicting the development of cardiogenic shock in patients with an MI [21,28]. However, because of a low predictive ability, we do not recommend their use.

CLINICAL PRESENTATION — 

The cardinal features of shock, irrespective of shock type, include clinical manifestations of hypoperfusion such as hypotension (which occurs in most patients), oliguria, abnormal mental status, cold clammy skin, and evidence of metabolic acidosis on laboratory testing (eg, arterial lactate >2.0 mmol/L). (See "Definition, classification, etiology, and pathophysiology of shock in adults", section on 'Classification and etiology'.)

The "classic" patient with cardiogenic shock has severe systemic hypotension, signs of systemic hypoperfusion (eg, cool extremities, oliguria, and/or alteration in mental status), and respiratory distress due to pulmonary congestion. However, not all patients present with this syndrome.

As the mortality associated with cardiogenic shock in the setting of acute MI is high and as the ability of therapies to improve this outcome declines with delays, the clinical evaluation (history and physical examination, as well as early laboratory testing) should be carried out expeditiously.

The Society for Cardiovascular Angiography and Interventions (SCAI) has developed a classification system for cardiogenic shock that categorizes the condition into five stages, labeled A through E. This system is designed to provide a standardized framework for assessing the severity of cardiogenic shock and guiding clinical management and research [29,30]. The stages are as follows:

●Stage A – "At risk" for cardiogenic shock but without clinical evidence of shock.

●Stage B – "Beginning" shock, characterized by hypotension or tachycardia without hypoperfusion.

●Stage C – "Classic" cardiogenic shock, with hypotension and hypoperfusion (lactate >2 mmol/L).

●Stage D – "Deteriorating" shock, where initial interventions have failed to restore stability and adequate perfusion.

●Stage E – "Extremis," indicating a highly unstable patient often with cardiovascular collapse.

This classification system was endorsed by multiple societies, including the American College of Cardiology, the American Heart Association, the Society of Critical Care Medicine, and the Society of Thoracic Surgeons [30,31]. Importantly, the SCAI stage often changes, with >50 percent of patients initially classified as SCAI stage B or C progressing to a more advanced stage [32]. SCAI stages correlate with hospital mortality rates. As an example, in one study, unadjusted hospital mortality rates increased progressively from Stage A (3 percent) to Stage E (67 percent) [33].

History and physical examination — Most patients with acute MI who develop cardiogenic shock do so after initial presentation (see 'Time of onset' below). These individuals often complain of the acute onset of recurrent chest pain and difficulty breathing. On examination, patients in cardiogenic shock often have new or worsening hypotension, tachycardia, and tachypnea. The following are variably present [4,34]: distended neck veins, coolness of the skin, rales, gallop rhythm or new heart murmur on examination, and decreased volume and intensity of the distal pulses. In the SHOCK trial registry, pulmonary congestion was absent at presentation in about one-third of patients [4] and 5.2 percent did not have overt hypotension (defined as a systolic pressure below 90 mmHg) despite signs of peripheral hypoperfusion [34].

Clinical manifestations are often different in patients with predominant right ventricular shock, which usually occurs in the setting of an acute inferior wall MI. This disorder is typically characterized by the absence of pulmonary congestion and the presence of jugular venous distension. (See "Right ventricular myocardial infarction".)

Laboratory findings — The following laboratory abnormalities are seen in patients who present with cardiogenic shock in the setting of acute MI:

●New or recurrent electrocardiographic evidence of ischemia. (See "Diagnosis of acute myocardial infarction", section on 'ECG'.)

●New or worsening pulmonary congestion on a chest radiograph. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults" and "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Chest radiograph'.)

●Evidence of metabolic acidosis – In particular, elevated lactate level and reduced pH. (See "Approach to the adult with metabolic acidosis".)

●Evidence of renal hypoperfusion – increasing blood urea nitrogen and creatinine. (See "Definition and staging criteria of acute kidney injury in adults".)

●Evidence of pump failure and associated mechanical complications on echocardiography. (See 'Echocardiography' below.)

Time of onset — The majority of patients have cardiogenic shock at admission. Presentation after hospital admission is less common [20,21,35-38]. Patients who develop delayed cardiogenic shock following MI often progress to shock and more severe SCAI shock stages [31], with clinical evidence of a low cardiac output prior to the development of hypotension. The delay in the development of cardiogenic shock is likely due to the eventual failure of the initial compensatory mechanisms that protect against the adverse hemodynamic consequences of a large infarction and associated mechanical complications. (See 'Etiology' above and 'Pathophysiology' above.)

A community-based observational study of 5782 patients with acute MI who were admitted to 11 hospitals in Massachusetts between 2001 and 2011, of whom 5.2 percent were diagnosed with cardiogenic shock, examined the frequency, timing, and outcome of cardiogenic shock that developed pre-hospital, within the first 24 hours (early) after admission, and thereafter (late). The proportion with prehospital cardiogenic shock (1.6 percent) and late cardiogenic shock (1.5 percent) remained stable over time, but the proportion with early cardiogenic shock declined from 2.2 percent in 2001 to 2003 to 1.2 percent in 2009 to 2011. Of those with STEMI (n = 1853), 2.5 percent had pre-hospital, 4.3 percent had early, and 2.1 percent had late development of cardiogenic shock. For those with non-ST elevation MI (n = 3929), the proportions were 1.2 percent at each time point (p<0.001). This confirms older data from clinical trials.

The development of late cardiogenic shock may be related to recurrent ischemia or reinfarction or to mechanical complications, such as rupture of the ventricular septum, ventricular free wall, or papillary muscle. The clinical presentation of recurrent ischemia or reinfarction usually consists of recurrent chest pain, recurrent or new ST segment elevation, and hypotension; some patients, however, have the sudden onset of dyspnea rather than chest pain. (See "Acute myocardial infarction: Mechanical complications".)

Some cases of late cardiogenic shock are iatrogenic in nature. For example, early intravenous beta blockade in those with multiple risk factors for shock (eg, age, increased heart rate, decreased blood pressure, Killip class >1, prior hypertension, late time to treatment), the use of multiple blood pressure lowering drugs (eg, beta blockers, angiotensin converting enzyme inhibitors, nitrates, and diuretics), and overly vigorous therapy of acute pulmonary edema [39]. (See 'Contributing factors' above.)

DIAGNOSIS — 

The diagnosis of cardiogenic shock in the setting of acute MI can be made or strongly suspected from clinical manifestations presented above, including a history of (recurrent) chest pain or difficulty breathing, and findings of hypotension (in most patients), hypoperfusion, and (generally) pulmonary congestion on examination. (See 'History and physical examination' above.)

When a patient is strongly suspected of having cardiogenic shock, the diagnostic evaluation should be carried out in conjunction with resuscitative efforts. Patients who present with acute MI with clear evidence of cardiogenic shock and major electrocardiographic abnormalities that can explain the degree of hemodynamic abnormalities (eg, ST-elevation and/or evolving Q waves in multiple leads [typically anterior] or profound ST depressions [including the apical leads]) should undergo rapid cardiac catheterization with coronary angiography. Rapid evaluation should be performed if there is suspicion of mechanical complication, which may be present on hospital admission (eg, first inferior MI or murmur). (See "Evaluation and management of suspected sepsis and septic shock in adults", section on 'Immediate evaluation and management' and "Treatment and prognosis of cardiogenic shock complicating acute myocardial infarction".)

In patients suspected of cardiogenic shock, a repeat electrocardiogram and an echocardiogram should be performed immediately. The electrocardiogram may confirm the presence of recurrent ischemia, particularly in patients who have been reperfused and, in most cases, the echocardiogram can confirm the diagnosis and exclude other cardiac etiologies. Patients in whom the diagnosis remains uncertain, or if the patient has not responded to initial resuscitative efforts, may undergo placement of a balloon-tipped pulmonary artery (Swan-Ganz) catheter to confirm diagnosis and/or to guide management. (See 'Hemodynamic assessment' below.)

Additional laboratory testing should include complete blood count, chemistry screen (including assessment of renal function and electrolyte status), prothrombin and partial thromboplastin times, serial troponin measurements, and a chest radiograph.

Echocardiography — The findings of severely depressed global left or right ventricular systolic function (or both), decreased stroke volume, and suggestion of elevated filling pressures on echocardiography support the diagnosis [1,40]. In addition, the study can assess regional left and right ventricular function, and can detect the cause or contributing factors to cardiogenic shock such as pericardial fluid with tamponade (movie 1 and movie 2), severe mitral regurgitation (movie 3), which may be seen with flail mitral leaflet (movie 4 and movie 5 and movie 6); ventricular septal rupture (movie 7); and proximal aortic dissection (movie 8), which may cause aortic insufficiency and/or tamponade, concomitant aortic, or mitral stenosis. (See "Role of echocardiography in acute myocardial infarction" and "Role of echocardiography in acute myocardial infarction", section on 'Detecting complications after MI'.)

Transthoracic echocardiography is usually performed initially. However, it may be difficult to obtain an adequate image with this modality in critically ill patients, particularly those supported by mechanical ventilation. If the patient is taken for a cardiac catheterization, a ventriculogram may be useful to assess LV function and diagnose mechanical complications if adequate echocardiographic images could not be obtained. If the initial echocardiogram images are limited or echocardiography is unavailable, a transesophageal echocardiography (TEE) may provide important information. There are, for example, cases in which moderate mitral regurgitation was visualized on transthoracic echocardiography but subsequent TEE revealed a flail mitral leaflet with severe mitral regurgitation. TEE may also more clearly demonstrate ventricular septal rupture with a shunt visualized by color flow Doppler (movie 5).

Hemodynamic assessment — The diagnosis of cardiogenic shock is confirmed when the hemodynamic profile shows arterial hypotension (a persistent systolic blood pressure below 80 to 90 mmHg or a mean blood pressure 30 mmHg lower than the patient's baseline level), a severe reduction in the cardiac index (<1.8 L/min/m² without support or <2.2 L/min/m² with support), and an elevated pulmonary capillary wedge pressure (PCWP) above approximately 15 mmHg. An elevated PCWP is often present in patients with and without pulmonary congestion (24 versus 22 mmHg in the SHOCK registry) [4]. In some cases, a normal or borderline elevated PCWP is present initially and then becomes clearly elevated after a fluid challenge.

Hemodynamic evaluation is also useful in assessing the degree of vasoconstriction or vasodilation and in identifying patients with low left-sided filling pressures due to inadequate intravascular volume or to right ventricular infarction, a setting in which right atrial pressure will be increased [40]. If an echocardiogram has not been performed or is not available, the following should be performed to diagnose mechanical complications such as ventricular septal rupture, mitral regurgitation, and tamponade: an oxygen series looking for a step-up in oxygen saturation from right atrium to right ventricle, the PCWP tracing examined for large v waves, and right atrium and PCWP compared for equalization of pressures. Some patients have vasodilatory shock after MI [2]. (See 'Pathophysiology' above.) Identification of these patients may influence therapy. We recommend PAC to help guide therapy if the patient does not respond to initial stabilization efforts. (See "Treatment and prognosis of cardiogenic shock complicating acute myocardial infarction".)

Coronary angiography and ventriculography — Coronary angiography (or repeat coronary angiography) should be performed in all patients with cardiogenic shock in whom acute MI is suspected and who are candidates for revascularization with either percutaneous coronary intervention or coronary artery bypass graft surgery [40]. It may also contribute to the diagnostic evaluation. In addition, if a transthoracic echocardiogram has not been performed or is not available, then a ventriculogram may be useful to assess LV function and diagnose mechanical complications. All patients who are candidates for aggressive care and have undergone reperfusion with fibrinolytic therapy should be evaluated emergently for failure of reperfusion if they exhibit new or persistent signs of cardiogenic shock. (See "Treatment and prognosis of cardiogenic shock complicating acute myocardial infarction" and "Acute ST elevation myocardial infarction: Failed fibrinolysis" and "Primary percutaneous coronary intervention in acute ST-elevation myocardial infarction: Periprocedural management", section on 'Intraaortic balloon counterpulsation'.)

DIFFERENTIAL DIAGNOSIS — 

For patients with diagnosed or suspected acute MI who have or develop symptoms and signs of hypoperfusion, shock is almost always due to the MI. However, other clinical scenarios may mimic this presentation and fall into two general categories:

●Acute MI with shock due to noncardiac causes such as sepsis from an indwelling catheter or hypovolemia caused by overaggressive diuresis. The hemodynamic profile of patients with shock due to sepsis or hypovolemia generally differs from that of patients with cardiogenic shock (table 1). (See 'Hemodynamic assessment' above.)

●Cardiovascular diseases in which the primary problem is not acute MI (table 2):

•Takotsubo syndrome, also called "transient LV apical ballooning" and "broken heart syndrome" – This disorder is typically precipitated by intense psychologic stress and primarily occurs in postmenopausal women. The characteristic finding of apical ballooning is seen on left ventriculography or echocardiography with ST elevation on the surface electrocardiogram. Dynamic LV outflow tract (LVOT) obstruction has been described in up to 20 percent of patients with stress cardiomyopathy and may contribute to hemodynamic instability and development of cardiogenic shock. Echocardiography is key for making the diagnosis [27]. As transient, nonsignificant LVOT obstruction is likely more common than severe, obstruction-inducing hypotension, correlating severity and timing of LVOT obstruction to instability and hypotension is of paramount importance to establishing the clinical significance of the finding and making appropriate therapeutic adjustments. Despite frequent hemodynamic compromise or even cardiogenic shock, patients recover, often completely, within one to four weeks. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".)

•Hypertrophic cardiomyopathy or acute myopericarditis – These may present with any combination of chest pain, ST or T wave changes on an electrocardiogram suggestive of acute infarction, and an elevated troponin. Clinically significant worsening of LVOT obstruction can also be seen in patients with hypertrophic cardiomyopathy due to excessive vasodilation, as with induction of general anesthesia or in other settings of vasodilation (eg, sepsis) or intravascular volume depletion. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation" and "Clinical manifestations and diagnosis of myocarditis in adults".)

•Pulmonary embolism. (See "Pulmonary embolism: Epidemiology and pathogenesis in adults".)

•Acute regurgitant valvular heart disease. (See "Acute aortic regurgitation in adults" and "Acute mitral regurgitation in adults".)

•Acute MI due to ascending aortic dissection. Shock in this setting can result from the infarction caused by occlusion of one or more coronary arteries, acute aortic insufficiency, and/or cardiac tamponade. (See "Clinical features and diagnosis of acute aortic dissection".)

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Non-ST-elevation acute coronary syndromes (non-ST-elevation myocardial infarction)" and "Society guideline links: ST-elevation myocardial infarction (STEMI)".)

SUMMARY AND RECOMMENDATIONS

●Etiology – In patients with myocardial infarction (MI), cardiac dysfunction is usually due to severe left ventricular (muscle) failure. However, mechanical complications such as acute mitral regurgitation or rupture of either the ventricular septal or free walls may be contributive or causative. (See 'Etiology' above.)

●Clinical presentation – The clinical presentation often includes a history of recurrent chest pain or difficulty breathing. Findings on examination usually include hypotension, cool extremities, oliguria, alteration in mental status, cool clammy skin, and respiratory distress. There is evidence of metabolic acidosis (low serum bicarbonate and elevated serum lactate) on laboratory testing. (See 'Clinical presentation' above.)

●Diagnosis – The diagnosis of cardiogenic shock after acute MI can be made or strongly suspected from the clinical manifestations presented above; an electrocardiogram showing evidence of new or recurrent myocardial ischemia is supportive. In most cases, the diagnosis can be confirmed with echocardiography. (See 'Diagnosis' above.)

•Hemodynamic assessment – Cardiogenic shock is characterized by severe reduction in the cardiac index (<1.8 L/min/m² without support or <2.2 L/min/m² with support) and elevated filling pressures of the left, right, or both ventricles, and is typically associated with persistent hypotension (systolic blood pressure <80 to 90 mmHg or mean arterial pressure 30 mmHg lower than baseline).

•Imaging – Echocardiography is helpful in supporting the diagnosis in the first group and coronary angiography will usually refute (or support) a diagnosis of myocardial ischemia. Hemodynamic monitoring may be used to identify other causes of shock and to assist in management of patients not responding to initial resuscitative efforts. (See 'Echocardiography' above.)

●Differential diagnosis – In patients with acute MI, shock is often directly attributable to MI, though other diatheses (eg, bleeding, hypovolemia) may contribute to the severity of shock. (See 'Differential diagnosis' above.)

ACKNOWLEDGMENTS — 

The UpToDate editorial staff acknowledges Venu Menon, MD, and Judith Hochman, MD, who contributed to earlier versions of this topic review.