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Clinical manifestations and diagnosis of cardiogenic shock in

acute myocardial infarction
Authors: Judith S Hochman, MD, Alex Reyentovich, MD
Section Editor: Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Deputy Editor: Gordon M Saperia, MD, FACC

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Oct 2019. | This topic last updated: Dec 18, 2017.

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'.)  

Acute myocardial infarction (MI) is the most common cause of cardiogenic shock and is defined as a
clinical event consequent to the death of cardiac myocytes (myocardial necrosis) that is caused by
ischemia (as opposed to other etiologies such as myocarditis or trauma). (See "Diagnosis of acute
myocardial infarction", section on 'Definitions'.)

Cardiogenic shock is the leading cause of death in patients with acute MI, with hospital mortality
rates approaching 50 percent [1]. Short-term prognosis is directly related to the severity of the
hemodynamic disorder. The clinical manifestations and diagnosis of cardiogenic shock in acute MI
will be reviewed here. The prognosis and treatment are discussed separately. (See "Prognosis and
treatment 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 end-organ hypoperfusion, such as poor mentation or low urine
output. Patients with cardiogenic shock have a low cardiac index (<2.2 L/min/m2), elevated filling
pressures of the left, right, or both ventricles, and a decreased mixed venous oxygen saturation (table
1) [2-4]. Some patients have only modest elevation of left ventricular filling pressures despite
depressed left ventricular ejection faction. These patients more often have baseline preserved renal
function and first myocardial infarction (MI) [5]. The systemic vascular resistance is often high, but it
may be in the normal or low range. 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  [4].

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 per m2 without support or <2.2 L/min
per 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 may result in a marked reduction in tissue perfusion.

The associated decrease in coronary perfusion pressure can lead to a vicious cycle of ischemia,
further myocardial dysfunction, and a downward spiral with progressive end-organ hypoperfusion and
ultimately death [6,7].

Hypotension and elevation of SVR occur in the presence of an elevated pulmonary capillary wedge
pressure if left ventricular dysfunction is the primary cardiac disorder. (See "Pathophysiology of heart
failure with reduced ejection fraction: Hemodynamic alterations and remodeling", section on 'Normal
LV pressure-volume relationship'.) Elevation of the right ventricular (RV) filling pressure occurs when
isolated RV shock is present, such as might occur with a large RV infarction [2,8]. (See 'Etiology'
below and "Right ventricular myocardial infarction".)

Acute MI, due to acute occlusion of one or more coronary arteries, is the most common clinical entity
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. In the SHOCK trial of patients with
confirmed cardiogenic shock developing within 36 hours of an acute MI, the mean left ventricular
ejection fraction on echocardiography was unexpectedly high at 31 percent [9]. Furthermore,
calculated systemic vascular resistance varied widely and on average was not elevated despite
vasopressor use [3]. 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 [3,4]. (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 [4]. 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
[10,11]. 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 [3,12]. 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'.)

EPIDEMIOLOGY

The incidence of cardiogenic shock after myocardial infarction (MI) was constant in the 1970s and
1980s and complicated approximately 5 to 9 percent of acute ST-elevation MI (STEMI) [2,13-16]. More
data (between the late 1990s and 2006) from large registries have shown a decrease in the rate of
cardiogenic shock by as much as 25 percent [1,17,18].

As an example, three nationwide French registries conducted five years apart and including 7531
individuals were used to evaluate the incidence of and outcomes after cardiogenic shock in the
setting of MI (STEMI and non-ST elevation MI) between 1995 and 2005 [19]. The incidence decreased
significantly from 6.9 percent in 1995 to 5.7 percent in 2005. Over this period, mortality fell from 70 to
51 percent, though mortality in patients over the age of 85 remained very high (64.7 percent) [18].
Trends from the CathPCI registry demonstrated an increase in cardiogenic shock in-hospital mortality
in 2011 to 2013 compared with 2005 to 2006 (27.6 percent in 2005 to 2006 versus 30.6 percent in
2011 to 2013, adjusted OR 1.09, CI 1.005-1.173; p = 0.04). Patients in the latter period had more
medical comorbidities including diabetes, hypertension, dyslipidemia, and end stage renal disease
[20].

ETIOLOGY

Severe dysfunction of the left ventricle (LV) is the most common presentation of cardiogenic shock in
the setting of acute myocardial infarction (MI) (table 2) [6,21]. 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 [2,22,23]. 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) [24]. 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 [2]. 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 "Mechanical
complications of acute myocardial infarction".) 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 [9].

● 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)
[25].
 ● Cardiac tamponade due to either rupture of the LV free wall or a hemorrhagic pericardial
effusion. Rupture of the LV free wall may rapidly temporarily 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 left ventricular 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 stress-induced cardiomyopathy 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, or those who are on the verge of developing it, may have other factors that
contribute to hypotension:

● Hemorrhagic shock due to treatment with fibrinolytic agents and/or anticoagulants. (See
"Fibrinolysis for acute ST-elevation myocardial infarction: Initiation of therapy", 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 myocardial infarction (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 [2,28].

Based upon these and other variables, models have been devised for predicting the development of
cardiogenic shock in patients with an MI [23,28]. 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. (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 myocardial infarction (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.

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 [5,29]: 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 [5] and 5.2
percent did not have overt hypotension (defined as a systolic pressure below 90 mmHg) despite
signs of peripheral hypoperfusion [29].

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 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: elevated lactate level and decreased serum bicarbonate. (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 — Most patients who develop cardiogenic shock due to acute MI do so after hospital
admission [13,14,22,23,30]. Patients who develop delayed cardiogenic shock following MI often slip
slowly into shock, 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.)
The time course was evaluated in a report from the GUSTO-I trial of 41,000 patients with acute MI
who were treated with fibrinolytic therapy [14]. The following observations were made with respect to
cardiogenic shock:

● Shock was present on admission in 0.8 percent at hospital presentation and an additional 5.3
percent developed shock after admission, either as a sudden event or as a gradual fall in blood
pressure.

● Approximately 50 percent of patients who developed shock after admission did so within the first
24 hours after the infarct; most remaining cases occurred in the following days, with a few cases
being delayed for up to one week. Similar findings were noted in the SHOCK trial in which the
median time from MI to onset of cardiogenic shock was 5.5 hours and 75 percent of patients
who developed shock did so within 24 hours [30].

A community-based observational study of 5782 patients with acute myocardial infarction 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 "Mechanical complications of acute
myocardial infarction".)

Some cases of late cardiogenic shock are in part iatrogenic due, for example, to 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 [31]. (See 'Contributing factors'
above.)
DIAGNOSIS

The diagnosis of cardiogenic shock in the setting of acute myocardial infarction (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
myocardial infarction or murmur). (See "Evaluation and management of suspected sepsis and septic
shock in adults", section on 'Immediate evaluation and management' and "Prognosis and treatment 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. 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
monitoring' 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 [2,32]. 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, then a ventriculogram may be useful to
assess left ventricular function and diagnose mechanical complications. 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 monitoring — 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 catheter (PAC) to confirm diagnosis and/or to guide management and assess the need for
more aggressive mechanical cardiac support [7,32,33]. Although there are no randomized trials
evaluating the utility of PAC use in patients with cardiogenic shock, it is notable that 95 percent of
patients in the SHOCK Trial were managed with pulmonary artery catheters [34]. (See "Pulmonary
artery catheterization: Interpretation of hemodynamic values and waveforms in adults" and
"Pulmonary artery catheters: Insertion technique in adults" and "Indications, interpretation, and
techniques for arterial catheterization for invasive monitoring" and "Prognosis and treatment of
cardiogenic shock complicating acute myocardial infarction" and "Prognosis and treatment of
cardiogenic shock complicating acute myocardial infarction", section on 'Hemodynamic support'.)

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 per
m2 without support or <2.2 L/ min per m2 with support), and an elevated pulmonary capillary wedge
pressure (PCWP) above approximately15 mmHg. An elevated PCWP is often present in patients with
and without pulmonary congestion (24 versus 22 mmHg in the SHOCK registry) [5]. 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 [32]. 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 [3]. (See 'Pathophysiology'
above.) Identification of these patients may influence therapy. (See "Prognosis and treatment 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 [32]. 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 left ventricular 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 "Prognosis and treatment of cardiogenic shock
complicating acute myocardial infarction" and "Management of failed fibrinolysis (thrombolysis) or
threatened reocclusion in acute ST elevation myocardial infarction" 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 myocardial infarction (MI) who have or develop
symptoms and signs of hypoperfusion, shock is almost always due to a complication of the MI. (See
'Etiology' above.) The diagnosis of cardiogenic shock is usually confirmed with a bedside
echocardiogram or (on occasion) hemodynamic monitoring. (See 'Diagnosis' above.)

However, other clinical scenarios may mimic this presentation and fall into two general categories:

● Acute MI with shock due to non-cardiac 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 monitoring' above.)

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

• Stress-induced cardiomyopathy, also called “transient left ventricular apical ballooning,”

“takotsubo cardiomyopathy,” 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 left
ventricular outflow tract (LVOT) obstruction has been described in up to 20 percent of
patients with stress-induced 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, almost all patients recover
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 "Overview of acute pulmonary embolism 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

● Cardiogenic shock is a clinical condition resulting from inadequate tissue (end-organ) perfusion
due to cardiac dysfunction; it occurs most often in the setting of acute myocardial infarction
(MI). It is characterized by severe reduction in the cardiac index (<1.8 L/ min per m2 without
support or <2.2 L/min per 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).

However, there is a spectrum of severity of cardiogenic shock and marked elevation of systemic
vascular resistance may maintain blood pressure despite end-organ hypoperfusion and low
cardiac index. (See 'Introduction' above.)

● In patients with 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 and
'Pathophysiology' above.)

● In patients with acute MI, cardiogenic shock often develops after hospital admission. 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.)

● 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 'Echocardiography' above.)

● Other clinical scenarios may mimic the presentation of acute MI followed by cardiogenic shock
and fall into two general categories: those with clinical events consistent with acute MI but in
whom myocardial ischemia is not the primary event, such as acute myopericarditis or ascending
aortic dissection; and those with other causes of shock in a patient with MI, such as line sepsis
or hypovolemia due to overdiuresis. (See 'Differential diagnosis' above.)

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 'Hemodynamic monitoring' above.)
 ● Additional testing should include a chest radiograph, complete blood count, chemistry screen
(including assessment of renal function and electrolyte status), prothrombin and partial
thromboplastin times, and serial troponin measurements. (See 'Laboratory findings' above.)

ACKNOWLEDGMENT

The UpToDate editorial staff would like to thank Dr. Venu Menon for his contributions as an author to
previous versions of this topic review.

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Topic 44 Version 23.0

GRAPHICS

Hemodynamic profiles of the types of shock in children

Physiologic Tissue Tissue

Preload Pump function Afterload
variable perfusion perfusion

Clinical signs* or
Clinical central venous Cardiac output or Systemic vascular Capillary refill Mixed venous
measurement pressure (if index ¶ resistance time Δ oxygen saturation ◊
measured)

Hypovolemic ↓ ↓ ↑ ↑ Low

Cardiogenic ↑ ↓ ↑ ↑ Low

Distributive ↓ or ↔ ↑ ↓ ↓ (initial) High

Obstructive ↑§ ↓ ↑ ↑ Low

* Clinical signs of decreased preload include tachycardia, tachypnea, decreased or absent peripheral pulses; normal or weak central pulses;
capillary refill time >2 seconds; skin that is pale, mottled, cold or diaphoretic; dusky or pale extremities, altered mental status, decreased urine
output, and flat jugular veins. Clinical signs of increased preload include jugular venous distension, pulmonary edema, and hepatomegaly. These
patients are also typically tachycardic and poorly perfused. Refer to topics on evaluation of shock in children.
¶ Cardiac index (cardiac output per body surface area) is typically what is measured during clinical care.
Δ In patients with shock, capillary refill time >2 seconds is associated with low mixed venous oxygen saturation while flash capillary refill
suggests increased mixed venous oxygen saturation.
◊ A low mixed oxygen saturation is <70 percent when measured through a triple lumen catheter and <65 percent when measured through a
pulmonary artery catheter.
§ In patients with obstructive shock caused by tension pneumothorax, the patient typically displays clinical signs of increased preload. However,
because blood return to the heart is obstructed by compression or occlusion of the superior and inferior vena cavae, physiologic preload is
decreased. 

Graphic 73000 Version 6.0

Causes of cardiogenic shock

Acute myocardial infarction

Pump failure
Large infarction, generally involving ≥40 percent of the left ventricle
Smaller infarction with preexisting left ventricular dysfunction or a prior infarction
Infarction extension or expansion
Reinfarction

Mechanical complications
Acute mitral regurgitation caused by rupture of a papillary muscle or chordae tendinae or severe papillary muscle dysfunction
Ventricular septal defect caused by rupture of the interventricular septum
Left ventricular free wall rupture
Pericardial tamponade due to rupture of the left ventricular free wall or hemorrhagic pericardial effusion

Right ventricular infarction

Other conditions
End-stage cardiomyopathy

Myocarditis

Septic shock with severe myocardial depression

Left ventricular outflow tract obstruction

Aortic stenosis
Hypertrophic obstructive cardiomyopathy

Obstruction to left ventricular filling

Mitral stenosis
Left atrial myxoma

Acute mitral regurgitation (chordal rupture)

Acute aortic insufficiency

Myocardial contusion

Prolonged cardiopulmonary bypass

Adapted from Hollenberg SM, Kavinsky CJ, Parrillo JE. Ann Intern Med 1999; 131:47.

Graphic 69673 Version 2.0

Contributor Disclosures
Judith S Hochman, MD Grant/Research/Clinical Trial Support: AstraZeneca [SIHD (Rosuvastatin, ticagrelor)],
associated research funding for drug distribution to NYU School of Medicine for the NIH-funded ISCHEMIA
Study. Alex Reyentovich, MD Speaker’s Bureau: Novartis [Heart failure (Entresto)]; United Therapeutics
[Pulmonary Hypertension]. Consultant/Advisory Boards: Alnylam [Amyloidosis]; Pfizer [Amyloidosis]. Bernard J
Gersh, MB, ChB, DPhil, FRCP, MACC Consultant/Advisory Boards: Boston Scientific Corporation [Data Safety
Monitoring Board (REPRISE study)]; Cardiovascular Research Foundation [Data Safety Monitoring Board
(RELIEVE-HF Trial)]; Duke Clinical Research Institute [Data Safety Monitoring Board (PIONEER HCM)]; Icahn
School of Medicine at Mount Sinai [Data Safety Monitoring Board (ENVISAGE-TAVI study)]; Janssen Scientific
Affairs [Executive committee (ORBIT Registries); Chairman (DSMB); Steering Committee & Writing Committee
(REVEAL Trial)]; Kowa Research Institute [Data Safety Monitoring Board (PROMINENT study)]; Medtronic
[REVEAL AF study]; Mount Sinai St Luke's [Chairman (TWILIGHT study)]; Thrombosis Research Institute [Data
Safety Monitoring Board (GARFIELD study)]; Baim Institute [CRO for trials involving Edwards Percutaneous Valve
Devices]. Gordon M Saperia, MD, FACC Nothing to disclose

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