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Cardiogenic Shock
Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director,
Respiratory Medicine, St Boniface General Hospital
Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private
Practice
Updated: Aug 20, 2008
Introduction
Background
Cardiogenic shock is a major, and frequently fatal, complication of a variety of acute and chronic disorders that impair the ability of the
heart to maintain adequate tissue perfusion. Cardiac failure with cardiogenic shock continues to be a frustrating clinical problem; the
management of this condition requires a rapid and well-organized approach.
Cardiogenic shock is a physiologic state in which inadequate tissue perfusion results from cardiac dysfunction, most commonly following
acute myocardial infarction (MI). Although ST-elevation MI (STEMI, previously termed Q-wave MI) is encountered in most patients,
cardiogenic shock may also develop in patients with non–ST-elevation acute coronary syndrome (NSTEMI, NSTACS, or unstable
angina). The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of
adequate intravascular volume. Hemodynamic criteria for cardiogenic shock are sustained hypotension (systolic blood pressure <90 mm
Hg for at least 30 min) and a reduced cardiac index (<2.2 L/min/m2) in the presence of elevated pulmonary capillary occlusion pressure
(>15 mm Hg).
The diagnosis of cardiogenic shock can sometimes be made at the bedside by observing hypotension and clinical signs of poor tissue
perfusion, which include oliguria, cyanosis, cool extremities, and altered mentation. These signs usually persist after attempts have been
made to correct hypovolemia, arrhythmia, hypoxia, and acidosis.
Historical aspects
MI is the most common cause of cardiogenic shock in modern times. Morgagni first recognized MI in 1761, and it was subsequently
described by Caleb Parry in 1788 and by Heberden in 1802. John Hunter, a surgeon at St. George's Hospital in London, England
described his personal experience with MI in 1773. Adam Hammer, a physician in Mannheim, Germany, identified the role of coronary
thrombosis in the causation of MI in 1878. The clinical features of acute MI and survival of patients after such an event were reported in
1912 in the Journal of the American Medical Association by James Herrick, a Chicago physician. In the late 20th century, clinicians
recognized cardiogenic shock as a low cardiac output state secondary to extensive left ventricular infarction, development of a
mechanical defect (eg, ventricular septal defect or papillary muscle rupture), and right ventricular (RV) infarction.
Pathophysiology
Disorders that can result in the acute deterioration of cardiac function and can lead to cardiogenic shock include MI or myocardial
ischemia, acute myocarditis, sustained arrhythmia, acute valvular catastrophe, and decompensation of end-stage cardiomyopathy from
multiple etiologies. Autopsy studies show that cardiogenic shock is generally associated with the loss of more than 40% of the left
ventricular myocardial muscle. The pathophysiology of cardiogenic shock, which is well understood in the setting of coronary artery
disease, is described below.
Myocardial pathology
Cardiogenic shock is characterized by both systolic and diastolic dysfunction. Patients who develop cardiogenic shock from acute MI
consistently have evidence of progressive myocardial necrosis with infarct extension. Decreased coronary perfusion pressure and
increased myocardial oxygen demand play a role in the vicious cycle that leads to cardiogenic shock. These patients often have
multivessel coronary artery disease with limited coronary blood flow reserve. Ischemia remote from the infarcted zone is an important
contributor to shock. Myocardial diastolic function is also impaired because ischemia causes decreased myocardial compliance, thereby
increasing left ventricular filling pressure, which may lead to pulmonary edema and hypoxemia.
Cellular pathology
Tissue hypoperfusion, with consequent cellular hypoxia, causes anaerobic glycolysis, the accumulation of lactic acid, and intracellular
acidosis. Also, myocyte membrane transport pumps fail, which decreases transmembrane potential and causes intracellular
accumulation of sodium and calcium, resulting in myocyte swelling. If ischemia is severe and prolonged, myocardial cellular injury
becomes irreversible and leads to myonecrosis, which includes mitochondrial swelling, the accumulation of denatured proteins and
chromatin, and lysosomal breakdown. These pathophysiologic events induce fracture of the mitochondria, nuclear envelopes, and
plasma membranes. Additionally, apoptosis (programmed cell death) may occur in peri-infarcted areas and may contribute to myocyte
loss. Activation of inflammatory cascades, oxidative stress, and stretching of the myocytes produces mediators that overpower inhibitors
of apoptosis, thus activating the apoptosis.
Reversible myocardial dysfunction
Understanding that large areas of dysfunctional but viable myocardium can contribute to the development of cardiogenic shock in
patients with MI is important. This potentially reversible dysfunction is often described as myocardial stunning or hibernating myocardium.
Myocardial stunning represents postischemic dysfunction that persists despite restoration of normal blood flow. By definition, myocardial
dysfunction from stunning eventually resolves completely. The mechanism of myocardial stunning involves a combination of oxidative
stress, abnormalities of calcium homeostasis, and circulating myocardial depressant substances.
Hibernating myocardium is a state of persistently impaired myocardial function at rest, which occurs because of the severely reduced
coronary blood flow. Hibernation appears to be an adaptive response to hypoperfusion that may minimize the potential for further
ischemia or necrosis. Revascularization of the hibernating (and/or stunned) myocardium generally leads to improved myocardial function.
Consideration for the presence of myocardial stunning and hibernation is vital in patients with cardiogenic shock because of the
therapeutic implications of these conditions. Hibernating myocardium improves with revascularization, whereas the stunned myocardium
retains inotropic reserve and can respond to inotropic stimulation. Although hibernation is considered a different physiologic process than
that of myocardial stunning, the conditions are difficult to distinguish in the clinical setting and they often coexist.
Cardiovascular mechanics of cardiogenic shock
The main mechanical defect in cardiogenic shock is that the left ventricular end-systolic pressure-volume curve shifts to the right because
of a marked reduction in contractility. As a result, at a similar or even lower systolic pressure, the ventricle is able to eject less blood
volume per beat. Therefore, the end-systolic volume is usually greatly increased in persons with cardiogenic shock. The stroke volume is
decreased. To compensate for the diminished stroke volume, the curvilinear diastolic pressure-volume curve also shifts to the right, with
a decrease in diastolic compliance. This leads to increased diastolic filling that is associated with an increase in end-diastolic pressure.
The attempt to enhance cardiac output by this mechanism comes at the cost of having a higher left ventricular diastolic filling pressure,
which ultimately increases myocardial oxygen demand and causes pulmonary edema.
As a result of decreased contractility, the patient develops elevated left ventricular and RV filling pressures and low cardiac output. Mixed
venous oxygen saturation falls because of the increased tissue oxygen extraction, which is due to the low cardiac output. This, combined
with the intrapulmonary shunting that is often present, contributes to substantial arterial oxygen desaturation.
Systemic effects
When a critical mass of left ventricular myocardium becomes ischemic and fails to pump effectively, stroke volume and cardiac output
are curtailed. Myocardial ischemia is further exacerbated by compromised myocardial perfusion due to hypotension and tachycardia. The
pump failure increases ventricular diastolic pressures concomitantly, causing additional wall stress, hence elevating myocardial oxygen
requirements. Systemic perfusion is compromised by decreased cardiac output, with tissue hypoperfusion intensifying anaerobic
metabolism and instigating the formation of lactic acid, which further deteriorates the systolic performance of the myocardium.
Depressed myocardial function also leads to the activation of several physiologic compensatory mechanisms. These include sympathetic
stimulation, which increases the heart rate and cardiac contractility and causes renal fluid retention, hence augmenting the left ventricular
preload. The raised heart rate and contractility increases myocardial oxygen demand, further worsening myocardial ischemia. Fluid
retention and impaired left ventricular diastolic filling triggered by tachycardia and ischemia contribute to pulmonary venous congestion
and hypoxemia. Sympathetically mediated vasoconstriction to maintain systemic blood pressure amplifies myocardial afterload, which
additionally impairs cardiac performance. Finally, excessive myocardial oxygen demand with simultaneous inadequate myocardial
perfusion worsens myocardial ischemia, initiating a vicious cycle that ultimately ends in death, if uninterrupted.
Usually, both systolic myocardial dysfunction and diastolic myocardial dysfunction are present in patients with cardiogenic shock.
Metabolic derangements that impair myocardial contractility further compromise systolic ventricular function. Myocardial ischemia
decreases myocardial compliance, thereby elevating left ventricular filling pressure at a given end-diastolic volume (diastolic dysfunction),
which leads to pulmonary congestion and congestive heart failure. For more information, see Medscape's Heart Failure Resource
Center.
Shock state
Shock state, irrespective of the etiology, is described as a syndrome initiated by acute systemic hypoperfusion that leads to tissue
hypoxia and vital organ dysfunction. All forms of shock are characterized by inadequate perfusion to meet the metabolic demands of the
tissues. A maldistribution of blood flow to end organs begets cellular hypoxia and end organ damage, the well-described multisystem
organ dysfunction syndrome. The organs of vital importance are the brain, heart, and kidneys.
A decline in higher cortical function may indicate diminished perfusion of the brain, which leads to an altered mental status ranging from
confusion and agitation to flaccid coma. The heart plays a central role in propagating shock. Depressed coronary perfusion leads to
worsening cardiac dysfunction and a cycle of self-perpetuating progression of global hypoperfusion. Renal compensation for reduced
perfusion results in diminished glomerular filtration, causing oliguria and subsequent renal failure.
Frequency
United States
The incidence rate of cardiogenic shock ranges from 5-10% in patients with acute MI. In the Worcester Heart Attack Study, a communitywide analysis, the reported incidence rate is 7.5%.[13 ]The literature contains few data on cardiogenic shock in patients without ischemia.
International
Several multicenter thrombolytic trials in Europe report a prevalence rate of cardiogenic shock following MI of approximately 7%.
Mortality/Morbidity
The historic mortality rates from cardiogenic shock are 80-90%; more recent studies have reported somewhat lower in-hospital mortality
rates, in the range of 56-67%. With the advent of thrombolytics, improved interventional procedures, and better medical therapies for
heart failure, the mortality rates from cardiogenic shock are expected to decline.

The following predictors of mortality were identified from the GUSTO-I trial[14 ]: increasing age; prior MI; altered sensorium; cold,
clammy skin; and oliguria.

Mortality rates are similar in patients with cardiogenic shock secondary to STEMI and NSTACS.

Echocardiographic predictors such as left ventricular ejection fraction (EF) and mitral regurgitation are independent predictors. EF
of less than 28% is associated with a survival rate of 24% at 1 year compared to a survival rate of 56% with a higher EF.
Moderate or severe mitral regurgitation led to a 1-year survival rate of 31% compared to a survival rate of 58% in those with no
regurgitation.
Sex
The overall incidence of cardiogenic shock is higher in men compared to women because of the increased prevalence of coronary artery
disease in males. However, the percentage of female patients with MI who develop cardiogenic shock is higher compared to their male
counterparts.
Clinical
History
Cardiogenic shock is a medical emergency. A complete clinical assessment is critical to understanding the cause of the shock and to
targeting therapy for correcting the cause.

Cardiogenic shock following acute MI generally develops after admission to the hospital, although a small number of patients are
in shock at presentation. Patients demonstrate clinical evidence of hypoperfusion (low cardiac output), which is manifested by
sinus tachycardia, low urine output, and cool extremities. Systemic hypotension, defined as systolic blood pressure below 90 mm
Hg or a decrease in mean blood pressure by 30 mm Hg, ultimately develops and further propagates tissue hypoperfusion.

Most patients who develop acute MI present with an abrupt onset of squeezing or heavy substernal chest pain; the pain may
radiate to the left arm or the neck. The chest pain may be atypical, the location being epigastric or only in the neck or arm. The
pain quality may be burning, sharp, or stabbing. The pain may be absent in persons with diabetes or in elderly individuals.

Patients also may report associated autonomic symptoms, including nausea, vomiting, and sweating.

A history of previous cardiac disease, use of cocaine, previous MI, or previous cardiac surgery should be obtained. A patient
thought to have myocardial ischemia should have an assessment for cardiac risk factors. The evaluation should reveal a history of
hyperlipidemia, left ventricular hypertrophy, hypertension, or cigarette smoking or should reveal a family history of premature
coronary artery disease. The presence of 2 or more risk factors increases the likelihood of acute MI.

Other associated symptoms are diaphoresis, exertional dyspnea, or dyspnea at rest. Presyncope or syncope, palpitations,
generalized anxiety, and depression are other features indicative of poor cardiac function.
Physical
Cardiogenic shock is diagnosed after documentation of myocardial dysfunction and exclusion of alternative causes of hypotension, such
as hypovolemia, hemorrhage, sepsis, pulmonary embolism, pericardial tamponade, aortic dissection, or preexisting valvular disease.
Shock is present if evidence of multisystem organ hypoperfusion is detected upon physical examination.

Patients in shock usually appear ashen or cyanotic and have cool skin and mottled extremities.

Peripheral pulses are rapid and faint and may be irregular if arrhythmias are present.

Jugular venous distention and crackles in the lungs are usually (but not always) present. Peripheral edema also may be present.

Heart sounds are usually distant, and both third and fourth heart sounds may be present.

The pulse pressure may be low, and patients are usually tachycardic.

Patients show signs of hypoperfusion, such as altered mental status and decreased urine output.

A systolic murmur is generally heard in patients with acute mitral regurgitation or ventricular septal rupture.

The associated parasternal thrill indicates the presence of a ventricular septal defect, whereas the murmur of mitral regurgitation
may be limited to early systole.

The systolic murmur, which becomes louder upon Valsalva and prompt standing, suggests hypertrophic obstructive
cardiomyopathy (idiopathic hypertropic subaortic stenosis).
Causes
Based on the etiology and pathophysiology, cardiogenic shock can be divided into systolic dysfunction, diastolic dysfunction, valvular
dysfunction, cardiac arrhythmias, coronary artery disease, and mechanical complications.
Systolic dysfunction
The primary abnormality in systolic dysfunction is abated myocardial contractility. Acute MI or ischemia is the most common cause;
cardiogenic shock is more likely to be associated with anterior MI. The other causes of systolic dysfunction leading to cardiogenic shock
are severe myocarditis, end-stage cardiomyopathy (including valvular causes), myocardial contusion, and prolonged cardiopulmonary
bypass.
Diastolic dysfunction
Increased left ventricular diastolic chamber stiffness contributes to cardiogenic shock during cardiac ischemia, but also in the late stages
of hypovolemic shock and septic shock. Increased diastolic dysfunction is particularly detrimental when systolic contractility is also
depressed. The causes of cardiogenic shock due primarily to diastolic dysfunction are listed in Diastolic dysfunction.
Valvular dysfunction
Valvular dysfunction may immediately lead to cardiogenic shock or may aggravate other etiologies of shock. Acute mitral regurgitation
secondary to papillary muscle rupture or dysfunction is caused by ischemic injury. Rarely, acute obstruction of the mitral valve by left
atrial thrombus may result in cardiogenic shock by means of severely decreased cardiac output. Aortic and mitral regurgitation reduce
forward flow, raise end-diastolic pressure, and aggravate shock associated with other etiologies.
Cardiac arrhythmias
Ventricular tachyarrhythmias are often associated with cardiogenic shock. Furthermore, bradyarrhythmias may cause or aggravate shock
due to another etiology. Sinus tachycardia and atrial tachyarrhythmias contribute to hypoperfusion and aggravate shock.
Coronary artery disease
Cardiogenic shock is generally associated with the loss of more than 40% of the left ventricular myocardium, although in patients with
previously compromised left ventricular function, even a small infarction may precipitate shock. Cardiogenic shock is more likely to
develop in people who are elderly or diabetic or in those who have had a previous inferior infarction.
Mechanical complications
Complication of acute MI, such as acute mitral regurgitation, large RV infarction, and rupture of the interventricular septum or left
ventricular free wall, are other causes of cardiogenic shock.
Specific causes of cardiogenic shock include the following:
Left ventricular failure

Systolic dysfunction (decreased contractility)

Ischemia/MI

Global hypoxemia

Valvular disease (see Valvular or structural abnormality)

Myocardial depressant drugs (eg, beta-blockers, calcium channel blockers, antiarrhythmics)





Myocardial contusion

Respiratory acidosis

Metabolic derangements (eg, acidosis, hypophosphatemia, hypocalcemia)
Diastolic dysfunction/increased myocardial diastolic stiffness

Ischemia

Ventricular hypertrophy

Restrictive cardiomyopathy

Consequence of prolonged hypovolemic or septic shock

Ventricular interdependence

External compression by pericardial tamponade
Greatly increased afterload

Aortic stenosis

Hypertrophic cardiomyopathy

Dynamic aortic outflow tract obstruction

Coarctation of the aorta

Malignant hypertension
Valvular or structural abnormality

Mitral stenosis

Endocarditis

Mitral aortic regurgitation

Obstruction due to atrial myxoma or thrombus

Papillary muscle dysfunction or rupture

Ruptured septum or free wall arrhythmias
Decreased contractility

RV infarction

Ischemia

Hypoxia

Acidosis
Right ventricular failure


Greatly increased afterload

Pulmonary embolism

Pulmonary vascular disease (eg, pulmonary arterial hypertension, veno-occlusive disease)

Hypoxic pulmonary vasoconstriction

Peak end-expiratory pressure

High alveolar pressure

Acute respiratory distress syndrome

Pulmonary fibrosis

Sleep disordered breathing

Chronic obstructive pulmonary disease
Arrhythmias

Atrial and ventricular arrhythmias (tachycardia-mediated cardiomyopathy)

Conduction abnormalities (eg, atrioventricular blocks, sinus bradycardia)
Differential Diagnoses
Myocardial Infarction
Septic Shock
Myocardial Ischemia
Shock, Distributive
Myocardial Rupture
Shock, Hemorrhagic
Myocarditis
Systemic Inflammatory Response Syndrome
Pulmonary Edema, Cardiogenic
Pulmonary Embolism
Sepsis, Bacterial
Other Problems to Be Considered
Approach to the initial clinical evaluation of a patient in shock
Any patient presenting with shock must receive an early working diagnosis, urgent resuscitation, and subsequent confirmation of the
working diagnosis. Shock is identified in most patients based on findings of hypotension and inadequate organ perfusion, which may be
caused by either low cardiac output or low systemic vascular resistance (SVR). Circulatory shock can be subdivided into 4 distinct
classes based on the underlying mechanism and characteristic hemodynamic findings. In all patients, before establishing a definite
diagnosis of septic shock, the following 4 classes of shock should be considered and systematically differentiated.

Hypovolemic shock: Hypovolemic shock results from loss of blood volume caused by conditions such as gastrointestinal bleeding,
extravasation of plasma, major surgery, trauma, and severe burns.

Obstructive shock: Obstructive shock results from impedance of circulation by an intrinsic or extrinsic obstruction. Pulmonary
embolism, dissecting aneurysm, and pericardial tamponade all result in obstructive shock.

Distributive shock: Distributive shock is caused by conditions producing direct arteriovenous shunting and is characterized by
decreased SVR or increased venous capacitance because of the vasomotor dysfunction. These patients have high cardiac
output, hypotension, high pulse pressure, low diastolic pressure, and warm extremities with good capillary refill. Such findings
upon physical examination strongly suggest a working diagnosis of septic shock.

Cardiogenic shock: Cardiogenic shock characterized by primary myocardial dysfunction causes the heart to be unable to maintain
adequate cardiac output. These patients demonstrate clinical signs of low cardiac output, with adequate intravascular volume.
The patients have cool and clammy extremities, poor capillary refill, tachycardia, narrow pulse pressure, and low urine output.
Workup
Laboratory Studies

Biochemical profile: Measurement of routine biochemistry parameters, such as electrolytes, renal function (eg, urea and
creatinine), and liver function tests (eg, bilirubin, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase
[LDH]), are all useful for assessing proper functioning of vital organs.

CBC count: A CBC count is generally helpful to exclude anemia; a high WBC count may indicate an underlying infection, and the
platelet count may be low because of coagulopathy related to sepsis.

Cardiac enzymes


The diagnosis of acute MI is aided by a variety of serum markers, which include creatine kinase and its subclasses,
troponin, myoglobin, and LDH. The value for the isoenzyme of creatine kinase with muscle and blood subunits is most
specific but may be falsely elevated in persons with myopathy, hypothyroidism, renal failure, or skeletal muscle injury.

The rapid release and metabolism of myoglobin occurs in persons with MI. A 4-fold rise of myoglobin over 2 hours appears
to be a test result sensitive for MI. The serum LDH value increases approximately 10 hours after the onset of MI, peaks at
24-48 hours, and gradually returns to normal in 6-8 days. The LDH fraction 1 isoenzyme is primarily released by the heart
but also may come from the kidneys, stomach, pancreas, and red blood cells.

Cardiac troponins T and I are widely used for the diagnosis of myocardial injury. Troponin elevation in the absence of
clinical evidence of ischemia should prompt a search for other causes of cardiac damage, such as myocarditis. Troponin I
and T can be detected in serum within the first few hours after onset of acute myocardial infarction. Troponin levels peak at
14 hours after acute myocardial infarction, peak again several days later (biphasic peak), and remain abnormal for 10
days. This characteristic could make troponin T (in combination with CK-MB) useful for retrospective diagnosis of acute
myocardial infarction in patients who seek care very late. Troponin T is an independent prognosticator of adverse
outcomes and can be used as a patient risk-stratifying tool in patients with unstable angina or non – Q-wave myocardial
infarction.
Arterial blood gases: Arterial blood gas values indicate overall acid-base homeostasis and the level of arterial blood oxygenation.
A base deficit elevation (reference range is +3 to -3 mmol/L) correlates with the occurrence and severity of shock. A base deficit is
also an important marker to follow during resuscitation of a patient from shock.

Lactate: Serial lactate measurements are useful markers of hypoperfusion and are also used as indicators of prognosis. Elevated
lactate values in a patient with signs of hypoperfusion indicate a poor prognosis; rising lactate values during resuscitation portend
a very high mortality rate.
Imaging Studies


Echocardiography should be performed early to establish the cause of cardiogenic shock.

Echocardiography provides information on global and regional systolic function and on diastolic dysfunction.

Echocardiography findings can also lead to a rapid diagnosis of mechanical causes of shock, such as papillary muscle
rupture causing acute myocardial regurgitation, acute ventricular septal defect, free myocardial wall rupture, and pericardial
tamponade.
Chest radiography findings are useful for excluding other causes of shock or chest pain.

A widened mediastinum may indicate aortic dissection.

Tension pneumothorax or pneumomediastinum readily detected on x-ray films may manifest as low-output shock.

Most patients with established cardiogenic shock exhibit findings of left ventricular failure. The radiological features of left
ventricular failure include pulmonary vascular redistribution, interstitial pulmonary edema, enlarged hilar shadows, the
presence of Kerley B lines, cardiomegaly, and bilateral pleural effusions; alveolar edema manifests as bilateral perihilar
opacities in a so-called butterfly distribution.
Other Tests

Electrocardiogram: Acute myocardial ischemia is diagnosed based on the presence of ST-segment elevation, ST-segment
depression, or Q waves. T-wave inversion, although a less sensitive finding, may be seen in persons with myocardial ischemia.
Therefore, perform electrocardiography immediately to help diagnose MI, myocardial ischemia, or both.
Procedures


Invasive hemodynamic monitoring

Invasive hemodynamic monitoring (Swan-Ganz catheterization) is very useful for helping exclude other causes of shock,
eg, volume depletion, or obstructive and septic shock.

The hemodynamic measurements of cardiogenic shock are a pulmonary capillary wedge pressure (PCWP) greater than 15
mm Hg and a cardiac index of less than 2.2 L/min/m2.

The presence of large V waves on the PCWP tracing suggests severe mitral regurgitation.

A step-up in oxygen saturation between the right atrium and the right ventricle is diagnostic of ventricular septal rupture.

High right-sided filling pressures in the absence of an elevated PCWP, when accompanied with electrocardiographic
criteria, indicate RV infarction.
Coronary artery angiography

Coronary angiography is urgently indicated in patients with myocardial ischemia or MI who also develop cardiogenic shock.
Angiography is required to help assess the anatomy of the coronary arteries and the need for urgent revascularization.

Coronary angiography findings often demonstrate multivessel coronary artery disease in persons with cardiogenic shock.
In these patients, a compensatory hyperkinesis cannot occur in the noninfarct territory because of the severe coronary
artery atherosclerosis.

The most common cause of cardiogenic shock is extensive MI, although a smaller infarction in a previously compromised
left ventricle also may precipitate shock. Following MI, large areas of nonfunctional but viable myocardium (hibernating
myocardium) can also cause or contribute to cardiogenic shock.
Treatment
Medical Care
Initial management includes fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema is present. Central
venous and arterial lines are often required. Swan-Ganz catheterization and continuous percutaneous oximetry are routine. Oxygenation
and airway protection are critical; intubation and mechanical ventilation are commonly required. Correction of electrolyte and acid-base
abnormalities, such as hypokalemia, hypomagnesemia, and acidosis, are essential.

Patients with MI or acute coronary syndrome are given aspirin and heparin. Both of these medications have been shown to be
effective in reducing mortality in separate studies.

The glycoprotein IIb/IIIa inhibitors improve the outcome of patients with NSTACS. Their benefit has been proven in reducing
recurrent MI following percutaneous coronary intervention (PCI) and in cardiogenic shock.

All patients with cardiogenic shock require close hemodynamic monitoring, volume support to ensure adequate sufficient preload,
and ventilatory support as discussed in Respiratory Failure.

Hemodynamic support



Dopamine, norepinephrine, and epinephrine are vasoconstricting drugs that help maintain adequate blood pressure during
life-threatening hypotension and help preserve perfusion pressure for optimizing flow in various organs. The mean blood
pressure required for adequate splanchnic and renal perfusion (mean arterial pressure [MAP] of 60 or 65 mm Hg) is based
on clinical indices of organ function.

In patients with inadequate tissue perfusion and adequate intravascular volume, initiation of inotropic and/or vasopressor
drug therapy may be necessary. Dopamine increases myocardial contractility and supports the blood pressure; however, it
may increase myocardial oxygen demand. Dobutamine may be preferable if the systolic blood pressure is higher than 80
mm Hg and has the advantage of not affecting myocardial oxygen demand as much as dopamine. However, the resulting
tachycardia may preclude the use of this inotropic agent in some patients.

Dopamine is usually initiated at a rate of 5-10 mcg/kg/min intravenously, and the infusion rate is adjusted according to the
blood pressure and other hemodynamic parameters. Often, patients may require high doses of dopamine (as much as 20
mcg/kg/min). If the patient remains hypotensive despite moderate doses of dopamine, a direct vasoconstrictor (eg,
norepinephrine) should be started at a dose of 0.5 mcg/kg/min and titrated to maintain an MAP of 60 mm Hg. The potent
vasoconstrictors (eg, norepinephrine) have traditionally been avoided because of their adverse effects on cardiac output
and renal perfusion.
Vasopressor supportive therapy: The following is a brief review of the mechanism of action and indications for drugs used for
hemodynamic support of cardiogenic shock.

Dopamine is a precursor of norepinephrine and epinephrine and has varying effects according to the doses infused. A
dose of less than 5 mcg/kg/min causes vasodilation of renal, mesenteric, and coronary beds. At a dose of 5-10
mcg/kg/min, beta1-adrenergic effects induce an increase in cardiac contractility and heart rate. At doses of approximately
10 mcg/kg/min, alpha-adrenergic effects lead to arterial vasoconstriction and an elevation in blood pressure. The blood
pressure increases primarily as a result of inotropic effect, and the undesirable effects are (1) tachycardia and increased
pulmonary shunting and (2) the potential to decrease splanchnic perfusion and increase pulmonary arterial wedge
pressure.

Norepinephrine is a potent alpha-adrenergic agonist with minimal beta-adrenergic agonist effects. Norepinephrine can
increase blood pressure successfully in patients who remain hypotensive following dopamine. The dose of norepinephrine
may vary from 0.2-1.5 mcg/kg/min, and large doses, as high as 3.3 mcg/kg/min, have been used because of the alphareceptor down-regulation in persons with sepsis.

Epinephrine can increase the MAP by increasing the cardiac index and stroke volume, along with an increase in SVR and
heart rate. Epinephrine may increase oxygen delivery and consumption and decreases the splanchnic blood flow.
Administration of this agent is associated with an increase in systemic and regional lactate concentrations. The use of
epinephrine is recommended only in patients who are unresponsive to traditional agents. The undesirable effects are an
increase in lactate concentration, a potential to produce myocardial ischemia, the development of arrhythmias, and a
reduction in splanchnic flow.
Inotropic supportive therapy

Dobutamine (sympathomimetic agent) is a beta1-receptor agonist, although it has some beta2-receptor and minimal alphareceptor activity. Intravenous dobutamine induces significant positive inotropic effects with mild chronotropic effects. It also
induces mild peripheral vasodilation (decrease in afterload). The combined effect of increased inotropy and decreased
afterload induces a significant increase in cardiac output. In the setting of acute MI, dobutamine use could increase the
size of the infarct because of the increase in myocardial oxygen consumption that may ensue. In general, avoid
dobutamine in patients with moderate or severe hypotension (eg, systolic blood pressure <80 mm Hg) because of the
peripheral vasodilation.

Phosphodiesterase inhibitors (PDIs), currently inamrinone (formerly amrinone) and milrinone, are the PDI inotropes that
have proved valuable.
 These are inotropic agents with vasodilating properties, and each has a long half-life. The hemodynamic properties
of PDIs are (1) a positive inotropic effect on the myocardium and peripheral vasodilation (decreased afterload) and
(2) a reduction in pulmonary vascular resistance (decreased preload).
 PDIs are beneficial in persons with cardiac pump failure, but they may require concomitant vasopressor
administration. Unlike catecholamine inotropes, these drugs are not dependent on adrenoreceptor activity;
therefore, patients are less likely to develop tolerance to these medications.
 PDIs are less likely than catecholamines to cause adverse effects known to be associated with adrenoreceptor
activity (eg, increased myocardial oxygen demand, myocardial ischemia). They are also associated with less
tachycardia and myocardial oxygen consumption. However, the incidence of tachyarrhythmias is greater with PDIs
compared to dobutamine.



Thrombolytic therapy

Although thrombolytic therapy (TT) reduces mortality rates in patients with acute MI, its benefits for patients with
cardiogenic shock secondary to MI are disappointing. When used early in the course of MI, TT reduces the likelihood of
subsequent development of cardiogenic shock after the initial event.

In the Gruppo Italiano Per lo Studio Della Streptokinase Nell'Infarto Miocardio trial, 30-day mortality rates were 69.9% in
patients with cardiogenic shock who received streptokinase, compared to 70.1% in patients who received a placebo.
Similarly, other studies with a tissue plasminogen activator did not show any benefit in mortality rates from cardiogenic
shock. Lower rates of reperfusion of the infarct-related artery in patients with cardiogenic shock might help explain the
disappointing results from TT. The other reasons for the decreased efficacy of TT are the presence of hemodynamic,
mechanical, and metabolic factors causative of cardiogenic shock; these factors are unaffected by TT.

A recent prospective study investigated the potential benefit of TT and intra-aortic balloon pump (IABP) counterpulsation
on in-hospital mortality rates of patients with MI complicated by cardiogenic shock.
 Out of 1190 patients enrolled, the treatments were (1) no TT and no IABP counterpulsation (33%, n = 285), (2)
IABP counterpulsation only (33%, n = 279), (3) TT only (15%, n = 132), and (4) TT and IABP counterpulsation
(19%, n = 160).
 Patients in cardiogenic shock treated with TT had lower in-hospital mortality rates compared to those who did not
receive TT (54% vs 64%, P = .005), and those selected for IABP counterpulsation had lower in-hospital mortality
rates compared to those who did not receive IABP counterpulsation (50% vs 72%, P <.0001).
 Furthermore, a significant difference was noted in in-hospital mortality rates among the 4 treatment groups, ie, TT
plus IABP counterpulsation (47%), IABP counterpulsation only (52%), TT only (63%), no TT and no IABP
counterpulsation (77%) (P <.0001).
 Revascularization influenced in-hospital mortality rates significantly (39% with revascularization vs 78% without
revascularization, P <.0001).

Patients who are unsuitable for invasive therapy should be treated with a thrombolytic agent in the absence of
contraindications. This is a class I recommendation by American College of Cardiology (ACC)/American Heart Association
(AHA) guidelines.
Intra-aortic balloon pump

The use of the IABP reduces systolic left ventricular afterload and augments diastolic coronary perfusion pressure, thereby
increasing cardiac output and improving coronary artery blood flow. The IABP is effective for the initial stabilization of
patients with cardiogenic shock. However, an IABP is not definitive therapy; the IABP stabilizes the patients so that
definitive diagnostic and therapeutic interventions can be performed.

The IABP also may be a useful adjunct to thrombolysis for initial stabilization and transfer of patients to a tertiary care
facility. Some studies have shown lower mortality rates in patients with MI and cardiogenic shock treated with an IABP and
subsequent revascularization, as previously mentioned.

Complications may be documented in up to 30% of patients who undergo IABP therapy and mainly relate to local vascular
problems, embolism, infection, and hemolysis. The impact of an IABP on long-term survival is controversial and depends
on the hemodynamic status and etiology of the cardiogenic shock. Patient selection is the key issue; early insertion of the
IABP may result in clinical benefit, rather than waiting until full-blown cardiogenic shock has developed.
Ventricular assist devices

In recent years, left ventricular assist devices (LVADs) capable of providing complete short-term hemodynamic support
have been developed. The application of LVAD during reperfusion, after acute coronary occlusion, causes reduction of the
left ventricular preload, increases regional myocardial blood flow and lactate extraction, and improves general cardiac
function. The LVAD makes it possible to maintain the collateral blood flow as a result of maintaining the cardiac output and
aortic pressure, keeping wall tension low, and reducing the extent of microvascular reperfusion injury.

The pooled analysis from 17 studies showed that the mean age of this group of patients was 59.5 ± 4.5 years, mean
support duration was 146.2 ± 60.2 hours. In 78.5% of patients (range, 53.8-100%), adjunctive reperfusion therapy, mainly
PTCA, was used. Mean weaning and survival rates were 58.5% (range, 46-75%) and 40% (range, 29-58%), respectively.
In any case, comparing studies is difficult because important data are usually missing, patients were younger, and time to
treatment is not standardized. Hemodynamic presentation seems to be worse compared with data reported in the SHOCK
trial, with lower cardiac index, lower systolic aortic pressure, and higher serum lactates. Taking these considerations into
account, LVAD support seems to give no survival improvement in patients with CS complicating acute MI, compared with
early reperfusion alone or in combination with IABP.

One randomized controlled trial assigned 129 patients with end-stage heart failure who were ineligible for cardiac
transplantation to receive a left ventricular assist device (68 patients) or optimal medical management. Survival analysis
that received left ventricular assist devices as compared with the medical therapy group (relative risk, 0.52; 95%
confidence interval, 0.34-0.78; P=0.001). The rates of survival at 1 year were 52% in the device group and 25% in the
medical therapy group (P=0.002), and the rates at 2 years were 23% and 8% (P=0.09), respectively. The quality of life was
significantly improved at 1 year in the device group.[49 ]

Implantable LVAD is being used as a bridge-to-heart transplantation for patients with acute MI and CS. Farrar and
colleagues reported the best outcome in a multicenter trial that included 17 patients in CS from acute MI.[48 ]Thirteen
patients (76%) underwent HTx and all were discharged after support with the Thoratec LVAD. According to the HeartMate
Data Registry[50 ], from 1986-1998, 41 patients (5% of the total number of HeartMate IP patients) were supported with this
implantable pneumatic device for acute MI and 25 (61%) were successfully bridged to heart transplantation. However,
LVADs as a bridging option for patients with CS must be considered cautiously and must be avoided in patients unlikely to
survive or unlikely to be transplant candidates. Further investigations are required to better define indications, support
modalities, and outcomes.

The indications for insertion of a ventricular assist device are controversial. Such an aggressive approach to support the
circulatory system in cardiogenic shock is appropriate (1) after the failure of medical treatment and the IABP and (2) when
the cause of cardiogenic shock is potentially reversible or as a bridging option.
Surgical Care
The retrospective and prospective data favor aggressive mechanical revascularization in patients with cardiogenic shock secondary to
MI.



Percutaneous transluminal coronary angioplasty

Reestablishing blood flow in the infarct-related artery may improve left ventricular function and survival following MI. In
acute MI, studies show that percutaneous transluminal coronary angioplasty (PTCA) can achieve adequate flow in 80-90%
of patients, compared with 50-60% of patients after TT.

Several retrospective clinical trials have shown that patients with cardiogenic shock due to myocardial ischemia benefitted
(reduction in 30-d mortality rates) when treated with angioplasty. A recent study of direct (primary) PTCA in patients with
cardiogenic shock reports lower mortality rates in patients treated with angioplasty combined with the use of stents,
compared to medical therapy.

To study the relationship of time to treatment and mortality in patients with acute MI, a series of 1336 patients who
underwent successful primary PTCA were stratified into low-risk and not low–risk patient groups. The 6-month mortality
rate was 9.3% for not low–risk patients and 1.3% for the low-risk patients (P <.001). An increase in the mortality rate from
4.8% to 12.9% with increasing time to reperfusion was observed in the not low–risk group. A delay from symptom onset to
treatment resulted in higher mortality rates for the not low–risk patients.[4 ]
Coronary artery bypass grafting

Critical left main artery disease and 3-vessel coronary artery disease are common findings in patients who develop
cardiogenic shock. The potential contribution of ischemia in the noninfarcted zone contributes to the deterioration of
already compromised myocardial function.

Coronary artery bypass grafting (CABG) in the setting of cardiogenic shock is generally associated with high surgical
morbidity and mortality rates. Because the results of percutaneous interventions can be favorable, routine bypass surgery
is often discouraged for these patients.

A 2004 task force of the ACC and the AHA gave a class I recommendation to the performance of primary PCI or emergent
CABG in patients younger than 75 years who have STEMI and who develop shock within 36 hours of MI and can be
treated within 18 hours of onset of shock. Performance of primary PCI or emergent CABG was considered reasonable in
patients older than 75 years (class IIa recommendation).
SHOCK trial

A recent study known as the SHOCK (ie, SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK)
trial addressed the question of revascularization in patients with cardiogenic shock. Patients were assigned to receive
either optimal medical management, including an IABP and TT, or cardiac catheterization followed by revascularization
using PTCA or CABG.[18 ]

The 1-month and 6-month survival rates were reported from the SHOCK Trial.[19 ]The mortality rates at 30 days were
46.7% in the early intervention group and 56% in patients treated with optimal medical management. Although this did not
reach a statistical significance at 1 month, the mortality rate at 6 months was significantly lower in the early intervention
group (50.3% vs 63.1%, P = .027). The results of this study support the superiority of a strategy that combines early
revascularization with medical management in patients with cardiogenic shock.

The 1-year survival rates were also reported from the SHOCK Trial.[20 ]The survival rate at 1-year was 46.7% for patients in
the early revascularization group and was 33.6% in the conservative management (absolute difference in survival, 13.2%;
95% confidence interval, 2.2-24.1%; P <.03; relative risk for death, 0.72; 95% confidence interval, 0.54-0.95) group. The
treatment benefit was apparent only for patients younger than 75 years (51.6% survival rate in early revascularization
group vs 33.3% in patients treated with optimal medical management). Based on the outcome of this study, the
recommendation is that patients with acute MI complicated by cardiogenic shock, particularly those younger than 75 years,
should be rapidly transferred to a center with personnel capable of performing early angiography and revascularization
procedures.
Consultations
Consultation with a cardiologist and/or an intensivist should be sought early in the patient's clinical course. The patient is usually admitted
to a coronary care unit or intensive care unit. All patients with cardiogenic shock should be cared for in a facility at which right heart
catheterization, coronary arteriography, and revascularization facilities are readily available.
Medication
Vasopressors augment the coronary and cerebral blood flow during the low-flow state associated with shock. Sympathomimetic amines
with both alpha- and beta-adrenergic effects are indicated for persons with cardiogenic shock. Dopamine and dobutamine are the drugs
of choice to improve cardiac contractility, with dopamine the preferred agent in patients with hypotension.
Vasodilators relax vascular smooth muscle and reduce the SVR, allowing for improved forward flow, which improves cardiac output.
Adequate pain control is essential for quality patient care and patient comfort. Diuretics are used to decrease plasma volume and
peripheral edema. The reduction in extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac output
and, consequently, blood pressure, with a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, the
plasma volume and peripheral vascular resistance usually return to pretreatment values.
Vasopressors/inotropic agents
Augment coronary and cerebral blood flow during low-flow state associated with cardiogenic shock.
Dopamine (Intropin)
Stimulates adrenergic and dopaminergic receptors. Hemodynamic effect depends on dose. Lower doses stimulate mainly dopaminergic
receptors that produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and vasoconstriction.
Dosing
Adult
5-20 mcg/kg/min IV continuous infusion; dose may be increased by 1-4 mcg/kg/min q10-30min until optimal response is achieved; >50%
of patients are maintained satisfactorily on doses <20 mcg/kg/min
Pediatric
Administer as in adults
Interactions
Phenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects
Contraindications
Documented hypersensitivity; pheochromocytoma; ventricular fibrillation
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Must be administered via central vein; closely monitor urine flow, cardiac output, pulmonary wedge pressure, and blood pressure during
infusion; prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated; monitoring central venous pressure or left
ventricular filling pressure may be helpful for detecting and treating hypovolemia
Dobutamine (Dobutrex)
Sympathomimetic amine with stronger beta than alpha effects. Produces systemic vasodilation and increases the inotropic state. Higher
doses may cause increase in heart rate, exacerbating myocardial ischemia.
Dosing
Adult
5-20 mcg/kg/min IV continuous infusion, titrate to desired response; not to exceed 40 mcg/kg/min
Pediatric
Administer as in adults
Interactions
Beta-adrenergic blockers antagonize effects; general anesthetics may increase toxicity
Contraindications
Documented hypersensitivity; hypertrophic cardiomyopathy, atrial fibrillation or flutter, severe tachycardia
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Following MI, use with extreme caution; correct hypovolemic state before using; may exacerbate hypotension; use with caution when
ventricular or life-threatening tachyarrhythmias present
Phosphodiesterase enzyme inhibitors
Induce peripheral vasodilation and provide inotropic support.
Milrinone (Primacor)
Positive inotrope and vasodilator with little chronotropic activity. Different in mode of action from either cardiac glycosides (digoxin) or
catecholamines.
Dosing
Adult
50 mcg/kg IV loading dose over 10 min, followed by 0.375-0.75 mcg/kg/min continuous IV infusion
Pediatric
Administer as in adults; although DOC in many pediatric ICUs, safety and efficacy are not well established
Interactions
May precipitate if infused in same IV line as furosemide
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor fluid, electrolyte changes, and renal function during therapy; excessive diuresis may cause increase in potassium loss and
predispose digitalized patients to arrhythmias (correct hypokalemia by potassium supplementation prior to treatment); slow or stop
infusion in patients showing excessive decreases in blood pressure; if vigorous diuretic therapy causes significant decreases in cardiac
filling pressure, cautiously administer drug and monitor blood pressure, heart rate, and clinical symptomatology
Inamrinone (Inocor)
Formerly known as amrinone. Phosphodiesterase inhibitor with positive inotropic and vasodilator activity. Produces vasodilation and
increases inotropic state. More likely to cause tachycardia than dobutamine and may exacerbate myocardial ischemia.
Dosing
Adult
Initial dose: 0.75 mg/kg IV bolus slowly over 2-3 min
Maintenance infusion: 5-10 mcg/kg/min; not to exceed 10 mg/kg; adjust dose according to patient response
Pediatric
Administer as in adults; safety and efficacy not well established
Interactions
Diuretics may cause significant hypovolemia and a decrease in filling pressure; has additive effects with cardiac glycosides
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Causes thrombocytopenia in 2-3% of patients; hypotension may occur following a loading dose; requires adequate preload; ventricular
dysrhythmias may occur but may be related to underlying condition; do not use in patients with cardiac outlet obstruction (eg, aortic
stenosis, pulmonic stenosis, hypertrophic cardiomyopathy); discontinue therapy if clinical symptoms of liver toxicity occur; correct
hypokalemic states before using
Vasodilators
Decrease preload and/or afterload.
Nitroglycerin (Nitro-Bid)
Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Result is a
decrease in preload and blood pressure (ie, afterload).
Dosing
Adult
10-200 mcg/min IV continuous infusion
Pediatric
0.1-1 mcg/kg/min IV infusion
Interactions
Aspirin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministration of
calcium channel blockers (dose adjustment of either agent may be necessary)
Contraindications
Documented hypersensitivity; severe anemia, shock, postural hypotension, head trauma, closed-angle glaucoma, cerebral hemorrhage
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in 3-vessel, left main coronary artery disease, aortic stenosis, or low systolic blood pressure
Analgesics
Reduce pain, which decreases sympathetic stress, in addition to providing some preload reduction.
Morphine sulfate (Duramorph, Astramorph, MS Contin)
DOC for narcotic analgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various IV
doses are used, commonly titrated until desired effect is achieved.
Dosing
Adult
Initial dose: 0.1 mg/kg IV/IM/SC
Maintenance dose: 5-20 mg/70 kg IV/IM/SC q4h
Relatively hypovolemic patients: Start with 2 mg IV/IM/SC, reassess hemodynamic effects of dose
Pediatric
0.1-0.2 mg/kg/dose IV/IM/SC q2-4h prn; not to exceed 15 mg/dose; may initiate at 0.05 mg/kg/dose
Interactions
Phenothiazines may antagonize analgesic effects of opiate agonists; TCAs, MAOIs, and other CNS depressants may potentiate adverse
effects
Contraindications
Documented hypersensitivity; hypotension, potentially compromised airway in patient in whom establishing rapid airway control would be
difficult
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; caution in atrial flutter and other
supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
Diuretics
Decrease plasma volume and peripheral edema. Excessive reduction in plasma volume and stroke volume associated with diuresis may
decrease cardiac output and, consequently, blood pressure.
Furosemide (Lasix)
Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride
reabsorption in ascending loop of Henle and distal renal tubule.
Individualize dose to patient. Depending on response, administer at increments of 20-40 mg no sooner than 6-8 h after previous dose,
until desired diuresis occurs. When treating infants, titrate in increments of 1 mg/kg/dose until satisfactory effect is achieved.
Dosing
Adult
20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states; also may be administered as continuous infusion
Pediatric
1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg
Interactions
Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of
tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides; hearing loss of varying degrees may
occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are
possible when taken concurrently
Contraindications
Documented hypersensitivity, hepatic coma, anuria, and a state of severe electrolyte depletion
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Observe for blood dyscrasias, liver or kidney damage, or idiosyncratic reactions; perform frequent serum electrolyte, carbon dioxide,
glucose, uric acid, calcium, creatinine, and BUN determinations during first few months of therapy and periodically thereafter; loop
diuretics may increase urinary excretion of magnesium and calcium
Follow-up
Further Inpatient Care
Cardiogenic shock is an emergency, requiring immediate resuscitative therapy before shock irreversibly damages vital organs.
Simultaneously, identifying the cause of shock is important so that therapy can be directed to amending the cause.
Transfer
Immediately transfer a patient who develops cardiogenic shock to an institution at which invasive monitoring, coronary revascularization,
and skilled personnel are available to provide expert care to the patient.
Prognosis
In the absence of aggressive, highly experienced technical care, mortality rates among patients with cardiogenic shock are exceedingly
high (up to 70-90%). The key to achieving a good outcome is rapid diagnosis, prompt supportive therapy, and expeditious coronary
artery revascularization in patients with myocardial ischemia and infarction. The mortality rate is reduced to 40-60% if patients are treated
aggressively. The prognosis for patients who survive cardiogenic shock is not well studied but may be favorable if the underlying cause
of shock is expeditiously corrected.
Patient Education
For excellent patient education resources, visit eMedicine's Shock Center and Public Health Center. Also, see eMedicine's patient
education articles Shock and Cardiopulmonary Resuscitation (CPR).
Miscellaneous
Medicolegal Pitfalls

Cardiogenic shock has a very high mortality rate (60-80%), although mortality rates have decreased over the last 2 decades.

Areas of nonfunctioning but viable (hibernating) myocardium can cause or contribute to the development of cardiogenic shock.

The key to a good outcome in patients with cardiogenic shock is an organized approach, with rapid diagnosis and prompt initiation
of pharmacologic therapy to maintain blood pressure and cardiac output.

Early and definitive restoration of coronary blood flow is the most important intervention for producing an improvement in survival,
and, at present, it represents standard therapy for patients with cardiogenic shock due to myocardial ischemia.

Cardiogenic shock may be prevented with early revascularization in patients with MI and with required intervention in patients with
structural heart disease.

Patients with cardiogenic shock who are admitted to hospitals without facilities for revascularization should be immediately
transferred to a tertiary care center with such facilities. If time to PCI is more than 1 hour and onset of symptoms is within 3 hours,
rapid administration of thrombolytic therapy is recommended.
Special Concerns

RV infarction

RV infarction occurs in up to 30% of patients with inferior MI and becomes hemodynamically unstable in 10% of these
patients. The diagnosis is made by identifying an ST-segment elevation in the right precordial leads (V3 or V4 R) and/or
typical hemodynamic findings after right heart catheterization. These are elevated right atrial and RV end-diastolic
pressures with normal-to-low pulmonary artery wedge pressure and low cardiac output. Echocardiography findings can
also be very helpful in the diagnosis of RV infarction. Patients with cardiogenic shock due to RV infarction have a better
prognosis when compared to those with cardiogenic shock due to left ventricular systolic failure.


Regarding the management of cardiogenic shock due to RV infarction, supportive therapy begins with the restoration and
maintenance of RV preload with fluid administration. However, excessive fluid resuscitation may compromise left
ventricular filling by introducing an interventricular septal shift. Inotropic therapy with dobutamine may be effective in
increasing cardiac output in patients with RV infarction. Maintenance of systemic arterial pressure in order to maintain
adequate coronary artery perfusion may require vasoconstricting agents, such as norepinephrine. In unstable patients, an
IABP may be useful for ensuring adequate blood supply to the already compromised right ventricle. Revascularization of
the occluded coronary artery, preferably by PTCA, is crucial for management and has shown to dramatically improve
outcome.
Acute mitral regurgitation

Acute mitral regurgitation is usually associated with inferior MI due to ischemia or infarction of the papillary muscle. The
incidence rate is approximately 1% of MI, and posteromedial papillary muscle is involved more frequently than
anterolateral muscle. Acute mitral regurgitation usually occurs 2-7 days following acute MI and manifests with an abrupt
onset of pulmonary edema, hypotension, and cardiogenic shock.




Echocardiography findings are extremely useful in making a diagnosis. The 2-dimensional echocardiogram image shows
the malfunctioning mitral valve, and findings from a Doppler study can be used to document the severity of mitral
regurgitation. Right heart catheterization is often required for stabilizing the patient. Tall V waves identified on pulmonary
arterial and wedge pressure waveforms indicate acute mitral regurgitation. However, the diagnosis must be confirmed
based on echocardiography or left ventriculography findings before definitive therapy or surgery is initiated.

Hemodynamic stabilization by reducing afterload, either with nitroprusside or IABP, is often instituted. Definitive therapy
requires revascularization, if ischemia is present, and/or surgical valve repair or replacement, if a structural valvular lesion
is present. The mortality rate in the presurgical era was 50% in the first 24 hours, with a 2-month survival rate of 6%.
Cardiac rupture

Rupture of the free wall of the left ventricle occurs within 2 weeks of the MI and may occur within the first 24 hours. The
rupture may involve the anterior, posterior, or lateral wall of the ventricle.

Cardiac rupture often presents as sudden cardiac death. Premortem symptoms include chest pain, agitation, tachycardia,
and hypotension. This diagnosis should be considered in patients with electromechanical dissociation who have a history
of anginal pain. Patients rarely, if ever, survive cardiac rupture.
Ventricular septal rupture

Approximately 1-3% of acute MIs are associated with ventricular septal rupture. Most septal ruptures occur within the week
following MI. Patients with acute ventricular septal rupture develop acute heart failure and/or cardiogenic shock, with
physical findings of a harsh holosystolic murmur and left parasternal thrill. A left-to-right intracardiac shunt, as
demonstrated by a step-up (>5% increase in oxygen saturation) between the right atrium and right ventricle, confirms the
diagnosis. Alternatively, 2-dimensional and Doppler echocardiography findings can be used to identify the location and
severity of the left-to-right shunt.

Rapid stabilization using IABP and pharmacologic measures, followed by emergent surgical repair, is life saving. The
timing of surgical intervention is controversial, but most experts suggest operative repair within 48 hours of the rupture.
Ventricular septal rupture portends a poor prognosis unless management is aggressive. Immediate surgical repair of
patients with ventricular septal rupture is reported to be associated with survival rates of 42-75%; therefore, prompt
surgical therapy is imperative as soon as possible after the diagnosis of ventricular septal rupture is confirmed.
Reversible myocardial dysfunction

Other causes of severe reversible myocardial dysfunction are sepsis-associated myocardial depression, myocardial
depression following cardiopulmonary bypass, or inflammatory myocarditis. In older literature, this presentation is often
referred to as cold septic shock. In these situations, myocardial dysfunction occurs from the effects of inflammatory
cytokines, such as tumor necrosis factor and interleukin-1.

Myocardial dysfunction may vary from mild to severe and may lead to cardiogenic shock. For patients in cardiogenic
shock, cardiovascular support with inotropic agents may be required until recovery, which generally occurs after the
underlying disease process resolves.
Multimedia
Media file 1: This ECG shows evidence of an extensive anterolateral myocardial infarction; this patient
subsequently developed cardiogenic shock.
Media file 2: Same patient as in Image 1. ECG tracing shows further evolutionary changes in a patient with
cardiogenic shock.
Media file 3: In contrast to the patient in images 1 and 2, another patient developed cardiogenic shock secondary
to pericarditis and pericardial tamponade.
Media file 4: A 63-year-old man admitted to the emergency department with clinical features of cardiogenic
shock. The ECG revealed findings indicative of wide-complex tachycardia, likely ventricular tachycardia. Following
cardioversion, his shock state improved. The cause of ventricular tachycardia was myocardial ischemia.
Media file 5: Patient with an acute anterolateral myocardial infarction who developed cardiogenic shock. Coronary
angiography images showed severe stenosis of the left anterior descending coronary artery, which was dilated by
percutaneous transluminal coronary angioplasty.
Media file 6: A coronary angiogram image of a patient with cardiogenic shock demonstrates severe stenosis of the
left anterior descending coronary artery.
Media file 7: Same patient as in Image 6. Following angioplasty of the critical stenosis, coronary flow is
reestablished. The patient recovered from cardiogenic shock.
Media file 8: Echocardiogram image from a patient with cardiogenic shock shows enlarged cardiac chambers; the
motion study showed poor left ventricular function. Courtesy of R. Hoeschen, MD.
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Keywords
cardiogenic shock, cardiac failure, heart failure, myocardial infarction, MI, ST-elevation MI, ST-elevation myocardial infarction, STEMI,
non–ST-elevation acute coronary syndrome, NSTEMI, unstable angina, myocardial ischemia, heart attack, cardiac dysfunction, acute
myocarditis, sustained arrhythmia, acute valvular catastrophe, end-stage cardiomyopathy, coronary artery disease, CAD, myocardial
pathology, myocardial stunning, hibernating myocardium, systolic dysfunction, diastolic dysfunction, valvular dysfunction, cardiac
arrhythmias, mechanical heart complications, left ventricular end-systolic pressure-volume curve, curvilinear diastolic pressure-volume
curve, shock state, hemodynamic support, vasopressor supportive therapy, inotropic supportive therapy, thrombolytic therapy, intra-aortic
balloon pump, ventricular assist device, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting, coronary artery
bypass grafting, shock trial
Contributor Information and Disclosures
Author
Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of
Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of
Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical
Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and
World Medical Association
Disclosure: Nothing to disclose.
Coauthor(s)
Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School;
Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians,
American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.
Medical Editor
Russell F Kelly, MD, Program Director, Assistant Professor, Department of Internal Medicine, Division of Cardiology, Cook County
Hospital, Rush Medical College
Russell F Kelly, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Managing Editor
Ronald J Oudiz, MD, FACP, FACC, Associate Professor of Medicine, Division of Cardiology, The David Geffen School of Medicine at
UCLA; Director, Liu Center for Pulmonary Hypertension, LA Biomedical Research Institute at Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC is a member of the following medical societies: American College of Cardiology, American College of
Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials +
honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United
Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx Clinical
Trials + honoraria
CME Editor
Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of
Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association,
American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal
Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.
Chief Editor
Thomas G Di Salvo, MD, Associate Professor of Medicine, Medical Director, Vanderbilt Heart and Vascular Institute, Vanderbilt
University Medical Center
Disclosure: Nothing to disclose.
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