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Practice Essentials

The clinical definition of cardiogenic shock is decreased cardiac output and evidence of
tissue hypoxia in the presence of adequate intravascular volume. Cardiogenic shock is the
leading cause of death in acute myocardial infarction (MI), with mortality rates as high as 70-
90% in the absence of aggressive, highly experienced technical care. See the image below.

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.
View Media Gallery
Signs and symptoms
The diagnosis of cardiogenic shock can sometimes be made at the bedside by observing the
following:
Hypotension
Absence of hypovolemia
Clinical signs of poor tissue perfusion (ie, oliguria, cyanosis, cool extremities, altered
mentation)
Findings on physical examination include the following:
Skin is usually ashen or cyanotic and cool; extremities are mottled
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 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
Ultimately, patients develop systemic hypotension (ie, systolic blood pressure below
90 mm Hg or a decrease in mean blood pressure by 30 mm Hg)
See Clinical Presentation for more detail.
Diagnosis
Laboratory studies
Biochemical profile
CBC
Cardiac enzymes (eg, creatine kinase and CK-MB, troponins, myoglobin, LDH)
Arterial blood gases
Lactate
Brain natriuretic peptide
Imaging studies
Echocardiography should be performed early to establish the cause of cardiogenic
shock
Chest radiographic findings are useful for excluding other causes of shock or chest
pain (eg, aortic dissection, tension pneumothorax, pneumomediastinum)
Ultrasonography can be used to guide fluid management
Coronary angiography is urgently indicated in patients with myocardial ischemia or
MI who also develop cardiogenic shock
Electrocardiography
Perform electrocardiography immediately to help diagnose MI and/or myocardial
ischemia
A normal ECG, however, does not rule out the possibility of acute MI
Invasive hemodynamic monitoring
Swan-Ganz catheterization is very useful for helping exclude other causes and types
of shock (eg, volume depletion, obstructive shock, and shock)
The hemodynamic measurements of cardiogenic shock are a pulmonary capillary
wedge pressure (PCWP) greater than 15 mm Hg and a cardiac index less than 2.2
L/min/m 2
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 by ECG criteria, indicate right ventricular infarction
See Workup for more detail.
Management
Cardiogenic shock is an emergency requiring the following:
Fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema
is present
Prompt initiation of pharmacologic therapy to maintain blood pressure and cardiac
output
Admission to an intensive care setting (eg, cardiac catheterization suite or ICU or
critical care transport to a tertiary care center)
Early and definitive restoration of coronary blood flow; at present, this represents
standard therapy for patients with cardiogenic shock due to myocardial ischemia
Correction of electrolyte and acid-base abnormalities (eg, hypokalemia,
hypomagnesemia, acidosis)
Invasive procedures include the following:
Placement of a central line may facilitate volume resuscitation, provide vascular
access for multiple infusions, and allow invasive monitoring of central venous
pressure
An arterial line may be placed to provide continuous blood pressure monitoring
An intra-aortic balloon pump may be placed as a bridge to percutaneous coronary
intervention (PCI) or coronary artery bypass grafting (CABG)
Pharmacologic therapy
Patients with MI or acute coronary syndrome are given aspirin and heparin
Inotropic and/or vasopressor drug therapy may be necessary in patients with
inadequate tissue perfusion and adequate intravascular volume, so as to maintain
mean arterial pressure (MAP) of 60 or 65 mm Hg
Diuretics are used to decrease plasma volume and peripheral edema
Features of dopamine are as follows:
Dopamine is the drug of choice to improve cardiac contractility in patients with
hypotension
Dopamine may increase myocardial oxygen demand
Dopamine is usually initiated at a rate of 5-10 mcg/kg/min IV
The infusion rate is adjusted according to the blood pressure and other hemodynamic
parameters
Often, patients may require doses as high as 20 mcg/kg/min
Features of dobutamine are as follows:
Dobutamine may be preferable to dopamine if the systolic blood pressure is higher
than 80 mm Hg
Compared with dopamine, dobutamine has less effect on myocardial oxygen demand
Tachycardia from dobutamine may preclude its use in some patients
If the patient remains hypotensive despite moderate doses of dopamine, a direct
vasoconstrictor may be administered, as follows:
Norepinephrine is started at a dose of 0.5 mcg/kg/min and titrated to maintain an
MAP of 60 mm Hg
The dose of norepinephrine may vary from 0.2-1.5 mcg/kg/min
Doses as high as 3.3 mcg/kg/min have been used
Phosphodiesterase inhibitors (eg, inamrinone [formerly amrinone], milrinone) are inotropic
agents with vasodilating properties and long half-lives that are beneficial in patients with
cardiac pump failure, but they may require concomitant vasopressor administration
PCI and CABG
Either PCI or CABG is the treatment of choice for cardiogenic shock
PCI should be initiated within 90 minutes after presentation
PCI remains helpful, as an acute intervention, within 12 hours after presentation
Thrombolytic therapy is second best but should be considered if PCI and CABG are
not immediately available
See Treatment and Medication for more detail.
Background
Cardiogenic shock is a physiologic state in which inadequate tissue perfusion results from
cardiac dysfunction, most often systolic. It is a major, and frequently fatal, complication of a
variety of acute and chronic disorders, occurring most commonly following acute myocardial
infarction (MI). (See Pathophysiology, Etiology, and Prognosis.)
Although ST-segment elevation MI (STEMI, previously termed Q-wave MI) is encountered
in most patients, cardiogenic shock may also develop in patients with non ST-segment
elevation acute coronary syndrome (NSTEMI, NSTACS, or unstable angina). (See the image
below.)

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.
View Media Gallery

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 30
min) and a reduced cardiac index (<2.2 L/min/m2) in the presence of normal or elevated
pulmonary capillary wedge pressure (>15 mm Hg) or right ventricular end-diastolic pressure
(RVEDP) (>10 mm Hg). (See DDx, Workup.)

Cardiogenic shock continues to be a difficult clinical problem; the management of this


condition requires a rapid and well-organized approach. (See Prognosis, Treatment, and
Medication.)

The diagnosis of cardiogenic shock may be made at the bedside by observing hypotension,
absence of hypovolemia, 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. (See
Presentation, DDx.)

Types of circulatory shock

Shock is identified in most patients on the basis of 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 four distinct classes according to
the underlying mechanism and characteristic hemodynamic findings. In all patients, before a
definite diagnosis of septic shock is established, the following four classes of shock should be
considered and systematically differentiated. (See Pathophysiology, Etiology, Presentation
and Workup.)

Cardiogenic shock

Cardiogenic shock characterized by primary myocardial dysfunction renders 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.

Hypovolemic shock

Hypovolemic shock results from loss of blood volume, the possible reasons for which include
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.

Patient education

Patients should receive instruction regarding the early warning signs of acute MI and how to
access the emergency medical system (eg, calling 911).

Patients must also be instructed on cardiac risk factors, particularly those that are reversible
and subject to change (eg, smoking, diet, exercise).

For patient education information, see the First Aid and Injuries Center and the Healthy
Living Center, as well as Shock and Cardiopulmonary Resuscitation (CPR).
Pathophysiology
Cardiogenic shock is recognized as a low-cardiac-output state secondary to extensive left
ventricular (LV) infarction, development of a mechanical defect (eg, ventricular septal defect
or papillary muscle rupture), or right ventricular (RV) infarction.

Autopsy studies show that cardiogenic shock is generally associated with the loss of more
than 40% of the LV myocardial muscle. [1] The pathophysiology of cardiogenic shock in the
setting of coronary artery disease, is described below.

Myocardial pathology

Cardiogenic shock is characterized by systolic and diastolic dysfunction leading to end organ
hypoperfusion. The interruption of blood flow in an epicardial coronary artery causes the
zone of myocardium supplied by that vessel to lose the ability to shorten and perform
contractile work. If a sufficient area of myocardium undergoes ischemic injury, LV pump
function become depressed and systemic hypotension develops.

Patients who develop cardiogenic shock from acute MI consistently have evidence of
progressive myocardial necrosis with infarct extension. Decreased coronary perfusion
pressure and cardiac output as well as increased myocardial oxygen demand play a role in the
vicious cycle that leads to cardiogenic shock and potentially death. [2]

Patients suffering from cardiogenic shock 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
decreases myocardial compliance and impairs filling, thereby increasing LV filling pressure
and leading 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 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

Large areas of myocardium that are dysfunctional but still viable can contribute to the
development of cardiogenic shock in patients with MI. This potentially reversible dysfunction
is often described as myocardial stunning or as hibernating myocardium. Although
hibernation is considered a different physiologic process than myocardial stunning, the
conditions are difficult to distinguish in the clinical setting and they often coexist.

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 of 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.

Cardiovascular mechanics of cardiogenic shock

Cardiogenic shock is the most severe clinical expression of LV failure. The primary
mechanical defect in cardiogenic shock is a shift to the right for the LV end-systolic pressure-
volume curve, 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
degree to which LV end systolic volume increases is a powerful hemodynamic predictor of
mortality following STEMI. [3]

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 and increased LV end-diastolic pressure. The attempt to enhance cardiac
output by this mechanism comes at the cost of having a higher LV diastolic filling pressure,
which ultimately increases myocardial oxygen demand and can lead to pulmonary edema.

As a result of decreased contractility, the patient develops elevated LV 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 LV myocardium becomes ischemic and fails to pump effectively,
stroke volume and cardiac output are curtailed. The LV pump function becomes depressed;
cardiac output, stroke volume, and blood pressure decline while end-systolic volume
increases. [4] Myocardial ischemia is further exacerbated by impaired myocardial perfusion
due to hypotension and tachycardia.

The LV pump failure increases ventricular diastolic pressures concomitantly, causing


additional wall stress and thereby 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 (lactic
acidosis), 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 [5] and causes renal salt and fluid retention, hence augmenting the
LV preload. The elevated heart rate and contractility increases myocardial oxygen demand,
further worsening myocardial ischemia.

Fluid retention and impaired LV diastolic filling triggered by tachycardia and ischemia
worsen 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. [2]

Usually, a combination of systolic and diastolic myocardial dysfunction is present in patients


with cardiogenic shock. Metabolic derangements that impair myocardial contractility further
compromise systolic ventricular function. Myocardial ischemia decreases myocardial
compliance, thereby elevating LV filling pressure at a given end-diastolic volume (diastolic
dysfunction), which leads to pulmonary congestion and congestive heart failure.

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.

Etiology
Cardiogenic shock can result from the following types of cardiac dysfunction:

Systolic dysfunction

Diastolic dysfunction

Valvular dysfunction

Cardiac arrhythmias

Coronary artery disease

Mechanical complications

The vast majority of cases of cardiogenic shock in adults are due to acute myocardial
ischemia. Indeed, cardiogenic shock is generally associated with the loss of more than 40% of
the LV myocardium, although in patients with previously compromised LV function, even a
small infarction may precipitate shock. Cardiogenic shock is more likely to develop in people
who are elderly or diabetic or in persons who have had a previous inferior MI.

Complications of acute MI, such as acute mitral regurgitation, large RV infarction, rupture of
the interventricular septum or LV free wall, and tamponade can result in cardiogenic shock.
Conduction abnormalities (eg, atrioventricular blocks, sinus bradycardia) are also risk factors.

Many cases of cardiogenic shock occurring after acute coronary syndromes may be due to
medication administration. The use of beta blockers and angiotensin-converting enzyme
(ACE) inhibitors in acute coronary syndromes must be carefully timed and monitored. [2, 6, 7]

In children, preceding viral infection may cause myocarditis. In addition, children and infants
may have unrecognized congenital structural heart defects that are well compensated until
there is a stressor. These etiologies plus toxic ingestions make up the three primary causes of
cardiogenic shock in children.

A systemic inflammatory response syndrometype mechanism has also been implicated in


the etiology of cardiogenic shock. Elevated levels of white blood cells, body temperature,
complement, interleukins, and C-reactive protein are often seen in large myocardial
infarctions. Similarly, inflammatory nitric oxide synthetase (iNOS) is also released in high
levels during myocardial stress. Nitric oxide production induced by iNOS may uncouple
calcium metabolism in the myocardium resulting in a stunned myocardium. Additionally,
iNOS leads to the expression of interleukins, which may themselves cause hypotension.

Left ventricular failure


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 causes of systolic dysfunction leading to cardiogenic shock can be
summarized as follows:

Ischemia/MI

Global hypoxemia

Valvular disease

Myocardial depressant drugs (eg, beta blockers, calcium-channel blockers, and


antiarrhythmics)

Myocardial contusion

Respiratory acidosis

Metabolic derangements (eg, acidosis, hypophosphatemia, and hypocalcemia)

Severe myocarditis

End-stage cardiomyopathy (including valvular causes)

Prolonged cardiopulmonary bypass.

Cardiotoxic drugs (eg, doxorubicin [Adriamycin])

Diastolic dysfunction

Increased LV diastolic chamber stiffness contributes to cardiogenic shock during cardiac


ischemia, as well as 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 can be summarized as
follows:

Ischemia

Ventricular hypertrophy

Restrictive cardiomyopathy

Prolonged hypovolemic or septic shock

Ventricular interdependence
External compression by pericardial tamponade

Greatly increased afterload

Increased afterload, which can impair cardiac function, can be caused by the following:

Aortic stenosis

Hypertrophic cardiomyopathy

Dynamic aortic outflow tract obstruction

Coarctation of the aorta

Malignant hypertension

Valvular and structural abnormality

Valvular dysfunction may immediately lead to cardiogenic shock, or it 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 a
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.

Valvular and structural abnormalities associated with cardiogenic shock include the
following:

Mitral stenosis

Endocarditis

Mitral aortic regurgitation

Obstruction due to atrial myxoma or thrombus

Papillary muscle dysfunction or rupture

Ruptured septum or free wall arrhythmias

Tamponade

Decreased contractility

Reduced myocardial contractility can result from the following:

RV infarction
Ischemia

Hypoxia

Acidosis

Right ventricular failure

Greatly increased afterload

Afterload increase associated with RV failure can result from the following:

Pulmonary embolism (PE)

Pulmonary vascular disease (eg, pulmonary arterial hypertension and veno-occlusive


disease)

Hypoxic pulmonary vasoconstriction

Peak end-expiratory pressure (PEEP)

High alveolar pressure

Acute respiratory distress syndrome (ARDS)

Pulmonary fibrosis

Sleep-disordered breathing

Chronic obstructive pulmonary disease (COPD)

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.

Epidemiology
United States statistics

The incidence rate of cardiogenic shock ranges from 5% to 10% in patients with acute MI. [8]
In the Worcester Heart Attack Study, a community-wide analysis, the reported incidence rate
was 7.5%. [9] The literature contains few data on cardiogenic shock in patients without
ischemia.
A 2014 review of the 2003-2010 Nationwide Inpatient Sample (NIS) databases revealed a
7.9% incidence in patients with STEMI. [8] Overall, of cases with cardiogenic shock and
STEMI, 42.3% were located in the anterior wall, 38.6% in the inferior wall, and 19.1% at
other sites. [8]

As many as 3% of patients with NSTACS develop cardiogenic shock. [10]

International statistics

Several multicenter thrombolytic trials in Europe reported a prevalence rate of cardiogenic


shock following MI of approximately 7%.

Race-, sex-, and age-related demographics

Asian/Pacific Islanders have a higher incidence of cardiogenic shock (11.4%) than white
(8%), black (6.9%), and Hispanic (8.6%) patients. [8]

Although the overall incidence of cardiogenic shock has traditionally been higher in men than
in women, a difference resulting from the increased prevalence of coronary artery disease in
males, the 2003-2010 NIS data revealed women had a higher overall incidence of cardiogenic
shock (8.5%) than men (76%) during this period. [8] Moreover, a higher percentage of female
patients with MI developed cardiogenic shock than did males with MI. [8]

Median age for cardiogenic shock mirrors the bimodal distribution of disease. For adults, the
median age ranges from 65-66 years. For children, cardiogenic shock presents as a
consequence of fulminant myocarditis or congenital heart disease.

Overall, the 2003-2010 NIS data revealed patients aged 75 years and older suffered
cardiogenic shock more often than those younger than 75 years. [8]

Prognosis
Cardiogenic shock is the leading cause of death in acute MI. [11] 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. [12, 13, 14] Thus, with the implementation of prompt
revascularization, improved interventional procedures, and better medical therapies and
mechanical support devices, the mortality rates from cardiogenic shock may continue to
decline.

The overall in-hospital mortality rate for patients with cardiogenic shock is 39%. [8] For
persons 75 years and older, the mortality rate is 55%; for those younger than 75 years, it is
29.8%. For women, it is 44.4% compared to 35.5% in men. [8]

Race-stratified inpatient mortality rates from cardiogenic shock are as follows (race-based
mortality differences persisted even after adjustment for early mechanical revascularization
status) [8] :
Hispanic patients - 40.6%

Black patients - 39.9%

White patients - 38.9%

Asians/others - 37.6%

Mortality rates are similar for patients with cardiogenic shock secondary to STEMI or
NSTACS. [15, 16]

Evidence of RV dilatation on an echocardiogram may indicate a worse outcome in patients


with cardiogenic shock, as may RV infarction on a right-side electrocardiogram. [17] 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.

Morbidity and mortality

Complications of cardiogenic shock may include the following:

Cardiopulmonary arrest

Dysrhythmia

Renal failure

Multisystem organ failure

Ventricular aneurysm

Thromboembolic sequelae

Stroke

Death

The following predictors of mortality were identified from the Global Utilization of
Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I)
trial [18] :

Increasing age

Prior MI

Altered sensorium

Cold, clammy skin


Oliguria

Echocardiographic findings such as LV ejection fraction (LVEF) and mitral regurgitation are
independent predictors of mortality. An ejection fraction of less than 28% has been associated
with a survival rate of 24% at 1 year, compared to a survival rate of 56% with a higher
ejection fraction. [19] Moderate or severe mitral regurgitation was found to be associated with a
1-year survival rate of 31%, compared to a survival rate of 58% in patients with no
regurgitation. [19] The time to reperfusion is an important predictor of mortality in acute MI
complicated by cardiogenic shock. In patients with shock, the in-hospital mortality rate
increased progressively with increasing time-to-reperfusion.

Outcomes in cardiogenic shock significantly improve only when rapid revascularization can
be achieved. The SHOCK (Should We Emergently Revascularize Occluded Coronaries for
Cardiogenic Shock?) trial demonstrated that overall mortality when revascularization occurs
is 38%. [20] When rapid revascularization is not attempted, mortality rates approach 70%.
Rates vary depending on the procedure (eg, percutaneous transluminal coronary angioplasty,
stent placement, thrombolytic therapy).

Author

Xiushui (Mike) Ren, MD Cardiologist, The Permanente Medical Group; Associate Director
of Research, Cardiovascular Diseases Fellowship, California Pacific Medical Center
Xiushui (Mike) Ren, MD is a member of the following medical societies: Alpha Omega
Alpha, American College of Cardiology, American Society of Echocardiography

Disclosure: Nothing to disclose.


Coauthor(s)

Andrew Lenneman

Disclosure: Nothing to disclose.


Chief Editor

Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant
Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine,
Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.


Acknowledgements

Ethan S Brandler, MD, MPH Clinical Assistant Professor, Attending Physician,


Departments of Emergency Medicine and Internal Medicine, University Hospital of
Brooklyn, Kings County Hospital

Ethan S Brandler, MD, MPH is a member of the following medical societies: American
College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard
Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General
Hospital

David FM Brown, MD is a member of the following medical societies: American College of


Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency
Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of
Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies:
American Academy of Clinical Toxicology, American Academy of Emergency Medicine,
American Academy of Pediatrics, American College of Emergency Physicians, and
Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Mark A Hostetler, MD, MPH Associate Professor of Pediatrics, University of Chicago;


Chief, Section of Emergency Medicine, Department of Pediatrics, Medical Director of
Pediatric Emergency Department, University of Chicago Children's Hospital

Disclosure: Nothing to disclose.

A Antoine Kazzi MD, Deputy Chief of Staff, American University of Beirut Medical Center;
Associate Professor, Department of Emergency Medicine, American University of Beirut,
Lebanon

A Antoine Kazzi is a member of the following medical societies: American Academy of


Emergency Medicine

Disclosure: Nothing to disclose.

Russell F Kelly MD, Assistant Professor, Department of Internal Medicine, Rush Medical
College; Chairman of Adult Cardiology and Director of the Fellowship Program, Cook
County Hospital

Russell F Kelly is a member of the following medical societies: American College of


Cardiology

Disclosure: Nothing to disclose.

Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of


California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for
Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at
Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC, FCCP 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; Bayer Grant/research funds Consulting

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.

Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant


Professor of Medicine, Research Director, State University of New York College of
Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital
Center

Richard H Sinert, DO is a member of the following medical societies: American College of


Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska


Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment