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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.
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.)
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.)
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
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
Distributive 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.
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.
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.
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.
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.
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.
Shock state
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
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.
Ischemia/MI
Global hypoxemia
Valvular disease
Myocardial contusion
Respiratory acidosis
Severe myocarditis
Diastolic dysfunction
Ischemia
Ventricular hypertrophy
Restrictive cardiomyopathy
Ventricular interdependence
External compression by pericardial tamponade
Increased afterload, which can impair cardiac function, can be caused by the following:
Aortic stenosis
Hypertrophic cardiomyopathy
Malignant hypertension
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
Tamponade
Decreased contractility
RV infarction
Ischemia
Hypoxia
Acidosis
Afterload increase associated with RV failure can result from the following:
Pulmonary fibrosis
Sleep-disordered breathing
Arrhythmias
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]
International statistics
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%
Asians/others - 37.6%
Mortality rates are similar for patients with cardiogenic shock secondary to STEMI or
NSTACS. [15, 16]
Cardiopulmonary arrest
Dysrhythmia
Renal 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
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
Andrew Lenneman
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
Ethan S Brandler, MD, MPH is a member of the following medical societies: American
College of Emergency Physicians and Society for Academic Emergency Medicine
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
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
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
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