Shock, Cardiogenic



Ethan S Brandler, MD, MPH, Clinical Assistant Professor, Attending Physician, Departments of Emergency Medicine and Internal Medicine, University Hospital of Brooklyn, Kings County Hospital

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

Nothing to disclose.

Specialty Editor(s)

A Antoine Kazzi, MD, Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon

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

Talecris Biotherapeutics Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

eMedicine Salary Employment

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

Nothing to disclose.

Chief Editor

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

Nothing to disclose.


Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state (ie, global hypoperfusion). It most commonly occurs in association with, and as a direct result of, acute myocardial infarction (AMI).

Similar to other shock states, cardiogenic shock is considered to be a clinical diagnosis characterized by decreased urine output, altered mentation, and hypotension. Other clinical characteristics include jugular venous distension, cardiac gallop, and pulmonary edema. The most recent prospective study of cardiogenic shock defines cardiogenic shock as sustained hypotension (systolic blood pressure [BP] less than 90 mm Hg lasting more than 30 min) with evidence of tissue hypoperfusion with adequate left ventricular (LV) filling pressure.[1] Tissue hypoperfusion was defined as cold peripheries (extremities colder than core), oliguria (< 30 mL/h), or both.

For related information, see Medscape's Cardiology Resource Centers.


The most common initiating event in cardiogenic shock is AMI. Dead myocardium does not contract, and classical teaching has been that when more than 40% of the myocardium is irreversibly damaged (particularly, the anterior cardiac wall), cardiogenic shock may result. On a mechanical level, a marked decrease in contractility reduces the ejection fraction and cardiac output. These lead to increased ventricular filling pressures, cardiac chamber dilatation, and ultimately univentricular or biventricular failure that result in systemic hypotension and/or pulmonary edema. The SHOCK trial, however, demonstrated that left ventricular ejection fraction is not always depressed in the setting of cardiogenic shock. Additional surprising findings included nonelevated systemic vascular resistance on vasopressors and that most survivors have only New York Heart Association (NYHA) class I congestive heart failure.

A systemic inflammatory response syndrome–type mechanism has been implicated in the pathophysiology 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. iNOS induces nitric oxide production, which 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.

Myocardial ischemia causes a decrease in contractile function, which leads to left ventricular dysfunction and decreased arterial pressure; these, in turn, exacerbate the myocardial ischemia. The end result is a vicious cycle that leads to severe cardiovascular decompensation. Other pathophysiological mechanisms responsible for cardiogenic shock include papillary muscle rupture leading to acute mitral regurgitation (4.4%); decreased forward flow, ejection fraction, and ventricular septal defect (1.5%); and free wall rupture (4.1%) as a consequence of AMI.

Right ventricular (RV) infarct, by itself, may lead to hypotension and shock because of reduced preload to the left ventricle. The management of RV infarcts is discussed elsewhere but should be considered in the setting of inferior wall MI.

Cardiac tamponade may result as a consequence of pericarditis, uremic pericardial effusion, or in rare cases systemic lupus erythematosus.

Whenever patients who present in shock have been exposed to medications that may cause hypotension, these drugs should be considered as possible culprits in the disease. Calcium channel blockers may cause profound hypotension with a normal or elevated heart rate. Beta-blocking agents may also cause hypotension. Hypotension can be seen with or without bradycardia, or AV node block can be seen with either of these types of medications. If these medications are the culprits, therapy directed at these toxicities is beneficial. Nitroglycerin, angiotensin-converting enzyme inhibitors, opiate, and barbiturates can all cause a shock state and may be difficult to distinguish from cardiogenic shock.

Initiating events other than AMI and ischemia include infection, drug toxicity, and pulmonary embolus.

For children, the causes of cardiogenic shock are vastly different. The 3 primary causes of cardiogenic shock in children and infants are viral myocarditis, congenital heart disease, and toxic ingestions. For details, see eMedicine's Pediatric Critical Care Medicine article on Shock.



United States

Cardiogenic shock occurs in 8.6% of patients with ST-segment elevation MI with 29% of those presenting to the hospital already in shock. It occurs only in 2% of patients with non–ST-segment elevation MI.


Cardiogenic shock is the leading cause of death in acute myocardial infarction (AMI).



Women comprise 42% of all patients with cardiogenic shock.


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.


Most patients with cardiogenic shock have an AMI and, therefore, present with the constellation of symptoms of acute cardiac ischemia (eg, chest pain, shortness of breath, diaphoresis, nausea, vomiting). Patients experiencing cardiogenic shock also may present with pulmonary edema, acute circulatory collapse, and presyncopal or syncopal symptoms.

View Video

Pleural sliding in an intercostal space demonstrating increased lung comet artifacts suggestive of pulmonary edema. Courtesy of Michael Stone, MD, RDMS.

Pediatric patients may present with listlessness, decreased feeding, and tachypnea.


The physical examination findings are consistent with shock. Patients are in frank distress, are profoundly diaphoretic with mottled extremities, and are usually visibly dyspneic. Clinical assessment begins with attention to the ABCs and vital signs.


The vast majority of cases of cardiogenic shock in adults are due to acute myocardial ischemia. Many cases of cardiogenic shock occurring after acute coronary syndromes may be due to medication administration. The use of beta-blockers and ACE inhibitors in acute coronary syndromes must be carefully timed and monitored.[5, 6, 7]

Laboratory Studies

No one test is completely sensitive or specific for cardiogenic shock. Laboratory studies are directed at the potential underlying cause.

In most cases, the usual workup includes tests of all of the following, which usually are assessed in cases of suspected cardiac ischemia:

Imaging Studies

A portable chest radiograph is helpful because it gives an overall impression of the cardiac size, pulmonary vascularity, and coexistent pulmonary pathology, and it provides a rough estimate of mediastinal and aortic sizes in the event that an aortic etiology is being considered.

Other Tests


Prehospital Care

Prehospital care is aimed at minimizing any further ischemia and shock.

Emergency Department Care

ED care of cardiogenic shock is aimed at making the diagnosis, preventing further ischemia, and treating the underlying cause. Treatment of the underlying cause is directed in the case of acute myocardial infarction (AMI) at coronary artery reperfusion. This is best accomplished with rapid transfer of the patient to a cardiac catheterization laboratory.

Clinicians should be alert to the fact that the SHOCK trial demonstrated that percutaneous coronary intervention (PCI) or coronary artery bypass are the treatments of choice and that they have been shown to markedly decrease mortality rates at 1 year. PCI should be initiated within 90 minutes of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation. If such a facility is not immediately available, thrombolytics should be considered. However, this treatment is second best. An increased mortality is seen in situations where thrombolytics are used instead of PCI. This is due to the relative ineffectiveness of the thrombolytic medications to lyse clots in low blood pressure situations.[10, 5]

Treatment begins with assessment and management of the ABCs.

The airway should be assessed for patency and breathing evaluated for effectiveness and increased work of breathing. Endotracheal intubation and mechanical ventilation should be considered for patients with excessive work of breathing. Positive pressure ventilation may improve oxygenation but may also compromise venous return, preload, to the heart. In any event, the patient should be treated with high-flow oxygen. Recent studies in patients with acute cardiogenic pulmonary edema have shown noninvasive ventilation to improve hemodynamics and reduce the intubation rate. Mortality is, however, unaffected.

Other interventions are directed at supporting myocardial perfusion and maximizing cardiac output. Intravenous fluids should be provided to maintain adequate preload. The administration of such fluids should be guided by central venous pressure, pulmonary capillary wedge pressure monitoring, or sonographic assessment of IVC filling.

Anticoagulants and aspirin should be used as in other cases of acute myocardial infarctions. Care should be taken to ensure that the patient does not have myocardial wall rupture that is amenable to surgery before initiating therapy. There is no need to start clopidogrel until after angiography as this may determine a need for urgent coronary bypass.[5]

Intravenous vasopressors provide inotropic support increasing perfusion of the ischemic myocardium and all body tissues. However, extreme heart rates should be avoided because they may increase myocardial oxygen consumption, increase infarct size, and further impair the pumping ability of the heart. No particular vasopressor has been shown to be superior to another. Carefully chosen combinations of pressors may be useful.[11, 12]

Nitrates and/or morphine are advised for the management of pain; however, they must be used with caution because these patients are in shock, and excessive use of either of these agents can produce profound hypotension. Neither of these options has been shown to improve outcomes in cardiogenic shock.

Other supportive medications to be considered include nesiritide (Natrecor) and levosimendan.

Mechanical device supports may be used to support patients in cardiogenic shock.


Consult a cardiologist at the earliest opportunity because his or her insight and expertise may be invaluable for facilitating echocardiographic support, placement of an IABP, and transfer to more definitive care (eg, cardiac catheterization suite, intensive care unit, operating room). In severe cases, also consider discussing the case with a cardiothoracic surgeon.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Class Summary

These drugs augment both coronary and cerebral blood flow present during the low-flow state associated with shock. Sympathomimetic amines with both alpha-adrenergic and beta-adrenergic effects are indicated. Dopamine and dobutamine are the drugs of choice to improve cardiac contractility.

Norepinephrine (Levophed)

Clinical Context:  Naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. Stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. Increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia. Generally reserved for use in patients with severe hypotension (eg, systolic blood pressure < 70 mm Hg) or hypotension unresponsive to other medication.

Dopamine (Intropin)

Clinical Context:  Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that, in turn, produce renal and mesenteric vasodilation. Higher doses cause cardiac stimulation and renal vasodilation.

Dobutamine (Dobutrex)

Clinical Context:  Sympathomimetic amine with stronger beta effects than alpha effects. Produces vasodilation and increases inotropic state. Higher doses may increase heart rate, exacerbating myocardial ischemia.

Class Summary

These agents improve cardiac output in refractory hypotension and shock. Milrinone and inamrinone (formerly amrinone) may be used.

Milrinone (Primacor)

Clinical Context:  Bipyridine with positive inotropic and vasodilator effects; little chronotropic activity; mode of action differs from that of digitalis glycosides and catecholamines.

Inamrinone (Inocor)

Clinical Context:  Phosphodiesterase inhibitor with positive inotropic and vasodilator activity. Produces vasodilation and increases inotropic state. More likely than dobutamine to cause tachycardia; may exacerbate myocardial ischemia.

Class Summary

Agents that irreversibly inhibit platelet aggregation may improve morbidity.

Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin)

Clinical Context:  Odorless white powdery substance available in 81 mg, 325 mg, and 500 mg for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids.

Stronger inhibitor of both prostaglandin synthesis and platelet aggregation than other salicylic acid derivatives. Acetyl group is responsible for inactivation of cyclooxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics.

Irreversibly inhibits platelet aggregation by inhibiting platelet cyclooxygenase. This, in turn, inhibits conversion of arachidonic acid to PGI2 (potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (potent vasoconstrictor and platelet aggregate). Platelet-inhibition lasts for life of cell (approximately 10 d). May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis. Reduces likelihood of myocardial infarction. Also very effective in reducing risk of stroke. Early administration of aspirin in patients with AMI may reduce cardiac mortality in first mo.

Class Summary

Smooth-muscle relaxers and vasodilators that can reduce systemic vascular resistance, allowing more forward flow and improving cardiac output.

Nitroglycerin IV (Nitro-Bid)

Clinical Context:  Relaxes vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production to decrease BP.

Class Summary

Pain control is essential to quality patient care. It ensures patient comfort and promotes pulmonary toilet.

Morphine sulfate (Duramorph, MS Contin)

Clinical Context:  DOC for analgesia because of reliable and predictable effects, safety profile, and ease of reversibility with naloxone.

Class Summary

These drugs cause diuresis to decrease plasma volume and edema and thereby decrease cardiac output BP. The initial decrease in cardiac output causes a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, extracellular fluid and plasma volumes almost return to pretreatment levels. Peripheral vascular resistance decreases below that of pretreatment baseline.

Furosemide (Lasix)

Clinical Context:  Inhibits reabsorption of sodium and chloride in the ascending loop of Henle and distal renal tubule; this inhibition interferes with the chloride-binding cotransport system, causing increased excretion of water, sodium, chloride, magnesium, and calcium.

Class Summary

These drugs cause arterial and venous dilation by binding to cyclic GMP receptor on vascular smooth muscle causing smooth muscle relaxation. This medication produces dose-dependent decreases in pulmonary capillary wedge pressure and systemic arterial pressure.

Nesiritide (Natrecor)

Clinical Context:  Recombinant DNA form of human B-type natriuretic peptides (hBNP), which dilate veins and arteries.

Human BNP binds to particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells. Binding to receptor causes increase in cyclic GMP, which serves as second messenger to dilate veins and arteries. Reduces pulmonary capillary wedge pressure and improves dyspnea in patients with acutely decompensated congestive heart failure.

Further Inpatient Care

All patients require admission to an intensive care setting, which may involve emergent transfer to the cardiac catheterization suite, critical care transport to a tertiary care center, or internal transfer to the ICU.


By definition, these patients are in shock, and their condition is unstable. Attempts to transfer the patient must be made only when everything possible has been done to stabilize their condition, when the level of care during the transfer does not significantly decrease, and when a higher level of care is available at the transfer location. Remember that survival is best when PCI is performed early.



Complications of cardiogenic shock may include the following:



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Pleural sliding in an intercostal space demonstrating increased lung comet artifacts suggestive of pulmonary edema. Courtesy of Michael Stone, MD, RDMS.

Short axis view of left ventricle demonstrating small pericardial effusion, low ejection fraction, and segmental wall motion abnormalities. Courtesy of Michael Stone, MD, RDMS.

Pleural sliding in an intercostal space demonstrating increased lung comet artifacts suggestive of pulmonary edema. Courtesy of Michael Stone, MD, RDMS.