Ethan S Brandler, MD, MPH,
Clinical Assistant Professor, Attending
Physician, Departments of Emergency Medicine and Internal
Medicine, University Hospital of Brooklyn, Kings County
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
Nothing to disclose.
A Antoine Kazzi, MD,
Chair and Medical Director, Department of
Emergency Medicine, American University of Beirut,
Nothing to disclose.
Daniel J Dire, MD, FACEP, FAAP,
Clinical Professor, Department of Emergency
Medicine, University of Texas-Houston; Clinical Professor,
Department of Pediatrics, University of Texas Health Sciences
Center, San Antonio, Texas
Biotherapeutics Honoraria Speaking and
Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor,
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
Nothing to disclose.
David FM Brown, MD,
Associate Professor, Division of Emergency
Medicine, Harvard Medical School; Vice Chair, Department of
Emergency Medicine, Massachusetts General
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. 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.
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).
The overall in-hospital mortality rate is 57%. For persons older than 75 years, the mortality rate is 64.1%. For those younger than 75 years, the mortality rate is 39.5%.
Outcomes significantly improve only when rapid revascularization can be achieved. The SHOCK trial demonstrated that overall mortality when revascularization occurs is 38%. 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), but they have been reported to be as low as 30-50%.
Mortality rates have declined over time. In the National Registry of Myocardial Infarction covering the period from 1995-2004, in-hospital mortality declined from 60.3% to 47.9%. This improvement has been attributed to the increasing frequency of the use percutaneous coronary intervention (PCI) and other revascularization procedures. Mortality rates attributable to cardiogenic shock are also thought to be due to the increased frequency of use of PCI, antiplatelet therapies, and lipid-lowering agents in patients with acute coronary syndromes. This has decreased the incidence of cardiogenic shock developing in the hospital due to acute coronary syndromes. The incidence of cardiogenic shock on arrival to the hospital has not changed significantly.[3, 4]
Race-stratified mortality rates are as follows: Hispanics, 74%; African Americans, 65%; whites, 56%; and Asians/others, 41%.
Race-based differences in mortality disappear with revascularization.
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.
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.
Although the patient may eventually require endotracheal intubation, the airway usually is patent initially.
Breathing may be labored, with audible coarse crackles or wheezing.
As in any shocklike state, circulation is markedly impaired. Tachycardia, delayed capillary refill, hypotension, diaphoresis, and poor peripheral pulses are frequent findings.
Other signs of end-organ dysfunction (eg, decreased mental function, urinary output) may be present.
Initial vital sign assessment should include BP measurements in both arms to evaluate possible thoracic aortic aneurysm or dissection. Vital signs should be regularly updated with continuous noninvasive physiologic monitoring.
Neck examination may reveal jugular venous distention, which may be prominent. This finding is evidence of RV failure.
LV dysfunction, characterized by florid pulmonary edema, can be auscultated as crackles with or without wheezing.
Careful cardiac examination may reveal mechanical causes of cardiogenic shock.
Loud murmurs may indicate a valvular dysfunction, whereas muffled heart tones with jugular venous distention and pulsus paradoxus may suggest tamponade (Beck's triad).
A gallop may also be heard. The presence of an S3 heart sound is pathognomonic of congestive heart failure. The presence of pulmonary edema increases the likelihood of cardiogenic shock in the setting of hypotension.
In children, hepatomegaly may also be present. Murmurs may be difficult to detect in children and in infants due to rapid heart rates.
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]
Mechanisms not related to acute infarction include the following:
Diastolic - Ventricular hypertrophy and restrictive cardiomyopathies
After load -Aortic stenosis, hypertrophic cardiomyopathy, dynamic outflow obstruction, aortic coarctation, and malignant hypertension
Valvular/structural -Mitral stenosis, endocarditis, mitral or aortic regurgitation, atrial myxoma or thrombus, and tamponade
In children, preceding viral infection may cause myocarditis. Children and infants may have unrecognized congenital structural heart defects that are well compensated until there is a stressor.
Risk factors for the development of cardiogenic shock include preexisting myocardial damage or disease (eg, diabetes, advanced age, previous AMI), AMI (eg, Q-wave, large or anterior wall AMIs), congenital heart disease, and dysrhythmia.
Coagulation profile (eg, prothrombin time, activated partial thromboplastin time)
An ABG may be useful to evaluate acid-base balance because acidosis can have a particularly deleterious effect on myocardial function. Elevated serum lactate level is an indicator of shock.
Brain natriuretic peptide (BNP) may be useful as an indicator of congestive heart failure and as an independent prognostic indicator of survival. A low BNP level may effectively rule out cardiogenic shock in the setting of hypotension; however, an elevated BNP level does not rule in the disease.
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.
An ECG is helpful if it reveals an acute injury pattern consistent with an AMI. A normal ECG, however, does not rule out the possibility. ECGs are often most helpful when they can be compared with previous tracings.
A ECG with right-sided chest leads may document RV infarction and may be useful in prognosis in addition to diagnosis.
A bedside echocardiogram can be performed in the emergency department and may offer useful diagnostic information.
It may be diagnostic and reveal akinetic or dyskinetic areas of ventricular wall motion. Ejection fraction may also be estimated.
It may reveal surgically correctable causes, such as valvular dysfunction and tamponade.
If a hyperdynamic left ventricle is found, the echocardiogram may suggest other potentially correctable causes of shock such as sepsis or anemia.
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.
Ultrasonography can also used to guide fluid management. In the spontaneously breathing patient, inferior vena cava (IVC) collapse with respiration suggests dehydration, whereas a lack of IVC collapse suggests intravascular euvolemia.
Placement of a central line may facilitate volume resuscitation, provide vascular access for multiple infusions, and allow invasive monitoring of central venous pressure. Central venous pressure may also be used to guide fluid resuscitation.
Although not necessary for the diagnosis of cardiogenic shock, invasive monitoring with a pulmonary artery catheter may be helpful in guiding fluid resuscitation in situations in which LV preload is difficult to determine. Cardiogenic shock may be indicated by a cardiac index of less than 1.8-2.2 L/min/m2 with a pulmonary capillary wedge pressure greater than 15-18 mm Hg.
Pulmonary artery (PA) catheter pressure measurements may also be useful in prognosis. Retrospective evaluation of PA catheter measurements from the SHOCK trial demonstrate that stroke volume index (SVI) and stroke work index (SWI) vary inversely with mortality.
An arterial line may be placed to provide continuous blood pressure monitoring. This is particularly useful if the patient requires inotropic medications.
An intra-aortic balloon pump may be placed in the ED as a bridge to percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) to decrease myocardial workload and to improve end-organ perfusion.
Prehospital care is aimed at minimizing any further ischemia and shock.
All patients require intravenous access, high-flow oxygen administered by mask, and cardiac monitoring.
Twelve-lead electrocardiography performed in the field by appropriately trained paramedics may be useful in decreasing door to PCI times and/or thrombolytics because acute ST-segment elevation myocardial infarctions can be identified earlier. The ED, can thus be alerted, and may mobilize the appropriate resources.
Inotropic medications should be considered in systems with appropriately trained paramedical personnel.
When clinically necessary, positive pressure ventilation and endotracheal intubation should be performed.
Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) support can be considered in appropriately equipped systems.
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.
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]
Dopamine may provide vasopressor support. With higher doses, it has the disadvantage of increasing the heart rate and myocardial oxygen consumption.
Dobutamine, inamrinone (formerly amrinone), or milrinone may provide inotropic support. In addition to their positive inotropic effects, inamrinone and milrinone have a beneficial vasodilator effect, which reduces preload and afterload.
Norepinephrine infusion can also be considered in refractory cardiogenic shock, though it significantly increases afterload.
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.
Nesiritide (Natrecor) may be considered. Although nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied as a treatment of acute congestive heart failure and currently retains Food and Drug Administration (FDA) approval. It should be used with caution in the setting of cardiogenic shock because it has been shown to cause hypotension.
Levosimendan, though not approved for use in the United States, can be considered in conjunction with vasopressors. It should be used with caution as it can cause hypotension. Used with vasopressors, levosimendan may improve hemodynamics and improve coronary blood flow.[13, 14]
Mechanical device supports may be used to support patients in cardiogenic shock.
The use of an intra-aortic balloon pump (IABP) is recommended for cardiogenic shock not quickly reversed with pharmacologic therapy. It is also recommended as a stabilizing measure combined with thrombolytic therapy when angiography and revascularization are not readily available. Counterpulsation of the IABP reduces LV afterload and improves coronary artery blood flow. Although this procedure is generally not performed in the ED, planning is essential, and early consultation with a cardiologist regarding this option is recommended. Although complications may occur in up to 30% of patients, extensive retrospective data support its use.[15, 16]
Left-ventricular assist devices (LVAD) may be used in selected patients with refractory shock as a bridge to cardiac transplantation. This is still controversial and requires the assistance of cardiologists and cardiac surgeons.[17, 15] LVADs have not been shown to be superior in terms of outcomes.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Although cardiogenic shock is not entirely preventable, measures can be taken to minimize the risk of occurrence, recognize it at earlier stages, and begin corrective therapy more expeditiously. Deterrence and prevention require a high degree of suspicion and heightened awareness.
Care is required in treating patients with acute coronary syndromes not yet in cardiogenic shock. Careful use of beta-blockers and ACE inhibitors in these patients is essential to avoid hypotension leading to cardiogenic shock.