AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Background

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.

Pathophysiology

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.

Frequency

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.

Mortality/Morbidity

Cardiogenic shock is the leading cause of death in 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%.

Race

• 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.

Sex

Women comprise 42% of all patients with cardiogenic shock.

CLINICAL

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

History

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.

Physical

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 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.

Causes

The vast majority of cases of cardiogenic shock are due to acute myocardial ischemia.

• Mechanisms not related to acute infarction include the following:
• • Systolic - Beta-blocker overdose, calcium channel blocker overdose, myocardial contusion, respiratory acidosis, hypocalcemia, hypophosphatemia, and cardiotoxic drugs (eg, doxorubicin [Adriamycin])
  • 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
• 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), and dysrhythmia.

DIFFERENTIALS

Section 4 of 12  

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• Multimedia
• References

Other Problems to be Considered

Papillary muscle rupture
Acute valvular dysfunction

WORKUP

Section 5 of 12  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab 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:
• • Cardiac enzymes (eg, creatine kinase, troponin, myoglobin)
  • CBC
  • Electrolytes
  • 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.

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

• 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 bedside echocardiogram can be performed by emergency physicians 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.
  • 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.

Procedures

• Placement of a central line may facilitate volume resuscitation, provide vascular access for multiple infusions, and allow invasive monitoring of central venous pressure and pulmonary capillary wedge pressure. 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. Central venous pressure may also be used to guide fluid resuscitation. Cardiogenic shock may be indicated by a cardiac index of less than 1.8 L/min/m² with a pulmonary capillary wedge pressure greater than 18 mm Hg.
• 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.

TREATMENT

Section 6 of 12  

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• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Prehospital Care

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 physician, 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.

Emergency Department Care

ED care 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. 

The ED physician should be alert to the fact that the SHOCK trial demonstrated that 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.

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.
• 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.  
• • 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.
  • Natrecor (nesiritide) may be considered. Although nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied as a treatment for 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.
  • 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.
  • Newer agents such as levosimendan and tilarginine should not be considered for routine use as their effectiveness and safety in cardiogenic shock has not yet been proven.
• 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.

Consultations

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).

MEDICATION

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

Drug Category: Vasopressors

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.

Drug Category: Phosphodiesterase enzyme inhibitors

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

Drug Category: Vasodilators

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

Drug Category: Analgesics

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

Drug Category: Diuretics

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.

Drug Category: Natriuretic peptide

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.

FOLLOW-UP

Section 8 of 12  

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• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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.

Transfer

• 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.

Deterrence/Prevention

• 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.

Complications

• Cardiopulmonary arrest
• Dysrhythmia
• Renal failure
• Multisystem organ failure
• Ventricular aneurysm
• Thromboembolic sequelae
• Stroke
• Death

Prognosis

• The mortality rate is more than 55% in patients treated medically. At best, the rate is 38% in those in whom surgical reperfusion is achieved.
• Evidence of right ventricular dilation on echocardiogram may indicate worse outcomes.

Patient Education

• Patients should be educated regarding the early warning signs of AMI and how to access the emergency medical system (eg, calling 911).
• Patients also must be educated regarding cardiac risk factors, particularly those that are reversible and subject to change (eg, smoking, diet, exercise).
• For excellent patient education resources, visit eMedicine's Shock Center and Public Health Center. Also, see eMedicine's patient education articles Shock and Cardiopulmonary Resuscitation (CPR).

MISCELLANEOUS

Section 9 of 12  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to recognize cardiogenic shock in the early stages before severe decompensation occurs
• Failure to consult a cardiologist early to obtain early
• Failure to focus on revascularization, which delays reperfusion
• Failure to give sufficient volume (eg, RV infarct without evidence of pulmonary edema)
• Failure to consider other potentially reversible or contributory causes of shock (eg, valvular dysfunction, tamponade)
• Failure to adequately resuscitate the patient prior to transfer
• Failure to have an appropriately trained transport team transfer the patient

ACKNOWLEDGMENTS

Section 10 of 12  

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• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Mark A Hostetler, MD, to the development and writing of this article.

MULTIMEDIA

Section 11 of 12  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Media file 1:  Short axis view of left ventricle demonstrating small pericardial effusion, low ejection fraction, and segmental wall motion abnormalities. Courtesy of Michael Stone, MD, RDMS.
	View Full Size Image
Media type:  Echo

Media file 2:  Pleural sliding in an intercostal space demonstrating increased lung comet artifacts suggestive of pulmonary edema. Courtesy of Michael Stone, MD, RDMS.
	View Full Size Image
Media type:  Echo

REFERENCES

Section 12 of 12

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• Introduction
• Clinical
• Differentials
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• Miscellaneous
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• References

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Article Last Updated: Apr 2, 2008