Shock, Cardiogenic

Back

Author

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.

Coauthor(s)

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

Nothing to disclose.

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.

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.

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.

Epidemiology

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 acute myocardial infarction (AMI).

Race

Sex

Women comprise 42% of all patients with cardiogenic shock.

Age

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.

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.


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.

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.

Causes

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

Procedures

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.

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). 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.

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

Complications

Complications of cardiogenic shock may include the following:

Prognosis

References

  1. Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med. Aug 26 1999;341(9):625-34.[View Abstract]
  2. Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS. Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. JAMA. Jul 27 2005;294(4):448-54.[View Abstract]
  3. Fox KA, Steg PG, Eagle KA, Goodman SG, Anderson FA Jr, Granger CB. Decline in rates of death and heart failure in acute coronary syndromes, 1999-2006. JAMA. May 2 2007;297(17):1892-900.[View Abstract]
  4. Jeger RV, Radovanovic D, Hunziker PR, Pfisterer ME, Stauffer JC, Erne P, et al. Ten-year trends in the incidence and treatment of cardiogenic shock. Ann Intern Med. Nov 4 2008;149(9):618-26.[View Abstract]
  5. Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation. Feb 5 2008;117(5):686-97.[View Abstract]
  6. Al-Reesi A, Al-Zadjali N, Perry J, Fergusson D, Al-Shamsi M, Al-Thagafi M, et al. Do beta-blockers reduce short-term mortality following acute myocardial infarction? A systematic review and meta-analysis. CJEM. May 2008;10(3):215-23.[View Abstract]
  7. Chen ZM, Pan HC, Chen YP, Peto R, Collins R, Jiang LX. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet. Nov 5 2005;366(9497):1622-32.[View Abstract]
  8. Hamon M, Agostini D, Le Page O, Riddell JW, Hamon M. Prognostic impact of right ventricular involvement in patients with acute myocardial infarction: meta-analysis. Crit Care Med. Jul 2008;36(7):2023-33.[View Abstract]
  9. Jeger RV, Lowe AM, Buller CE, Pfisterer ME, Dzavik V, Webb JG, et al. Hemodynamic parameters are prognostically important in cardiogenic shock but similar following early revascularization or initial medical stabilization: a report from the SHOCK Trial. Chest. Dec 2007;132(6):1794-803.[View Abstract]
  10. Hochman JS, Sleeper LA, White HD. One-year survival following early revascularization for cardiogenic shock. JAMA. Jan 10 2001;285(2):190-2.[View Abstract]
  11. Ellender TJ, Skinner JC. The use of vasopressors and inotropes in the emergency medical treatment of shock. Emerg Med Clin North Am. Aug 2008;26(3):759-86, ix.[View Abstract]
  12. Naples RM, Harris JW, Ghaemmaghami CA. Critical care aspects in the management of patients with acute coronary syndromes. Emerg Med Clin North Am. Aug 2008;26(3):685-702, viii.[View Abstract]
  13. Fuhrmann JT, Schmeisser A, Schulze MR, Wunderlich C, Schoen SP, Rauwolf T. Levosimendan is superior to enoximone in refractory cardiogenic shock complicating acute myocardial infarction. Crit Care Med. Aug 2008;36(8):2257-66.[View Abstract]
  14. De Luca L, Colucci WS, Nieminen MS, Massie BM, Gheorghiade M. Evidence-based use of levosimendan in different clinical settings. Eur Heart J. Aug 2006;27(16):1908-20.[View Abstract]
  15. Garatti A, Russo C, Lanfranconi M, Colombo T, Bruschi G, Trunfio S, et al. Mechanical circulatory support for cardiogenic shock complicating acute myocardial infarction: an experimental and clinical review. ASAIO J. May-Jun 2007;53(3):278-87.[View Abstract]
  16. Cheng JM, den Uil CA, Hoeks SE, van der Ent M, Jewbali LS, van Domburg RT, et al. Percutaneous left ventricular assist devices vs. intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: a meta-analysis of controlled trials. Eur Heart J. Sep 2009;30(17):2102-8.[View Abstract]
  17. Windecker S. Percutaneous left ventricular assist devices for treatment of patients with cardiogenic shock. Curr Opin Crit Care. Oct 2007;13(5):521-7.[View Abstract]
  18. Amin AP, Nathan S, Prodduturi P, D'Silva O, Gupta A, Kumar A. Survival benefit from early revascularization in elderly patients with cardiogenic shock after acute myocardial infarction: a cohort study. J Invasive Cardiol. Jul 2009;21(7):305-12.[View Abstract]
  19. Ander DS, Jaggi M, Rivers E, Rady MY, Levine TB, Levine AB, et al. Undetected cardiogenic shock in patients with congestive heart failure presenting to the emergency department. Am J Cardiol. Oct 1 1998;82(7):888-91.[View Abstract]
  20. Antoniucci D, Valenti R, Santoro GM, Bolognese L, Trapani M, Moschi G, et al. Systematic direct angioplasty and stent-supported direct angioplasty therapy for cardiogenic shock complicating acute myocardial infarction: in-hospital and long-term survival. J Am Coll Cardiol. Feb 1998;31(2):294-300.[View Abstract]
  21. Archan S, Toller W. Levosimendan: current status and future prospects. Curr Opin Anaesthesiol. Feb 2008;21(1):78-84.[View Abstract]
  22. Barry WL, Sarembock IJ. Cardiogenic shock: therapy and prevention. Clinical Cardiology. 1998;21:72-80.[View Abstract]
  23. Bellone A, Monari A, Cortellaro F, Vettorello M, Arlati S, Coen D. Myocardial infarction rate in acute pulmonary edema: noninvasive pressure support ventilation versus continuous positive airway pressure. Crit Care Med. Sep 2004;32(9):1860-5.[View Abstract]
  24. Bengtson JR, Kaplan AJ, Pieper KS, Wildermann NM, Mark DB, Pryor DB, et al. Prognosis in cardiogenic shock after acute myocardial infarction in the interventional era. J Am Coll Cardiol. Dec 1992;20(7):1482-9.[View Abstract]
  25. Brodie BR, Stuckey TD, Hansen C, Muncy D. Intra-aortic balloon counterpulsation before primary percutaneous transluminal coronary angioplasty reduces catheterization laboratory events in high-risk patients with acute myocardial infarction. Am J Cardiol. Jul 1 1999;84(1):18-23.[View Abstract]
  26. Bur A, Bayegan K, Holzer M, Herkner H, Schreiber W, Siostrzonek P, et al. Intra-aortic balloon counterpulsation in the emergency department: a 7-year review and analysis of predictors of survival. Resuscitation. Jun 2002;53(3):259-64.[View Abstract]
  27. Burger AJ, Elkayam U, Neibaur MT. Comparison of the occurrence of ventricular arrhythmias in patients with acutely decompensated congestive heart failure receiving dobutamine versus nesiritide therapy. Am J Cardiol. Jul 1 2001;88(1):35-9.[View Abstract]
  28. Ciccone TJ, Grossman SA. Cardiac ultrasound. Emerg Med Clin North Am. Aug 2004;22(3):621-40.[View Abstract]
  29. den Uil CA, Lagrand WK, Valk SD, Spronk PE, Simoons ML. Management of cardiogenic shock: focus on tissue perfusion. Curr Probl Cardiol. Aug 2009;34(8):330-49.[View Abstract]
  30. Doust JA, Pietrzak E, Dobson A, Glasziou P. How well does B-type natriuretic peptide predict death and cardiac events in patients with heart failure: systematic review. BMJ. Mar 19 2005;330(7492):625.[View Abstract]
  31. Dzavik V, Sleeper LA, Cocke TP, Moscucci M, Saucedo J, Hosat S, et al. Early revascularization is associated with improved survival in elderly patients with acute myocardial infarction complicated by cardiogenic shock: a report from the SHOCK Trial Registry. Eur Heart J. May 2003;24(9):828-37.[View Abstract]
  32. Dzavík V, Burton JR, Kee C, Teo KK, Ignaszewski A, Lucas AR, et al. Changing practice patterns in the management of acute myocardial infarction complicated by cardiogenic shock: elderly compared with younger patients. Can J Cardiol. Jul 1998;14(7):923-30.[View Abstract]
  33. Fuhrmann JT, Schmeisser A, Schulze MR, Wunderlich C, Schoen SP, Rauwolf T, et al. Levosimendan is superior to enoximone in refractory cardiogenic shock complicating acute myocardial infarction. Crit Care Med. Aug 2008;36(8):2257-66.[View Abstract]
  34. Goldberg RJ, Samad NA, Yarzebski J, Gurwitz J, Bigelow C, Gore JM. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med. Apr 15 1999;340(15):1162-8.[View Abstract]
  35. Gowda RM, Fox JT, Khan IA. Cardiogenic shock: basics and clinical considerations. Int J Cardiol. Jan 24 2008;123(3):221-8.[View Abstract]
  36. Gurm HS, Bates ER. Cardiogenic shock complicating myocardial infarction. Crit Care Clin. Oct 2007;23(4):759-77, vi.[View Abstract]
  37. Hasdai D, Califf RM, Thompson TD, Hochman JS, Ohman EM, Pfisterer M, et al. Predictors of cardiogenic shock after thrombolytic therapy for acute myocardial infarction. J Am Coll Cardiol. Jan 2000;35(1):136-43.[View Abstract]
  38. Hasdai D, Holmes DR Jr, Califf RM, Thompson TD, Hochman JS, Pfisterer M, et al. Cardiogenic shock complicating acute myocardial infarction: predictors of death. GUSTO Investigators. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries. Am Heart J. Jul 1999;138(1 Pt 1):21-31.[View Abstract]
  39. Hochman JS, Buller CE, Sleeper LA, Boland J, Dzavik V, Sanborn TA, et al. Cardiogenic shock complicating acute myocardial infarction--etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1063-70.[View Abstract]
  40. Hollenberg SM, Kavinsky CJ, Parrillo JE. Cardiogenic shock. Ann Intern Med. Jul 6 1999;131(1):47-59.[View Abstract]
  41. Holmes CL, Walley KR. The evaluation and management of shock. Clin Chest Med. Dec 2003;24(4):775-89.[View Abstract]
  42. Holmes DR Jr, Califf RM, Van de Werf F, Berger PB, Bates ER, Simoons ML, et al. Difference in countries' use of resources and clinical outcome for patients with cardiogenic shock after myocardial infarction: results from the GUSTO trial. Lancet. Jan 11 1997;349(9045):75-8.[View Abstract]
  43. Iakobishvili Z, Behar S, Boyko V, Battler A, Hasdai D. Does current treatment of cardiogenic shock complicating the acute coronary syndromes comply with guidelines?. Am Heart J. Jan 2005;149(1):98-103.[View Abstract]
  44. Jacobs AK, French JK, Col J, Sleeper LA, Slater JN, Carnendran L, et al. Cardiogenic shock with non-ST-segment elevation myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded coronaries for Cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1091-6.[View Abstract]
  45. Jones AE, Craddock PA, Tayal VS, Kline JA. Diagnostic accuracy of left ventricular function for identifying sepsis among emergency department patients with nontraumatic symptomatic undifferentiated hypotension. Shock. Dec 2005;24(6):513-7.[View Abstract]
  46. Katayama T, Nakashima H, Takagi C. Predictors of mortality in patients with acute myocardial infarction and cardiogenic shock. Circ J. Jan 2005;69(1):83-8.[View Abstract]
  47. Klocke RK, Mager G, Kux A, Hopp HW, Hilger HH. Effects of a twenty-four-hour milrinone infusion in patients with severe heart failure and cardiogenic shock as a function of the hemodynamic initial condition. Am Heart J. Jun 1991;121(6 Pt 2):1965-73.[View Abstract]
  48. Kohsaka S, Menon V, Lowe AM. Systemic inflammatory response syndrome after acute myocardial infarction complicated by cardiogenic shock. Arch Intern Med. Jul 25 2005;165(14):1643-50.[View Abstract]
  49. Mark DG, Ku BS, Carr BG, Everett WW, Okusanya O, Horan A, et al. Directed bedside transthoracic echocardiography: preferred cardiac window for left ventricular ejection fraction estimation in critically ill patients. Am J Emerg Med. Oct 2007;25(8):894-900.[View Abstract]
  50. Mendes LA, Picard MH, Sleeper LA, Thompson CR, Jacobs AK, White HD, et al. Cardiogenic shock: predictors of outcome based on right and left ventricular size and function at presentation. Coron Artery Dis. Jun 2005;16(4):209-15.[View Abstract]
  51. Menon V, Hochman JS, Stebbins A. Lack of progress in cardiogenic shock: lessons from the GUSTO trials. Eur Heart J. Dec 2000;21(23):1928-36.[View Abstract]
  52. Mukae S, Yanagishita T, Geshi E, Umetsu K, Tomita M, Itoh S, et al. The effects of dopamine, dobutamine and amrinone on mitochondrial function in cardiogenic shock. Jpn Heart J. Jul 1997;38(4):515-29.[View Abstract]
  53. Palmeri ST, Lowe AM, Sleeper LA. Racial and ethnic differences in the treatment and outcome of cardiogenic shock following acute myocardial infarction. Am J Cardiol. Oct 15 2005;96(8):1042-9.[View Abstract]
  54. Perez-Castellano N, Garcia E, Serrano JA, Elizaga J, Soriano J, Abeytua M, et al. Efficacy of invasive strategy for the management of acute myocardial infarction complicated by cardiogenic shock. Am J Cardiol. Apr 1 1999;83(7):989-93.[View Abstract]
  55. Rackley CE, Russell RO Jr, Mantle JA, Rogers WJ. Cardiogenic shock. Cardiovasc Clin. 1981;11(3):15-24.[View Abstract]
  56. Randazzo MR, Snoey ER, Levitt MA, Binder K. Accuracy of emergency physician assessment of left ventricular ejection fraction and central venous pressure using echocardiography. Acad Emerg Med. Sep 2003;10(9):973-7.[View Abstract]
  57. Russ MA, Prondzinsky R, Christoph A, Schlitt A, Buerke U, Soffker G, et al. Hemodynamic improvement following levosimendan treatment in patients with acute myocardial infarction and cardiogenic shock. Crit Care Med. Dec 2007;35(12):2732-9.[View Abstract]
  58. [Guideline] Ryan TJ, Antman EM, Brooks NH, Califf RM, Hillis LD, Hiratzka LF, et al. 1999 update: ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction: Executive Summary and Recommendations: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). Circulation. Aug 31 1999;100(9):1016-30.[View Abstract]
  59. Sackner-Bernstein JD, Skopicki HA, Aaronson KD. Risk of worsening renal function with nesiritide in patients with acutely decompensated heart failure. Circulation. Mar 29 2005;111(12):1487-91.[View Abstract]
  60. Sanborn TA, Sleeper LA, Bates ER. Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1123-9.[View Abstract]
  61. Singh M, White J, Hasdai D, Hodgson PK, Berger PB, Topol EJ. Long-term outcome and its predictors among patients with ST-segment elevation myocardial infarction complicated by shock: insights from the GUSTO-I trial. J Am Coll Cardiol. Oct 30 2007;50(18):1752-8.[View Abstract]
  62. [Best Evidence] Sleeper LA, Ramanathan K, Picard MH, Lejemtel TH, White HD, Dzavik V, et al. Functional status and quality of life after emergency revascularization for cardiogenic shock complicating acute myocardial infarction. J Am Coll Cardiol. Jul 19 2005;46(2):266-73.[View Abstract]
  63. Smilth L, Hernan L. Shock States. In: Fuhrman BP, Zimmerman JJ, eds. Pediatric Critical Care. 3rd ed. Philadelphia, PA: Mosby Inc; 2006:chap 27.
  64. Stone PH, Raabe DS, Jaffe AS, et al. Prognostic significance of location and type of myocardial infarction: independent adverse outcome associated with anterior location. J Am Coll Cardiol. Mar 1988;11(3):453-63.[View Abstract]
  65. Tan LB, Littler WA. Measurement of cardiac reserve in cardiogenic shock: implications for prognosis and management. Br Heart J. Aug 1990;64(2):121-8.[View Abstract]
  66. Topalian S, Ginsberg F, Parrillo JE. Cardiogenic shock. Crit Care Med. Jan 2008;36(1 Suppl):S66-74.[View Abstract]
  67. Topalian S, Ginsberg F, Parrillo JE. Cardiogenic shock. Crit Care Med. Jan 2008;36(1 Suppl):S66-74.[View Abstract]
  68. [Best Evidence] TRIUMPH Investigators, Alexander JH, Reynolds HR, Stebbins AL, Dzavik V, Harrington RA. Effect of tilarginine acetate in patients with acute myocardial infarction and cardiogenic shock: the TRIUMPH randomized controlled trial. JAMA. Apr 18 2007;297(15):1657-66.[View Abstract]
  69. Tung RH, Garcia C, Morss AM. Utility of B-type natriuretic peptide for the evaluation of intensive careunit shock. Crit Care Med. Aug 2004;32(8):1643-7.[View Abstract]
  70. Urban P, Stauffer JC, Bleed D, Khatchatrian N, Amann W, Bertel O, et al. A randomized evaluation of early revascularization to treat shock complicating acute myocardial infarction. The (Swiss) Multicenter Trial of Angioplasty for Shock-(S)MASH. Eur Heart J. Jul 1999;20(14):1030-8.[View Abstract]
  71. Valente S, Lazzeri C, Chiostri M, Sori A, Giglioli C, Salvadori C, et al. Time of onset and outcome of cardiogenic shock in acute coronary syndromes. J Cardiovasc Med (Hagerstown). Dec 2008;9(12):1235-40.[View Abstract]
  72. [Best Evidence] Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Does this dyspneic patient in the emergency department have congestive heart failure?. JAMA. Oct 19 2005;294(15):1944-56.[View Abstract]
  73. Webb JG. Interventional management of cardiogenic shock. Can J Cardiol. Feb 1998;14(2):233-44.[View Abstract]
  74. Webb JG, Carere RG, Hilton JD, Rabinowitz A, Buller E, Dodek AA, et al. Usefulness of coronary stenting for cardiogenic shock. Am J Cardiol. Jan 1 1997;79(1):81-4.[View Abstract]
  75. Webb JG, Lowe AM, Sanborn TA, White HD, Sleeper LA, Carere RG, et al. Percutaneous coronary intervention for cardiogenic shock in the SHOCK trial. J Am Coll Cardiol. Oct 15 2003;42(8):1380-6.[View Abstract]
  76. Webb JG, Sleeper LA, Buller CE. Implications of the timing of onset of cardiogenic shock after acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1084-90.[View Abstract]
  77. White HD, Assmann SF, Sanborn TA, Jacobs AK, Webb JG, Sleeper LA, et al. Comparison of percutaneous coronary intervention and coronary artery bypass grafting after acute myocardial infarction complicated by cardiogenic shock: results from the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial. Circulation. Sep 27 2005;112(13):1992-2001.[View Abstract]
  78. White HD, Palmeri ST, Sleeper LA, French JK, Wong CK, Lowe AM, et al. Electrocardiographic findings in cardiogenic shock, risk prediction, and the effects of emergency revascularization: results from the SHOCK trial. Am Heart J. Nov 2004;148(5):810-7.[View Abstract]
  79. Wong SC, Sanborn T, Sleeper LA, Webb JG, Pilchik R, Hart D, et al. Angiographic findings and clinical correlates in patients with cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1077-83.[View Abstract]
  80. Wong SC, Sleeper LA, Monrad ES, Menegus MA, Palazzo A, Dzavik V, et al. Absence of gender differences in clinical outcomes in patients with cardiogenic shock complicating acute myocardial infarction. A report from the SHOCK Trial Registry. J Am Coll Cardiol. Nov 1 2001;38(5):1395-401.[View Abstract]

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.