Cardiogenic Shock Workup
- Author: Xiushui (Mike) Ren, MD; Chief Editor: Henry H Ooi, MD, MRCPI more...
As previously discussed, the key to achieving a good outcome in patients with cardiogenic shock is rapid diagnosis, prompt supportive therapy, and expeditious coronary artery revascularization in patients with myocardial ischemia and infarction.
Any patient presenting with shock must receive an early working diagnosis, urgent resuscitation, and subsequent confirmation of the working diagnosis.
In addition to laboratory studies, workup in cardiogenic shock can include imaging studies such as echocardiography, chest radiography, and angiography; electrocardiography; and invasive hemodynamic monitoring.
Measurement of routine biochemical parameters, such as electrolytes, renal function (eg, urea and creatinine levels), and liver function tests (eg, bilirubin, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase [LDH]), are useful for assessing proper functioning of vital organs.
A complete blood count (CBC) is generally helpful to exclude anemia. A high white blood cell (WBC) count may indicate an underlying infection, and the platelet count may be low because of coagulopathy related to sepsis.
The diagnosis of acute myocardial infarction (MI) is aided by a variety of serum markers, which include creatine kinase and its subclasses, troponin, myoglobin, and LDH. The value for the isoenzyme of creatine kinase with muscle and blood subunits is most specific, but it may be falsely elevated in persons with myopathy, hypothyroidism, renal failure, or skeletal muscle injury.
The rapid release and metabolism of myoglobin occurs in persons with MI. A 4-fold rise of myoglobin over 2 hours appears to be a test result that is sensitive for MI. The serum LDH value increases approximately 10 hours after the onset of MI, peaks at 24-48 hours, and gradually returns to normal in 6-8 days. The LDH fraction 1 isoenzyme is primarily released by the heart, but it also may come from the kidneys, stomach, pancreas, and red blood cells.
Cardiac troponins T and I are widely used for the diagnosis of myocardial injury. Troponin elevation in the absence of clinical evidence of ischemia should prompt a search for other causes of cardiac damage, such as myocarditis.
Troponin T and I can be detected in serum within the first few hours after onset of acute MI. Troponin levels peak at 14 hours after acute MI, peak again several days later (biphasic peak), and remain abnormal for 10 days. This characteristic could make troponin T (in combination with CK-MB) useful for retrospective diagnosis of acute MI in patients who seek care very late.
Troponin T is an independent prognostic indicator of adverse outcomes and can be used as a patient risk-stratifying tool in patients with unstable angina or non–Q-wave MI.
Arterial blood gases
Arterial blood gas values indicate overall acid-base homeostasis and the level of arterial blood oxygenation. (Acidosis can have a particularly deleterious effect on myocardial function.) A base deficit elevation (reference range is +3 to -3 mmol/L) correlates with the occurrence and severity of shock. A base deficit is also an important marker to follow during resuscitation of a patient from shock.
An elevated serum lactate level is an indicator of shock. Serial lactate measurements are useful markers of hypoperfusion and are also used as indicators of prognosis. Elevated lactate values in a patient with signs of hypoperfusion indicate a poor prognosis; rising lactate values during resuscitation portend a very high mortality rate.
Brain natriuretic peptide
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.
Echocardiography should be performed early to establish the cause of cardiogenic shock. Echocardiography provides information on global and regional systolic function and on diastolic dysfunction. Echocardiography findings can also lead to a rapid diagnosis of mechanical causes of shock, such as acute ventricular septal defect, free myocardial wall rupture, pericardial tamponade, and papillary muscle rupture causing acute myocardial regurgitation.
In addition, an echocardiogram may reveal akinetic or dyskinetic areas of ventricular wall motion or may demonstrate valvular dysfunction. Ejection fraction may be estimated as well (although results from the SHOCK trial indicated that left ventricular ejection fraction is not always depressed in the setting of cardiogenic shock). If a hyperdynamic left ventricle is found, the echocardiogram may suggest other causes of shock such as sepsis or anemia. (See the images below.)
Chest radiographic findings are useful for excluding other causes of shock or chest pain. The presence of a widened mediastinum may indicate aortic dissection. Tension pneumothorax or pneumomediastinum that are readily detected on radiographic films may manifest as low-output shock.
Most patients with established cardiogenic shock exhibit findings of left ventricular failure, the radiologic features of which include pulmonary vascular redistribution, interstitial pulmonary edema, enlarged hilar shadows, the presence of Kerley B lines, cardiomegaly, and bilateral pleural effusions. Alveolar edema manifests as bilateral perihilar opacities in a so-called butterfly distribution.
Ultrasonography can be 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.
Coronary artery angiography
Coronary angiography is urgently indicated in patients with myocardial ischemia or myocardial infarction (MI) who also develop cardiogenic shock. Angiography is required to help assess the anatomy of the coronary arteries as well as evaluate the need for urgent revascularization.
Coronary angiography findings often demonstrate multivessel coronary artery disease in persons with cardiogenic shock. In these patients, a compensatory hyperkinesis cannot occur in the noninfarct territory because of the severe coronary artery atherosclerosis.
The most common cause of cardiogenic shock is extensive MI, although a smaller infarction in a previously compromised left ventricle also may precipitate shock. Following MI, large areas of nonfunctional, but viable, myocardium (hibernating myocardium) can also cause or contribute to cardiogenic shock. (See the images below.)
Acute myocardial ischemia is diagnosed based on the presence of ST-segment elevation, ST-segment depression, or Q waves. T-wave inversion, although a less sensitive finding, may also be seen in persons with myocardial ischemia. An ECG with right-sided chest leads may document right ventricular infarction and may be prognostically, as well as diagnostically, useful.[17, 21]
Perform electrocardiography immediately to help diagnose myocardial infarction (MI) and/or myocardial ischemia. A normal ECG, however, does not rule out the possibility of acute MI. (See the images below.)
Invasive Hemodynamic Monitoring
Invasive hemodynamic monitoring (Swan-Ganz catheterization) is very useful for helping to exclude other causes and types of shock (eg, volume depletion, obstructive shock, and septic shock).
The hemodynamic measurements of cardiogenic shock are a pulmonary capillary wedge pressure (PCWP) of greater than 15 mm Hg and a cardiac index of less than 2.2 L/min/m2.
The presence of large V waves on the PCWP tracing suggests severe mitral regurgitation, whereas a step-up in oxygen saturation between the right atrium and the right ventricle is diagnostic of ventricular septal rupture.
High right-sided filling pressures in the absence of an elevated PCWP, when accompanied by electrocardiographic criteria, indicate right ventricular infarction.
Alonso DR, Scheidt S, Post M, Killip T. Pathophysiology of cardiogenic shock. Quantification of myocardial necrosis, clinical, pathologic and electrocardiographic correlations. Circulation. 1973 Sep. 48 (3):588-96. [Medline].
Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation. 2008 Feb 5. 117(5):686-97. [Medline].
Funaro S, La Torre G, Madonna M, et al, for the AMICI Investigators. Incidence, determinants, and prognostic value of reverse left ventricular remodelling after primary percutaneous coronary intervention: results of the Acute Myocardial Infarction Contrast Imaging (AMICI) multicenter study. Eur Heart J. 2009 Mar. 30 (5):566-75. [Medline].
Forrester JS, Wyatt HL, Da Luz PL, Tyberg JV, Diamond GA, Swan HJ. Functional significance of regional ischemic contraction abnormalities. Circulation. 1976 Jul. 54 (1):64-70. [Medline].
Beyersdorf F, Buckberg GD, Acar C, et al. Cardiogenic shock after acute coronary occlusion. Pathogenesis, early diagnosis, and treatment. Thorac Cardiovasc Surg. 1989 Feb. 37 (1):28-36. [Medline].
Al-Reesi A, Al-Zadjali N, Perry J, et al. Do beta-blockers reduce short-term mortality following acute myocardial infarction? A systematic review and meta-analysis. CJEM. 2008 May. 10(3):215-23. [Medline].
Chen ZM, Pan HC, Chen YP, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet. 2005 Nov 5. 366(9497):1622-32. [Medline].
Kolte D, Khera S, Aronow WS, et al. Trends in incidence, management, and outcomes of cardiogenic shock complicating ST-elevation myocardial infarction in the United States. J Am Heart Assoc. 2014 Jan 13. 3 (1):e000590. [Medline].
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. 1999 Apr 15. 340(15):1162-8. [Medline].
Roffi M, Patrono C, Collet JP, et al, for the European Society of Cardiology Task Force. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2015 Aug 29. [Medline].
Graf T, Desch S, Eitel I, Thiele H. Acute myocardial infarction and cardiogenic shock: pharmacologic and mechanical hemodynamic support pathways. Coron Artery Dis. 2015 Sep. 26 (6):535-44. [Medline].
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. 2005 Jul 27. 294(4):448-54. [Medline].
Fox KA, Steg PG, Eagle KA, Goodman SG, Anderson FA Jr, Granger CB, et al. Decline in rates of death and heart failure in acute coronary syndromes, 1999-2006. JAMA. 2007 May 2. 297(17):1892-900. [Medline].
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. 2008 Nov 4. 149(9):618-26. [Medline].
Amsterdam EA, Wenger NK, Brindis RG, et al, for the ACC, AHA Task Force on Practice Guidelines, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014 Dec 23. 64 (24):e139-228. [Medline].
Kunadian V, Qiu W, Ludman P, et al, for the National Institute for Cardiovascular Outcomes Research. Outcomes in patients with cardiogenic shock following percutaneous coronary intervention in the contemporary era: an analysis from the BCIS database (British Cardiovascular Intervention Society). JACC Cardiovasc Interv. 2014 Dec. 7 (12):1374-85. [Medline].
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. 2008 Jul. 36(7):2023-33. [Medline].
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. 2000 Jan. 35(1):136-43. [Medline].
Picard MH, Davidoff R, Sleeper LA, and the SHOCK Trial investigators. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK. Echocardiographic predictors of survival and response to early revascularization in cardiogenic shock. Circulation. 2003 Jan 21. 107 (2):279-84. [Medline].
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. 2007 Dec. 132(6):1794-803. [Medline].
O'Gara PT, Kushner FG, Ascheim DD, et al, for the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013 Jan 29. 127 (4):e362-425. [Medline].
Hochman JS, Sleeper LA, White HD, Dzavik V, Wong SC, Menon V, et al. One-year survival following early revascularization for cardiogenic shock. JAMA. 2001 Jan 10. 285(2):190-2. [Medline].
Shin TG, Choi JH, Jo IJ, Sim MS, Song HG, Jeong YK, et al. Extracorporeal cardiopulmonary resuscitation in patients with inhospital cardiac arrest: A comparison with conventional cardiopulmonary resuscitation. Crit Care Med. 2011 Jan. 39(1):1-7. [Medline].
De Backer D, Biston P, Devriendt J, et al, for the SOAP II Investigators. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010 Mar 4. 362 (9):779-89. [Medline].
Ellender TJ, Skinner JC. The use of vasopressors and inotropes in the emergency medical treatment of shock. Emerg Med Clin North Am. 2008 Aug. 26(3):759-86, ix. [Medline].
Naples RM, Harris JW, Ghaemmaghami CA. Critical care aspects in the management of patients with acute coronary syndromes. Emerg Med Clin North Am. 2008 Aug. 26(3):685-702, viii. [Medline].
Felker GM, Benza RL, Chandler AB, et al, for the OPTIME-CHF Investigators. Heart failure etiology and response to milrinone in decompensated heart failure: results from the OPTIME-CHF study. J Am Coll Cardiol. 2003 Mar 19. 41 (6):997-1003. [Medline].
Gheorghiade M, Gattis WA, Klein L. OPTIME in CHF trial: rethinking the use of inotropes in the management of worsening chronic heart failure resulting in hospitalization. Eur J Heart Fail. 2003 Jan. 5 (1):9-12. [Medline].
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. 2008 Aug. 36(8):2257-66. [Medline].
De Luca L, Colucci WS, Nieminen MS, Massie BM, Gheorghiade M. Evidence-based use of levosimendan in different clinical settings. Eur Heart J. 2006 Aug. 27(16):1908-20. [Medline].
Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet. 1986 Feb 22. 1 (8478):397-402. [Medline].
Gruppo Italiano per lo Studio della Streptochi-nasi nell'Infarto Miocardico (GISSI). Long-term effects of intravenous thrombolysis in acute myocardial infarction: final report of the GISSI study. Lancet. 1987 Oct 17. 2 (8564):871-4. [Medline].
Sanborn TA, Sleeper LA, Bates ER, et al. 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 cardiogenic shocK?. J Am Coll Cardiol. 2000 Sep. 36(3 Suppl A):1123-9. [Medline].
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. 2007 May-Jun. 53(3):278-87. [Medline].
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. 2009 Sep. 30(17):2102-8. [Medline].
Sjauw KD, Engstrom AE, Vis MM, et al. A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines?. Eur Heart J. 2009 Feb. 30 (4):459-68. [Medline].
Ramanathan K, Farkouh ME, Cosmi JE, French JK, Harkness SM, Džavík V, et al. Rapid complete reversal of systemic hypoperfusion after intra-aortic balloon pump counterpulsation and survival in cardiogenic shock complicating an acute myocardial infarction. Am Heart J. 2011 Aug. 162(2):268-75. [Medline]. [Full Text].
Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med. 2012 Oct 4. 367(14):1287-96. [Medline].
Windecker S. Percutaneous left ventricular assist devices for treatment of patients with cardiogenic shock. Curr Opin Crit Care. 2007 Oct. 13(5):521-7. [Medline].
Rose EA, Gelijns AC, Moskowitz AJ, Heitjan DF, Stevenson LW, Dembitsky W, et al. Long-term use of a left ventricular assist device for end-stage heart failure. N Engl J Med. 2001 Nov 15. 345(20):1435-43. [Medline].
Farrar DJ, Lawson JH, Litwak P, Cederwall G. Thoratec VAD system as a bridge to heart transplantation. J Heart Transplant. 1990 Jul-Aug. 9(4):415-22; discussion 422-3. [Medline].
Damme L, Heatley J, Radovancevic B. Clinical results with the HeartMate LVAD: Worldwide Registry update. J Congestive Heart Failure Circ Support. 2001. 2:5-7(3).
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. 1999 Aug 26. 341(9):625-34. [Medline].
Antoniucci D, Valenti R, Migliorini A, Moschi G, Trapani M, Buonamici P, et al. Relation of time to treatment and mortality in patients with acute myocardial infarction undergoing primary coronary angioplasty. Am J Cardiol. 2002 Jun 1. 89(11):1248-52. [Medline].
Antman EM, Anbe DT, Armstrong PW, et al, for the American College of Cardiology, American Heart Association, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol. 2004 Aug 4. 44 (3):671-719. [Medline].
Hochman JS, Boland J, Sleeper LA, Porway M, Brinker J, Col J, et al. Current spectrum of cardiogenic shock and effect of early revascularization on mortality. Results of an International Registry. SHOCK Registry Investigators. Circulation. 1995 Feb 1. 91(3):873-81. [Medline].
Jeger RV, Harkness SM, Ramanathan K, et al, for the SHOCK Investigators. Emergency revascularization in patients with cardiogenic shock on admission: a report from the SHOCK trial and registry. Eur Heart J. 2006 Mar. 27 (6):664-70. [Medline].
Hochman JS, Sleeper LA, Webb JG, et al, for the SHOCK Investigators. Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction. JAMA. 2006 Jun 7. 295 (21):2511-5. [Medline].
Slottosch I, Liakopoulos O, Kuhn E, Deppe AC, Scherner M, Madershahian N, Choi YH, Wahlers T. Outcomes after peripheral extracorporeal membrane oxygenation therapy for postcardiotomy cardiogenic shock: a single-center experience. J Surg Res. 2013 May 15;181(2):e47-55. doi: 10.1016/j.jss.2012.07.030. Epub 2012 Aug 1. [Medline].
Anderson ML, Peterson ED, Peng SA, et al. Differences in the profile, treatment, and prognosis of patients with cardiogenic shock by myocardial infarction classification: A report from NCDR. Circ Cardiovasc Qual Outcomes. 2013 Nov. 6 (6):708-15. [Medline].
Menon V, White H, LeJemtel T, et al. The clinical profile of patients with suspected cardiogenic shock due to predominant left ventricular failure: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK?. J Am Coll Cardiol. 2000 Sep. 36 (3 suppl A):1071-6. [Medline].
Koprivanac M, Kelava M, Soltesz E, et al. Advances in temporary mechanical support for treatment of cardiogenic shock. Expert Rev Med Devices. 2015 Nov. 12 (6):689-702. [Medline].
Susen S, Rauch A, Van Belle E, Vincentelli A, Lenting PJ. Circulatory support devices: fundamental aspects and clinical management of bleeding and thrombosis. J Thromb Haemost. 2015 Oct. 13 (10):1757-67. [Medline].