eMedicine Specialties > Cardiology > Myocardial Disease and Cardiomyopathies

Cardiogenic Shock: Differential Diagnoses & Workup

Author: Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Coauthor(s): Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Contributor Information and Disclosures

Updated: Aug 20, 2008

Differential Diagnoses

Myocardial Infarction
Septic Shock
Myocardial Ischemia
Shock, Distributive
Myocardial Rupture
Shock, Hemorrhagic
Myocarditis
Systemic Inflammatory Response Syndrome
Pulmonary Edema, Cardiogenic
Pulmonary Embolism
Sepsis, Bacterial

Other Problems to Be Considered

Approach to the initial clinical evaluation of a patient in shock

Any patient presenting with shock must receive an early working diagnosis, urgent resuscitation, and subsequent confirmation of the working diagnosis. Shock is identified in most patients based on findings of hypotension and inadequate organ perfusion, which may be caused by either low cardiac output or low systemic vascular resistance (SVR). Circulatory shock can be subdivided into 4 distinct classes based on the underlying mechanism and characteristic hemodynamic findings. In all patients, before establishing a definite diagnosis of septic shock, the following 4 classes of shock should be considered and systematically differentiated.

  • Hypovolemic shock: Hypovolemic shock results from loss of blood volume caused by conditions such as gastrointestinal bleeding, extravasation of plasma, major surgery, trauma, and severe burns.
  • Obstructive shock: Obstructive shock results from impedance of circulation by an intrinsic or extrinsic obstruction. Pulmonary embolism, dissecting aneurysm, and pericardial tamponade all result in obstructive shock.
  • Distributive shock: Distributive shock is caused by conditions producing direct arteriovenous shunting and is characterized by decreased SVR or increased venous capacitance because of the vasomotor dysfunction. These patients have high cardiac output, hypotension, high pulse pressure, low diastolic pressure, and warm extremities with good capillary refill. Such findings upon physical examination strongly suggest a working diagnosis of septic shock.
  • Cardiogenic shock: Cardiogenic shock characterized by primary myocardial dysfunction causes the heart to be unable to maintain adequate cardiac output. These patients demonstrate clinical signs of low cardiac output, with adequate intravascular volume. The patients have cool and clammy extremities, poor capillary refill, tachycardia, narrow pulse pressure, and low urine output.

Workup

Laboratory Studies

  • Biochemical profile: Measurement of routine biochemistry parameters, such as electrolytes, renal function (eg, urea and creatinine), and liver function tests (eg, bilirubin, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase [LDH]), are all useful for assessing proper functioning of vital organs.
  • CBC count: A CBC count is generally helpful to exclude anemia; a high WBC count may indicate an underlying infection, and the platelet count may be low because of coagulopathy related to sepsis.
  • Cardiac enzymes
    • The diagnosis of acute 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 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 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 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 I and T can be detected in serum within the first few hours after onset of acute myocardial infarction. Troponin levels peak at 14 hours after acute myocardial infarction, 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 myocardial infarction in patients who seek care very late. Troponin T is an independent prognosticator of adverse outcomes and can be used as a patient risk-stratifying tool in patients with unstable angina or non – Q-wave myocardial infarction.
  • Arterial blood gases: Arterial blood gas values indicate overall acid-base homeostasis and the level of arterial blood oxygenation. 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.
  • Lactate: 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.

Imaging Studies

  • 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 papillary muscle rupture causing acute myocardial regurgitation, acute ventricular septal defect, free myocardial wall rupture, and pericardial tamponade.
  • Chest radiography findings are useful for excluding other causes of shock or chest pain.
    • A widened mediastinum may indicate aortic dissection.
    • Tension pneumothorax or pneumomediastinum readily detected on x-ray films may manifest as low-output shock.
    • Most patients with established cardiogenic shock exhibit findings of left ventricular failure. The radiological features of left ventricular failure 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.

Other Tests

  • Electrocardiogram: 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 be seen in persons with myocardial ischemia. Therefore, perform electrocardiography immediately to help diagnose MI, myocardial ischemia, or both.

Procedures

  • Invasive hemodynamic monitoring
    • Invasive hemodynamic monitoring (Swan-Ganz catheterization) is very useful for helping exclude other causes of shock, eg, volume depletion, or obstructive and septic shock.
    • The hemodynamic measurements of cardiogenic shock are a pulmonary capillary wedge pressure (PCWP) 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.
    • 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 with electrocardiographic criteria, indicate RV infarction.
  • Coronary artery angiography
    • Coronary angiography is urgently indicated in patients with myocardial ischemia or MI who also develop cardiogenic shock. Angiography is required to help assess the anatomy of the coronary arteries and 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.

More on Cardiogenic Shock

Overview: Cardiogenic Shock
Differential Diagnoses & Workup: Cardiogenic Shock
Treatment & Medication: Cardiogenic Shock
Follow-up: Cardiogenic Shock
Multimedia: Cardiogenic Shock
References
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Further Reading

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Keywords

cardiogenic shock, cardiac failure, heart failure, myocardial infarction, MI, ST-elevation MI, ST-elevation myocardial infarction, STEMI, non–ST-elevation acute coronary syndrome, NSTEMI, unstable angina, myocardial ischemia, heart attack, cardiac dysfunction, acute myocarditis, sustained arrhythmia, acute valvular catastrophe, end-stage cardiomyopathy, coronary artery disease, CAD, myocardial pathology, myocardial stunning, hibernating myocardium, systolic dysfunction, diastolic dysfunction, valvular dysfunction, cardiac arrhythmias, mechanical heart complications, left ventricular end-systolic pressure-volume curve, curvilinear diastolic pressure-volume curve, shock state, hemodynamic support, vasopressor supportive therapy, inotropic supportive therapy, thrombolytic therapy, intra-aortic balloon pump, ventricular assist device, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting, coronary artery bypass grafting, shock trial

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Contributor Information and Disclosures

Author

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Russell F Kelly, MD, Program Director, Assistant Professor, Department of Internal Medicine, Division of Cardiology, Cook County Hospital, Rush Medical College
Russell F Kelly, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Ronald J Oudiz, MD, FACP, FACC, Associate Professor of Medicine, Division of Cardiology, The David Geffen School of Medicine at UCLA; Director, Liu Center for Pulmonary Hypertension, LA Biomedical Research Institute at Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx  Clinical Trials + honoraria

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Thomas G Di Salvo, MD, Associate Professor of Medicine, Medical Director, Vanderbilt Heart and Vascular Institute, Vanderbilt University Medical Center
Disclosure: Nothing to disclose.

 
 
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