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Cardiogenic Shock Differential Diagnoses

  • Author: Xiushui (Mike) Ren, MD; Chief Editor: Henry H Ooi, MD, MRCPI  more...
 
Updated: Dec 13, 2015
 
 

Diagnostic ConsiderationsRight ventricular infarctionAcute mitral regurgitationCardiac ruptureVentricular septal ruptureReversible myocardial dysfunction

Conditions to consider in the differential diagnosis of cardiogenic shock include the following:

  • Systemic inflammatory response syndrome
  • Acute coronary syndrome
  • Aortic regurgitation
  • Dilated cardiomyopathy
  • Restrictive cardiomyopathy
  • Congestive heart failure and pulmonary edema
  • Mitral regurgitation
  • Pericarditis and cardiac tamponade
  • Hypovolemic shock
  • Papillary muscle rupture
  • Acute valvular dysfunction

Right ventricular infarction occurs in up to 30% of patients with inferior myocardial infarction (MI) and becomes hemodynamically unstable in 10% of these patients. The diagnosis is made by identifying an ST-segment elevation in the right precordial leads (V3 or V4 R) and/or typical hemodynamic findings after right heart catheterization. These are elevated right atrial and right ventricular end-diastolic pressures with normal to low pulmonary artery wedge pressure and low cardiac output.

Echocardiography findings can also be very helpful in the diagnosis of right ventricular infarction. Patients with cardiogenic shock due to this condition have a better prognosis than do patients when compared to those with cardiogenic shock due to left ventricular systolic failure.

Regarding the management of cardiogenic shock due to right ventricular infarction, supportive therapy begins with the restoration and maintenance of right ventricular preload with fluid administration. However, excessive fluid resuscitation may compromise left ventricular filling by introducing an interventricular septal shift.

Inotropic therapy with dobutamine may be effective in increasing cardiac output in patients with right ventricular infarction. Maintenance of systemic arterial pressure in order to maintain adequate coronary artery perfusion may require vasoconstricting agents, such as norepinephrine. In unstable patients, an intra-aortic balloon pump (IABP) may be useful for ensuring adequate blood supply to the already compromised right ventricle.

Revascularization of the occluded coronary artery, preferably by percutaneous transluminal coronary angioplasty (PTCA), is crucial for management and has shown to dramatically improve outcome.

Acute mitral regurgitation is usually associated with inferior MI due to ischemia or infarction of the papillary muscle. It occurs in approximately 1% of MIs, and posteromedial papillary muscle is involved more frequently than anterolateral muscle. Acute mitral regurgitation usually happens 2-7 days following acute MI and manifests with an abrupt onset of pulmonary edema, hypotension, and cardiogenic shock.

Echocardiography findings are extremely useful in making a diagnosis. The 2-dimensional (2-D) echocardiographic image shows the malfunctioning mitral valve, and findings from a Doppler study can be used to document the severity of mitral regurgitation. Right heart catheterization is often required for stabilizing the patient. Tall V waves identified on pulmonary arterial and wedge pressure waveforms indicate acute mitral regurgitation. However, the diagnosis must be confirmed based on echocardiography or left ventriculography findings before definitive therapy or surgery is initiated.

Hemodynamic stabilization by reducing afterload, either with nitroprusside or an IABP, is often instituted. Definitive therapy requires revascularization, if ischemia is present, and/or surgical valve repair or replacement, if a structural valvular lesion is present. The mortality rate in the presurgical era was 50% in the first 24 hours, with a 2-month survival rate of 6%.

Rupture of the free wall of the left ventricle occurs within 2 weeks of the MI and may occur within the first 24 hours. The rupture may involve the anterior, posterior, or lateral wall of the ventricle.

Cardiac rupture often presents as sudden cardiac death. Premortem symptoms include chest pain, agitation, tachycardia, and hypotension. This diagnosis should be considered in patients with electromechanical dissociation who have a history of anginal pain. Patients rarely, if ever, survive cardiac rupture.

Approximately 1-3% of acute MIs are associated with ventricular septal rupture. Most septal ruptures occur within the week following MI. Patients with acute ventricular septal rupture develop acute heart failure and/or cardiogenic shock, with physical findings of a harsh holosystolic murmur and left parasternal thrill.

A left-to-right intracardiac shunt, as demonstrated by a step-up (>5% increase in oxygen saturation) between the right atrium and right ventricle, confirms the diagnosis. Alternatively, 2-D and Doppler echocardiographic findings can be used to identify the location and severity of the left-to-right shunt.

Rapid stabilization using an IABP and pharmacologic measures, followed by emergent surgical repair, is lifesaving. The timing of surgical intervention is controversial, but most experts suggest operative repair within 48 hours of the rupture.

Ventricular septal rupture portends a poor prognosis unless management is aggressive. Immediate surgical repair of patients with ventricular septal rupture is reported to be associated with survival rates of 42-75%; therefore, prompt surgical therapy is imperative as soon as possible after the diagnosis of ventricular septal rupture is confirmed.

Other causes of severe, reversible myocardial dysfunction are sepsis-associated myocardial depression, myocardial depression following cardiopulmonary bypass, and inflammatory myocarditis. In older literature, this presentation is often referred to as cold septic shock. In these situations, myocardial dysfunction occurs from the effects of inflammatory cytokines, such as tumor necrosis factor and interleukin 1.

Myocardial dysfunction may vary from mild to severe and may lead to cardiogenic shock. For patients in cardiogenic shock, cardiovascular support with inotropic agents may be required until recovery, which generally occurs after the underlying disease process resolves.

Differential Diagnoses

 
 
Contributor Information and Disclosures
Author

Xiushui (Mike) Ren, MD Cardiologist, The Permanente Medical Group; Associate Director of Research, Cardiovascular Diseases Fellowship, California Pacific Medical Center

Xiushui (Mike) Ren, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Society of Echocardiography

Disclosure: Nothing to disclose.

Coauthor(s)

Andrew Lenneman 

Disclosure: Nothing to disclose.

Chief Editor

Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Ethan S Brandler, MD, MPH Clinical Assistant Professor, Attending Physician, Departments of Emergency Medicine and Internal Medicine, University Hospital of Brooklyn, Kings County Hospital

Ethan S Brandler, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Mark A Hostetler, MD, MPH Associate Professor of Pediatrics, University of Chicago; Chief, Section of Emergency Medicine, Department of Pediatrics, Medical Director of Pediatric Emergency Department, University of Chicago Children's Hospital

Disclosure: Nothing to disclose.

A Antoine Kazzi MD, Deputy Chief of Staff, American University of Beirut Medical Center; Associate Professor, Department of Emergency Medicine, American University of Beirut, Lebanon

A Antoine Kazzi is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Russell F Kelly MD, Assistant Professor, Department of Internal Medicine, Rush Medical College; Chairman of Adult Cardiology and Director of the Fellowship Program, Cook County Hospital

Russell F Kelly is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center

Ronald J Oudiz, MD, FACP, FACC, FCCP 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; Bayer Grant/research funds Consulting

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.

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

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Patient with an acute anterolateral myocardial infarction who developed cardiogenic shock. Coronary angiography images showed severe stenosis of the left anterior descending coronary artery, which was dilated by percutaneous transluminal coronary angioplasty.
A coronary angiogram image of a patient with cardiogenic shock demonstrates severe stenosis of the left anterior descending coronary artery.
A coronary angiogram image of a patient with cardiogenic shock demonstrates severe stenosis of the left anterior descending coronary artery. Following angioplasty of the critical stenosis, coronary flow is reestablished. The patient recovered from cardiogenic shock.
This ECG shows evidence of an extensive anterolateral myocardial infarction; this patient subsequently developed cardiogenic shock.
ECG tracing shows further evolutionary changes in a patient with cardiogenic shock.
ECG tracing in a patient who developed cardiogenic shock secondary to pericarditis and pericardial tamponade.
A 63-year-old man admitted to the emergency department with clinical features of cardiogenic shock. The ECG revealed findings indicative of wide-complex tachycardia, likely ventricular tachycardia. Following cardioversion, his shock state improved. The cause of ventricular tachycardia was myocardial ischemia.
Short-axis view of the 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.
HeartMate II Left Ventricular Assist Device. Reprinted with the permission of Thoratec Corporation.
 
 
 
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