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Cardiogenic Shock Workup

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

Approach Considerations

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.

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Laboratory Studies

Biochemical profile

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.

CBC count

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.

Cardiac enzymes

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.

Troponins

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.

Lactate

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.

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Imaging Studies

Echocardiography

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.[21]

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.)

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.

Chest radiography

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

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.)

Patient with an acute anterolateral myocardial inf 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 cardi 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 cardi 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.
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Electrocardiography

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.)

This ECG shows evidence of an extensive anterolate This ECG shows evidence of an extensive anterolateral myocardial infarction; this patient subsequently developed cardiogenic shock.
ECG tracing shows further evolutionary changes in ECG tracing shows further evolutionary changes in a patient with cardiogenic shock.
ECG tracing in a patient who developed cardiogenic ECG tracing in a patient who developed cardiogenic shock secondary to pericarditis and pericardial tamponade.
A 63-year-old man admitted to the emergency depart 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.
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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.[21]

High right-sided filling pressures in the absence of an elevated PCWP, when accompanied by electrocardiographic criteria, indicate right ventricular infarction.

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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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