Cardiogenic Shock Workup

Updated: Aug 06, 2019
  • Author: Xiushui (Mike) Ren, MD; Chief Editor: Henry H Ooi, MD, MRCPI  more...
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Approach Considerations

As previously discussed, the keys to achieving a good outcome in patients with cardiogenic shock are 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 (ECG); and invasive hemodynamic monitoring to determine the primary mechanism causing the acute hemodynamic instability. [1, 24]  In the evaluation of hemodynamic status, pulmonary artery catheterization is a potentially important diagnostic and therapeutic tool in cardiogenic shock, including assessing the following [1, 24] :

  • The presence and severity of cardiogenic shock
  • Right ventricular involvement
  • Pulmonary artery pressures
  • Transpulmonary gradient
  • Vascular resistance of the pulmonary and systemic arterial beds

If not contraindicated and appropriate, consider further imaging if suspicion exists for acute aortic syndrome or pulmonary embolism with computed tomography (CT) scanning or transesophageal echocardiography (TEE). [1]


Laboratory Studies

The 2019 American Heart Association (AHA) scientific statement on contemporary management of cardiogenic shock recommends including the following laboratory studies: complete blood cell (CBC) count; levels of electrolytes, creatinine, lactate, and serial cardiac troponin; hepatic function studies; and arterial blood gas (ABG) [1]

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 [AST], alanine aminotransferase [ALT], and lactate dehydrogenase [LDH]), are useful for assessing proper functioning of vital organs.

Complete blood cell count

A 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 (CK) 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 fourfold 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

ABG 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, +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 (CHF) 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.


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 acute ventricular septal defect, free myocardial wall rupture, pericardial tamponade, and papillary muscle rupture causing acute myocardial regurgitation. [25]

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 [LV] ejection fraction [LVEF] is not always depressed in the setting of cardiogenic shock). If a hyperdynamic LV is found, the echocardiogram may suggest other causes of shock such as sepsis or anemia. (See the images below.)

Cardiogenic shock. A short-axis view of the left ventricle demonstrates small pericardial effusion, low ejection fraction, and segmental wall motion abnormalities. Courtesy of Michael Stone, MD, RDMS.
Cardiogenic shock. Pleural sliding in an intercostal space demonstrates 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 LV 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 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 (CAD) 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, though a smaller infarction in a previously compromised LV also may precipitate shock. After MI, large areas of nonfunctional, but viable, myocardium (hibernating myocardium) can also cause or contribute to cardiogenic shock. (See the images below.)

Cardiogenic shock. This image was obtained from a Cardiogenic shock. This image was obtained from a 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.
Cardiogenic shock. This coronary angiogram from a Cardiogenic shock. This coronary angiogram from a patient with cardiogenic shock demonstrates severe stenosis of the right coronary artery.
Cardiogenic shock. This coronary angiogram from a Cardiogenic shock. This coronary angiogram from a patient with cardiogenic shock reveals severe stenosis of the right coronary artery. Following angioplasty of the critical stenosis, coronary flow was reestablished. The patient recovered from cardiogenic shock.


Acute myocardial ischemia is diagnosed on the basis of the presence of ST-segment elevation, ST-segment depression, or Q waves. T-wave inversion, though a less sensitive finding, may also be seen in persons with myocardial ischemia. An ECG with right-side chest leads may document right ventricular (RV) infarction and may be prognostically, as well as diagnostically, useful. [19, 25]

Perform electrocardiography immediately to help diagnose MI and/or myocardial ischemia. A normal ECG, however, does not rule out the possibility of acute MI. (See the images below.)

Cardiogenic shock. This electrocardiogram shows ev Cardiogenic shock. This electrocardiogram shows evidence of an extensive anterolateral myocardial infarction. The patient subsequently developed cardiogenic shock.
Cardiogenic shock. The electrocardiogram tracing s Cardiogenic shock. The electrocardiogram tracing shows further evolutionary changes in a patient with cardiogenic shock.
Cardiogenic shock. The electrocardiogram tracing w Cardiogenic shock. The electrocardiogram tracing was obtained from a patient who developed cardiogenic shock secondary to pericarditis and pericardial tamponade.
Cardiogenic shock. A 63-year-old man was admitted Cardiogenic shock. A 63-year-old man was admitted to the emergency department with clinical features of cardiogenic shock. The electrocardiogram revealed findings indicative of wide-complex tachycardia, likely ventricular tachycardia. Following cardioversion, his shock state improved. Myocardial ischemia was the cause of the ventricular tachycardia.

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) higher than 15 mm Hg and a cardiac index lower 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 (RA) and the RV is diagnostic of ventricular septal rupture. [25]

High right-side filling pressures in the absence of an elevated PCWP, when accompanied by ECG criteria, indicate RV infarction.