Cardiogenic Shock: Laboratory Evaluation, Noninvasive Testing, and Hemodynamic Monitoring – Part 3 Of Excerpts From The 2017 AHA Guidelines

This post is third of a series I’ve made for my study notes on Cardiogenic Shock. This post contains links to and excerpts from the  Laboratory Evaluation, Noninvasive Testing, and Hemodynamic section of  Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association [PubMed Abstract] [Full Text HTML] [Full Text PDF]. Circulation. 2017 Oct 17;136(16):e232-e268.

The above article has been cited by 38 PubMed Central articles.

Here are excerpts [Note to myself, I’ve linked the title headings below directly to the title headings of the article-so I can easily read the full section]:


Laboratory Evaluation

Biomarkers of cardiac myonecrosis are useful to gauge the severity of acute underlying myocardial injury in conditions such as fulminant myocarditis. In ACS, cardiac troponin is noted to be elevated and has a rise-and-fall pattern consistent with acute ischemic injury.81

Natriuretic peptides are significantly elevated in the setting of acute HF culminating in CS and are associated with mortality in
MI-associated CS.82,83

Elevated arterial lactic acid levels are nonspecifically indicative of tissue hypoxia but are associated with mortality in CS.84,85

A peripheral oxygen demand-delivery mismatch will result in low central venous oxygen measurements.

Serial measurements of arterial lactate and mixed venous oxygen saturation levels may be helpful to temporally monitor responses to therapeutic interventions.

Acute kidney injury, which is reflected by a rise in serum creatinine and a potential reduction in urinary output, in the setting of CS may indicate renal hypoperfusion and is associated with poor outcomes.87,88

Acute ischemic or congestive liver injury can occur in the setting of CS and manifests as a marked elevation in serum aspartate aminotransferase, alanine aminotransferase, serum bilirubin, and lactate dehydrogenase levels, often accompanied by an increase in prothrombin time with a peak at 24 to 72 hours that subsequently recovers to baseline within 5 to 10 days, and a ratio of alanine aminotransferase to lactate dehydrogenase of <1.5.89,90

This should be differentiated from chronic to subacute elevation of liver function abnormalities in the setting of venous congestion resulting from right-sided HF.

Noninvasive Testing

[Useful testing includes a chest x-ray, 12-lead electrocardiogram, a transesophageal echo, and]  When images are inadequate or the diagnosis remains uncertain, a transesophageal echocardiogram should be considered.

An overview of invasive hemodynamic testing and monitoring is provided later in Management of CS.

Suggestions for Clinical Practice

We suggest that all patients with CS be evaluated with an ECG, chest x-ray, and comprehensive echocardiogram with the specific purpose of understanding the dominant mechanism responsible for acute hemodynamic instability.

In the absence of contraindications, additional imaging with a computed tomography scan or transesophageal echocardiogram (as appropriate) if an acute aortic syndrome or pulmonary embolism is suspected is appropriate.

Suggested laboratory tests include a complete blood count, electrolytes, creatinine, hepatic function tests, arterial blood gas and lactate, and serial cardiac troponin levels.

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