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. A mismatch between the degree of segmental dysfunction on imaging and troponin release may be noted in the setting of stunned/hibernating myocardium or when presentation is significantly delayed after the ischemic insult. Myocardial necrosis biomarker levels may provide an idea of the extent of myocardial injury, whereas serial measurements are useful in assessing early washout after successful reperfusion and in estimating the amount of cardiac necrosis. Natriuretic peptides are significantly elevated in the setting of acute HF culminating in CS and are associated with mortality in MI-associated CS. Oxygen-carrying capacity is the product of cardiac output and the oxygen content of blood. Thus, an ineffective CI will result in inadequate peripheral tissue oxygen delivery. Elevated arterial lactic acid levels are nonspecifically indicative of tissue hypoxia but are associated with mortality in CS.The pathogenesis of lactate production in CS is uncertain, although impaired oxygen delivery, stress-induced hyperlactatemia, and impaired clearance are likely contributors. A peripheral oxygen demand-delivery mismatch will result in low central venous oxygen measurements. A mixed venous oxygen saturation sample is ideally obtained from the distal port of a pulmonary artery catheter (PAC) and is a reflection of oxygen saturation from blood returning to the heart via the superior and inferior vena cava, as well as the coronary sinus. Serial measurements of arterial lactate and mixed venous oxygen saturation levels may be helpful to temporally monitor responses to therapeutic interventions. Arterial blood gas measurements also permit the assessment of [[arterial] oxygenation and ventilation, as well as metabolic and respiratory acid-base disorders. 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. It should be noted that novel renal biomarkers such as neutrophil gelatinase–associated lipocalcin, kidney injury molecule 1, and cystatin C were not more effective than standard evaluation with serum creatinine for assessing risk. 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. This should be differentiated from chronic to subacute elevation of liver function abnormalities in the setting of venous congestion resulting from right-sided HF.
Cardiogenic shock laboratory findings
Cardiogenic shock diagnostic criteria
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Cardiac tamponade electrocardiogram
Cardiogenic shock electrocardiogram
Cardiogenic shock chest x ray
Sinoatrial arrest laboratory findings
ST elevation myocardial infarction laboratory findings