Cardiogenic shock laboratory findings
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Attending to the catastrophic outcome of cardiogenic shock in a very short time span, its diagnosis must be reached as early as possible in order for proper therapy to be started. This period until diagnosis and treatment initiation is particularly important in the case of cardiogenic shock since the mortality rate of this condition complicating acute-MI is very high, along with the fact that the ability to revert the damage caused, through reperfusion techniques, declines considerably with diagnostic delays. Therefore and due to the unstable state of these patients, the diagnostic evaluations are usually performed as supportive measures are initiated. The diagnostic measures should start with the proper history and physical examination, including blood pressure measurement, followed by an EKG, chest x-ray and collection of blood samples for evaluation. The physician should have in mind the common features of shock, irrespective of the type of shock, in order to avoid delays in the diagnosis. Although not all shock patients present in the same way, these features include: abnormal mental status, cool extremities, clammy skin, manifestations of hypoperfusion, such as hypotension and oliguria, as well as evidence of metabolic acidosis on the blood results.[1]
Laboratory Findings
As in all laboratory tests, these must be ordered in order to confirm, sustain or rule out a clinical diagnosis that has been reached after proper history and physical examination have been made. In the case of cardiogenic shock, these may include:[2][3]
Arterial Blood Gas
- Hypoxemia
- Metabolic acidosis, possibly compensated by respiratory alkalosis
Cardiac Markers
- Elevated cardiac markers, such as:
- Troponin I and Troponin T
- Elevated CK MB
Complete Blood Count
- Elevated white blood cell count (WBC), typically with a left shift. It should be noted that the WBC may be elevated in STEMI and shock in general, due to demargination of neutrophils.
- Leukopenia may be present later in shock or in alternate diagnosis of sepsis
- Platelet count may be elevated in early stages of shock due to the stress caused by this condition, however, thrombocytopenia may be noted later, in situations of resuscitation from massive hemorrhage, or in alternate diagnosis of sepsis.
Renal Function
- Elevated blood urea nitrogen
- Elevated creatinine
In case of prior normal renal function, BUN and creatinine will only be elevated later on the course of the disease. If there is prior renal insufficiency, these values will be elevated earlier.
Hypophosphatemia should be excluded as an underlying cause. Myonecrosis following hypophosphatemia may be observed in refeeding syndrome, as phosphate is used to convert glucose to glycogen.
Liver Function
- Elevated hepatic transaminases, following liver hypoperfusion
Serum Lactate
- Lactic acidosis (Anion Gap Acidosis). The level of lactic acid, particularly its serial determinations, along with compensatory decrease in serum bicarbonate, are markers of the extent of hypoperfusion and valuable in gauging a patient's prognosis. However, its utility is limited by the fact that lactic acid rises later in tissue hypoperfusion therefore, by the time it is elevated, severe tissue ischemia will already have occurred. This downside is aggravated by the constant clearance of lactic acid by the liver in the presence of normal hepatic function.[4]
References
- ↑ Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ Parrillo, Joseph (2013). Critical care medicine principles of diagnosis and management in the adult. Philadelphia, PA: Elsevier/Saunders. ISBN 0323089291.
- ↑ Cilley RE, Scharenberg AM, Bongiorno PF, Guire KE, Bartlett RH (1991). "Low oxygen delivery produced by anemia, hypoxia, and low cardiac output". J Surg Res. 51 (5): 425–33. PMID 1758176.