Cardiogenic shock history and symptoms
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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 beasurements, 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, oliguria and evidence of metabolic acidosis on the blood results.[1]
History and Symptoms
Cardiogenic shock may be a complication of different conditions. Despite a common pattern of symptoms, each condition may have its specific history and presentation. Irrespective to the form of shock, most patients will present with manifestations of hypoperfusion, such as altered mental status, hypotension, oliguria, cool extremities, clammy skin, blood results with evidence of lactic acidosis and pulmonary congestion causing respiratory distress. The patient may present these symptoms immediately after the myocardial infarction, therefore manifesting them on admission, or as happens in most cases, develop them later during hospital admission.[2][3][4] These patients tend to evolve slowly into shock, first experiencing a decrease in cardiac output before hypotension is installed. This delay is thought to be due either to the failure of the compensatory mechanisms, that were initially protecting the body against the hemodynamic repercussions of the MI or, to a possible reinfarction or occurrence of mechanical complications.
Attending to the fact that acute-MI is the most common cause of this form of shock, most patients
- Anxiety, agitation, restlessness, and an altered mental state including flacid coma may be present due to decreased cerebral perfusion and ensuing hypoxia.
- Fatigue may be present due to the work of breathing and hypoxia.
References
- ↑ Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS; et al. (2005). "Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock". JAMA. 294 (4): 448–54. doi:10.1001/jama.294.4.448. PMID 16046651.
- ↑ Holmes DR, Bates ER, Kleiman NS, Sadowski Z, Horgan JH, Morris DC; et al. (1995). "Contemporary reperfusion therapy for cardiogenic shock: the GUSTO-I trial experience. The GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries". J Am Coll Cardiol. 26 (3): 668–74. PMID 7642857.
- ↑ Webb JG, Sleeper LA, Buller CE, Boland J, Palazzo A, Buller E; et al. (2000). "Implications of the timing of onset of cardiogenic shock after acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?". J Am Coll Cardiol. 36 (3 Suppl A): 1084–90. PMID 10985709.