Cardiogenic shock overview: Difference between revisions
No edit summary |
No edit summary |
||
| Line 53: | Line 53: | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Cardiovascular diseases]] | [[Category:Cardiovascular diseases]] | ||
Revision as of 21:29, 28 February 2013
|
Cardiogenic Shock Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Cardiogenic shock overview On the Web |
|
American Roentgen Ray Society Images of Cardiogenic shock overview |
|
Risk calculators and risk factors for Cardiogenic shock overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Cardiogenic shock is defined as an insufficient forward cardiac output to maintain adequate perfusion of vital organs to meet ongoing demands for oxygenation and metabolism. Cardiogenic shock is due to either inadequate left ventricular pump function (such as in congestive heart failure) or inadequate left ventricular filling (such as in cardiac tamponade or mitral stenosis with tachycardia). In so far as the course of treatment differs substantially, cardiogenic shock should be distinguished from other forms of shock such as septic shock, distributive shock, hypovolemic shock and neurogenic shock.
Definition
Cardiogenic shock is defined as sustained hypotension (>30 minutes) with evidence of tissue hypoperfusion despite adequate left ventricular filling pressure. Signs of tissue hypoperfusion include oliguria (<30 mL/h), cool extremities, cyanosis and altered mentation.
The pathophysiology of cardiogenic shock is complex and multifactorial. Furthermore, there are a variety of compensatory mechanisms in response to the pathophysiology that can mask the underlying hemodynamic derangements that may be present. As a result, the diagnostic criteria for cardiogenic shock are complex and have been debated.
Given that the condition is a form of "shock", many clinicians argue that by definition "shock" must therefore be present. However, some clinicians argue that hypotension alone should not be the key criteria in so far as compensatory tachycardia and vasoconstriction may compensate for the reduced cardiac output to yield only a mildly depressed systolic blood pressure. These clinicians advocate a hemodynamic definition with greater reliance placed on hemodynamic measures and interpretation of the cardiac output in the context of left ventricular filling pressure as often gauged by the pulmonary capillary wedge pressure. For instance, a patient who has a history of hypertension who now has a blood pressure of 100 mm Hg with a markedly elevated systemic vascular resistance (SVR) and pronounced tachycardia with a markedly reduced cardiac output, would be in cardiogenic shock in the judgement of some clinicians despite the absence of hypotension. Some definitions require a drop in systolic blood pressure of 30 mm Hg.
In clinical trials, cardiogenic shock has been defined as follows by the SHOCK investigators: [1]
Clinical Criteria
- Systolic blood pressure <90 mm Hg for at least 30 minutes
- Evidence of hypoperfusion
- Cool, clammy periphery
- Decreased urine output
- Decreased level of consciousness
Hemodynamic Criteria
- Left ventricular end diastolic pressure or pulmonary capillary wedge pressure >15 mm Hg
- Cardiac index <2.2 L/min/m2
Pathophysiology
Cardiogenic shock is inadequate cardiac output due to myocardial depression caused by various factors. Inflammatory mediators generated due to infarction or ischemia cause myocardial muscle depression causing a loss in the contractile ability of the heart and in turn hypotension. Lactic acidosis that develops as a result of poor systemic perfusion also depresses the myocardium.
Epidemiology and Demographics
The incidence of cardiogenic shock among patients with acute MI is approximately 5% to 10% [2][3]
Because atherosclerosis and myocardial infarction are both more frequent among men, the number of men developing cardiogenic shock exceeds that of women. However, because women present with acute myocardial infarction at a later age than men, and because they may have more multivessel disease when they do present at a later age, a greater proportion of women with acute MI develop cardiogenic shock.[4]
Risk Factors
Several triggers have been associated with an increased risk of developing cardiogenic shock. Advanced age and MI are among the most common predisposing risk factors.
Diagnosis
Electrocardiogram
An electrocardiogram may be useful in distinguishing cardiogenic shock from septic shock or neurogenic shock. A diagnosis of cardiogenic shock is suggested by the presence of ST segment changes, new left bundle branch block or signs of a cardiomyopathy. Cardiac arrhythmias may also be present.
Chest X Ray
The chest x ray will show pulmonary edema, pulmonary vascular redistribution, enlarged hila, Kerley's B lines, and bilateral pleural effusions in patients with left ventricular failure. In contrast, a pneumonia may be present in the patient with septic shock.
The heart may be enlarged (cardiomegaly) in the patient with tamponade. A widened mediastinum may be present in the patient with aortic dissection.
The chest x ray may also be useful in excluding a tension pneumothorax that may be associated with hypotension.
Echocardiography
Echocardiography is important imaging modality in the evaluation of the patient with cardiogenic shock. It allows the clinician to distinguish cardiogenic shock from septic shock and neurogenic shock. In cardiogenic shock due to acute MI, poor wall motion will be present. In septic shock, a hypercontractile ventricle may be present. Mechanical complications such as papillary muscle rupture, pseudoaneurysm, and a ventricular septal defect may also be visualized. Valvular heart disease such as aortic stenosis, aortic insufficiency and mitral stenosis can also be assessed. Dynamic outflow obstruction such as HOCM can also be indentified and quantified. The magnitude of left ventricular dysfunction in patients with cardiomyopathy can be evaluated.
References
- ↑ Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med 1999; 341 (9) : 625–34.
- ↑ Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med. Apr 15 1999;340(15):1162-8.
- ↑ Hasdai D, Holmes DR, Topol EJ, et al. Frequency and clinical outcome of cardiogenic shock during acute myocardial infarction among patients receiving reteplase or alteplase. Results from GUSTO-III. Global Use of Strategies to Open Occluded Coronary Arteries. Eur Heart J. Jan 1999;20(2):128-35.
- ↑ Hasdai D, Califf RM, Thompson TD, et al. Predictors of cardiogenic shock after thrombolytic therapy for acute myocardial infarction. J Am Coll Cardiol. Jan 2000;35(1):136-43.