Cardiogenic shock physical examination
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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 and oliguria, as well as evidence of metabolic acidosis on the blood results.[1]
Physical Examination
Patients in cardiogenic shock, generally complicating acute-MI, often present to the hospital with signs of end-organ hypoperfusion, such as altered mentation and agitated. The typical physical examination may include:[2]
- Vital Signs
- Hypotension with narrow pulse pressure. However, due to increased SVR blood pressure may be normal
- Tachycardia (90-110 beats/min) with a weak pulse or bradycardia if in the presence of high-grade heart block
- Neck
- Distended jugular veins due to increased jugular venous pressure
- Skin
- Heart
- Soft S1
- S3 gallop
- Systolic murmurs if in the presence of mechanical complications, such as mitral regurgitation or ventricle septal rupture:
- Acute mitral regurgitation - there may be a soft pansystolic murmur heard best at the apex area, radiating to the axilla, with no thrill (may be absent in left ventricle systolic function impairment or in increased left atrial pressure)[3][4][5]
- Ventricle Septal Rupture - there may be a harsh pansystolic murmur, heard best at the lower left sternal border and with a thrill in 50% of the cases, however, its absence does not rule out VSR. This finding in the setting of hemodynamic compromise following an MI may be mistaken for acute mitral regurgitation, with which it may occur simultaneously[3][6][7]
- Lungs
- Tachypnea due to sympathetic nervous system stimulation by stretch receptors and as compensation for metabolic acidosis
- Cheyne-Stokes respiration
- Pulmonary edema (fluid in the lungs) due to insufficient pumping of the heart, leading to fluid accumulation
- Rales on auscultation, commonly in left ventricle failure
- Genitourinary
On the particular case of right ventricle myocardial infarction, the physical examination will generally reveal a clear lung auscultation. There will also often be a so called triad of signs (with poor sensitivity for diagnosis):[3][8][9]
There may also be findings of:[10]
- Tricuspid regurgitation
- Right ventricle gallop
- Atrio-ventricular block
- Pulsus paradoxus
- Kussmaul's sign, often present in constrictive pericarditis
(The presence of increased JVP and Kussmaul's sign is both specific and sensitive for the diagnosis of right ventricle myocardial infarction)
In the case of occurrence of free wall rupture, the physical examination may be consistent with the findings in cardiac tamponade and therefore include:
- Softened heart sounds
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.
- ↑ 3.0 3.1 3.2 Ng, R.; Yeghiazarians, Y. (2011). "Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies". Journal of Intensive Care Medicine. 28 (3): 151–165. doi:10.1177/0885066611411407. ISSN 0885-0666.
- ↑ Braunwald, Eugene (2012). Braunwald's heart disease : a textbook of cardiovascular medicine. Philadelphia: Saunders. ISBN 1437703984.
- ↑ Stout KK, Verrier ED (2009). "Acute valvular regurgitation". Circulation. 119 (25): 3232–41. doi:10.1161/CIRCULATIONAHA.108.782292. PMID 19564568.
- ↑ Reeder GS (1995). "Identification and treatment of complications of myocardial infarction". Mayo Clin Proc. 70 (9): 880–4. doi:10.1016/S0025-6196(11)63946-3. PMID 7643642.
- ↑ Cohn, Lawrence (2012). Cardiac surgery in the adult. New York: McGraw-Hill Medical. ISBN 007163312X.
- ↑ Cohn JN, Guiha NH, Broder MI, Limas CJ (1974). "Right ventricular infarction. Clinical and hemodynamic features". Am J Cardiol. 33 (2): 209–14. PMID 4810018.
- ↑ Dell'Italia LJ, Starling MR, O'Rourke RA (1983). "Physical examination for exclusion of hemodynamically important right ventricular infarction". Ann Intern Med. 99 (5): 608–11. PMID 6638720.
- ↑ Haji SA, Movahed A (2000). "Right ventricular infarction--diagnosis and treatment". Clin Cardiol. 23 (7): 473–82. PMID 10894433.