A 69-year-old man was treated 3 hours ago 81 - highsky

[ArchivalUser]

BB

[ArchivalUser]

bbb

[ArchivalUser]

SUPPOSE THE Dx IS RT H FAIL (acute ST-elevation myocardial infarction involving leads II, III, and aVF ) YHEN WHAT S THE Rx

[ArchivalUser]

even i think its B!!!!

[ArchivalUser]

(Correct Answer = A)

Hypotension in the setting of a myocardial infarction is potentially life-threatening and requires prompt diagnostic evaluation and treatment. The potential causes are diverse and include tachyarrhythmias or bradyarrhythmias, heart block, cardiogenic shock from extensive left ventricular infarction, ventricular septal rupture, papillary muscle rupture with severe mitral regurgitation, right ventricular infarction, and even ventricular free wall rupture with cardiac tamponade. The pertinent constellation of findings in this patient is hypotension, elevated jugular venous pressure with clear lung fields, and no dyspnea. Although this constellation is not very sensitive, it is highly specific for right ventricular infarction.

These manifestations represent right ventricular dysfunction out of proportion to left ventricular impairment. The lack of pulmonary congestion on examination helps to exclude other potential etiologies, such as extensive left ventricular infarction, papillary muscle rupture, and ventricular septal rupture. Right ventricular infarction is typically seen in association with left ventricular inferior myocardial infarction, as evidenced in this patient by the acute ST-segment changes in the inferior electrocardiography leads. As further illustrated by this case example, the absence of angina for more than 1 week prior to an inferior myocardial infarction predicts a higher risk for the development of right ventricular infarction, hypotension, and shock.

In patients with hypotension from a right ventricular infarction, particularly if there is no prior myocardial infarction, emergency empiric intravenous volume expansion is indicated as first-line treatment. It is important to avoid excessive volume expansion as left ventricular failure may ensue.

Inotropic support (dobutamine) or vasopressor support (dopamine) may be indicated if volume expansion is inadequate. However, these interventions are best guided by intracardiac hemodynamic monitoring of right atrial pressure, pulmonary capillary wedge pressure, and cardiac output. Empiric use of dopamine thus is not appropriate empiric therapy at this point. Readministration of a thrombolytic is not advisable owing to the risk of bleeding complications, particularly stroke.

Transcutaneous pacing would be indicated as a bridge to dual-chamber transvenous pacing for bradycardia-induced hypotension. However, a heart rate of 64/min is unlikely to account for a systolic blood pressure of 74 mm Hg. Although intra-aortic balloon pump counterpulsation has been used for shock from right ventricular infarction with variable success, it is not a first choice for empiric therapy. If medical treatment fails to correct the hemodynamic instability, this patient would warrant urgent cardiac catheterization and possible percutaneous intervention.
Bibliography

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thanks

[ArchivalUser]

thanks highsky