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  •    In the setting of an acute MI, hypotension is not infrequent when powerful vasodilating agents like morphine sulfate and/or nitroglycerin are administered in the emergency room. Patients with acute inferior wall MI tend to be "parasympathetic" and have a high vagal tone. This explains the sinus bradycardia and lower blood pressure manifested by such patients. Relative volume contraction (caused by anorexia, nausea, vomiting and diaphoresis) coupled with drug-induced vasodilation may frequently precipitate hypotension. This is usually reversed with an aggressive fluid challenge.
  • The engorged neck veins in this patient is probably due to RV involvement and points against hypovolemic shock. Obtaining right-sided chest leads and demonstrating ST elevation in the right precordial leads will help in making the diagnosis. Evaluation of the function of the RV by echocardiography is an invaluable tool in such cases.
  • Clear lung fields, absence of tachycardia plus a warm and dry skin points against cardiogenic shock induced by primary LV pump failure.
  • Murmurs may be absent, atypical or unimpressive in nearly 50% of patients with severe papillary muscle dysfunction or rupture. However, acute pulmonary congestion or edema is present if the mitral regurgitation is severe enough to cause hypotension.
  • Please remember that rales may be absent in the early phase of acute pulmonary edema when the fluid is primarily localized in the interstitial spaces and have not made their way to the alveolar sacs (where the combination of air and fluid create the characteristic inspiratory rales of failure).
  • Although aortic dissection with involvement of the right coronary artery may be a cause of acute inferior wall MI, there is nothing in the history or physical exam to help substantiate this diagnosis.
  • Myocardial rupture is not a consideration in the acute phase of an MI since they are more likely to occurs 3-7 days after the onset of acute myocardial infarction.

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