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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