The bedside examination in our patient with an inferior wall myocardial infarction is important. Certainly the history is very important and the electrocardiogram. But beware, the history may be atypical and the electrocardiogram, not uncommonly, at least initially, may be entirely normal. So we must call upon all our resources and, in this case, our bedside skills to help us with the diagnosis. Now, we do this for those very good three reasons: 1) we can help to determine the severity or extent of the infarction; 2) we can help to determine if there are complication; and 3) every examination is a baseline for the next – so that if something changes, you are aware of the baseline and then of the change. It’s very important to follow patients historically, in terms of their electrocardiograms, and their bedside examination, with repetitive observations during their hospital course.
Now, sometimes very simple bedside observations are very important. For example, if the appearance of the patient reflects an anxious, diaphoretic, cold, clammy patient, then beware. In that case maybe there is an extensive infarction. A second type of very simple observation is something as simple as the heart rate. A rapid heart rate – a sinus tachycardia – could be the first clue to an extensive infarction; and a low rate – a sinus bradycardia – could be a clue that there is involvement of the right coronary artery, often associated with inferior wall infarction and the blood supply to the sa node is diminished.
Now, in our patient we did not have very many impressive bedside findings. The carotid arterial impulse, the jugular venous pulse, chest wall movement, all entirely normal, and on auscultation, the expected finding, that low-frequency fourth sound at the apex [sounds] and, of course, another subtle observation, a diminution of the first heart sound, possibly due to reduced ventricular contractility in the context of an infarction or possibly due to a long pr interval in the context of an inferior infarction.
Now, one very important point, we must ask ourselves is why was our patient’s bedside examination not that impressive? Well, possibly one reason is that we had the opportunity in this case to observe the patient early, to diagnose early, and to intervene. “time is muscle,” and just possibly, our early intervention obviated, prevented problems, and because of that, we have preserved myocardium, and that was reflected in the nearly normal bedside examination.
Our patient's course
A summary of our patient's course to this point includes the following key features: His diagnosis is an acute inferior wall myocardial infarction based on his history and the indicative changes seen in his initial electrocardiogram. He was treated with aspirin and thrombolytic therapy to be followed by angiography as soon as possible. This combined treatment given during the first few hours of an evolving infarction results in a striking decrease in mortality. After urgent treatment was begun, and the patient was pain free and stable a focused, but thorough, cardiovascular examination was carried out. It was unremarkable but for a fourth sound at the apex, an expected finding in this clinical setting. His baseline blood work drawn in the emergency department revealed a normal CBC, chemistries and clotting studies. His initial cardiac biomarkers were normal.
Acute MI cardiac markers in plasma
In the presence of acute myocardial infarction, intracellular cardiac markers appear in the plasma due to necrosis of myocardial tissue. These curves illustrate the activity and timeline for their appearance. The troponins are extremely sensitive and specific markers for myocardial necrosis. Elevated levels provide diagnostic and prognostic information. They are particularly valuable for the late diagnosis of myocardial infarction, as they remain elevated up to two weeks. The elevations in myocardial creatine kinase, or CPK, creatine kinase isoenzyme, or CK-MB, and troponins all begin approximately four hours after the onset of infarction. They are reliable for initial diagnosis twelve to sixteen hours after infarction and peak at about twenty-four hours. As with our patient, in the first three to six hours after infarction, markers might not be elevated. Tests that may detect myocardial injury in this time frame include CK-MB isoforms and myoglobin.