Our patient's diagnosis is pulmonary hypertension. The diagnosis is supported by the patient's history of recent dyspnea on exertion, exertional syncope, angina and lower extremity edema. We will now review our patient's cardiac bedside examination.
Summary of Hx and Px
By using our bedside skills we have together defined the pathophysiology of our patient. Starting out by simply taking the blood pressure, we found it to be a bit reduced with a narrow pulse pressure and when combined with a hypokinetic, or small, carotid impulse, we started thinking: this is a patient who may have obstruction somewhere or a reduced cardiac output or a combination of the two.
When we looked at the jugular venous pulse and we saw the giant "a" wave, the atrium struggling to put blood into the right ventricle, we defined the problem as a right sided heart disease problem. And then, when we examined the chest wall, we confirmed that. There were no findings to suggest left heart disease, we could not palpate the apical impulse. Rather, at the sternal edge we felt a right ventricular impulse and we felt an enlarged pulmonary artery, and not only did we find the sustained right ventricular impulse, but we confirmed the type of finding we saw in the neck, with the giant "a" wave that reflected the atrium contracting against increased resistance, we palpated a presystolic impulse at the lower left sternal edge which also tells us the same thing.
After we completed our precordial examination, we listened to the patient. A compelling finding at the upper right sternal edge, not [sounds], but [sounds], telling us that there was an increased second heart sound. And, as we completed the auscultatory examination, we defined that increased second sound as due to an increase in the pulmonary component of the second heart sound. We have a category of heart disease now, it is pulmonary hypertension with a loud, increased pulmonary component of the second heart sound. Then we listened at the upper left sternal edge. First, we tuned in on murmurs and we heard both a systolic and a diastolic murmur, and those murmurs increased with inspiration, telling us that they were emanating from the right side, the diastolic decrescendo, sometimes called the Graham-Steele murmur [sounds]. Very well heard, especially at the lower left sternal edge. And the short, early flow murmur [sounds] generated by increased flow in a dilated pulmonary artery in early systole. And then we tuned in on the heart sounds and we heard an ejection sound. More information that the pulmonary artery was dilated as can be seen in pulmonary hypertension.
Then, after listening at the lower left sternal edge, we went to the apex. But, before we go to the apex now, I want to remind you that at the lower left sternal edge you may not always hear the Graham-Steele murmur or at the upper left sternal edge. In patients with severe pulmonary hypertension, you may hear tricuspid regurgitation. It is quite common in that context. And when the patient breathes in you hear [sounds] and when they breathe out [sounds]. In other words, it augments with inspiration, telling you that that regurgitation is right sided. And finally, we went to the apex, and at the apex we got no help listening for low frequency sounds. We were searching for left heart disease as a cause of the pulmonary hypertension, but we heard no reflectors of left heart disease.
We have, therefore, using our bedside skills defined a patient with pulmonary hypertension. We have not only defined pulmonary hypertension, we have defined that it is severe and now we must go further to define the exact etiology, because the exact etiology determines the exact therapy.