1. What are the three general types of pulmonary hypertension?
ANS: a. Hyperkinetic pulmonary hypertension, i.e., that due to excess volume flow, as in large left-to-right shunts. The pulmonary arterioles can dilate to accommodate up to three times the normal cardiac output before the pulmonary artery pressure must rise.
b. Vasoactive pulmonary hypertension, i.e., that due primarily to pulmonary arteriolar constriction, as in response to either hypoxia or to a high left atrial pressure, as in patients with mitral stenosis (MS).
c. Obstructive pulmonary hypertension, i.e., that due to fixed lumen obliteration, as with pulmonary emboli, or to narrowing, as with the endothelial and medial hypertrophy seen in some ASDs, PDAs, and VSDs with bidirectional shunting (Eisenmenger reaction), or with primary pulmonary hypertension.
2. How much obstruction is necessary before an acute pulmonary embolism can produce wide, relatively fixed splitting of the S2?
ANS: Almost the entire pulmonary tree on both sides must be obstructed. If, however, pulmonary hypertension is already present due to previous disease, a further embolus to one branch may cause wide, fixed splitting.
3. Why does the S2 of a VSD with an Eisenmenger reaction become single?
ANS: This occurs because only a large VSD could produce an Eisenmenger reaction, and such a large communication between the ventricles tends to make them function as a single chamber.
4. How does the S2 differ among the three different levels of Eisenmenger syndromes, i.e., VSD, ASD, and PDA?
ANS: In VSDs the S2 is single; in ASDs it is split and fixed (often widely split); in PDAs it is normally or narrowly split and when split, it moves normally with respiration.
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