During labor, the mother with signiicant heart disease should be kept in a semirecumbent position with a lateral tilt. Vital signs are taken frequently between contractions. Increases in pulse rate much above 100 beats per minute (bpm) or respiratory rate above 24 per minute, particularly when associated with dyspnea, may suggest impending ventricular failure. For evidence of cardiac decompensation, intensive medical management must be instituted immediately. Delivery itself does not necessarily improve the maternal condition and, in fact, may worsen it. Moreover, emergency cesarean delivery may be particularly hazardous. Clearly, both maternal and fetal status must be considered in the decision to hasten delivery under these circumstances.
Relief from pain and from apprehension is important. Although women, continuous epidural analgesia is recommended for most. The major problem with conduction analgesia is mater nal hypotension (Chap. 25, p. 491). This is especially danger ous in women with intracardiac shunts in whom low may be reversed. Hypotension can also be life-threatening if there is pulmonaY arterial hypertension or aortic stenosis because ven tricular output is dependent on adequate preload. In women with these conditions, narcotic regional analgesia or general anesthesia may be preferable.
For vaginal delivery in women with only mild cardiovas cular compromise, epidural analgesia given with intravenous sedation oten suices. his has been shown to minimize intra uum-assisted delivery. Subarachnoid blockade is not generally recommended in women with significant heart disease due to associated hypotension. For cesarean delivery, epidural analge sia is preferred by most clinicians with caveats for its use with pulmonary arterial hypertension (p. 962).
Cardiovascular decompensation during labor may manifest as pulmonary edema with hypoxia or as hypotension, or both. The proper therapeutic approach depends on the speciic hemodynamic status and the underlying cardiac lesion. For example, decompensated mitral stenosis with pulmonary edema due to luid overload is often best treated with aggressive diuresis. If precipitated by tachycardia, heart rate control with �-blocking agents is preferred. Conversely, the same treatment in a woman sufering decompensation and hypotension due to aortic stenosis could prove fatal. Unless the underlying pathophysiology is understood and the cause of the decompensation is clear, empirical therapy may be hazardous.
Women who have shown little or no evidence of cardiac compromise during pregnancy, labor, or delivery may still decompensate postpartum. Fluid mobilized into the intravascular compartment and reduced peripheral vascular resistance place higher demands on myocardial performance. Therefore, meticulous care is continued into the puerperium (Keizer, 2006; Zeeman, 2006). Postpartum hemorrhage, anemia, infection, and thromboembolism are much more serious complications with heart disease. Indeed, these factors often act in concert to precipitate postpartum heart failure. In addition, sepsis and severe preeclampsia cause or worsen pulmonary edema because of endothelial activation and capillary-alveolar leakage (Chap. 47, p. 917).
For puerperal tubal sterilization after vaginal delivery, the procedure can be delayed up to several days to ensure that the mother has normalized hemodynamically and that she is afebrile, not anemic, and ambulating normally. Alternatively, for those desiring future fertility, detailed contraceptive advice is available in the u. Medical Eligibiliy Criteria or Contraceptive Use guidelines (Curtis, 2016).