One of the most common cardiac problems seen in pregnancy is maternal congenital heart disease. We describe a PDA in a pregnant patient and its effect on cardiopulmonary pathophysiology.
A 24 y.o. gravid woman with an uncorrected PDA presented at term with severe dyspnea. Vital signs: blood pressure 149/65, pulse 105, respirations 25, SaO2 97% on room air. On exam a 5/6 continuous murmur, palpable thrill and bilateral crackles were noted. A chest roentogram was consistent with congestive heart failure. Due to preeclampsia and fetal distress, caesarean section was performed. Upon intubation, frank blood was noted in the endotracheal tube. Oxygen saturations fell to 50%-70% and ventilation was difficult. A chest roentogram demonstrated bilateral fluffy infiltrates. Mechanical ventilation was initiated with high oxygen requirements. ABG revealed mild respiratory acidosis and a PaO2/FiO2 ratio of 125 mmHg. Bronchoscopy revealed blood clots throughout mainstems and in distal airways. Sequential bronchoalveolar lavage (BAL) had consistently bloody return, compatible with alveolar hemorrhage. Cytopathology revealed hemosiderin-laden macrophages. Laboratory studies revealed normal platelet count, coagulation, and renal function. Pulmonary artery (PA) pressures were elevated at 88/58 mmHg with wedge systolic of 32 mmHg. Echocardiogram showed left atrial and ventricular (LV) dilatation, dilated PA, mild LV hypertrophy, PHTN, and large PDA with left-to-right shunting. After aggressive diuresis, PA pressures and oxygen requirements improved. Repeat bronchoscopy revealed less bloody return. Patient was successfully extubated 5 days post-delivery. Follow-up echocardiogram was unchanged except for significant reduction in PA pressures. Pediatric cardiology evaluated the patient for possible PDA closure.
Pregnancy is associated with significant alterations in the cardiovascular system. A 50% increase in blood volume and cardiac output (CO) may occur. In the 1st trimester, the increase in CO is due to larger stroke volume, while higher heart rates account for later rise.1 While most patients tolerate these hemodynamic changes, those with underlying congenital heart disease are at increased risk for cardiovascular complications. In general, PDA in gravid patients carries a favorable outcome. There is increased risk if pulmonary hypertension is present, as often occurs by the time adulthood is reached. If the systemic blood pressure falls and elevated pulmonary pressures are present, shunt reversal may occur. Overall, by age 40, one-third of patients with uncorrected PDAs succumb to heart failure, endarteritis or PHTN. Our patient developed alveolar hemorrhage in association with PHTN both of which resolved post-partum. Based on studies by West et al. this is likely due to “stress failure” of pulmonary capillaries. In animal models, when capillary pressures rise, there is microscopic evidence of breakdown of the alveolar-capillary membrane, or “stress failure”. This produces edema fluid with higher protein concentrations or “high-permeability” edema rather than “hydrostatic” edema. Development of “high-permeability” edema, which includes leakage of red blood cells (RBC’s) and alveolar hemorrhage, increases as capillary pressures rise. Although not specifically recognized in patients with PDA, similar phenomena are well described in mitral stenosis, whereby increased pulmonary venous pressures lead to edema and extravasation of RBC’s, manifesting as hemoptysis. Athletes who train intensely, raising their CO and necessitating higher filling pressures, thus creating increased capillary pressures, have also presented with hemorrhagic pulmonary edema.2.
The interplay of pregnancy related hemodynamic changes and underlying PDA can lead to significant PHTN and increased capillary pressures which may present as pulmonary edema and alveolar hemorrhage. Knowledge of the hemodynamic changes associated with congenital heart disease and pregnancy will aid in understanding the pathophysiology of resulting alveolar hemorrhage and its treatment.
Amee Patrawalla, None.