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PowerPoint Discussion of the Diagnosis and Management of Pulmonary Edema and Peripartum Cardiomyopathy
Pulmonary edema is a secondary disease process characterized by pulmonary interstitial and alveolar fluid collection resulting in hypoxemia and increased work of breathing. Conceptually, pulmonary edema may be classified into the four categories of hydrostatic, increased capillary permeability, lymphatic insufficiency, and unclear etiology ( Fig. 7-1 ). As Figure 7-1 implies, pregnancy-related causes of pulmonary edema typically encompass three of the four categories. The most frequent causes of pulmonary edema in pregnancy postpartum are listed in Table 7-1 . Both tocolytic-associated pulmonary edema ( Table 7-2 ) and pulmonary edema from preeclampsia ( Table 7-3 ) are complex entities about which some controversy still exists regarding their etiology; however, changes in vascular permeability and gradient between pulmonary wedge pressure and colloid oncotic pressure play an important role in its etiology ( Fig. 7-2 ). Nonetheless, successful management of pulmonary edema is logically addressed in a standardized fashion.
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Peripartum cardiomyopathy in which maternal cardiac left ventricular systolic dysfunction and symptoms of heart failure develop between the last month of pregnancy and the fifth month postpartum. The disorder is of unknown cause and is a diagnosis of exclusion in pregnant or puerperal patients who present in congestive heart failure late in pregnancy or early in the postpartum period. Despite being traditionally classified as a late pregnancy or postpartum entity, a similar clinical presentation may be seen earlier in pregnancy and has been reported early in the second trimester of pregnancy. In the United States, the incidence of peripartum cardiomyopathy is estimated to be 1 in 3000 to 4000 live births. The worldwide incidence varies; certain populations have a reported risk of 1 in 100. Characteristics and associations seen with the diagnosis of peripartum cardiomyopathy are listed in Table 7-4 . Pulmonary edema in the patient with peripartum cardiomyopathy typically is hydrostatic in nature, with mechanistic specifics from left ventricular systolic dysfunction.
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Case 1: Peripartum Cardiomyopathy
A 34-year-old G3P2 presents to labor and delivery 6 weeks postpartum complaining of profound lower extremity edema and shortness of breath. Review of her pregnancy history indicates that she delivered a 36 twin gestation via vaginal delivery after spontaneously presenting in labor. Her pregnancy was complicated by gestational hypertension, although she never manifested the criteria to make the diagnosis of mild preeclampsia. Since discharge she has felt tired, with a progressive increase in fatigue that she initially attributed to around-the-clock care of newborn twins. Approximately 2 days prior to her presentation to the emergency department, she developed a cough, and increasing dyspnea on exertion. In the evening prior to presentation, she awoke unable to remain supine in her bed.
On admission her blood pressure was 140/65 mm Hg and her pulse was 130 beats per minute (bpm). Respirations were labored, with a respiratory rate of 35 per minute. Digital pulse oximetry saturation (room air) was 86%. Temperature was normal. Physical exam of the patient’s cardiovascular system demonstrated diffuse rales and rhonchi during lung auscultation, an S 3 gallop, and jugular venous distention. Pitting lower extremity edema was also observed. Initial arterial blood gas (100% Fi o 2 ) revealed a pH of 7.46 Pa o 2 of 140 mm Hg, Pa co 2 of 32 mm Hg, and HCO 3 – of 24 mEq/L.
The patient was immediately managed with oxygen administration, bilevel positive airway pressure (BIPAP), judicious administration of 2 mg morphine sulfate IV and furosemide 40 mg IV. Portable chest x-ray showed bilateral air-space disease, perihilar infiltrates, and bilateral small pleural effusions. Cardiomegaly was also suspected. Complete blood count (CBC) and metabolic panel were drawn; results were unremarkable. Electrocardiogram (ECG) was consistent with left atrial enlargement, sinus tachycardia, diffuse T-wave inversion, increased QRS voltage in horizontal plane leads (V 1 -V 6 ) and low QRS amplitude in limb leads. D-dimer and cardiac enzyme panel results were normal. B-type natriuretic peptide (BNP) was elevated at 900 pg/mL.
As initial therapy and diagnostic workup were begun, the patient received a bedside echocardiograph. Diffuse hypokinesis of the dilated left ventricle was immediately evident. There was also mitral valve regurgitation, left atrial enlargement, and a calculated left ventricular ejection fraction (LVEF) of 23%. A diagnosis of dilated cardiomyopathy, congestive heart failure, and pulmonary edema were made. The patient’s management rapidly became multidisciplinary in nature, with cardiovascular and ventilatory management directed by appropriately credentialed acute care physicians. The patient received her care in an acute care unit that provides continuous monitoring of ECG, blood pressure, pulse oximetry, and clinical assessment. The ability to manage acute cardiovascular and/or respiratory instability was present.
After load reduction with the angiotensin-converting enzyme inhibitor (ACE) captopril was begun. Judicious additional diuresis with furosemide (20 to 40 mg IV) was accomplished. Venous thromboembolic prophylaxis with 40 mg enoxaparin subcutaneously daily was ordered. Dobutamine and IV nitroglycerin were initiated. However, the patient became hypotensive (<90/60 mm Hg). Noninvasive assessment of cardiac output demonstrated a reduced cardiac output. At the recommendation of the patient’s consulting cardiologist, norepinephrine was started IV at 2 mcg/min, with titration to blood pressure as obtained by continuous arterial blood pressure monitoring. A central venous catheter was placed. Hypoxemia worsened and the patient was intubated, sedated, and maintained on mechanical ventilation. The use of a pulmonary artery catheter was considered, however, the patient’s condition stabilized and noninvasive assessment of the patient was sufficient for management.
On hospital day 3, the dose of norepinephrine was gradually reduced and was eventually discontinued. The patient’s systolic blood pressure remained above 90 mm Hg. Nesiritide, a recombinant human BNP used for acute decompensated heart failure, was begun by the cardiologist as a 2-mcg/kg bolus followed by continuous infusion at 0.01 mcg/kg/min. Hypoxemia resolved and work of breathing lessened as the hydrostatic pulmonary edema caused by congestive heart failure improved. The patient was successfully extubated and progressively weaned from oxygen. Nesiritide was discontinued and the patient was maintained on a daily regimen of furosemide, captopril, and eplerenone, an aldosterone agonist. The patient was eventually discharged and had an improving clinical status and echocardiographic picture. Metoprolol was begun early in the outpatient period. A search for other specific causes of the patient’s dilated cardiomyopathy was not suggestive of any other likely etiology. A presumptive diagnosis of peripartum cardiomyopathy was made. The patient was discouraged from becoming pregnant immediately and had a careful 6-month follow-up of her status by both her OB-GYN provider and her cardiologist arranged. Review of status at that time formed the basis of long-term recommendations for both general and reproductive follow up.
Discussion
This case entails both the immediate management of hydrostatic pulmonary edema and the underlying initiating pathophysiologic process of peripartum cardiomyopathy. This case is typical in that the presentation is suggestive of a cardiorespiratory process. The case example as presented is straightforward in that sufficient time has elapsed from delivery to lessen confusion from most other primary pregnancy-related diagnoses ( Table 7-5 ). Presentation of peripartum cardiomyopathy in the antenatal period or within the first 2 weeks postpartum is often confounded by confusion on the part of physicians caring for the patient in eliciting the primary diagnosis. Preeclampsia and other pregnancy-related diagnoses may be initially confused with the primary cardiac etiology of peripartum cardiomyopathy.
