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Peripartum Cardiomyopathy
principles and practice Peripartum Cardiomyopathy JUDY SCHMIDT, RNC, MSN, MA, MITZI BOILANGER, RNC, MS, AND SUSAN ABBOTT, RN, NP, BA Peripartum cardiomyopathy is a rare and devastating disease of unknown etiology that manifests between the last trimester of pregnancy and five postpartum months. This disease often is confused with many other illnesses, and even with hemodynamic changes in normal pregnancy. Pathophysiology, signs, and symptoms of this unique cardiomyopathy are presented and case studies offered. Since outcome of this disease is directly related to duration of the illness, nurses must be aware of the symptoms and investigate them immediately. The nurse must support the patient and involve the family and social services in the patient's recovery.
Peripartum cardiomyopathy is a rare, but devastating, disease. Seemingly triggered by pregnancy, the disease manifests between the last trimester of pregnancy and five postpartum months without obvious cause or history of heart disease (Table 1). A dilated, congestive cardiomyopathy appears. Symptoms include shortness of breath, particularly with exertion; edema; pleuritic chest pain; palpitations; tachycardia; productive cough, including hemoptysis; fatigue; and, in the extreme case, an emboli (Table 2). Actual incidence of peripartum cardiomyopathy is difficult to assess because of the variety of symptoms exhibited, misdiagnosis, and late postpartum onset. When the onset is weeks o r months into the postpartum period, but still within the fivemonth criterion, the diagnosis
may state primary cardiomyopathy, instead of peripartum cardiomyopathy. The literature reports a wide range of incidences of peripartum cardiomyopathy in the United States-from 1:1,300 to 1:15,000 live births.'-3 In Sutter Perinatal Center at Sutter Memorial Hospital, a tertiary care center that handled 26,459 deliveries from January 1984 through May 1988, five cases met definitive criteria of peripartum cardiomyopathy-an incidence of 5,292 or 1:5,300. Two more cases did not meet definitive criteria,
but the mothers developed cardiomyopathy after pregnancy. One mother exceeded the time limit of five postpartum months, and the other mother, who had been doing well with a mechanical valve in place for several years, developed cardiomyopathy during late pregnancy. ETIOLOGY To date, the precise etiology of peripartum cardiomyopathy is unknown. Various suggestions have
Table 2. Symptoms of Peripartum Cardiomyopathy Table 1. Definition of Peripartum Cardiomyopathy
No recognizable etiology of heart failure, including occult or pre-existing disease unmasked by cardiovascular stress of pregnancy.12Symptoms appear between the last trimester and five postpartum rnonth~.',~.~,~
Edema Fatigue Hernoptysis Palpitations Pleuritic chest pain Productive cough Shortness of breath Tachycardia
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465
Table 3.
Associated Conditions
Black African race Multiparity Multiple gestation Postpartum hypertension Pregnancy-induced hypertension
been proposed, such a s protozoans, virus, metabolic, poor nutrition, small vessel abnormalities, hormonal changes, maternal-fetal immunologic response, physiological stress, toxic insult, and subclinical heart disease without prior diagnosis. A look a t t h e charts and the literature shows that misdiagnoses have included pregnancy-induced hypertension, congestive heart failure, pulmonary embolus, myocardial infarction, asthma, and combinations of the aforementioned, such as pregnancy-induced hypertension complicated by congestive heart failure and asthma. Symptoms also have been attributed to variations of normal hemodynamic changes that occur in pregnancy. Increased incidence of the disease occurs with multiparity, twinning, pregnancy-induced hypertension, postpartum hypertension, and in Black African and African-American women (Table 3). All of the women reported in the following case studies a r e more than 25 years of age. Usually the family has no history of cardiomyopathy. Homans questions the increased incidence reported by o t h e r s relating t o maternal age (mature gravidas) and multiparity.’
riod, the patient may be more susceptible to developing peripartum cardiomyopathy related to the depression of left ventricular function.2 A prolongation of the preejection period and shortening of left ventricular ejection time occurs.’ Changes that transpire a r e nonspecific for peripartum cardiomyopathy, and are similar to those found in idiopathic dilated cardiomyopathy.‘ Changes include disintegration of muscle fibers, a pale and flabby heart, four chamber dilatation (especially of the left ventricle), endocardia1 thickening, mural thrombi, and myocardial fibrosis; yet the heart valves remain normal (Figure Reduction of the ejection fraction of the left ventricle and impairment of ventricular contractile
power are the main pathological features of peripartum cardiomyopathy.’ Left ventricular failure can lead to increased pulmonary artery pressure and pulmonary vascular resistance.’ The pulmonary capillary wedge pressure also will increase.’ An initial tachycardia may compensate for decreased cardiac output from the decreased stroke volume. Persistent heart failure will lead to further decreases in cardiac output and stroke volume.’*’ Left heart failure will lead to increased right atrial and ventricular pressures’*’ until cardiac failure progresses to pulmonary edema and/or effusion.’ DIAGNOSTIC~EX AMIN
ATIG
The diagnostic work-up includes a chest roentgenogram, ra-
Mitral Regurgitation
PATHOPHYSIOLOGY Because of the normal hemodynamic changes that occur during pregnancy, health-care professionals may have difficulty determining when pathological changes begin and what might trigger them. During the postpartum pe-
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Hypoki nesi s Dilated Ventricle
Figure 1. Cardiac changes associated with peripartum cardiomyopathy.
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diologic examination, electrocardiogram (ECG), echocardiogram, and laboratory tests. When cardiomyopathy is present, the radiologic exam will reveal cardiac enlargement, especially of the left ~ e n t r i c l e . ’ ~Pulmonary ’~~ congestion and pleural effusion may be present.'.'^^ The echocardiogram displays the left ventricular and left atrial dilation, as well as decreased left ventricular systolic performance. Caution must b e used if left ventricular enlargement is the only abnormality, as this could be associated with normal pregnancy.’ Ventricular thrombi also may be
Awareness of this disease is essential for proper diagnosis, treatment, and improved outcome.
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In cardiomyopathy, pulmonary vasculature is increased, showing pulmonary congestion, which can lead to pulmonary edema.6 The ECG shows nonspecific findings,’,’ which include signs of left ventricular hypertrophy; arrhythmias; occasional left bundle branch block (LBBB); changes in the QRS complex, S-T segment, and Twave; and prolongation of the P-R i n t e r ~ a l . ’ ~These ’ ~ ~ ECG changes slowly regress but may still be evident up to six months after onset of the cardiomyopathy.’ ECG changes may even persist when clinical improvement is apparent.’ In the most severe cases, a cardiac catheterization and biopsy may be necessary, which may reveal cellular hypertrophy and degenerat i o n . ’ ~Myocarditis ~ also could be diagnosed.’
PROGNOSIS Prognosis varies depending upon when, and if, the cardiomegaly resolves. Recovery within six months is considered favorable
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for long-term prognosis.’S6 A 20-60% mortality rate is associated with this condition if recovery does not occur within six months. The mortality percentage increases in patients with persistent ~ a r d i o m e g a l y . ’ ~Death ~~~ occurs usually from progressive heart failure but may be attributed to pulmonary or cerebral emboli and ventricular arrhythmia.’ Deaths have been reported to have occurred as long as eight years after the initial episode.’
TREATMENT Treatment of peripartum cardiomyopathy varies depending upon the existing signs and symptoms, as well as the gestational age of the pregnancy versus postpartum status. The first line of treatment is hospitalization and bed rest,'^^-^ which help reduce preload and benefits cardiac function.’ The use of elastic support stockings and leg exercises is beneficial in preventing emb01i.~Other treatments include aggressive cardiac care, consisting of diuretics, digitalization, afterload reduction, anticoagulation, sodium restriction, vasodilating agents, and steroid^.^.'*^ Digitalization should be gradual, since risk of digoxin toxicity increases in pregnant women.’ Care should be exercised in the use of vasodilating agents during pregnancy to maintain adequate uteroplacental perfusion.’ During pregnancy, heparin is the anticoagulant of choice. Arrhythmias are treated symptomatically after health-care professionals assess whether o r not the arrhythmias a r e related to digoxin toxicity.’ Physicians will consider cesarean delivery only for obstetrical indic a t i o n ~ . ’“Epidural ~~ anesthesia is safe in skilled hands.”’ A shortened second stage may be appropriate in vaginal delivery.’t5 Peripartum cardiomyopathy usually occurs in healthy women
with no history of cardiac disease. Cardiac transplant may be a viable treatment for those showing rapid deterioration or little or no improvement in their clinical condit i o n ~ . These ~ ’ ~ patients need intensive care and hemodynamic monitoring, since health-care professionals must stay abreast of the patients’ changing cardiac statuses.
Misdiagnoses of this devastating disease have included pregnancyinduced hypertension, asthma, congestive heart failure, pulmonary embolus, myocardial infarction, and normal pregnancy changes. PREVIOUS STUDIES One of the largest and longest studies on peripartum cardiomyopathy, by Demakis et al., followed 27 patients in Cook County, Illinois, from 1947 to 1967.3The disease’s status six months after delivery became an important prognostic indication during the 20-year study. In the Cook County group, 14 patients demonstrated normal heart size at six months after delivery and did well thereafter. Eight patients were categorized as having functional class I murmurs and four had class I1 murmurs. N o deaths occurred due to cardiomyopathy; one patient died of cervical carcinoma and one of renal disease. Eight of the 14 patients in the first (normal heart size) group had subsequent pregnancies, and 3 of those patients temporarily had recurring symptoms of peripartum cardiomyopathy. Of the remaining 13 patients who suffered from persistent cardiomegaly after the sixth postpartum month, 10 died from cardiomyopathy within 8 years (7
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within 5 years and 3 within 8 years) and 1 died after 16 years. Six of these patients had subsequent pregnancies, resulting in three maternal deaths. Hence, patients with persistent cardiomegaly after six months should not experience subsequent pregnancies.
The prognosis is related to the severity of symptoms and their postpartum durations.
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Walsh studied 15 peripartum cardiomyopathy patients who were described a s having extremely deficient nutrition.’ Only 3 of these patients resumed normal heart size by 6 months, and 9 of the 15 patients died within 29 months.’ In Seftel and Sussex’s study, 9 of 23 patients resumed normal heart size within 6 months after delivery, 5 died, 6 had persistent cardiomegaly, and 3 were unacc ~ u n t e dThis . ~ group, as with the Cook County group, was well nourished. Hughes et al. reported a peripartum cardiomyopathy death with no associated family history.” Sixteen years later, Honey wrote an additional report
t
regarding the patient’s family history.” As time progressed, this particular patient’s sisters and nephews demonstrated dilated cardiomyopathy (Figure 2). CASE STUDIES
The following five cases met definitive criteria at this tertiary hospital within a 4X-year time span. At the time of this writing, four of the women continued to experience varying severity of symptoms, and one was doing well following a cardiac transplant. Case 1
M.,a 25-year-old, married, Caucasian gravida l , para l , was brought to the emergency room three days after delivery complaining of severe and worsening shortness of breath, difficulty breathing at night, increased ankle and thigh edema, and a 20-pound weight gain. M. also experienced dizziness, abdominal distention, sore throat, fever, palpitations, chest pain, and arthralgia. When M. had seen her obstetrician she complained of increased lochia flow and general malaise, and she had severe edema of her entire lower body, which had practically doubled in size.
Older Sister
Patient
Peripartum cardiomyopathy 3 weeks’ postpartum onset Died within 10 months
-
38 years old; postpartum; First pregnancy Cardiomyopathy resolved
1st son 12 years old Dilated cardiomyopathy after coxsackie virus; cardiac transplant
Nurses play important roles in assisting with the diagnosis of peripartum cardiomyopathy.
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One month before delivery, M. complained of shortness of breath, significant fatigue, and pedal edema, which were attributed to her pregnancy. Her labor was induced, resulting in the vacuum extraction of an eight-pound, one-ounce female a t 41 weeks’ gestation. M. had epidural anesthesia during her labor, and edema was noted by the anesthesiologist. M.’s postpartum course required a blood patch for a severe headache and one episode of orthostatic hypotension. At that time, the anesthesiologist noted a II/VI systolic murmur. M.was discharged in stable condition. Three days after discharge, M. was admitted to the intensive-care unit. Several consultations were obtained, and a diagnosis of peripartum cardiomyopathy was made. A cardiac gated scan showed a right ventricular ejection fraction of 22% and a left ventricular ejection fraction of 24%, with markedly dilated chambers and general hypokinesis. M . ’ s condition progressively worsened, leading to further cardiac and renal failure. She was maintained on sodium nitroprusside, dopamine, isoproterenol, and propranolol, but her condition con-
1 Younger Sister
1
Died at 31 years of
- age of dilated
cardiomyopathy
I
2nd son Cardiomyopathy, died 2 years after ligated ductus
Figure 2. Family tree for patient who died from periparturn cardiomyopathy.
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M.’s medical history included a patent ductus arteriosus ligation at 11 months of age, a varicose vein stripping, and repair of a compressed abdominal artery. M. denied smoking, admitted to occasional alcohol use, and had used cocaine intravenously for three years, with seizures reported after one use. M. denied using cocaine since that time, which was approximately one year before her pregnancy.
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tinued to deteriorate rapidly. M. was transferred to the cardiac service and subsequently received a cardiac transplant. M. has done well since her transplant and her infant daughter also is doing well.
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The support and teaching provided by community nurses are vital parts of 0 patient care. Case 2
During her third pregnancy, F., a 33-year-old, divorced, Black, gravida 3, para 2 patient, suffered worsening shortness of breath (SOB) and dyspnea at 31 weeks’ gestation. At the time of delivery, she had two daughters, ages 15 and 1 1 , had no prior history of heart disease, and did not smoke or use alcohol or drugs. About 2% weeks after delivering a healthy female, F. experienced increasing dyspnea, orthopnea, chest pain, and congestive heart failure, for which she was hospitalized. Her ejection fractions, a t that time, were 27% on the left and 40% on the right ventricles. The left ventricle was hypertrophied. A diagnosis of probable peripartum cardiomyopathy was made with no specific treatment ordered at discharge. Plan of care included rest, a low-salt diet, and further observation. At 3% postpartum months, F. experienced bronchitis, wheezing, and coughing. Her PO, was 74, Pcol 26, and pH 7.51. F. was treated with diuretics for her congestive heart failure. She was also treated with antibiotics and a bronchodilator. Approximately one month later, F. was hospitalized and found to have severe mitral regurgitation, as well as moderate tricuspid regurgitation (measured 4+/4+ during cardiac catheterization), causing a worsening congestive heart failure. F. had atrial fibrillation, anemia, and hyperthyroidism. A
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mitral valve replacement, annuloplasty of the tricuspid valve, and left ventricular biopsy were performed in a single surgery. The left ventricle demonstrated hypertrophy with diffuse hypokinesis. F. was discharged on a regimen of furosemide, potassium, warfarin sodium, and digoxin. F. was readmitted to the emergency room o n e day after discharge, complaining of nausea, vomiting, and syncope. A toxic digoxin level and a normal potassium level were obtained. While still in the emergency room, before inpatient admission, F. experienced a cardiac arrest and a long anoxic seizure. Cardiopulmonary resuscitation and cardioversion were immediately initiated by the emergency room nurses and lidocaine therapy followed. F.’s digoxin level was allowed to drop to a low level, but arrhythmias and tachycardia persisted. The patient tolerated verapamil, which was used to lower her pulse to 100. An electrophysiology study was refused before discharge. Approximately five weeks later, F. was again admitted with a lower right quadrant pain and an elevated white blood cell count of 14,500. Health-care professionals initially diagnosed appendicitis. Surgery was scheduled late in the day, so that F. could leave the hospital temporarily to take care of personal business and make child-care arrangements. Upon readmission, F. felt better and her white blood cell count had improved. A pulmonary embolus was then suspected, but a negative echocardiogram was obtained. A cardiac evaluation showed ejection fractions a t 20-25%, an enlarged atria, a n enlarged right ventricle, and improved size of the left ventricle since F.’s valve replacement, with mild to moderate regurgitation. At eight postpartum months, F.’s home therapy consisted of a
low-sodium, low-cholesterol diet and a regimen of daily warfarin sodium, furosemide, potassium, and verapamil. F. experienced shortness of breath, congestive heart failure, and decreased exertion tolerance. (She could not even lift her infant.) F.’s older daughters were helpful and supportive. On occasion, F. was visited by a public health nurse, who provided moral support to the family and assisted in coordinating medical needs and resources, such as food stamps. F.’s prognosis is poor. Case 3
R., a 26-year-old, married, Black gravida 2, para 2, developed peripartum cardiomyopathy after her second pregnancy in September 1985. R. had no prior cardiovascular disease and a normal first pregnancy in 1981. R.’s dyspnea began one week before delivery and worsened after delivery with the onset of weakness and edema. After two visits to the emergency room, R. was diagnosed as having cardiomegaly, pulmonary venous hypertension, and alveolar and interstitial edema. R. was hospitalized, and cardiac consultation was requested. The cardiac diagnostic workup showed a dilated, hypokinetic,left ventricle with 1+ mitral regurgitation. R. was treated with furosemide, digoxin, and potassium. She was advised to follow a no-added salt diet and t o quit smoking. Over the next year, R. experienced decreasing stamina, chest discomfort, and worsening dyspnea on exertion. She did not suffer overt left heart failure. R.’s ejection fraction was 34%, and biopsy revealed hypokinesis and moderate enlargement of the left ventricle. Approximately 2% years after giving birth, R.’s symptoms still persist, but she has an improved ejection fraction and fewer symptoms. Her only routine medication
469
is indomethacin three times a day. R. is a passive and dependent person,ga tendency that was exaggerated during the initial stages of her illness. R. currently works a s a child-care supervisor; although, her prognosis is uncertain. Case 4
G., a 36-year-old, married, Hispanic, gravida 3, para 2 migrant worker, was 37 weeks’ gestation. After several emergency room visits, G. was admitted to her local hospital for complaints of respiratory difficulties for the past six weeks. The initial diagnosis had been bronchitis, for which C . had been treated with ampicillin and sent home from t h e emergency room. When C . showed no improvement, a diagnosis of asthma was made, which was treated with theophylline. Signs and symptoms included paroxysmal nocturnal dyspnea (PND), shortness of breath causing an inability to lie down, and a cough. G. had no history of respiratory or cardiac disease and had one episode of hypertension, without recurrence, 15 years earlier when s h e had thyroid surgery. C.’s family medical history included coronary artery disease in her father and asthma in her mother. Upon G.’s admission, a pulmonary specialist was consulted. He diagnosed congestive heart failure, not asthma, probably related to an infectious cause. G. was taken off theophylline and treated with erythromycin, without much improvement. Electrocardiogram showed a left bundle branch block, and a cardiac consultation was obtained. At this time, C. was thought t o have pregnancy-induced hypertension, and the cardiac consultation attributed the congestive heart failure t o t h e pregnancy-induced hypertension and pregnancy. C . was transferred
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to t h e intensive care unit and started on a regimen of intravenous apresoline, MgS04,2L O2 per cannula, and furosemide. A consultation from a tertiary center was obtained, and G. was transferred on 3 g/h of MgS04. G. also was noted t o have generalized edema and an S3 gallop. On admission to t h e tertiary center, G. was assessed and delivered, by primary cesarean section, of a male infant at 37 weeks’ gestation. A Swan-Ganz catheter was inserted before surgery to monitor G.’s fluid levels. The pulmonary artery diastolic pressures went as high as from 35 to 40 with surgery. A cardiac consultation was obtained. Postpartum, G. was admitted to the intensive care unit and placed on a regimen of nitroprusside. G. slowly improved and was transferred to the high-risk maternity unit. After G. experienced an acute episode of respiratory distress, a pulmonary angiogram showed pulmonary edema and a right pleural effusion with exudate of unknown etiology. C. also underwent echocardiogram, multiple gated acquisition scanning, cardiac catherization, and a thoracentesis during her postpartum course. Cardiac studies showed a borderline, increased, pulmonary wedge pressure of 13, with no evidence of increased vascular resistance; normal cardiac output; a dilated left ventricle with diffuse moderate hypokinesis; a normal right ventricle; and a left ventricular ejection fraction of 43%, with 49% in the right ventricle. The apex appeared to have an ischemic area. A discharge diagnosis of pulmonary edema secondary to hypertension and peripartum cardiomyopathy was made. C . was discharged on a regimen of captopril, clonidine, furosemide, and ktabs and restricted to a 2 g/day sodium diet. G.’s prognosis was
“somewhat guarded,” and she was advised to stay under the supervision of a cardiologist. At six postpartum weeks, follow-up on this patient was unknown. Case 5
C., a 29-year-old, married, Caucasian gravida 5, para 2, was hospitalized at 37 weeks’ gestation with a headache, hypertension, edema, anemia, and blurred vision. At 39 weeks, C. experienced her second cesarean section. Postoperative, C. was anemic, dyspneic, wheezing, and had a cough with hemoptysis. On the third postoperative day, C. received three units of packed cells. Following a pulmonary consultation and treatment for obstructive airway disease with decreased breath sounds, crackles, and wheeze, as well as a facial, sacral, and pedal edema, and an S3 gallop with a booming S1 and S2, C. was discharged with a diagnosis of fluid overload and allergic lung disease. Medications prescribed were digoxin, lasix, erythromycin, and an inhaler. A 20-pound weight loss immediately followed. Persistent symptoms led to the referral of a cardiology consult. An initial diagnosis of pulmonary hypertension was later changed to peripartum cardiomyopathy. C.’s ejection fractions worsened in four days’ time, from 35-40% to 25-30%, with pericardial effusion, mitral and tricuspid regurgitation, a palpable closure of the pulmonary valve, and congestive heart failure. C. had smoked for 15 years but had quit during the early stages of her last pregnancy. Prior to pregnancy, C. had a past history of six months’ cocaine abuse. C.’s family did not have a history of coronary disease. Although C.’s symptoms persisted one year after delivery, she had improved and was usually
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stable on a regimen of lasix, digoxin, and potassium. C. was eager to learn more about her disease and prognosis, which was uncertain. C. learned to use her medications, and discussed her activity, low-salt diet, treatment, and need for support and information with the cardiology clinical nurse spelong-term prognosis cialist. c . ’ ~ remains guarded, and she requires frequent monitoring of her cardiac status. NURSING IMPLICATIONS A nurse’s most important role in assisting peripartum cardiomyopathy patients may well lie in the ability to contribute to the initial diagnosis. An office, antepartum, or postpartum nurse may detect subtle changes occurring in a patient that might initially be attributed to normal physiological changes of pregnancy or the postpartum period. A perceptive nurse will notice these changes a r e beyond what is considered normal and will discuss any concerns with the patient’s physician, leading to further tests and possibly diagnosis. During the postpartum period, the office nurse also may detect the slow recovery or the worsening signs and symptoms of the disease. Hospital nurses may see more dramatic signs of peripartum cardiomyopathy related t o t h e stress of labor and the hemodynamic changes of the postpartum patient. When initial diagnosis is made; the nurse must provide emotional support, since uncertainty of the prognosis can leave a patient and her family in turmoil. Assessing a patient’s support system and coping strategies and recommending appropriate referrals, including social services and occupational therapy, are important. The family, which plays a major role in the patient’s support and prognosis,
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also may need counseling to cope during this difficult time. During pregnancy, fetal outcome is an additional concern. The nurse must be available to t h e patient and willing to listen to the patient’s concerns, which requires time and energy. A nurse’s responsibilities vary with the needs of each patient. Mild disease may only limit a patient’s activities, while severe disease can lead to intensive care and possibly a cardiac transplant. A patient who experiences shortness of breath, chest pain, fatigue, palpitations, and tachycardia will require frequent rest periods, timed activities, and a n altered lifestyle. Patients who experience severe edema should be reminded to rest frequently with their feet up and to wear prescribed antiembolic stockings. The nurse must understand a patient’s limitations, assist the patient with activities, and educate the patient and family on the disease process, limitations, and expectations. The nurse can help a patient tailor her activities t o meet her current status, understand medication instructions and the rationale behind the treatment, and review future reproductive considerations. Depending on her condition, the patient may breastfeed and still show improvement. Patients suffering from peripartum cardiomyopathy should be advised against using oral contraceptives, which increase the risk of pulmonary or systemic emboli. To date, however, the Pill is not linked to this peripartum cardiomyopathy.2 Patients should be advised against subsequent pregnancies, especially those patients with residual cardiac dysfuncti~n.’.‘.~ Nurses involved in the care of these patients need to be alert to changes in patients’ statuses and report the changes immediately to
the physicians. Nurses must be sensitive to the needs of the patients and their families during this devastating time.
SUMMARY Peripartum cardiomyopathy is a profoundly serious disease with no recognizable etiology. The signs and symptoms often a r e confused with a multiple of other illnesses or with normal hemodynamic changes in pregnancy. Peripartum cardiomyopathy may recur in subsequent pregnancies, especially if the heart has not returned to normal size within six months.’-3 Nurses play vital roles in the care of peripartum cardiomyopathy patients and their families. T h e most important areas in which nurses serve are in assisting with the initial diagnosis and in the continued education and support of these patients throughout the course of the disease. Further research needs to be conducted on peripartum cardiomyopathy. Areas that should be investigated include nutritional and genetic influences in the pathophysiology of this devastating disease.
REFERENCES 1. Homans, D. 1985. Peripartum cardiomyopathy-Medical intelligence. N Engl J Med. 312(22): 1432-37. 2. Julian, D., and P. Szekely. 1985. Peripartum cardiomyopathy. Prog Cardiouasc Dis. 27(4):223-40. 3. Demakis, J., et al. 1971. Natural course of peripartum cardiomyopathy. Circulation. 44: 1053-61. 4. Goodwin, J.F., and C.M. Oakley. 1972. The cardiomyopathies. Br Heart . I 34:545-52. . 5. Goodwin, J.F. 1975. Peripartal heart disease. Clin Obstet Cynecol. 18(3):125-31. 6. Weitz, C., and M. Spence. 1983. Peripartal cardiomyopathy. Obstet Cynecol. 62:555.
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7. Aroney, C., F. Khafagi, C. Boyle, et al. 1986. Peripartum cardiomyopathy: Echocardiographic features in five cases. Am J Obstet Gynecol. 155( 1): 103-6. 8. Walsh, J.J., G. Burch, W.C. Black, et al. 1965. Idiopathic myocardiopathy of the puerperium (postpartial heart disease). Br Heart J. 32:19-31. 9. Seftel, H., and M. Susser. 1961. Maternity & myocardiac failure in African women. Br Heart J. 23:4351. 10. Hughes, R.A., P. Kapur, G.C. Sutton, e t a]. 1970. A c a s e of fatal peri-partum cardiomyopathy. Br Heart J. 32:272-76. 11. Honey, M. 1986. A case of fatal
postpartum cardiomyopathy. Br Heart J. 55:1:114. 12. Cunningham, G., et al. 1986. Peripartum heart failure: Idiopathic cardiomyopathy o r compounding cardiovascular events? Obstet Gynecol. 67(2):157-67. A more extended bibliography is available from the author. Address for correspondence: J u d y Schmidt, R N , 11061 Autumnwind Lane, Rancho Cordova, CA 956704268. Judy Schmidt is an obstetrical clinical nurse specialist at Sutter Perinatal Center, Sutter
Memorial Hospital, in Sacramento, California. Ms. Schmidt is a member of NAACOG, the California Perinatal Association, and Sigma Theta Tau. Mitzi Boilanger is an obstetrical clinical nurse specialist at Sutter Perinatal Center, Sutter Memorial Hospital, in Sacramento, California. Ms. Boilanger is a member of NAACOG, the California Perinatal Association, and Sigma Theta Tau. Susan Abbott is in private practice as an obstetric-gynecologic nurse practitioner. Ms. Abbott is a member of NAACOG, the California Coalition of Nurse Practitioners,and the Preterm Advisory Committee, State of California.
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Peripartum cardiomyopathy is a rare, but devastating, disease. Seemingly triggered by pregnancy, the disease manifests between the last trimester of pregnancy and five postpartum months without obvious cause or history of heart disease (Table 1). A dilated, congestive cardiomyopathy appears. Symptoms include shortness of breath, particularly with exertion; edema; pleuritic chest pain; palpitations; tachycardia; productive cough, including hemoptysis; fatigue; and, in the extreme case, an emboli (Table 2). Actual incidence of peripartum cardiomyopathy is difficult to assess because of the variety of symptoms exhibited, misdiagnosis, and late postpartum onset. When the onset is weeks o r months into the postpartum period, but still within the fivemonth criterion, the diagnosis
may state primary cardiomyopathy, instead of peripartum cardiomyopathy. The literature reports a wide range of incidences of peripartum cardiomyopathy in the United States-from 1:1,300 to 1:15,000 live births.'-3 In Sutter Perinatal Center at Sutter Memorial Hospital, a tertiary care center that handled 26,459 deliveries from January 1984 through May 1988, five cases met definitive criteria of peripartum cardiomyopathy-an incidence of 5,292 or 1:5,300. Two more cases did not meet definitive criteria,
but the mothers developed cardiomyopathy after pregnancy. One mother exceeded the time limit of five postpartum months, and the other mother, who had been doing well with a mechanical valve in place for several years, developed cardiomyopathy during late pregnancy. ETIOLOGY To date, the precise etiology of peripartum cardiomyopathy is unknown. Various suggestions have
Table 2. Symptoms of Peripartum Cardiomyopathy Table 1. Definition of Peripartum Cardiomyopathy
No recognizable etiology of heart failure, including occult or pre-existing disease unmasked by cardiovascular stress of pregnancy.12Symptoms appear between the last trimester and five postpartum rnonth~.',~.~,~
Edema Fatigue Hernoptysis Palpitations Pleuritic chest pain Productive cough Shortness of breath Tachycardia
Accepted: December 1988
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465
Table 3.
Associated Conditions
Black African race Multiparity Multiple gestation Postpartum hypertension Pregnancy-induced hypertension
been proposed, such a s protozoans, virus, metabolic, poor nutrition, small vessel abnormalities, hormonal changes, maternal-fetal immunologic response, physiological stress, toxic insult, and subclinical heart disease without prior diagnosis. A look a t t h e charts and the literature shows that misdiagnoses have included pregnancy-induced hypertension, congestive heart failure, pulmonary embolus, myocardial infarction, asthma, and combinations of the aforementioned, such as pregnancy-induced hypertension complicated by congestive heart failure and asthma. Symptoms also have been attributed to variations of normal hemodynamic changes that occur in pregnancy. Increased incidence of the disease occurs with multiparity, twinning, pregnancy-induced hypertension, postpartum hypertension, and in Black African and African-American women (Table 3). All of the women reported in the following case studies a r e more than 25 years of age. Usually the family has no history of cardiomyopathy. Homans questions the increased incidence reported by o t h e r s relating t o maternal age (mature gravidas) and multiparity.’
riod, the patient may be more susceptible to developing peripartum cardiomyopathy related to the depression of left ventricular function.2 A prolongation of the preejection period and shortening of left ventricular ejection time occurs.’ Changes that transpire a r e nonspecific for peripartum cardiomyopathy, and are similar to those found in idiopathic dilated cardiomyopathy.‘ Changes include disintegration of muscle fibers, a pale and flabby heart, four chamber dilatation (especially of the left ventricle), endocardia1 thickening, mural thrombi, and myocardial fibrosis; yet the heart valves remain normal (Figure Reduction of the ejection fraction of the left ventricle and impairment of ventricular contractile
power are the main pathological features of peripartum cardiomyopathy.’ Left ventricular failure can lead to increased pulmonary artery pressure and pulmonary vascular resistance.’ The pulmonary capillary wedge pressure also will increase.’ An initial tachycardia may compensate for decreased cardiac output from the decreased stroke volume. Persistent heart failure will lead to further decreases in cardiac output and stroke volume.’*’ Left heart failure will lead to increased right atrial and ventricular pressures’*’ until cardiac failure progresses to pulmonary edema and/or effusion.’ DIAGNOSTIC~EX AMIN
ATIG
The diagnostic work-up includes a chest roentgenogram, ra-
Mitral Regurgitation
PATHOPHYSIOLOGY Because of the normal hemodynamic changes that occur during pregnancy, health-care professionals may have difficulty determining when pathological changes begin and what might trigger them. During the postpartum pe-
466
Hypoki nesi s Dilated Ventricle
Figure 1. Cardiac changes associated with peripartum cardiomyopathy.
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diologic examination, electrocardiogram (ECG), echocardiogram, and laboratory tests. When cardiomyopathy is present, the radiologic exam will reveal cardiac enlargement, especially of the left ~ e n t r i c l e . ’ ~Pulmonary ’~~ congestion and pleural effusion may be present.'.'^^ The echocardiogram displays the left ventricular and left atrial dilation, as well as decreased left ventricular systolic performance. Caution must b e used if left ventricular enlargement is the only abnormality, as this could be associated with normal pregnancy.’ Ventricular thrombi also may be
Awareness of this disease is essential for proper diagnosis, treatment, and improved outcome.
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In cardiomyopathy, pulmonary vasculature is increased, showing pulmonary congestion, which can lead to pulmonary edema.6 The ECG shows nonspecific findings,’,’ which include signs of left ventricular hypertrophy; arrhythmias; occasional left bundle branch block (LBBB); changes in the QRS complex, S-T segment, and Twave; and prolongation of the P-R i n t e r ~ a l . ’ ~These ’ ~ ~ ECG changes slowly regress but may still be evident up to six months after onset of the cardiomyopathy.’ ECG changes may even persist when clinical improvement is apparent.’ In the most severe cases, a cardiac catheterization and biopsy may be necessary, which may reveal cellular hypertrophy and degenerat i o n . ’ ~Myocarditis ~ also could be diagnosed.’
PROGNOSIS Prognosis varies depending upon when, and if, the cardiomegaly resolves. Recovery within six months is considered favorable
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for long-term prognosis.’S6 A 20-60% mortality rate is associated with this condition if recovery does not occur within six months. The mortality percentage increases in patients with persistent ~ a r d i o m e g a l y . ’ ~Death ~~~ occurs usually from progressive heart failure but may be attributed to pulmonary or cerebral emboli and ventricular arrhythmia.’ Deaths have been reported to have occurred as long as eight years after the initial episode.’
TREATMENT Treatment of peripartum cardiomyopathy varies depending upon the existing signs and symptoms, as well as the gestational age of the pregnancy versus postpartum status. The first line of treatment is hospitalization and bed rest,'^^-^ which help reduce preload and benefits cardiac function.’ The use of elastic support stockings and leg exercises is beneficial in preventing emb01i.~Other treatments include aggressive cardiac care, consisting of diuretics, digitalization, afterload reduction, anticoagulation, sodium restriction, vasodilating agents, and steroid^.^.'*^ Digitalization should be gradual, since risk of digoxin toxicity increases in pregnant women.’ Care should be exercised in the use of vasodilating agents during pregnancy to maintain adequate uteroplacental perfusion.’ During pregnancy, heparin is the anticoagulant of choice. Arrhythmias are treated symptomatically after health-care professionals assess whether o r not the arrhythmias a r e related to digoxin toxicity.’ Physicians will consider cesarean delivery only for obstetrical indic a t i o n ~ . ’“Epidural ~~ anesthesia is safe in skilled hands.”’ A shortened second stage may be appropriate in vaginal delivery.’t5 Peripartum cardiomyopathy usually occurs in healthy women
with no history of cardiac disease. Cardiac transplant may be a viable treatment for those showing rapid deterioration or little or no improvement in their clinical condit i o n ~ . These ~ ’ ~ patients need intensive care and hemodynamic monitoring, since health-care professionals must stay abreast of the patients’ changing cardiac statuses.
Misdiagnoses of this devastating disease have included pregnancyinduced hypertension, asthma, congestive heart failure, pulmonary embolus, myocardial infarction, and normal pregnancy changes. PREVIOUS STUDIES One of the largest and longest studies on peripartum cardiomyopathy, by Demakis et al., followed 27 patients in Cook County, Illinois, from 1947 to 1967.3The disease’s status six months after delivery became an important prognostic indication during the 20-year study. In the Cook County group, 14 patients demonstrated normal heart size at six months after delivery and did well thereafter. Eight patients were categorized as having functional class I murmurs and four had class I1 murmurs. N o deaths occurred due to cardiomyopathy; one patient died of cervical carcinoma and one of renal disease. Eight of the 14 patients in the first (normal heart size) group had subsequent pregnancies, and 3 of those patients temporarily had recurring symptoms of peripartum cardiomyopathy. Of the remaining 13 patients who suffered from persistent cardiomegaly after the sixth postpartum month, 10 died from cardiomyopathy within 8 years (7
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within 5 years and 3 within 8 years) and 1 died after 16 years. Six of these patients had subsequent pregnancies, resulting in three maternal deaths. Hence, patients with persistent cardiomegaly after six months should not experience subsequent pregnancies.
The prognosis is related to the severity of symptoms and their postpartum durations.
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Walsh studied 15 peripartum cardiomyopathy patients who were described a s having extremely deficient nutrition.’ Only 3 of these patients resumed normal heart size by 6 months, and 9 of the 15 patients died within 29 months.’ In Seftel and Sussex’s study, 9 of 23 patients resumed normal heart size within 6 months after delivery, 5 died, 6 had persistent cardiomegaly, and 3 were unacc ~ u n t e dThis . ~ group, as with the Cook County group, was well nourished. Hughes et al. reported a peripartum cardiomyopathy death with no associated family history.” Sixteen years later, Honey wrote an additional report
t
regarding the patient’s family history.” As time progressed, this particular patient’s sisters and nephews demonstrated dilated cardiomyopathy (Figure 2). CASE STUDIES
The following five cases met definitive criteria at this tertiary hospital within a 4X-year time span. At the time of this writing, four of the women continued to experience varying severity of symptoms, and one was doing well following a cardiac transplant. Case 1
M.,a 25-year-old, married, Caucasian gravida l , para l , was brought to the emergency room three days after delivery complaining of severe and worsening shortness of breath, difficulty breathing at night, increased ankle and thigh edema, and a 20-pound weight gain. M. also experienced dizziness, abdominal distention, sore throat, fever, palpitations, chest pain, and arthralgia. When M. had seen her obstetrician she complained of increased lochia flow and general malaise, and she had severe edema of her entire lower body, which had practically doubled in size.
Older Sister
Patient
Peripartum cardiomyopathy 3 weeks’ postpartum onset Died within 10 months
-
38 years old; postpartum; First pregnancy Cardiomyopathy resolved
1st son 12 years old Dilated cardiomyopathy after coxsackie virus; cardiac transplant
Nurses play important roles in assisting with the diagnosis of peripartum cardiomyopathy.
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One month before delivery, M. complained of shortness of breath, significant fatigue, and pedal edema, which were attributed to her pregnancy. Her labor was induced, resulting in the vacuum extraction of an eight-pound, one-ounce female a t 41 weeks’ gestation. M. had epidural anesthesia during her labor, and edema was noted by the anesthesiologist. M.’s postpartum course required a blood patch for a severe headache and one episode of orthostatic hypotension. At that time, the anesthesiologist noted a II/VI systolic murmur. M.was discharged in stable condition. Three days after discharge, M. was admitted to the intensive-care unit. Several consultations were obtained, and a diagnosis of peripartum cardiomyopathy was made. A cardiac gated scan showed a right ventricular ejection fraction of 22% and a left ventricular ejection fraction of 24%, with markedly dilated chambers and general hypokinesis. M . ’ s condition progressively worsened, leading to further cardiac and renal failure. She was maintained on sodium nitroprusside, dopamine, isoproterenol, and propranolol, but her condition con-
1 Younger Sister
1
Died at 31 years of
- age of dilated
cardiomyopathy
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2nd son Cardiomyopathy, died 2 years after ligated ductus
Figure 2. Family tree for patient who died from periparturn cardiomyopathy.
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M.’s medical history included a patent ductus arteriosus ligation at 11 months of age, a varicose vein stripping, and repair of a compressed abdominal artery. M. denied smoking, admitted to occasional alcohol use, and had used cocaine intravenously for three years, with seizures reported after one use. M. denied using cocaine since that time, which was approximately one year before her pregnancy.
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tinued to deteriorate rapidly. M. was transferred to the cardiac service and subsequently received a cardiac transplant. M. has done well since her transplant and her infant daughter also is doing well.
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The support and teaching provided by community nurses are vital parts of 0 patient care. Case 2
During her third pregnancy, F., a 33-year-old, divorced, Black, gravida 3, para 2 patient, suffered worsening shortness of breath (SOB) and dyspnea at 31 weeks’ gestation. At the time of delivery, she had two daughters, ages 15 and 1 1 , had no prior history of heart disease, and did not smoke or use alcohol or drugs. About 2% weeks after delivering a healthy female, F. experienced increasing dyspnea, orthopnea, chest pain, and congestive heart failure, for which she was hospitalized. Her ejection fractions, a t that time, were 27% on the left and 40% on the right ventricles. The left ventricle was hypertrophied. A diagnosis of probable peripartum cardiomyopathy was made with no specific treatment ordered at discharge. Plan of care included rest, a low-salt diet, and further observation. At 3% postpartum months, F. experienced bronchitis, wheezing, and coughing. Her PO, was 74, Pcol 26, and pH 7.51. F. was treated with diuretics for her congestive heart failure. She was also treated with antibiotics and a bronchodilator. Approximately one month later, F. was hospitalized and found to have severe mitral regurgitation, as well as moderate tricuspid regurgitation (measured 4+/4+ during cardiac catheterization), causing a worsening congestive heart failure. F. had atrial fibrillation, anemia, and hyperthyroidism. A
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mitral valve replacement, annuloplasty of the tricuspid valve, and left ventricular biopsy were performed in a single surgery. The left ventricle demonstrated hypertrophy with diffuse hypokinesis. F. was discharged on a regimen of furosemide, potassium, warfarin sodium, and digoxin. F. was readmitted to the emergency room o n e day after discharge, complaining of nausea, vomiting, and syncope. A toxic digoxin level and a normal potassium level were obtained. While still in the emergency room, before inpatient admission, F. experienced a cardiac arrest and a long anoxic seizure. Cardiopulmonary resuscitation and cardioversion were immediately initiated by the emergency room nurses and lidocaine therapy followed. F.’s digoxin level was allowed to drop to a low level, but arrhythmias and tachycardia persisted. The patient tolerated verapamil, which was used to lower her pulse to 100. An electrophysiology study was refused before discharge. Approximately five weeks later, F. was again admitted with a lower right quadrant pain and an elevated white blood cell count of 14,500. Health-care professionals initially diagnosed appendicitis. Surgery was scheduled late in the day, so that F. could leave the hospital temporarily to take care of personal business and make child-care arrangements. Upon readmission, F. felt better and her white blood cell count had improved. A pulmonary embolus was then suspected, but a negative echocardiogram was obtained. A cardiac evaluation showed ejection fractions a t 20-25%, an enlarged atria, a n enlarged right ventricle, and improved size of the left ventricle since F.’s valve replacement, with mild to moderate regurgitation. At eight postpartum months, F.’s home therapy consisted of a
low-sodium, low-cholesterol diet and a regimen of daily warfarin sodium, furosemide, potassium, and verapamil. F. experienced shortness of breath, congestive heart failure, and decreased exertion tolerance. (She could not even lift her infant.) F.’s older daughters were helpful and supportive. On occasion, F. was visited by a public health nurse, who provided moral support to the family and assisted in coordinating medical needs and resources, such as food stamps. F.’s prognosis is poor. Case 3
R., a 26-year-old, married, Black gravida 2, para 2, developed peripartum cardiomyopathy after her second pregnancy in September 1985. R. had no prior cardiovascular disease and a normal first pregnancy in 1981. R.’s dyspnea began one week before delivery and worsened after delivery with the onset of weakness and edema. After two visits to the emergency room, R. was diagnosed as having cardiomegaly, pulmonary venous hypertension, and alveolar and interstitial edema. R. was hospitalized, and cardiac consultation was requested. The cardiac diagnostic workup showed a dilated, hypokinetic,left ventricle with 1+ mitral regurgitation. R. was treated with furosemide, digoxin, and potassium. She was advised to follow a no-added salt diet and t o quit smoking. Over the next year, R. experienced decreasing stamina, chest discomfort, and worsening dyspnea on exertion. She did not suffer overt left heart failure. R.’s ejection fraction was 34%, and biopsy revealed hypokinesis and moderate enlargement of the left ventricle. Approximately 2% years after giving birth, R.’s symptoms still persist, but she has an improved ejection fraction and fewer symptoms. Her only routine medication
469
is indomethacin three times a day. R. is a passive and dependent person,ga tendency that was exaggerated during the initial stages of her illness. R. currently works a s a child-care supervisor; although, her prognosis is uncertain. Case 4
G., a 36-year-old, married, Hispanic, gravida 3, para 2 migrant worker, was 37 weeks’ gestation. After several emergency room visits, G. was admitted to her local hospital for complaints of respiratory difficulties for the past six weeks. The initial diagnosis had been bronchitis, for which C . had been treated with ampicillin and sent home from t h e emergency room. When C . showed no improvement, a diagnosis of asthma was made, which was treated with theophylline. Signs and symptoms included paroxysmal nocturnal dyspnea (PND), shortness of breath causing an inability to lie down, and a cough. G. had no history of respiratory or cardiac disease and had one episode of hypertension, without recurrence, 15 years earlier when s h e had thyroid surgery. C.’s family medical history included coronary artery disease in her father and asthma in her mother. Upon G.’s admission, a pulmonary specialist was consulted. He diagnosed congestive heart failure, not asthma, probably related to an infectious cause. G. was taken off theophylline and treated with erythromycin, without much improvement. Electrocardiogram showed a left bundle branch block, and a cardiac consultation was obtained. At this time, C. was thought t o have pregnancy-induced hypertension, and the cardiac consultation attributed the congestive heart failure t o t h e pregnancy-induced hypertension and pregnancy. C . was transferred
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to t h e intensive care unit and started on a regimen of intravenous apresoline, MgS04,2L O2 per cannula, and furosemide. A consultation from a tertiary center was obtained, and G. was transferred on 3 g/h of MgS04. G. also was noted t o have generalized edema and an S3 gallop. On admission to t h e tertiary center, G. was assessed and delivered, by primary cesarean section, of a male infant at 37 weeks’ gestation. A Swan-Ganz catheter was inserted before surgery to monitor G.’s fluid levels. The pulmonary artery diastolic pressures went as high as from 35 to 40 with surgery. A cardiac consultation was obtained. Postpartum, G. was admitted to the intensive care unit and placed on a regimen of nitroprusside. G. slowly improved and was transferred to the high-risk maternity unit. After G. experienced an acute episode of respiratory distress, a pulmonary angiogram showed pulmonary edema and a right pleural effusion with exudate of unknown etiology. C. also underwent echocardiogram, multiple gated acquisition scanning, cardiac catherization, and a thoracentesis during her postpartum course. Cardiac studies showed a borderline, increased, pulmonary wedge pressure of 13, with no evidence of increased vascular resistance; normal cardiac output; a dilated left ventricle with diffuse moderate hypokinesis; a normal right ventricle; and a left ventricular ejection fraction of 43%, with 49% in the right ventricle. The apex appeared to have an ischemic area. A discharge diagnosis of pulmonary edema secondary to hypertension and peripartum cardiomyopathy was made. C . was discharged on a regimen of captopril, clonidine, furosemide, and ktabs and restricted to a 2 g/day sodium diet. G.’s prognosis was
“somewhat guarded,” and she was advised to stay under the supervision of a cardiologist. At six postpartum weeks, follow-up on this patient was unknown. Case 5
C., a 29-year-old, married, Caucasian gravida 5, para 2, was hospitalized at 37 weeks’ gestation with a headache, hypertension, edema, anemia, and blurred vision. At 39 weeks, C. experienced her second cesarean section. Postoperative, C. was anemic, dyspneic, wheezing, and had a cough with hemoptysis. On the third postoperative day, C. received three units of packed cells. Following a pulmonary consultation and treatment for obstructive airway disease with decreased breath sounds, crackles, and wheeze, as well as a facial, sacral, and pedal edema, and an S3 gallop with a booming S1 and S2, C. was discharged with a diagnosis of fluid overload and allergic lung disease. Medications prescribed were digoxin, lasix, erythromycin, and an inhaler. A 20-pound weight loss immediately followed. Persistent symptoms led to the referral of a cardiology consult. An initial diagnosis of pulmonary hypertension was later changed to peripartum cardiomyopathy. C.’s ejection fractions worsened in four days’ time, from 35-40% to 25-30%, with pericardial effusion, mitral and tricuspid regurgitation, a palpable closure of the pulmonary valve, and congestive heart failure. C. had smoked for 15 years but had quit during the early stages of her last pregnancy. Prior to pregnancy, C. had a past history of six months’ cocaine abuse. C.’s family did not have a history of coronary disease. Although C.’s symptoms persisted one year after delivery, she had improved and was usually
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stable on a regimen of lasix, digoxin, and potassium. C. was eager to learn more about her disease and prognosis, which was uncertain. C. learned to use her medications, and discussed her activity, low-salt diet, treatment, and need for support and information with the cardiology clinical nurse spelong-term prognosis cialist. c . ’ ~ remains guarded, and she requires frequent monitoring of her cardiac status. NURSING IMPLICATIONS A nurse’s most important role in assisting peripartum cardiomyopathy patients may well lie in the ability to contribute to the initial diagnosis. An office, antepartum, or postpartum nurse may detect subtle changes occurring in a patient that might initially be attributed to normal physiological changes of pregnancy or the postpartum period. A perceptive nurse will notice these changes a r e beyond what is considered normal and will discuss any concerns with the patient’s physician, leading to further tests and possibly diagnosis. During the postpartum period, the office nurse also may detect the slow recovery or the worsening signs and symptoms of the disease. Hospital nurses may see more dramatic signs of peripartum cardiomyopathy related t o t h e stress of labor and the hemodynamic changes of the postpartum patient. When initial diagnosis is made; the nurse must provide emotional support, since uncertainty of the prognosis can leave a patient and her family in turmoil. Assessing a patient’s support system and coping strategies and recommending appropriate referrals, including social services and occupational therapy, are important. The family, which plays a major role in the patient’s support and prognosis,
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also may need counseling to cope during this difficult time. During pregnancy, fetal outcome is an additional concern. The nurse must be available to t h e patient and willing to listen to the patient’s concerns, which requires time and energy. A nurse’s responsibilities vary with the needs of each patient. Mild disease may only limit a patient’s activities, while severe disease can lead to intensive care and possibly a cardiac transplant. A patient who experiences shortness of breath, chest pain, fatigue, palpitations, and tachycardia will require frequent rest periods, timed activities, and a n altered lifestyle. Patients who experience severe edema should be reminded to rest frequently with their feet up and to wear prescribed antiembolic stockings. The nurse must understand a patient’s limitations, assist the patient with activities, and educate the patient and family on the disease process, limitations, and expectations. The nurse can help a patient tailor her activities t o meet her current status, understand medication instructions and the rationale behind the treatment, and review future reproductive considerations. Depending on her condition, the patient may breastfeed and still show improvement. Patients suffering from peripartum cardiomyopathy should be advised against using oral contraceptives, which increase the risk of pulmonary or systemic emboli. To date, however, the Pill is not linked to this peripartum cardiomyopathy.2 Patients should be advised against subsequent pregnancies, especially those patients with residual cardiac dysfuncti~n.’.‘.~ Nurses involved in the care of these patients need to be alert to changes in patients’ statuses and report the changes immediately to
the physicians. Nurses must be sensitive to the needs of the patients and their families during this devastating time.
SUMMARY Peripartum cardiomyopathy is a profoundly serious disease with no recognizable etiology. The signs and symptoms often a r e confused with a multiple of other illnesses or with normal hemodynamic changes in pregnancy. Peripartum cardiomyopathy may recur in subsequent pregnancies, especially if the heart has not returned to normal size within six months.’-3 Nurses play vital roles in the care of peripartum cardiomyopathy patients and their families. T h e most important areas in which nurses serve are in assisting with the initial diagnosis and in the continued education and support of these patients throughout the course of the disease. Further research needs to be conducted on peripartum cardiomyopathy. Areas that should be investigated include nutritional and genetic influences in the pathophysiology of this devastating disease.
REFERENCES 1. Homans, D. 1985. Peripartum cardiomyopathy-Medical intelligence. N Engl J Med. 312(22): 1432-37. 2. Julian, D., and P. Szekely. 1985. Peripartum cardiomyopathy. Prog Cardiouasc Dis. 27(4):223-40. 3. Demakis, J., et al. 1971. Natural course of peripartum cardiomyopathy. Circulation. 44: 1053-61. 4. Goodwin, J.F., and C.M. Oakley. 1972. The cardiomyopathies. Br Heart . I 34:545-52. . 5. Goodwin, J.F. 1975. Peripartal heart disease. Clin Obstet Cynecol. 18(3):125-31. 6. Weitz, C., and M. Spence. 1983. Peripartal cardiomyopathy. Obstet Cynecol. 62:555.
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7. Aroney, C., F. Khafagi, C. Boyle, et al. 1986. Peripartum cardiomyopathy: Echocardiographic features in five cases. Am J Obstet Gynecol. 155( 1): 103-6. 8. Walsh, J.J., G. Burch, W.C. Black, et al. 1965. Idiopathic myocardiopathy of the puerperium (postpartial heart disease). Br Heart J. 32:19-31. 9. Seftel, H., and M. Susser. 1961. Maternity & myocardiac failure in African women. Br Heart J. 23:4351. 10. Hughes, R.A., P. Kapur, G.C. Sutton, e t a]. 1970. A c a s e of fatal peri-partum cardiomyopathy. Br Heart J. 32:272-76. 11. Honey, M. 1986. A case of fatal
postpartum cardiomyopathy. Br Heart J. 55:1:114. 12. Cunningham, G., et al. 1986. Peripartum heart failure: Idiopathic cardiomyopathy o r compounding cardiovascular events? Obstet Gynecol. 67(2):157-67. A more extended bibliography is available from the author. Address for correspondence: J u d y Schmidt, R N , 11061 Autumnwind Lane, Rancho Cordova, CA 956704268. Judy Schmidt is an obstetrical clinical nurse specialist at Sutter Perinatal Center, Sutter
Memorial Hospital, in Sacramento, California. Ms. Schmidt is a member of NAACOG, the California Perinatal Association, and Sigma Theta Tau. Mitzi Boilanger is an obstetrical clinical nurse specialist at Sutter Perinatal Center, Sutter Memorial Hospital, in Sacramento, California. Ms. Boilanger is a member of NAACOG, the California Perinatal Association, and Sigma Theta Tau. Susan Abbott is in private practice as an obstetric-gynecologic nurse practitioner. Ms. Abbott is a member of NAACOG, the California Coalition of Nurse Practitioners,and the Preterm Advisory Committee, State of California.
NEONATAL MANUSCRIPTS SOUGHT
JOGNN welcomes the chance to review clinical and research manuscripts on the following topics. Neonatal Intensive Care Drug Therapy Update Adoption Hyaline Membrane Disease Fever in the Neonate Cardiac Catheterization in the Neonate Neonatal Emergencies Sudden Infant Death Syndrome Trends in Neonatal Technology Thermoregulation Ventilatory Care of the Neonate Editor, 409 12th St., S.W., For more topic information and author guidelines, write to JOG" Washington, DC 20024-21 91.
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