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Aortic Stenosis in Pregnancy: A Case Report
Aortic Stenosis in Pregnancy: A Case Report Kimberly A. Comport, RN, MSN, Janet K. Seng, RN, MSN
=This
case report describes a pregnant patient with severe aortic stenosis. A multidisciplinary plan of care was developed for the antepartum, intraparturn, postpartum, and, ultimately, postoperative clinical course. Salient points reviewed include normal cardiovascular anatomy and physiology, hemodynamic and physiologic changes of pregnancy, bicuspid aortic valvular stenosis, and the patient's clinical data profile. Numerous psychosocialstresses and the need for specialized nursing added to the complexity of caring for this patient. JOGNN, 26,67-77; 1997. Accepted: June 1995
agement of patients at high risk because of aortic stenosis is possible in part through the use of surveillance technologies previously available only in intensive care units. The newly established specialty area of critical care obstetrics presents an opportunity for collaboration and sharing of expertise between obstetric nurses and critical care nurses.
T h e newly established specialty area of critical care obstetrics presents a
The number of pregnant women presenting with preexisting valvular heart disease has increased during the past 2 decades. Advances in neonatal and pediatric medicine have allowed women with congenital heart defects to reach childbearing age. In addition, women with heart disease who previously were discouraged from becoming pregnant because of probable negative outcomes recently have been encouraged by reports of successful pregnancies. However, the maternal mortality rates for these patients remain disturbingly high, ranging from 5% to 20% for aortic stenosis (Clark, Cotton, Hankins, & Phelon, 1991; Ramin, Maberry, & Gilstrap, 1989).The incidence of aortic stenosis in pregnancy is relatively rare for two reasons. It is found more frequently in men than women, and severe stenosis is uncommon in women of childbearing age (Bashore & Lieberman, 1993; Easterling, Chadwick, Otto, & Benedetti, 1988; Creasy & Resnik, 1989). Successful man-
*Descriptive information has been altered to protect the confidentiality of the patient.
JanuaryIFebruary 1997
challenging opportunity for collaboration and sharing of expertise between obstetric nurses and critical care nurses.
This article describes the cooperative team approach used in the clinical management of an obstetric patient with severe aortic stenosis who underwent cardiac surgery after giving birth. Information on care of patients with this diagnosis is limited in nursing literature. The following case report presents cardiovascular and obstetric aspects of care.
Case Report D.Z., a white 22-year-old gravida 1, para 0, presented to our tertiary care center for antepartal care at 28 weeks gestation. She was referred by her obstetrician because of severe aortic stenosis. The perinatologist had asked the perinatal clinical JOGNN 67
nurse specialist (CNS) to meet with the patient to develop preadmission rapport and coordinate hospital care. The cardiovascular CNS subsequently became involved in developing the plan of care for the patient. During the initial interview, the perinatal CNS obtained a medical and psychosocial history. The patient had a history of congenital aortic stenosis, first diagnosed at age 7. She became symptomatic progressively during her childhood and young adulthood. At present, she was unable to work and her income was limited to disability payments. She reported a history of fatigue, orthopnea, and paroxysmal nocturnal dyspnea. Other pertinent medical history included Hashimoto’s thyroiditis and mitral valve prolapse. Medications included .125 mg levothyroxine daily, prenatal vitamins, and iron. The patient was unmarried, but maintained a close personal relationship with the baby’s father, who was her only source of emotional support. D.Z. and her partner voiced many concerns about their current living arrangement with her family. She reported a history of abusive relationships within the family, including emotional and sexual abuse. However, it was not possible financially for the couple to maintain an independent residence because D.Z.’s partner was unemployed and she was physically disabled. It became increasingly clear that nursing care of this patient would be complex, not only because of the underlying medical problems, but also because of numerous psychosocial concerns. An additional complicating factor was the limited intellectual capability of the patient and her partner. After the initial meeting between D.Z. and the perinatal CNS, a general outline of patient care was devised for antepartum, intrapartum, and postpartum management. Planning team members were the perinatal CNS, the cardiovascular CNS, the chief obstetric resident, and the perinatologist. The primary goals of treatment were to avoid hypotension and tachycardia by maintaining adequate intravascular volume status (Austin & Davis, 1991; Kirkland, 1992). Because the patient had transportation problems that prevented her from keeping prenatal care appointments, her next interaction with health care providers occurred when she was hospitalized for preterm labor and gastroenteritis at 34 weeks gestation. Contractions were occurring every 3 minutes; the cervix was closed, thick, and high; and membranes were intact. Sonography showed the fetus in a vertex presentation at the 40th percentile of growth and an anterior grade I placenta. Biornetrics confirmed appropriate growth in comparison with previous studies. Fetal assessment via biophysical profile was reassuring (score: 10/10). Umbilical artery doppler flow studies (continuous wave doppler) were slightly elevated, with a systolic/diastolic ratio of 3.73. The fetal heart rate tracing was reactive, with a baseline 68 JOGNN
rate of 140-150 beats per minute (bpm). A fetal echocardiogram had not been completed because the mother had missed prenatal care appointments. The potential risk of fetal congenital heart disease had been addressed extensively with the patient (Nora, Berg & Nora, 1991). The reported incidence of congenital heart defects in the offspring of women with heart defects ranges from 3.4% to 16.1% (Elkayam & Gleicher, 1990). D.Z.’s general physical appearance was cachectic and frail; her weight was 105 pounds (47.25 kg) on a 5foot (1.5 m) frame. She presented with a flat affect and avoided eye contact initially. She complained of shortness of breath and chest pain on exertion and occasionally at rest. Her lungs were clear to auscultation, and respirations were easy and unlabored on room air. Her skin was pale, warm, and dry to touch, with a capillary refill of less than 2 seconds. Blood pressure readings were in the range between 90 and 100 and more than 50 and 70. A grade IV-VM systolic murmur was present in the aortic area, with radiation to the back and carotids. All other physical findings were within normal limits. D.Z.’s preterm labor was stopped, using magnesium sulfate as the tocolytic drug. Ritodrine hydrochloride was contraindicated in this patient because beta-agonists often induce tachycardia. Maintaining the patient on an oral sympathomimetic agent (i.e., terbutaline) was contraindicated for the same reason. After the patient was stabilized, a cardiology workup was initiated to determine the extent of her aortic stenosis. A 12-lead electrocardiogram showed normal sinus rhythm with sinus arrhythmia (rate varied with the respiratory cycle). An echocardiogram revealed mild to moderate aortic stenosis, with an aortic valve gradient of 25-32 mm Hg. Three valve leaflets could not be visualized well. The study concluded that there was a congenital bicuspid aortic valve. In addition, the anterior leaflet of the mitral valve was thickened and redundant, allowing a trivial mitral regurgitation. Based on her clinical presentation and diagnostic findings, the patient’s condition was determined to be Class 11-111 in the New York Heart Association Functional Classification scheme for cardiac disease (Braunwald, 1992) (see Table 1) and Group I1 according to Clark’s classification system of risk status for pregnant women (Clark et al., 1991) (see Table 2). The patient was discharged after a 3-day hospital stay. Because of the nature of her condition, a detailed multidisciplinary plan for delivery was developed by the health care team with the assistance of an anesthesiologist and a cardiologist (see Table 3). Prophylatic antibiotic was recommended for prevention of subacute bacterial endocarditis associated with mitral valve prolapse and existing aortic valve disease. The cardiologist thought that a pulmonary artery catheter was indicated to monitor hemodynamic status because the patient’s clinical status might Volume 26, Number 1
Hemodynamics
Class
Definition
Class I
No limitation of physical activity. Ordinary activity does not cause undue fatigue, palpitations, dyspnea, or angina. Slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitations, dyspnea, or angina. Marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitations, dyspnea, or angina. Inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or angina may be present even at rest, and are intensified by activity.
Class I1
Class 111
Class IV
deteriorate with the stress of labor. Pulmonary artery data could be used to avoid hypovolemia throughout labor, delivery, and the postpartum recovery period. Continuous electrocardiogram monitoring was planned to detect possible cardiac rhythm disturbances, particularly atrial arrhythmia. The anesthesiology department was consulted about pulmonary artery catheter placement and pain management during labor and delivery. The consensus in the department was that regional anesthesia should be avoided with this patient because of the severity of her aortic stenosis, even though regional anesthesia (i.e., epidural, pudendal) can be used with caution for most cardiac patients. There is risk of hypotension in patients with tight aortic stenosis because their cardiac output cannot increase across the stenotic valve. Such patients depend on appropriate venous return (end-diastolic volume or preload). Decreased cardiac output results in a secondary reduction in myocardial perfusion via the coronary arteries (Gabbe, Niebyl, & Simpson, 1991). Planned interventions included follow-up by the perinatal and cardiovascular CNSs and nursing staff education about anticipated care and invasive hemodynamic monitoring. A patient care conference with the critical care obstetric nursing team was held to discuss the care plan for this patient. The social services department was consulted about assistance with psychosocial and financial aspects of care. The need for postpartum home follow-up was also identified and addressed at this time.
January/February 1997
Before addressing the pathophysiology of aortic stenosis, normal cardiac anatomy and physiology are presented (see Figure 1).Atria are low pressure chambers that serve as reservoirs of blood for the ventricles. The right atrium receives deoxygenated venous blood via the inferior and superior vena cavae. The left atrium receives oxygenated blood returning to the heart from the pulmonary veins. Blood flows from the atria to the ventricles during diastole because of the one-way action of the atrioventricular valves and the existing pressure differentials. The tricuspid valve lies between the right atrium and the right ventricle, whereas the mitral valve lies between the left atrium and the left ventricle. The ventricles serve as pumps to expel blood. The right ventricle pumps deoxygenated blood to the lungs via the pulmonary artery. The left ventricle pumps oxygenated blood into the systemic circulation via the aorta. Blood flow out of the ventricles to the great vessels during systole requires opening of the pulmonic and aortic valves. The pulmonic valve directs blood flow from the right ventricle into the pulmonary artery and blood flow from the left ventricle passes through the aortic valve into the aorta (Marieb, 1992). Cardiac output is the amount of blood ejected from the left ventricle and is the product of stroke volume and
TABLE 2 Mortality Risk Associated with Pregnancy GROUP 1: Mortality < 1% Atrial septal defect Ventricular septal defect (uncomplicated) Patent ductus arteriosus Pulmonic and tricuspid disease Corrected tetralogy of Fallot Biosynthetic valve prosthesis (porcine and human) Mitral stenosis, NYHA class I and I1 GROUP 2: Mortality 5% to 15% Mitral stenosis with atrial fibrillation Mechanical valve prosthesis Mitral stenosis, NYHA class 111 or IV Aortic stenosis Coarctation of the aorta (uncomplicated) Uncorrected tetralogy of Fallot Previous myocardial infarction Marfan’s syndrome with normal aorta GROUP 3: Mortality 25% to 50% Pulmonary hypertension Coarctation of the aorta (complicated) Marfan’s syndrome with aortic involvement Note. From Critical Cure Obstetrics. (2nd ed.)., by S. L. Clark, D. B. Cotton, G. D. Hawkins, & J. P. Phelan (Eds.), 1991, Boston, MA: Blackwell Scientific Publications. Copyright 1991 by Blackwell Scientific Publications. Adapted with permission.
JOGNN 69
TABLE 3
Plan of Care for Obstetric Patient With Aortic Stenosis C;O‘llS:
Adcquatc matern;il/utcro-pla~~ntal pertusion Stal7le hemodyn;imic st;itus Adequate fluid v o l u m e status Decrease ‘inxicry No evidence ot infection o r tliroinhoeinh~~lisin secondary to valvular heart disease Adcquntc pain control Ma tern a 1-i n fan t attach men t he ha v iors
Potential Problems
Hemodynamic Effects
Interventions
Arrhythmia: atrial arrhythmia, tachycardia
Decreased preload Decreased cardiac output Hypotension
Institute continuous ECG monitoring Maintain heart rate in range of 60-100 bpm Avoid beta agonists Initiate continuous pulse oximetry Monitor fetus with continuous external fetal monitoring Obtain intravenous access Control pain
Peripheral vasodilation
Decreased afterload Decreased preload Decreased cardiac output Hypotension
Avoid regional anesthesia (for D. Z.) Assess pulmonary artery pressure via pulmonary artery catheter if available
Fluid volume deficit
Decreased preload Decreased cardiac output Hypotension Decreased urine output
Avoid blood loss Intravenous pitocin after placental delivery Fundal massage Maintain pulmonary capillary wedge pressure at 16-18 mm Hg Titrate intravenous fluids to maintain adequate hydration per: -Hernodynamic parameters -Urine output (> 30 mihour) Gentle pushing to avoid erratic venous return associated with Valsalva
Fluid volume overload
Increased preload Pulmonary congestion
Fowler’s position (avoid lithotomy position) Double concentrate intravenous meds (i.e., Pitocin) Regulate intravenous fluids via infusor device Diuretics as ordered Strict intake and output Weigh patient daily Maintain pulmonary capillary wedge pressure at 16-18 mm Hg Anticipate postpartum autotransfusion Avoid infusion of colloids during delivery Close hemodynamic monitoring Auscultate lung sounds every hour during labor and postpartum
Increased risk of pulmonary edema
(continues)
70 JOGNN
Volume 26, Number 1
TABLE 3 (continued)
Plan of Care for Obstetric Patient With Aortic Stenosis Potential Probliwrs
Hivnodvnrrrnic- Effects
lrrtimriwtioris
Patient anxiety
Tachycardia Decreased cardiac output
Remain with patient during labor and delivery Provide adequate pain control Consult clinical nurse specialist, social service, neonatal intensive care unit as needed Educate patient about diagnosis, treatment of cardiac disease, labor and delivery, neonatal workup, well baby care and follow-up Keep patient informed of all tesdtreatments Teach and review relaxation and breathing techniques with patient Provide family-centered care Promote parentauinfant attachment behaviors Coordinate discharge planning
Hypoxemia
Tachycardia
Continuous pulse oximetry Oxygen and suction at bedside Apply oxygen via face mask for oxygen saturation < 92% Continuous electronic fetal monitoring to assess for fetal distress Consolidate nursing interventions to avoid patient's fatigue Limit activities Provide calm, quiet atmosphere
Thromboem boli
Decreased perfusion to affected organ
Apply thigh high thromboembolic support stockings Anticoagulation via subcutaneous heparin (does not cross placental barrier) Maintain adequate hydration Control arrhythmia
Infection
Tachycardia Increased cardiac output
Subacute bacterial endocarditis antibiotic prophylaxis Antipyretics as needed Strict sterile technique for line insertion Monitor for leukocytosis
heart rate. This parameter reflects the overall functional capacity of the left ventricle to maintain satisfactory blood pressure and organ perfusion. Cardiac output is affected by the heart rate as well as the interaction of three variables that influence stroke volume. These variables are preload, afterload, and contractility. Stroke volume is the amount of blood (in milliliters) ejected from the heart in one beat. JanuarylFebruary 1997
Preload is determined by intraventricular volume and pressure and is related to the existing myocardial muscle fiber length. Rising volume and pressure stretch the muscle fibers and, in a normal heart, increase cardiac output. As blood vessels relax or dilate, the cardiac output increases. Conversely, if blood vessels constrict, the cardiac output decreases. Contractility, or the inotropic state of the heart, is reflected in the force and velocity of JOG"
71
systemic vascular resistance (Easterling & Benedetti, 1991). The high volume, low resistance state that accounts for the characteristic hemodynamic profile in pregnancy is summarized in Table 5.
R e g n a n t women experience several significant changes from the normal hemodynamic profile.
FIGURE 1
Cardiac anatomy and normal pressures in pregnancy. IVC, inferior vena cava; SVC, superior vena cava; RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle; PA, pulmonary artery; AO, aorta; P C W , pulmonary capillary wedge pressure.
ventricular ejection when preload and afterload remain constant. Changes in intracardiac pressure generated by the contraction and relaxation of the cardiac muscle produce pressure gradients that facilitate the direction and velocity of blood flow into and out of the ventricles. The size and condition of the cardiac valves also affects the direction and velocity of flow. This is addressed in greater detail below.
Hemodynamics in Normal Pregnancy Several significant alterations from the normal hemodynamic profile occur in the pregnant patient as a result of the physiologic adaptation to the growing fetus (see Table 4). These adaptations include an increase in circulating blood volume to as much as 50% higher than in the nonpregnant state. The etiology of this hypervolemic state includes renin-induced aldosterone secretion associated with sodium and water retention and increased red blood cell mass (Hibbard, 1989).This higher volume status, accompanied by increases in maternal heart rate and stroke volume, leads to a 30% to 50% increase in the cardiac output. The increase in stroke volume occurs in early pregnancy but not as pregnancy advances. Heart rate and cardiac output continue to increase throughout pregnancy. Despite the dramatic increase in cardiac output associated with pregnancy, blood pressure is maintained at or near nonpregnant values because of a hormonally mediated decrease in the 72 JOGNN
Normal, healthy, expectant mothers adjust readily to the physiologic changes of pregnancy. In women with coexisting cardiac disease, the added workload of pregnancy can precipitate complications. This is most evident clinically between 26 and 34 weeks gestation, when blood volume reaches its peak. Immediately after delivery, an autotransfusion of approximately 1,000 ml of uterine blood shifts into the systemic circulation. This physiologic phenomenon represents another potentially dangerous time for the woman with aortic stenosis because of limitations of cardiovascular adaptation.
Valvular Heart Disease Valvular heart disease is acquired or congenital. Acquired valvular disease results primarily from inflammatory or degenerative changes over time, and therefore symptoms usually are not manifested until later in life. Congenital valvular disease is the result of a malformation present at birth. In the case of aortic stenosis, this malformation, present in 1% to 2% of the general population, is a bicuspid aortic valve rather than the normal three-cusp (leaflet) aortic valve (Schlant, 1991) (see Figure 2). The abnormal structure of a congenitally bicuspid valve, as found in this case, induces turbulent blood flow through the valve. This turbulence over time traumatizes the valve leaflets and ultimately leads to fibrosis, increased rigidity, and calcification of the leaflets. Subsequently, this results in narrowing (stenosis) of the aortic valve orifice (Braunwald, 1992). The basic hemodynamic feature of aortic stenosis is an obstruction to left ventricular ejection, which can lead ultimately to a low cardiac output. In general, the cross-sectional area of the valve orifice must be narrowed to less than one third of normal before clinically significant obstruction is produced. In response to this narrowing, the left ventricle hypertrophies to generate stronger contractions. These stronger contractions are Volume 26, Number 1
heart failure, angina pectoris, and syncope (Schlant, 1991). A grossly hypertrophied ventricle, as mentioned above, may compound symptoms via hypoperfusion and ischemia, which contribute further to the reduction in cardiac output.
TABLE 4
Cardiovascular Cbanges During Pregnancy ~~ ~~
Parmrietc~r
ALler'lgc <.'h'1tZge
Blood volume Cardiac output Stroke volume Heart rate Workload of heart Total peripheral resistance Mean arterial pressure Systolic blood pressure Diastolic blood pressure Central venous pressure
Increases 35% Increases 40% Increases 30% Increases 15% Increases 40% Decreases 15% Decreases 15 mm Hg Decreases 3-5 mm Hg Decreases 5-10 mm Hg No change
The Intraparturn Period
Nofe. From Crrtical Cure Obstetrical Nursing, by C. J. Harvey, 1991, Gaithersburg, MD: Aspen Publishers, Inc. Copyright 1991 by Aspen Publishers, Inc. Adapted with permsision.
necessary to maintain cardiac output. The result is a larger than normal pressure gradient between the left ventricle and the aorta. A pressure gradient greater than 50 mm Hg accompanied by a decrease in the aortic valve area to less than 0.8 cm2 (normal = 1.5-2.6 cm2) indicates significant aortic stenosis. At this level of stenosis, clinical symptoms emerge that progress from dyspnea and activity intolerance to the classic triad of congestive
When the patient was admitted to the delivery suite at 35-4/7 weeks gestation in active labor with contractions every 2-3 minutes, the possibility of reduced cardiac output caused concern. D.Z.'s weight was 110 pounds (49.5 kg), blood pressure 108/68, pulse rate 92, and respiratory rate 14. A care conference was held to review management of this patient during the intrapartum period. A decision was made not to place a pulmonary artery catheter at that time, but to insert a pulmonary artery catheter introducer to facilitate rapid insertion of the catheter if it became necessary. This conservative approach was an effort to minimize the risk of valvular infection. The team thought that the patient showed good cardiovascular stability. To avoid potentially deleterious tachycardia, pain control was achieved with intravenous narcotics. The perinatal CNS was present throughout labor, delivery, and the initial recovery period to provide support and coaching, with a goal of reducing anxiety. Continuous electrocardiographic monitoring was initiated to observe for cardiac arrhythmia, although none was noted. Intravenous ampicillin and gentamicin antibiotic prophylaxis were given when cervical dilation reached 8 cm (30 minutes before deliv-
TABLE 5
Hemodynamic Parameters in Pregnancy Pararn r ters
Assesses
Norninl Values
Cardiac output Stroke volume
Contractility Contractility
Stroke work index Mean arterial pressure Pulmonary vascular resistance Systemic vascular resistance Central venous pressure Pulmonary capillary wedge pressure Pulmonary artery pressure
Contractility
6-7 Uminute 50-60 ml 25% t 20-24 weeks 50% t by full-term 35-55 g M m 2 65-110 mm Hg 60-100 dynes/second/cm-s 1,000-1,600 dynes/second/cm-s 1-7 mm Hg 6-10 mm Hg Systolic 18-30 mm Hg Diastolic 6-10 mm Hg Mean 11-15 mm Hg 11-15 mm Hg
Mean pulmonary artery pressure (MPAP)
Right afterload Left afterload Right preload Left preload Right afterload
Note. From OB Critiitical Care Guide, by K. A. Comport, 1992, Pittsburgh, PA. Copyright 1992 by K. A. Comport. Reprinted with permission.
Januay/Februay 1997
JOGNN 73
newborn was admitted to the neonatal intensive care unit for initial assessment and to rule out cardiac anomalies. He was found to be normal and subsequently was transferred to the pediatric unit.
The Postparttlm Period
FIGURE 2
Comparison of normal tricuspid aortic valve and biscuspid valve with aortic stenosis. Top, normal tricuspid aortic valve; bottom, bicuspid valve with aortic stenosis.
ery) and again after delivery according to prophylaxis recommendations for subacute bacterial endocarditis. The patient remained stable throughout labor and delivery with normal vital signs (blood pressure, 100170; pulse rate, 80-90; and respiration rate, 20-24). D.Z. delivered a viable boy who weighed 5 pounds, 9 ounces (2,524 g) and had Apgar scores of 8 and 9 at 1 and 5 minutes, respectively. The placenta delivered spontaneously and was intact with a threevessel cord. Blood loss was kept to a minimum at delivery through the use of dilute intravenous pitocin. Because of patient nonadherence, a prenatal fetal echocardiogram was not performed. Therefore, the 74 JOG"
D.Z.'s initial postpartum recovery period was uneventful, and her vital signs remained at baseline. Her episiotomy was intact, and her uterine fundus remained firm and midline, with minimal lochia rubra. Her abdomen was nontender, her breasts were soft, and Homan's sign was negative. She experienced a hypotensive episode several hours after delivery, with her systolic readings in the 80s. A central venous pressure catheter was inserted via the introducer to assess for fluid volume deficit as a cause for hypotension. Her central venous pressure values ranged between 1-3 mm Hg, which are normal in postpartum women. No data were available showing a favorable correlation between the central venous pressure and the pulmonary capillary wedge pressure, especially when an optimal pulmonary capillary wedge pressure for aortic stenosis is 16-18 mm Hg. However, when her central venous pressure values were integrated with other assessment data, hypovolemia was ruled out as a cause for the low blood pressure. This pressure was believed to be linked to the cumulative effects of analgesics used before and after delivery for pain relief. Doses were reduced, and no further incidents occurred. The interventions described in Table 3 were planned, implemented, and evaluated primarily by the professional nursing staff of the critical care obstetric unit. The goals specified in the care plan were met through the teamwork, dedication, and expertise provided by this staff. Their efforts enabled the patient to have a normal labor, delivery, and recovery. After being observed during recovery for 12 hours, D.Z. was transferred to the postpartum unit for education about normal newborn care and self-care and for further stabilization. Maternal-infant attachment was facilitated through her frequent visits to the neonatal intensive care unit while the newborn was being evaluated for cardiac disease. D.Z. exhibited normal attachment behaviors with her son. The health care team recommended evaluation for reparative valvular surgery to D.Z. before her hospital discharge. This suggestion was based on the seriousness of her cardiac disorder and her history of poor adherence and access to health care. The patient consented to surgical evaluation and was transferred to the cardiac telemetry unit. Although D.Z. and her newborn were separated, the nurses arranged frequent visits for her between the cardiac and pediatric units. In addition, the father had been rooming-in on the pediatrics unit to learn normal newborn care and to faVolume 26, Number 1
LV Pressure
150r
120
FIGURE 3 A comparison of left ventricular and aortic pressures. A, Normal pressure tracing; B, the patient (D.Z.) pressure tracing- aortic stenosis with 32 mm Hg pressure gradient.
cilitate attachment because D.Z. would be incapacitated for a while. He was receptive and exhibited normal attachment behaviors. The patient’s clinical status remained stable, with infrequent reports of dyspnea and tachycardia with exertion. Four days after giving birth, she underwent cardiac catherization. It revealed a left ventricular systolic pressure of 142 mm Hg and an aortic systolic pressure of 110 mm Hg, indicating a valvular gradient of 32 mm Hg (see Figure 3). The aortic valve area was measured at 0.78 cm’. The clinical symptoms of severe dyspnea at rest and the catheterization findings led to a diagnosis of critical aortic stenosis, even though the pressure gradient was not as severe as expected. Left ventricular systolic function was slightly elevated, with an ejection fraction of 70% (normal range, 55% to 65%). Coronary arteries were normal. Pulmonary artery pressure was 13/5 mm Hg, with a wedge pressure of 7 mm Hg, indicating low volume status. Aortic valve replacement was recommended and scheduled for the following week.
Prosthetic Valve Replacement The CNS discussed birth control options with D.Z. in anticipation of anticoagulation therapy after the prosthetic valve replacement. Coumadin (Dupont Pharmaceutical, Wilmington DE), which is teratogenic, was the anticoagulant to be used. D.Z. did not wish to have a tuba1 ligation and selected levonorgestrel implants (Norplant, Wyeth-Ayerst Laboratories, Philadelphia, PA) as her method of birth control. She received standard subacute bacterial endocarditis prophylaxis before the surgery, but experienced a fever the next day, which necessitated cancellation of her surgery. After a 3-day delay, she underwent aortic valve replacement with insertion of a 21-mm valvular prosthesis. Her initial postoperative hemodynamic profile followed the expected pattern after cardiac surgery. Pregnancy values were used as the basis for comparison in this patient, who had given birth 10
JanuarylFebruary 1997
A) Normal
L
142
LV Pressure
B) DZ
days previously. Return to normal nonpregnant hemodynamic values is not expected for 2-4 weeks after delivery (Arditi, 1981; Clark et al., 1991). The higher systemic vascular resistance values represent vasoconstriction resulting from hypothermia induced to decrease metabolic demand during surgery. Endogenous catecholamine release (and other vasoconstrictor substances) also contributes to a high resistance state. The low cardiac output is a reflection of myocardial depression due to hypothermia and anesthesia effects. Values 6 hours later indicated some resolution of these usual effects. D.Z. experienced no complications during the recovery period (see Table 6). The patient was transferred to the cardiovascular progressive care unit the day after her surgery and remained there until discharge. She experienced anemia, with a hemoglobin of 6.8 and a hematocrit of 20.2%, which manifested with nausea, weakness, dizziness, and atrial tachycardia with premature atrial contractions. To avoid the risk of donor blood transfusions, she was treated with oral ferrous sulfate, which led to a rise in her hemoglobin and hematocrit levels. The patient’s heart rate of 140-150 bpm and rhythm abnormality were related to the anemia and to postoperative hypoxemia secondary to bilateral pleural effusions and atelectasis of the left lower lobe. The tachycardia and arrhythmia resolved as the patient’s anemia and lung status improved. Maternal-infant visits were reestablished by having the pediatric nurses bring the newborn to D.Z.’s room. Education about normal newborn care and normal infant development was repeated. Both parents were able to demonstrate competence in newborn care before discharge. The couple decided to marry and raise their child together in a new environment. They planned to move out of state away from the abusive home situation. The couple had supportive relatives in the new area, who were willing to assist them with their adjustments to a new life. JOGNN 75
TABLE 6
D.Z .s' Postoperative Hernodynamic Profile Parameter
Initial
6 Hours Postoperative
Temperature Pulmonary artery pressure
37.1 21/14
38.4 29/16
Pulmonary capillary wedge pressure Central venous pressure Cardiac output Cardiac index Systemic vascular resistance
14 11 4.2 2.9 1,294
15 11 5.6 3.9 942
C a r e of this patient required collaborative efforts from nurses, physicians, and ancillary health care professionals.
A planning meeting was conducted to coordinate aspects of discharge for D.Z. and the newborn. Home care visits were scheduled for prothrombin time analysis and maternal-infant assessment. Routine postdischarge care and follow-up responsibilities were transferred to her physician.
Summary Care of this patient required collaborative efforts from nurses, physicians, and ancillary support personnel. Care of this patient within a critical care obstetric unit was a culmination of consultation efforts between the perinatal and cardiovascular CNSs to determine the unit design, select equipment, develop policies, and establish standards for care. Staff development and a program for ongoing maintenance of clinical competence also were instituted. Development of the unit and ongoing operations was accomplished through the advanced practice nursing role (CNS). The key to this success was the dedication and commitment to excellence in patient care of the critical care obstetric nursing staff. This unit demonstrated nurses' ability to turn a vision into the reality of improved patient care. REFERENCES Arditi, L. (1981). Heart disease in pregnancy. In G. Schaefer & E. A. Graber, (Eds.), Complications in obstetric and
76 JOGNN
Nomral 37.0"C Systolic 18-30 mm Hg, diastolic 6-10 mm Hg 6-10 mm Hg 0-7 mm Hg 6-7 Uminute 2.5-4.0 Uminute 1,000-1,600 dynes/ second/cm- '
gynecologic surgery: Prevention, diagnosis and treatment (pp. 218-227). Philadelphia: J. B. Lippincott. Austin, D. A., & Davis, P. A. (1991).Valvular disease in pregnancy. Journal of Perinatal and Neonatal Nursing, 5(2), 13-24. Bashore, T. M., & Lieberman, E. B. (1993). Aortichnitral obstruction and coarctation of the aorta. Cardiology Clinics, 11(4),617-641. Braunwald, E. (Ed.) (1992). Heart disease: A textbook o f cardiovascular medicine (4th ed.). Philadelphia: W.B. Saunders. Clark, S. L., Cotton, D. B., Hankins, G. D., & Dhelan, J. P. (1991). Critical Care Obstetrics (2nd ed.). Boston: Blackwell Scientific Publications. Creasy, R. K., & Resnik, R. (1989). Maternal-fetal medicine: Principles and practice (2nd ed.). Philadelphia: W. B. Saunders. Dolan, J. T. (1991).Critical care nursing: Clinical management through the nursing process. Philadelphia: W. B. Saunders. Easterling, T. R., & Benedetti, T. J. (1991). Principles of invasive hernodynamic monitoring in pregnancy. In s. L. Clark, D. B. Cotton, G. D. Hankins, & J. P. Phelan (Eds.), Critical care obstetrics (2nd ed., pp. 72-85). Boston: Blackwell Scientific Publications. Easterling, T. R., Chadwick, H. S., Otto, C. M., & Benedetti, T. J. (1988).Aortic stenosis in pregnancy. Obstetrics and Gynecology, 72(1), 113-118. Elkayam, U., & Gleicher, N. (Eds.). (1990). Cardiac problems in pregnancy: Diagnosis and management of maternal/ fetal diagnosis (2nd ed.). New York: Alan R. Liss, Inc. Gabbe, S. G., Niebyl, J. R., & Simpson, J. L. (1991). Obstetrics: Normal and problem pregnancies (2nd ed.). New York: Churchill Livingstone. Harvey, C. J. (1991). Critical care obstetrical nursing. Gaithersburg, MD: Aspen Publications. Hibbard, L. T. (1989). Maternal mortality due to cardiac disease. Clinics in Obstetrics and Gynecology, 18,2736. Kirkland, C. J. (1992).The impact of pregnancy on the woman with congenital heart disease: Considerations for intra-
Volume 26, Number 1
parturn nursing care. NAACOG's Clinical Issues in Perinatal and Women's Health Nursing, 3, 429-436. Marieb, E. N. (1992). Human anatomy and physiology (2nd ed.). Redwood City, CA: Benjamin Cumrnings Publishing Co. Nora, J., Berg, K., & Nora, A. (1991).Cardiovasculardiseases, genetics, epidemiology and prevention. New York: Oxford University Association. Perloff, J. K. (1987). The clinical recognition of congenital heart disease (3rd ed.). Philadelphia: W. B. Saunders. Ramin, S. M., Maberry, M. C., & Gilstrap, L. C. (1989).Congenital heart disease. Clinical Obstetrics and GynecolO ~ Y ,32(l),41-53. Schlant, R. C. (1991). Aortic stenosis. In I. K. Chatterjee, J. Karliner, E. Rapaport, M. D. Cheitlin, W. W. Parrnley, & M. Scheinrnan, (Eds.), Cardiology:An illustrated text/
JanuarylFebruary 1997
reference 2, ( p p . 9.106-9.115). Philadelphia: J. B. Lippincott. Kimberly A. Comport is the clinical nurse specialist (CNS)for the Department of Maternal Fetal Medicine, Allegheny General Hospital, Pittsburgh, Pennsylvania. She was the perinatal CNS at the Western Pennsylvania Hospital in Pittsburgh, where she was program director for the critical care obstetric unit. Janet K. Seng was the cardiovascular CNS at the Western Pennsylvania Hospital, Pittsburgh, Pennsylvania, when this article was written. She is currently a case manager liaison for the Tristate Network in Pittsburgh. Address for correspondence:Kimberly A. Comport, RN, MSN, 160 Richard Drive, Glenshaw, PA 15116.
JOG"
77
=This
case report describes a pregnant patient with severe aortic stenosis. A multidisciplinary plan of care was developed for the antepartum, intraparturn, postpartum, and, ultimately, postoperative clinical course. Salient points reviewed include normal cardiovascular anatomy and physiology, hemodynamic and physiologic changes of pregnancy, bicuspid aortic valvular stenosis, and the patient's clinical data profile. Numerous psychosocialstresses and the need for specialized nursing added to the complexity of caring for this patient. JOGNN, 26,67-77; 1997. Accepted: June 1995
agement of patients at high risk because of aortic stenosis is possible in part through the use of surveillance technologies previously available only in intensive care units. The newly established specialty area of critical care obstetrics presents an opportunity for collaboration and sharing of expertise between obstetric nurses and critical care nurses.
T h e newly established specialty area of critical care obstetrics presents a
The number of pregnant women presenting with preexisting valvular heart disease has increased during the past 2 decades. Advances in neonatal and pediatric medicine have allowed women with congenital heart defects to reach childbearing age. In addition, women with heart disease who previously were discouraged from becoming pregnant because of probable negative outcomes recently have been encouraged by reports of successful pregnancies. However, the maternal mortality rates for these patients remain disturbingly high, ranging from 5% to 20% for aortic stenosis (Clark, Cotton, Hankins, & Phelon, 1991; Ramin, Maberry, & Gilstrap, 1989).The incidence of aortic stenosis in pregnancy is relatively rare for two reasons. It is found more frequently in men than women, and severe stenosis is uncommon in women of childbearing age (Bashore & Lieberman, 1993; Easterling, Chadwick, Otto, & Benedetti, 1988; Creasy & Resnik, 1989). Successful man-
*Descriptive information has been altered to protect the confidentiality of the patient.
JanuaryIFebruary 1997
challenging opportunity for collaboration and sharing of expertise between obstetric nurses and critical care nurses.
This article describes the cooperative team approach used in the clinical management of an obstetric patient with severe aortic stenosis who underwent cardiac surgery after giving birth. Information on care of patients with this diagnosis is limited in nursing literature. The following case report presents cardiovascular and obstetric aspects of care.
Case Report D.Z., a white 22-year-old gravida 1, para 0, presented to our tertiary care center for antepartal care at 28 weeks gestation. She was referred by her obstetrician because of severe aortic stenosis. The perinatologist had asked the perinatal clinical JOGNN 67
nurse specialist (CNS) to meet with the patient to develop preadmission rapport and coordinate hospital care. The cardiovascular CNS subsequently became involved in developing the plan of care for the patient. During the initial interview, the perinatal CNS obtained a medical and psychosocial history. The patient had a history of congenital aortic stenosis, first diagnosed at age 7. She became symptomatic progressively during her childhood and young adulthood. At present, she was unable to work and her income was limited to disability payments. She reported a history of fatigue, orthopnea, and paroxysmal nocturnal dyspnea. Other pertinent medical history included Hashimoto’s thyroiditis and mitral valve prolapse. Medications included .125 mg levothyroxine daily, prenatal vitamins, and iron. The patient was unmarried, but maintained a close personal relationship with the baby’s father, who was her only source of emotional support. D.Z. and her partner voiced many concerns about their current living arrangement with her family. She reported a history of abusive relationships within the family, including emotional and sexual abuse. However, it was not possible financially for the couple to maintain an independent residence because D.Z.’s partner was unemployed and she was physically disabled. It became increasingly clear that nursing care of this patient would be complex, not only because of the underlying medical problems, but also because of numerous psychosocial concerns. An additional complicating factor was the limited intellectual capability of the patient and her partner. After the initial meeting between D.Z. and the perinatal CNS, a general outline of patient care was devised for antepartum, intrapartum, and postpartum management. Planning team members were the perinatal CNS, the cardiovascular CNS, the chief obstetric resident, and the perinatologist. The primary goals of treatment were to avoid hypotension and tachycardia by maintaining adequate intravascular volume status (Austin & Davis, 1991; Kirkland, 1992). Because the patient had transportation problems that prevented her from keeping prenatal care appointments, her next interaction with health care providers occurred when she was hospitalized for preterm labor and gastroenteritis at 34 weeks gestation. Contractions were occurring every 3 minutes; the cervix was closed, thick, and high; and membranes were intact. Sonography showed the fetus in a vertex presentation at the 40th percentile of growth and an anterior grade I placenta. Biornetrics confirmed appropriate growth in comparison with previous studies. Fetal assessment via biophysical profile was reassuring (score: 10/10). Umbilical artery doppler flow studies (continuous wave doppler) were slightly elevated, with a systolic/diastolic ratio of 3.73. The fetal heart rate tracing was reactive, with a baseline 68 JOGNN
rate of 140-150 beats per minute (bpm). A fetal echocardiogram had not been completed because the mother had missed prenatal care appointments. The potential risk of fetal congenital heart disease had been addressed extensively with the patient (Nora, Berg & Nora, 1991). The reported incidence of congenital heart defects in the offspring of women with heart defects ranges from 3.4% to 16.1% (Elkayam & Gleicher, 1990). D.Z.’s general physical appearance was cachectic and frail; her weight was 105 pounds (47.25 kg) on a 5foot (1.5 m) frame. She presented with a flat affect and avoided eye contact initially. She complained of shortness of breath and chest pain on exertion and occasionally at rest. Her lungs were clear to auscultation, and respirations were easy and unlabored on room air. Her skin was pale, warm, and dry to touch, with a capillary refill of less than 2 seconds. Blood pressure readings were in the range between 90 and 100 and more than 50 and 70. A grade IV-VM systolic murmur was present in the aortic area, with radiation to the back and carotids. All other physical findings were within normal limits. D.Z.’s preterm labor was stopped, using magnesium sulfate as the tocolytic drug. Ritodrine hydrochloride was contraindicated in this patient because beta-agonists often induce tachycardia. Maintaining the patient on an oral sympathomimetic agent (i.e., terbutaline) was contraindicated for the same reason. After the patient was stabilized, a cardiology workup was initiated to determine the extent of her aortic stenosis. A 12-lead electrocardiogram showed normal sinus rhythm with sinus arrhythmia (rate varied with the respiratory cycle). An echocardiogram revealed mild to moderate aortic stenosis, with an aortic valve gradient of 25-32 mm Hg. Three valve leaflets could not be visualized well. The study concluded that there was a congenital bicuspid aortic valve. In addition, the anterior leaflet of the mitral valve was thickened and redundant, allowing a trivial mitral regurgitation. Based on her clinical presentation and diagnostic findings, the patient’s condition was determined to be Class 11-111 in the New York Heart Association Functional Classification scheme for cardiac disease (Braunwald, 1992) (see Table 1) and Group I1 according to Clark’s classification system of risk status for pregnant women (Clark et al., 1991) (see Table 2). The patient was discharged after a 3-day hospital stay. Because of the nature of her condition, a detailed multidisciplinary plan for delivery was developed by the health care team with the assistance of an anesthesiologist and a cardiologist (see Table 3). Prophylatic antibiotic was recommended for prevention of subacute bacterial endocarditis associated with mitral valve prolapse and existing aortic valve disease. The cardiologist thought that a pulmonary artery catheter was indicated to monitor hemodynamic status because the patient’s clinical status might Volume 26, Number 1
Hemodynamics
Class
Definition
Class I
No limitation of physical activity. Ordinary activity does not cause undue fatigue, palpitations, dyspnea, or angina. Slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitations, dyspnea, or angina. Marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitations, dyspnea, or angina. Inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or angina may be present even at rest, and are intensified by activity.
Class I1
Class 111
Class IV
deteriorate with the stress of labor. Pulmonary artery data could be used to avoid hypovolemia throughout labor, delivery, and the postpartum recovery period. Continuous electrocardiogram monitoring was planned to detect possible cardiac rhythm disturbances, particularly atrial arrhythmia. The anesthesiology department was consulted about pulmonary artery catheter placement and pain management during labor and delivery. The consensus in the department was that regional anesthesia should be avoided with this patient because of the severity of her aortic stenosis, even though regional anesthesia (i.e., epidural, pudendal) can be used with caution for most cardiac patients. There is risk of hypotension in patients with tight aortic stenosis because their cardiac output cannot increase across the stenotic valve. Such patients depend on appropriate venous return (end-diastolic volume or preload). Decreased cardiac output results in a secondary reduction in myocardial perfusion via the coronary arteries (Gabbe, Niebyl, & Simpson, 1991). Planned interventions included follow-up by the perinatal and cardiovascular CNSs and nursing staff education about anticipated care and invasive hemodynamic monitoring. A patient care conference with the critical care obstetric nursing team was held to discuss the care plan for this patient. The social services department was consulted about assistance with psychosocial and financial aspects of care. The need for postpartum home follow-up was also identified and addressed at this time.
January/February 1997
Before addressing the pathophysiology of aortic stenosis, normal cardiac anatomy and physiology are presented (see Figure 1).Atria are low pressure chambers that serve as reservoirs of blood for the ventricles. The right atrium receives deoxygenated venous blood via the inferior and superior vena cavae. The left atrium receives oxygenated blood returning to the heart from the pulmonary veins. Blood flows from the atria to the ventricles during diastole because of the one-way action of the atrioventricular valves and the existing pressure differentials. The tricuspid valve lies between the right atrium and the right ventricle, whereas the mitral valve lies between the left atrium and the left ventricle. The ventricles serve as pumps to expel blood. The right ventricle pumps deoxygenated blood to the lungs via the pulmonary artery. The left ventricle pumps oxygenated blood into the systemic circulation via the aorta. Blood flow out of the ventricles to the great vessels during systole requires opening of the pulmonic and aortic valves. The pulmonic valve directs blood flow from the right ventricle into the pulmonary artery and blood flow from the left ventricle passes through the aortic valve into the aorta (Marieb, 1992). Cardiac output is the amount of blood ejected from the left ventricle and is the product of stroke volume and
TABLE 2 Mortality Risk Associated with Pregnancy GROUP 1: Mortality < 1% Atrial septal defect Ventricular septal defect (uncomplicated) Patent ductus arteriosus Pulmonic and tricuspid disease Corrected tetralogy of Fallot Biosynthetic valve prosthesis (porcine and human) Mitral stenosis, NYHA class I and I1 GROUP 2: Mortality 5% to 15% Mitral stenosis with atrial fibrillation Mechanical valve prosthesis Mitral stenosis, NYHA class 111 or IV Aortic stenosis Coarctation of the aorta (uncomplicated) Uncorrected tetralogy of Fallot Previous myocardial infarction Marfan’s syndrome with normal aorta GROUP 3: Mortality 25% to 50% Pulmonary hypertension Coarctation of the aorta (complicated) Marfan’s syndrome with aortic involvement Note. From Critical Cure Obstetrics. (2nd ed.)., by S. L. Clark, D. B. Cotton, G. D. Hawkins, & J. P. Phelan (Eds.), 1991, Boston, MA: Blackwell Scientific Publications. Copyright 1991 by Blackwell Scientific Publications. Adapted with permission.
JOGNN 69
TABLE 3
Plan of Care for Obstetric Patient With Aortic Stenosis C;O‘llS:
Adcquatc matern;il/utcro-pla~~ntal pertusion Stal7le hemodyn;imic st;itus Adequate fluid v o l u m e status Decrease ‘inxicry No evidence ot infection o r tliroinhoeinh~~lisin secondary to valvular heart disease Adcquntc pain control Ma tern a 1-i n fan t attach men t he ha v iors
Potential Problems
Hemodynamic Effects
Interventions
Arrhythmia: atrial arrhythmia, tachycardia
Decreased preload Decreased cardiac output Hypotension
Institute continuous ECG monitoring Maintain heart rate in range of 60-100 bpm Avoid beta agonists Initiate continuous pulse oximetry Monitor fetus with continuous external fetal monitoring Obtain intravenous access Control pain
Peripheral vasodilation
Decreased afterload Decreased preload Decreased cardiac output Hypotension
Avoid regional anesthesia (for D. Z.) Assess pulmonary artery pressure via pulmonary artery catheter if available
Fluid volume deficit
Decreased preload Decreased cardiac output Hypotension Decreased urine output
Avoid blood loss Intravenous pitocin after placental delivery Fundal massage Maintain pulmonary capillary wedge pressure at 16-18 mm Hg Titrate intravenous fluids to maintain adequate hydration per: -Hernodynamic parameters -Urine output (> 30 mihour) Gentle pushing to avoid erratic venous return associated with Valsalva
Fluid volume overload
Increased preload Pulmonary congestion
Fowler’s position (avoid lithotomy position) Double concentrate intravenous meds (i.e., Pitocin) Regulate intravenous fluids via infusor device Diuretics as ordered Strict intake and output Weigh patient daily Maintain pulmonary capillary wedge pressure at 16-18 mm Hg Anticipate postpartum autotransfusion Avoid infusion of colloids during delivery Close hemodynamic monitoring Auscultate lung sounds every hour during labor and postpartum
Increased risk of pulmonary edema
(continues)
70 JOGNN
Volume 26, Number 1
TABLE 3 (continued)
Plan of Care for Obstetric Patient With Aortic Stenosis Potential Probliwrs
Hivnodvnrrrnic- Effects
lrrtimriwtioris
Patient anxiety
Tachycardia Decreased cardiac output
Remain with patient during labor and delivery Provide adequate pain control Consult clinical nurse specialist, social service, neonatal intensive care unit as needed Educate patient about diagnosis, treatment of cardiac disease, labor and delivery, neonatal workup, well baby care and follow-up Keep patient informed of all tesdtreatments Teach and review relaxation and breathing techniques with patient Provide family-centered care Promote parentauinfant attachment behaviors Coordinate discharge planning
Hypoxemia
Tachycardia
Continuous pulse oximetry Oxygen and suction at bedside Apply oxygen via face mask for oxygen saturation < 92% Continuous electronic fetal monitoring to assess for fetal distress Consolidate nursing interventions to avoid patient's fatigue Limit activities Provide calm, quiet atmosphere
Thromboem boli
Decreased perfusion to affected organ
Apply thigh high thromboembolic support stockings Anticoagulation via subcutaneous heparin (does not cross placental barrier) Maintain adequate hydration Control arrhythmia
Infection
Tachycardia Increased cardiac output
Subacute bacterial endocarditis antibiotic prophylaxis Antipyretics as needed Strict sterile technique for line insertion Monitor for leukocytosis
heart rate. This parameter reflects the overall functional capacity of the left ventricle to maintain satisfactory blood pressure and organ perfusion. Cardiac output is affected by the heart rate as well as the interaction of three variables that influence stroke volume. These variables are preload, afterload, and contractility. Stroke volume is the amount of blood (in milliliters) ejected from the heart in one beat. JanuarylFebruary 1997
Preload is determined by intraventricular volume and pressure and is related to the existing myocardial muscle fiber length. Rising volume and pressure stretch the muscle fibers and, in a normal heart, increase cardiac output. As blood vessels relax or dilate, the cardiac output increases. Conversely, if blood vessels constrict, the cardiac output decreases. Contractility, or the inotropic state of the heart, is reflected in the force and velocity of JOG"
71
systemic vascular resistance (Easterling & Benedetti, 1991). The high volume, low resistance state that accounts for the characteristic hemodynamic profile in pregnancy is summarized in Table 5.
R e g n a n t women experience several significant changes from the normal hemodynamic profile.
FIGURE 1
Cardiac anatomy and normal pressures in pregnancy. IVC, inferior vena cava; SVC, superior vena cava; RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle; PA, pulmonary artery; AO, aorta; P C W , pulmonary capillary wedge pressure.
ventricular ejection when preload and afterload remain constant. Changes in intracardiac pressure generated by the contraction and relaxation of the cardiac muscle produce pressure gradients that facilitate the direction and velocity of blood flow into and out of the ventricles. The size and condition of the cardiac valves also affects the direction and velocity of flow. This is addressed in greater detail below.
Hemodynamics in Normal Pregnancy Several significant alterations from the normal hemodynamic profile occur in the pregnant patient as a result of the physiologic adaptation to the growing fetus (see Table 4). These adaptations include an increase in circulating blood volume to as much as 50% higher than in the nonpregnant state. The etiology of this hypervolemic state includes renin-induced aldosterone secretion associated with sodium and water retention and increased red blood cell mass (Hibbard, 1989).This higher volume status, accompanied by increases in maternal heart rate and stroke volume, leads to a 30% to 50% increase in the cardiac output. The increase in stroke volume occurs in early pregnancy but not as pregnancy advances. Heart rate and cardiac output continue to increase throughout pregnancy. Despite the dramatic increase in cardiac output associated with pregnancy, blood pressure is maintained at or near nonpregnant values because of a hormonally mediated decrease in the 72 JOGNN
Normal, healthy, expectant mothers adjust readily to the physiologic changes of pregnancy. In women with coexisting cardiac disease, the added workload of pregnancy can precipitate complications. This is most evident clinically between 26 and 34 weeks gestation, when blood volume reaches its peak. Immediately after delivery, an autotransfusion of approximately 1,000 ml of uterine blood shifts into the systemic circulation. This physiologic phenomenon represents another potentially dangerous time for the woman with aortic stenosis because of limitations of cardiovascular adaptation.
Valvular Heart Disease Valvular heart disease is acquired or congenital. Acquired valvular disease results primarily from inflammatory or degenerative changes over time, and therefore symptoms usually are not manifested until later in life. Congenital valvular disease is the result of a malformation present at birth. In the case of aortic stenosis, this malformation, present in 1% to 2% of the general population, is a bicuspid aortic valve rather than the normal three-cusp (leaflet) aortic valve (Schlant, 1991) (see Figure 2). The abnormal structure of a congenitally bicuspid valve, as found in this case, induces turbulent blood flow through the valve. This turbulence over time traumatizes the valve leaflets and ultimately leads to fibrosis, increased rigidity, and calcification of the leaflets. Subsequently, this results in narrowing (stenosis) of the aortic valve orifice (Braunwald, 1992). The basic hemodynamic feature of aortic stenosis is an obstruction to left ventricular ejection, which can lead ultimately to a low cardiac output. In general, the cross-sectional area of the valve orifice must be narrowed to less than one third of normal before clinically significant obstruction is produced. In response to this narrowing, the left ventricle hypertrophies to generate stronger contractions. These stronger contractions are Volume 26, Number 1
heart failure, angina pectoris, and syncope (Schlant, 1991). A grossly hypertrophied ventricle, as mentioned above, may compound symptoms via hypoperfusion and ischemia, which contribute further to the reduction in cardiac output.
TABLE 4
Cardiovascular Cbanges During Pregnancy ~~ ~~
Parmrietc~r
ALler'lgc <.'h'1tZge
Blood volume Cardiac output Stroke volume Heart rate Workload of heart Total peripheral resistance Mean arterial pressure Systolic blood pressure Diastolic blood pressure Central venous pressure
Increases 35% Increases 40% Increases 30% Increases 15% Increases 40% Decreases 15% Decreases 15 mm Hg Decreases 3-5 mm Hg Decreases 5-10 mm Hg No change
The Intraparturn Period
Nofe. From Crrtical Cure Obstetrical Nursing, by C. J. Harvey, 1991, Gaithersburg, MD: Aspen Publishers, Inc. Copyright 1991 by Aspen Publishers, Inc. Adapted with permsision.
necessary to maintain cardiac output. The result is a larger than normal pressure gradient between the left ventricle and the aorta. A pressure gradient greater than 50 mm Hg accompanied by a decrease in the aortic valve area to less than 0.8 cm2 (normal = 1.5-2.6 cm2) indicates significant aortic stenosis. At this level of stenosis, clinical symptoms emerge that progress from dyspnea and activity intolerance to the classic triad of congestive
When the patient was admitted to the delivery suite at 35-4/7 weeks gestation in active labor with contractions every 2-3 minutes, the possibility of reduced cardiac output caused concern. D.Z.'s weight was 110 pounds (49.5 kg), blood pressure 108/68, pulse rate 92, and respiratory rate 14. A care conference was held to review management of this patient during the intrapartum period. A decision was made not to place a pulmonary artery catheter at that time, but to insert a pulmonary artery catheter introducer to facilitate rapid insertion of the catheter if it became necessary. This conservative approach was an effort to minimize the risk of valvular infection. The team thought that the patient showed good cardiovascular stability. To avoid potentially deleterious tachycardia, pain control was achieved with intravenous narcotics. The perinatal CNS was present throughout labor, delivery, and the initial recovery period to provide support and coaching, with a goal of reducing anxiety. Continuous electrocardiographic monitoring was initiated to observe for cardiac arrhythmia, although none was noted. Intravenous ampicillin and gentamicin antibiotic prophylaxis were given when cervical dilation reached 8 cm (30 minutes before deliv-
TABLE 5
Hemodynamic Parameters in Pregnancy Pararn r ters
Assesses
Norninl Values
Cardiac output Stroke volume
Contractility Contractility
Stroke work index Mean arterial pressure Pulmonary vascular resistance Systemic vascular resistance Central venous pressure Pulmonary capillary wedge pressure Pulmonary artery pressure
Contractility
6-7 Uminute 50-60 ml 25% t 20-24 weeks 50% t by full-term 35-55 g M m 2 65-110 mm Hg 60-100 dynes/second/cm-s 1,000-1,600 dynes/second/cm-s 1-7 mm Hg 6-10 mm Hg Systolic 18-30 mm Hg Diastolic 6-10 mm Hg Mean 11-15 mm Hg 11-15 mm Hg
Mean pulmonary artery pressure (MPAP)
Right afterload Left afterload Right preload Left preload Right afterload
Note. From OB Critiitical Care Guide, by K. A. Comport, 1992, Pittsburgh, PA. Copyright 1992 by K. A. Comport. Reprinted with permission.
Januay/Februay 1997
JOGNN 73
newborn was admitted to the neonatal intensive care unit for initial assessment and to rule out cardiac anomalies. He was found to be normal and subsequently was transferred to the pediatric unit.
The Postparttlm Period
FIGURE 2
Comparison of normal tricuspid aortic valve and biscuspid valve with aortic stenosis. Top, normal tricuspid aortic valve; bottom, bicuspid valve with aortic stenosis.
ery) and again after delivery according to prophylaxis recommendations for subacute bacterial endocarditis. The patient remained stable throughout labor and delivery with normal vital signs (blood pressure, 100170; pulse rate, 80-90; and respiration rate, 20-24). D.Z. delivered a viable boy who weighed 5 pounds, 9 ounces (2,524 g) and had Apgar scores of 8 and 9 at 1 and 5 minutes, respectively. The placenta delivered spontaneously and was intact with a threevessel cord. Blood loss was kept to a minimum at delivery through the use of dilute intravenous pitocin. Because of patient nonadherence, a prenatal fetal echocardiogram was not performed. Therefore, the 74 JOG"
D.Z.'s initial postpartum recovery period was uneventful, and her vital signs remained at baseline. Her episiotomy was intact, and her uterine fundus remained firm and midline, with minimal lochia rubra. Her abdomen was nontender, her breasts were soft, and Homan's sign was negative. She experienced a hypotensive episode several hours after delivery, with her systolic readings in the 80s. A central venous pressure catheter was inserted via the introducer to assess for fluid volume deficit as a cause for hypotension. Her central venous pressure values ranged between 1-3 mm Hg, which are normal in postpartum women. No data were available showing a favorable correlation between the central venous pressure and the pulmonary capillary wedge pressure, especially when an optimal pulmonary capillary wedge pressure for aortic stenosis is 16-18 mm Hg. However, when her central venous pressure values were integrated with other assessment data, hypovolemia was ruled out as a cause for the low blood pressure. This pressure was believed to be linked to the cumulative effects of analgesics used before and after delivery for pain relief. Doses were reduced, and no further incidents occurred. The interventions described in Table 3 were planned, implemented, and evaluated primarily by the professional nursing staff of the critical care obstetric unit. The goals specified in the care plan were met through the teamwork, dedication, and expertise provided by this staff. Their efforts enabled the patient to have a normal labor, delivery, and recovery. After being observed during recovery for 12 hours, D.Z. was transferred to the postpartum unit for education about normal newborn care and self-care and for further stabilization. Maternal-infant attachment was facilitated through her frequent visits to the neonatal intensive care unit while the newborn was being evaluated for cardiac disease. D.Z. exhibited normal attachment behaviors with her son. The health care team recommended evaluation for reparative valvular surgery to D.Z. before her hospital discharge. This suggestion was based on the seriousness of her cardiac disorder and her history of poor adherence and access to health care. The patient consented to surgical evaluation and was transferred to the cardiac telemetry unit. Although D.Z. and her newborn were separated, the nurses arranged frequent visits for her between the cardiac and pediatric units. In addition, the father had been rooming-in on the pediatrics unit to learn normal newborn care and to faVolume 26, Number 1
LV Pressure
150r
120
FIGURE 3 A comparison of left ventricular and aortic pressures. A, Normal pressure tracing; B, the patient (D.Z.) pressure tracing- aortic stenosis with 32 mm Hg pressure gradient.
cilitate attachment because D.Z. would be incapacitated for a while. He was receptive and exhibited normal attachment behaviors. The patient’s clinical status remained stable, with infrequent reports of dyspnea and tachycardia with exertion. Four days after giving birth, she underwent cardiac catherization. It revealed a left ventricular systolic pressure of 142 mm Hg and an aortic systolic pressure of 110 mm Hg, indicating a valvular gradient of 32 mm Hg (see Figure 3). The aortic valve area was measured at 0.78 cm’. The clinical symptoms of severe dyspnea at rest and the catheterization findings led to a diagnosis of critical aortic stenosis, even though the pressure gradient was not as severe as expected. Left ventricular systolic function was slightly elevated, with an ejection fraction of 70% (normal range, 55% to 65%). Coronary arteries were normal. Pulmonary artery pressure was 13/5 mm Hg, with a wedge pressure of 7 mm Hg, indicating low volume status. Aortic valve replacement was recommended and scheduled for the following week.
Prosthetic Valve Replacement The CNS discussed birth control options with D.Z. in anticipation of anticoagulation therapy after the prosthetic valve replacement. Coumadin (Dupont Pharmaceutical, Wilmington DE), which is teratogenic, was the anticoagulant to be used. D.Z. did not wish to have a tuba1 ligation and selected levonorgestrel implants (Norplant, Wyeth-Ayerst Laboratories, Philadelphia, PA) as her method of birth control. She received standard subacute bacterial endocarditis prophylaxis before the surgery, but experienced a fever the next day, which necessitated cancellation of her surgery. After a 3-day delay, she underwent aortic valve replacement with insertion of a 21-mm valvular prosthesis. Her initial postoperative hemodynamic profile followed the expected pattern after cardiac surgery. Pregnancy values were used as the basis for comparison in this patient, who had given birth 10
JanuarylFebruary 1997
A) Normal
L
142
LV Pressure
B) DZ
days previously. Return to normal nonpregnant hemodynamic values is not expected for 2-4 weeks after delivery (Arditi, 1981; Clark et al., 1991). The higher systemic vascular resistance values represent vasoconstriction resulting from hypothermia induced to decrease metabolic demand during surgery. Endogenous catecholamine release (and other vasoconstrictor substances) also contributes to a high resistance state. The low cardiac output is a reflection of myocardial depression due to hypothermia and anesthesia effects. Values 6 hours later indicated some resolution of these usual effects. D.Z. experienced no complications during the recovery period (see Table 6). The patient was transferred to the cardiovascular progressive care unit the day after her surgery and remained there until discharge. She experienced anemia, with a hemoglobin of 6.8 and a hematocrit of 20.2%, which manifested with nausea, weakness, dizziness, and atrial tachycardia with premature atrial contractions. To avoid the risk of donor blood transfusions, she was treated with oral ferrous sulfate, which led to a rise in her hemoglobin and hematocrit levels. The patient’s heart rate of 140-150 bpm and rhythm abnormality were related to the anemia and to postoperative hypoxemia secondary to bilateral pleural effusions and atelectasis of the left lower lobe. The tachycardia and arrhythmia resolved as the patient’s anemia and lung status improved. Maternal-infant visits were reestablished by having the pediatric nurses bring the newborn to D.Z.’s room. Education about normal newborn care and normal infant development was repeated. Both parents were able to demonstrate competence in newborn care before discharge. The couple decided to marry and raise their child together in a new environment. They planned to move out of state away from the abusive home situation. The couple had supportive relatives in the new area, who were willing to assist them with their adjustments to a new life. JOGNN 75
TABLE 6
D.Z .s' Postoperative Hernodynamic Profile Parameter
Initial
6 Hours Postoperative
Temperature Pulmonary artery pressure
37.1 21/14
38.4 29/16
Pulmonary capillary wedge pressure Central venous pressure Cardiac output Cardiac index Systemic vascular resistance
14 11 4.2 2.9 1,294
15 11 5.6 3.9 942
C a r e of this patient required collaborative efforts from nurses, physicians, and ancillary health care professionals.
A planning meeting was conducted to coordinate aspects of discharge for D.Z. and the newborn. Home care visits were scheduled for prothrombin time analysis and maternal-infant assessment. Routine postdischarge care and follow-up responsibilities were transferred to her physician.
Summary Care of this patient required collaborative efforts from nurses, physicians, and ancillary support personnel. Care of this patient within a critical care obstetric unit was a culmination of consultation efforts between the perinatal and cardiovascular CNSs to determine the unit design, select equipment, develop policies, and establish standards for care. Staff development and a program for ongoing maintenance of clinical competence also were instituted. Development of the unit and ongoing operations was accomplished through the advanced practice nursing role (CNS). The key to this success was the dedication and commitment to excellence in patient care of the critical care obstetric nursing staff. This unit demonstrated nurses' ability to turn a vision into the reality of improved patient care. REFERENCES Arditi, L. (1981). Heart disease in pregnancy. In G. Schaefer & E. A. Graber, (Eds.), Complications in obstetric and
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Nomral 37.0"C Systolic 18-30 mm Hg, diastolic 6-10 mm Hg 6-10 mm Hg 0-7 mm Hg 6-7 Uminute 2.5-4.0 Uminute 1,000-1,600 dynes/ second/cm- '
gynecologic surgery: Prevention, diagnosis and treatment (pp. 218-227). Philadelphia: J. B. Lippincott. Austin, D. A., & Davis, P. A. (1991).Valvular disease in pregnancy. Journal of Perinatal and Neonatal Nursing, 5(2), 13-24. Bashore, T. M., & Lieberman, E. B. (1993). Aortichnitral obstruction and coarctation of the aorta. Cardiology Clinics, 11(4),617-641. Braunwald, E. (Ed.) (1992). Heart disease: A textbook o f cardiovascular medicine (4th ed.). Philadelphia: W.B. Saunders. Clark, S. L., Cotton, D. B., Hankins, G. D., & Dhelan, J. P. (1991). Critical Care Obstetrics (2nd ed.). Boston: Blackwell Scientific Publications. Creasy, R. K., & Resnik, R. (1989). Maternal-fetal medicine: Principles and practice (2nd ed.). Philadelphia: W. B. Saunders. Dolan, J. T. (1991).Critical care nursing: Clinical management through the nursing process. Philadelphia: W. B. Saunders. Easterling, T. R., & Benedetti, T. J. (1991). Principles of invasive hernodynamic monitoring in pregnancy. In s. L. Clark, D. B. Cotton, G. D. Hankins, & J. P. Phelan (Eds.), Critical care obstetrics (2nd ed., pp. 72-85). Boston: Blackwell Scientific Publications. Easterling, T. R., Chadwick, H. S., Otto, C. M., & Benedetti, T. J. (1988).Aortic stenosis in pregnancy. Obstetrics and Gynecology, 72(1), 113-118. Elkayam, U., & Gleicher, N. (Eds.). (1990). Cardiac problems in pregnancy: Diagnosis and management of maternal/ fetal diagnosis (2nd ed.). New York: Alan R. Liss, Inc. Gabbe, S. G., Niebyl, J. R., & Simpson, J. L. (1991). Obstetrics: Normal and problem pregnancies (2nd ed.). New York: Churchill Livingstone. Harvey, C. J. (1991). Critical care obstetrical nursing. Gaithersburg, MD: Aspen Publications. Hibbard, L. T. (1989). Maternal mortality due to cardiac disease. Clinics in Obstetrics and Gynecology, 18,2736. Kirkland, C. J. (1992).The impact of pregnancy on the woman with congenital heart disease: Considerations for intra-
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parturn nursing care. NAACOG's Clinical Issues in Perinatal and Women's Health Nursing, 3, 429-436. Marieb, E. N. (1992). Human anatomy and physiology (2nd ed.). Redwood City, CA: Benjamin Cumrnings Publishing Co. Nora, J., Berg, K., & Nora, A. (1991).Cardiovasculardiseases, genetics, epidemiology and prevention. New York: Oxford University Association. Perloff, J. K. (1987). The clinical recognition of congenital heart disease (3rd ed.). Philadelphia: W. B. Saunders. Ramin, S. M., Maberry, M. C., & Gilstrap, L. C. (1989).Congenital heart disease. Clinical Obstetrics and GynecolO ~ Y ,32(l),41-53. Schlant, R. C. (1991). Aortic stenosis. In I. K. Chatterjee, J. Karliner, E. Rapaport, M. D. Cheitlin, W. W. Parrnley, & M. Scheinrnan, (Eds.), Cardiology:An illustrated text/
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reference 2, ( p p . 9.106-9.115). Philadelphia: J. B. Lippincott. Kimberly A. Comport is the clinical nurse specialist (CNS)for the Department of Maternal Fetal Medicine, Allegheny General Hospital, Pittsburgh, Pennsylvania. She was the perinatal CNS at the Western Pennsylvania Hospital in Pittsburgh, where she was program director for the critical care obstetric unit. Janet K. Seng was the cardiovascular CNS at the Western Pennsylvania Hospital, Pittsburgh, Pennsylvania, when this article was written. She is currently a case manager liaison for the Tristate Network in Pittsburgh. Address for correspondence:Kimberly A. Comport, RN, MSN, 160 Richard Drive, Glenshaw, PA 15116.
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