Medical-Surgical PROBLEMS  in Pregnancy



Effect of pregnancy on heart disease


Hematologic Changes During Pregnancy

u         Blood Volume:  ­ 45% (­ 1450-1750 ml)

l        Protects the mother from devastating hemorrhage at delivery

u         Plasma Volume:  ­ 45-50% (­ 1200-1300 ml)

l        Serves to dissipate fetal heat production

u         Red Cell Mass:  ­ 18-30% (­ 250-450 ml)

l        Necessary to ­ O2 transport to meet fetal needs

u         Based on the above, pregnancy normally results in a “physiologic anemia”

l        Hgb:   10-12 g/dL  (nonpregnant =  12-15 g/dL)

l        Hct:    32-40% (nonpregnant = 35-47%)


Hematologic Changes During Pregnancy—cont.

u        WBC: ­

l        1st Trimester:  3,000-15,000/mm3

l       (mean 9500/ mm3)

l        2nd & 3rd Trimesters:  6,000-16,000/mm3

l       (mean 10,500/ mm3)

l        Labor: 20,000-30,000/mm3


Clotting Factor Changes During Pregnancy

u        Fibrin: ­ 40% at term

u        Plasma Fibrinogen (Factor I): ­ 50%

u        Clotting time:  Unchanged

u        Coagulation Factors V, VII, VIII, IX, X, XII all ­

u        Coagulation Factors XI, XIII both ¯ slightly

u        Prothrombin time:  Unchanged or ­ slightly

u        Platelets:  Unchanged 


Hypertension in Pregnancy: Background Information

u         The most common complication of pregnancy

u         Complicates 7-10% of all pregnancies

u         Hypertension in pregnancy can lead to multisystem damage and failure with pathologic changes noted in the brain, kidney, liver, & cardiovascular systems as well as altered uteroplacental perfusion

u         Prediposes women to conditions such as abruptio placentae, DIC, cerebral hemorrhage, CVA, hepatic failure, and acute renal failure

u         Contributes to intrauterine growth restriction and fetal death


ACOG Hypertension Classifications

u        Chronic Hypertension

l        BP >140/90 mmHg present <20 weeks gestation or before pregnancy; HTN persisting for >42 days after delivery is also classified in this category

u        Preeclampsia / Eclampsia *

u        Preeclampsia Superimposed on Chronic Hypertension

u        Transient Hypertension (Pregnancy induced hypertension)

l        ­ in BP at >20 weeks or in the first 24 hours postdelivery without other preeclamptic signs or preexisting HTN



u        Preeclampsia ranks second only to embolic events as a cause of maternal mortality

u        It is unique to human pregnancy

u        Directly responsible for 15% of maternal deaths

u        The incidence ranges from 10-14% in primigravidas and from 5.7-7.3% in multiparas


What is preeclampsia?

Triad of criteria

u          ­ BP of ³30 mmHg systolic or ³ 15 mmHg diastolic as compared to BP prior to 20 weeks gestation. (The ­ BP must be present on 2 occasions taken 6 hours apart; if previous BP is unknown, 140/90 after 20 weeks gestation is considered diagnostic)



Severe Preeclampsia

u         BP ³160 mmHg systolic or ³110 mmHg diastolic on 2 occasions ³6 hours apart

u         Proteinuria ³5 grams in 24 hours

u         Oliguria £500 mL in 24 hours

u         HA (especially frontal)

u         Hyperreflexia

u         Scotomata and other visual changes

u         Epigastric pain

u         Pulmonary edema or cyanosis

u         Impaired liver function of unclear etiology

u         Thrombocytopenia



u        The occurrence of convulsions (seizures) or coma that is not attributable to other causes in the presence of preeclamptic signs and symptoms

u        Eclamptic seizures are grand mal in nature

Risk Factors for Preeclampsia


Pathophysiology of Preeclampsia

u         Exact etiology unknown

l        Multiple theories exist including abnormal trophoblast invasion, genetic predisposition, and dietary deficiencies or excesses

u         Damage to the maternal endothelium triggers systemic maternal vasospasm

l        (It is unclear if endothelial damage causes vasospasm or vice versa)

u         There is a restriction of blood flow

u         The amount of circulating maternal blood volume is altered

u         Damage to organ systems results from hypoxia that occurs 2º to vasospasm

u          ­ peripheral vascular resistance 2º to vasospasm causes ­ in BP

u         Connection to early placental ischemia


Clinical Manifestations of Preeclampsia:

Hematologic Changes

u          ¯ plasma volume / circulating volume

u          Hemoconcentration results from fluid shifts to extravascular space (Hgb & Hct ­)

l        The degree of hemoconcentration can be used as an indicator of the severity of preeclampsia

u          Thrombocytopenia results from endothelial damage 2º to vasospasm (platelets adhere to damaged sites)

l        A platelet count of <150,000/mm3 has been found in 32-50% of women with severe preeclampsia

l        ­ risk of hemorrhage at delivery


Clinical Manifestations of Preeclampsia:

Renal Changes

u        ¯ renal plasma flow

u        ¯ GFR (25% less than is normal in pregnancy)

u        ­ serum uric acid  (³4.5 mg/dL)

u        ­ serum creatinine (some sources say this does not commonly ­)

u        ­ serum blood urea nitrogen

u        Potential for oliguria (especially in severe preeclampsia) due to intracellular fluid moving to extracellular space.


Clinical Manifestations of Preeclampsia:
Hepatic Changes

u        The liver is not primarily involved in preeclampsia; involvement is seen in only ~10% of women with severe preeclampsia

u        Still, one may possibly assess RUQ or epigastric pain

l        May indicate liver damage due to vasospasm

u        ­ liver enzymes


Clinical Manifestations of Preeclampsia:

CNS Changes

u         ­ cerebrovascular resistance

u         Vision changes: scotomata (spots), diplopia (blurry), retinal detachment (usually unilateral; rare)

u         HA that is unrelieved by medication

u         Hyperreflexia / clonus

l        Clonus is involuntary, rapid, rhythmical CTXs and relaxations of a muscle when it is sharply stretched and maintained

u         Seizure activity with eclampsia which can occur antepartally, intrapartally, or postpartally


Clinical Manifestations of Preeclampsia:

Pulmonary Changes

u        Colloid oncotic pressure decreases even further than what is normal in pregnancy due to damaged vessels and proteinuria, potentially, resulting in generalized and/or pulmonary edema


Clinical Manifestations of Preeclampsia:

Uteroplacental Changes

u        ¯ uteroplacental perfusion due to vasospasm, ¯ circulating volume, vasospasm of spiral arteries, and possible lesions from damage to the endothelium.

l        Due to the above, there is an ­ chance of IUGR, oligohydramnios, & IUFD.


Non-Pharmacologic Care of the Preeclamptic Patient

Depends on Severity of Preeclampsia, Maternal and Fetal Status at time of evaluation,  Gestational Age, Bishop Cervical Score, and wishes of the Parents

u         If mild to moderate HTN, bedrest with BP and urine protein checks (1+ proteinuria), in addition to regular office visits including fetal evaluation (i.e., NSTs, BPP)

u         If fetal evaluation indicates compromise (IUGR, non-reactive NST) or maternal condition worsens (­ BP, ­ proteinuria), hospitalization is usually required for constant observation and therapy; continuous fetal monitoring is indicated


Normal Fetal Heart Pattern tracing at term

u         Reassuring pattern. Baseline fetal heart rate is 130 to 140 bpm, preserved beat-to-beat and long-term variability. Accelerations last for ³15 sec and peak at ³15 bpm above baseline.


During a normal pregnancy, the maternal cardiovascular system undergoes many changes that put a physiologic strain on the heart. The normal heart can compensate for the increased workload, so that pregnancy, labor, and birth are generally well tolerated, whereas the diseased heart is challenged hemodynamically. If the cardiovascular changes are not well tolerated, cardiac failure can develop during pregnancy, during labor, or during the postpartum period. In addition, if myocardial disease develops, if valvular disease exists, or if a congenital heart defect is present, cardiac decompensation is anticipated


Approximately 1% of pregnancies are complicated by heart disease, and half of all heart disease cases in pregnancy are congenital heart lesions (Cunningham et al., 2001). Box 1 lists maternal cardiac disease risk groups and their related mortality rates.


 The degree of disability experienced by the woman with cardiac disease often is more important in the treatment and prognosis during pregnancy than is the diagnosis of the type of cardiovascular disease. The New York Heart Association's functional classification of organic heart disease, a widely accepted standard, is as follows (New York Heart Association, 1964):


•  Class I: asymptomatic at normal levels of activity

•  Class II: symptomatic with increased activity

•  Class III: symptomatic with ordinary activity

•  Class IV: symptomatic at rest


No classification of heart disease can be considered rigid or absolute, but this one offers a basic practical guide for treatment, assuming that frequent prenatal visits, good patient cooperation, and appropriate obstetric care occur. Medical therapy is conducted as a team approach, including the cardiologist, obstetric physician, and nurses. The functional classification may change for the pregnant woman because of the hemodynamic changes that occur in the cardiovascular system, especially increased cardiac output. The functional classification of the disease is determined at 3 months and again at 7 or 8 months of gestation.


The incidence of miscarriage is increased, and preterm labor and birth are more prevalent in the pregnant woman with cardiac problems. In addition, IUGR is common, probably because of low oxygen pressure in the pregnant woman. The risk of congenital heart lesions is increased in children of mothers with congenital heart disease (Mendelson, 1997). A maternal mortality rate of more than 50% during pregnancy has been associated with pulmonary hypertension (Mendelson, 1997).





Peripartum cardiomyopathy is congestive heart failure with cardiomyopathy found in the last month of pregnancy or in the first 5 months postpartum (Easterling & Otto, 2002). The etiology of the disease is unknown; theories suggest genetic predisposition, autoimmunity, and viral infections.


Peripartum cardiomyopathy is more likely to occur in African-Americans, in a woman who is 30 years old or more with a twin pregnancy, and in the presence of preeclampsia (Mendelson & Lang, 1995). Maternal mortality rate has been estimated at 25% to 50% (Easterling & Otto, 2002). Clinical findings are those of congestive heart failure (left ventricular failure). Signs include breathless-ness, tachyarrhythmias, and edema with radiologic findings of cardiomegaly. Medical management of cardiomyopathy during pregnancy includes diuretics, potassium, anticoagulants, and digitalis. Intrapartum management includes hemodynamic monitoring; epidural analgesia is appropriate for pain control. The prognosis is good if cardiomegaly does not persist for 6 months postpartum (Easterling & Otto, 2002).




Rheumatic fever usually develops suddenly several symptom-free weeks after an inadequately treated group A beta-hemolytic streptococcal infection of the throat. Episodes of rheumatic fever create an autoimmune reaction in the heart tissue, leading to permanent damage of heart valves (usually the mitral valve) and the chordae tendineae cordis. This damage is referred to as rheumatic heart disease (RHD). RHD may be evident during acute rheumatic fever or discovered years later. Recurrences of rheumatic fever are common, each with the potential to increase the severity of heart damage. If a woman has had rheumatic fever in the past, a recurrence can occur during pregnancy, most likely early in the pregnancy. The American Heart Association recommends lifelong prophylaxis with benzathine penicillin, even during pregnancy. For those with penicillin allergies, erythromycin is an acceptable alternative during pregnancy. Heart murmurs resulting from stenosis, valvular insufficiency, or thickening of the walls of the heart characterize RHD. Abnormal pulse rate and rhythm and congestive heart failure are common.




Mitral valve stenosis (narrowing of the opening of the mitral valve caused by stiffening of valve leaflets, which obstructs blood flow from the atrium to the ventricle) accounts for 90% of RHD seen in pregnancy (McAnulty, Metcalfe, & Ueland, 1995). As the mitral valve narrows, dyspnea worsens, occurring first on exertion and eventually at rest. A tight stenosis plus the increase in blood volume and thus cardiac output of normal pregnancy may cause ventricular failure and pulmonary edema; hemoptysis may occur.


The care of the woman with mitral stenosis typically is managed by reducing her activity, restricting dietary sodium, and increasing bed rest. The pregnant woman with mitral stenosis should be followed clinically for symptoms and by echocardiograms to monitor the atrial and ventricular size, as well as heart valve function. Prophylaxis for intrapartum endocarditis and pulmonary infections is provided.




Mitral valve prolapse (MVP) is a common, usually benign, condition occurring in nearly 10% of women of reproductive age (Cunningham et al., 2001). The mitral valve leaflets prolapse into the left atrium during ventricular systole, allowing some backflow of blood. Midsystolic click and late systolic murmur are hallmarks of this syndrome. Most cases are asymptomatic. A few women have atypical chest pain (sharp and located in the left side of the chest) that occurs at rest and does not respond to nitrates. They may also have anxiety, palpitations, dyspnea on exertion, and syncope. Patients usually are treated with beta-blockers such as propranolol (Inderal). Pregnancy and its associated hemodynamic changes may change or alleviate the murmur and click of MVP, as well as symptoms. Pregnancy usually is well tolerated unless bacterial endocarditis occurs. As with RHD, antibiotic prophylaxis is given before invasive procedures for at-risk patients and for complicated vaginal births in patients with MVP.




Marfan syndrome is an autosomal dominant disorder characterized by generalized weakness of the connective tissue, resulting in joint deformities, ocular lens dislocation, and weakness of the aortic wall and root (McAnulty, Metcalfe, & Ueland, 1995). Approximately 90% of individuals with this syndrome have MVP and 25% have aortic insufficiency. There is an increased risk of aortic dissection and rupture during pregnancy. Excruciating chest pain is the most common symptom of aortic dissection. Preconception genetic counseling is recommended to make patients aware of the risks of pregnancy (Shabetai, 1999). Mortality rates may be as high as 50% in women who have significant cardiac disease. If the woman still desires to become pregnant, she should have baseline data gathered about the aortic root. Management during pregnancy is similar to women with class III and IV heart disease.




Infective endocarditis (inflammation of the innermost lining-endocardium-of the heart caused by invasion of microorganisms) is an uncommon disorder during pregnancy (Mendelson & Lang, 1995). It may be seen in women taking street drugs intravenously. Bacterial endocarditis, leading to incompetence of heart valves and thus congestive heart failure and cerebral emboli, can result in death. Treatment is with antibiotics.




Eisenmenger syndrome is a right-to-left or bidirectional shunting that can be at the atrial or ventricular level and is combined with elevated pulmonary vascular resistance (Easterling & Otto, 2002). The syndrome is associated with high mortality rates (30% to 50% in mothers and 50% in fetuses) and thus pregnancy is contraindicated (Kansaria & Salvi, 2000). Contraception is essential, and tubal ligation should be considered because oral contraceptives and intrauterine devices carry considerable risk (Mendelson & Lang, 1995). If pregnancy occurs, termination may be recommended if the woman has significant pulmonary hypertension.


In women who continue pregnancy, physical activity is strictly limited; prophylactic anticoagulation is considered (Mendelson & Lang, 1995). During labor and birth, Swan-Ganz monitoring is essential. Central hypovolemia should be avoided. Oxygen therapy is administered. There is controversy about use of epidural analgesia. If used, serial determinations of arterial oxygen concentrations should be done.




Assessment and Nursing Diagnoses


The presence of cardiac disease makes the decision to become pregnant more difficult. Planned pregnancy requires that the woman understand the peripartum risks. If the pregnancy is unplanned, the nurse needs to explore the woman's desire to continue the pregnancy after examining the risks in relation to the status of her cardiac condition. The woman's partner and family should be included in the discussion.


The pregnant woman with cardiac disease requires detailed assessment to determine the potential for optimal maternal health and a viable fetus throughout the peripartum period. If she chooses to continue the pregnancy, the high risk pregnant woman's condition may be assessed as often as weekly.




The nurse assesses for factors that would increase stress on the heart, such as anemia, infection, and edema, and how the woman is adapting to the physiologic changes of pregnancy. Special attention is given to the review of the cardiovascular and pulmonary systems. The nurse should determine whether the woman has experienced chest pain at rest or on exertion; edema of the face, hands, or feet; hypertension; heart murmurs; palpitations; paroxysmal nocturnal dyspnea; diaphoresis; pallor; or syncope. Pulmonary symptoms such as cough, hemoptysis, shortness of breath, and orthopnea can be signs of cardiac disease. Table 4 lists normal and abnormal cardiovascular signs during pregnancy.


The nurse documents all medication taken by the woman—including over-the-counter (OTC) medications such as supplemental iron—and is alert to their potential side effects and interactions. The woman is also assessed for undue emotional stress that might further compromise her cardiac status. Examples are depression, anxiety/fear of morbidity or mortality for herself and her fetus, financial concerns related to extended hospitalization, anger because of impaired social interaction, and feelings of inadequacy regarding her inability to meet family and household demands.


The woman's cultural background may affect the amount of support that she is able to receive from significant others. Family size (number of children and extended family members in the home), as well as role expectations within the family, may be dictated by cultural norms. For the woman with cardiac impairment, family expectations may prove to be a cause of major stress if she is unable to bear the expected number of children or if it is unacceptable to receive help with domestic chores.




•   Increasing fatigue or difficulty breathing, or both, with her usual activities

•   Feeling of smothering

•   Frequent cough

•   Palpitations; feeling that her heart is "racing"

•   Generalized edema: swelling of face, feet, legs, fingers (e.g., rings do not fit anymore)




•   Irregular, weak, rapid pulse (>100 beats/min)

•   Progressive, generalized edema

•   Crackles at base of lungs after two inspirations and exhalations that do not clear after coughing

•   Orthopnea; increasing dyspnea

•   Rapid respirations (>25 breaths/min)

•   Moist, frequent cough

•   Cyanosis of lips and nail beds


Physical assessment


Routine assessments continue during the prenatal period, including monitoring the amount and pattern of weight gain, edema, vital signs, and discomforts of pregnancy. Additionally, the woman is observed for signs of cardiac decompensation, that is, progressive generalized edema, crackles at the base of the lungs, or pulse irregularity (see Signs of Potential Complications box). Symptoms of cardiac decompensation may appear abruptly or gradually. Medical intervention must be instituted immediately to maintain optimal cardiac status. Dyspnea, palpitations, syncope, and edema occur commonly in pregnant women and can mask the symptoms of a developing or worsening cardiovascular disorder. A woman's sudden inability to perform activities that she previously was comfortable doing may indicate cardiac decompensation.