Normal physiological changes of the mother during pregnancy have the potential to exacerbate preexisting cardiorespiratory conditions or lead to new disorders.
By Bill Pruitt, MBA, RRT, CPFT, AE-C, FAARC
During pregnancy, many changes occur in the mother’s body to accommodate and support the developing fetus, from providing warmth, nutrients, and oxygen to removing waste products from the baby as metabolism occurs. These changes in the mother’s body have the potential to exacerbate preexisting medical conditions, or bring about new challenges to the mother’s health and well-being.
Mothers suffering from asthma, cystic fibrosis, systemic and/or pulmonary hypertension, valve diseases, arrhythmias, or other cardiac pathology may find their conditions worsen. In addition, new conditions may manifest during pregnancy, such as preeclampsia, gestational asthma, acute pulmonary edema, cardiomyopathy, or others. This article will focus on several of these maternal issues and discuss the pathology and the management needed to support the mother.
Normal Cardiovascular Changes in Maternal Physiology
As a fetus begins to develop, the mother’s body has to change to accommodate the demands required to support the process. Beginning at about 6 weeks, her blood volume begins to increase; by approximately 32 weeks gestation, it reaches a peak of about 4.7 to 5.2 liters total (about a 45% increase, or 1.2 to 1.6 liters of extra volume). During this time, the distribution of blood shifts as well. By the third trimester, there is an increase in interstitial and plasma volume. This hypervolemia has many possible causes, including increased sodium and the effects of estrogen on the renin-angiotensin system, a hormone system that regulates sodium balance, fluid volume, and blood pressure.
Fetal growth and the baby’s weight at birth correlate directly with the increase in plasma volume. Meanwhile, a reduction in plasma volume is linked to clinical issues such as intrauterine growth restriction (IUGR) and small for gestational age (SGA) in the newborn, and preeclampsia in the mother. Other cardiovascular changes include an increase in red blood cell production, with a 17% to 40% increase in red blood cell mass (between 250 mL and 450 mL). This ramp-up in red blood cell production requires about a 500 mg increase in iron. Despite the increase in red blood cell mass, the larger plasma volume results in a relative decrease in hemoglobin concentration (referred to as physiologic anemia of pregnancy).
Cardiac Output and Blood Pressure
Cardiac output increases during pregnancy and may hit a peak of 150% of normal. The time frame for this is near to that of the blood volume changes mentioned prior; cardiac output begins to increase during the first trimester and hits the maximum between 25 and 35 weeks gestation. Increased stroke volume provides the initial increase in cardiac output, but the mechanism shifts to an increase in heart rate as stroke volume increases up to the end of the second trimester, then plateaus. Heart rate increases by about 20 beats per minute by the time the pregnancy reaches week 32. Changes in maternal position will alter the cardiac output due to compression or release of the inferior vena cava (IVC). Positioning on the side allows for normal venous return, whereas a supine position will compress the IVC and have a marked effect on cardiac output levels. While measuring cardiac output using an invasive pulmonary artery catheter and the Fick method, the dye dilution method, or the thermodilution technique using a cold injectate has been recognized as the gold standard, M-mode Doppler echocardiography has gained recognition as having good correlation with the PA catheter methods, while avoiding the issues linked to invasive monitoring.
Meanwhile, blood pressure begins to decrease with the advancing pregnancy until about 20 to 24 weeks, then begins to rise to normal or above normal levels once term is reached. Systemic vascular resistance (SVR) also undergoes a significant decrease, with an approximate 10% reduction during the first trimester and reaching about 35% below normal at the midpoint of the gestation, where it remains fairly level. (It is thought that nitric oxide plays a part in the decrease in SVR.)
Normal Pulmonary Changes in Maternal Physiology
Oxygen consumption reflects the uptick in maternal metabolism by increasing between 20% and 30% by the time full term is reached. Early in the pregnancy, oxygen consumption is covered by the increase in cardiac output so the blood supply to the fetus is rich in oxygen. However, as the pregnancy progresses, O2 consumption continues to increase and overtakes the increase in cardiac output, resulting in a widening arterial-venous oxygen difference. The final a-v O2 difference at term returns to normal prepregnancy levels.
Pulmonary function is altered, with an increase in tidal volume of 30% to 40%, resulting in an increase in minute ventilation of approximately 40%. As a result of a drop in both the expiratory reserve volume and the residual volume, the functional residual capacity (FRC) is reduced by about 20%. These changes are brought on by the growth of the fetus in the abdomen, which causes the diaphragm to elevate approximately 4 cm. Total lung capacity is reduced by about 5%. The relative state of hyperventilation results in a respiratory alkalosis when arterial blood gases are checked. FEV1 and peak expiratory flow (PEF) are normally unchanged during normal pregnancy.[2,3] Despite the decrease in FRC, total lung capacity (TLC) will decrease only slightly due to a widening of the thoracic cage. Lung compliance remains stable during the pregnancy, but there is a decrease in chest wall and total respiratory compliance.
Cardiopulmonary Complications During Pregnancy: Asthma
Asthma is a common problem in the general population and may be an issue during pregnancy. This disease is estimated to affect between 3% and 8% of pregnancies. Asthma is said to follow the “Rule of Thirds” for pregnant women: about 28% of pregnancies with existing asthma show an improvement, about 33% of pregnant asthmatics have no change in their asthma, and about 35% get worse.[2,3] During pregnancy, an asthmatic has an increased risk of preeclampsia, excessive vomiting, gestational diabetes, low birth weight, and premature delivery. Issues during pregnancy that may aggravate asthma include gastroesophageal reflux disease (GERD), changes in the chest wall conformation, and increases in upper respiratory infections.
The National Heart, Lung, and Blood Institute began the National Asthma Education and Prevention Program (NAEPP) several years ago, which has released guidelines for the diagnosis and management of asthma in the form of the Expert Panel Report (EPR). The third report was released in 2007 and refers the reader to the 2004 NAEPP working group’s publication, “Working Group Report on Managing Asthma During Pregnancy: Recommendations for Pharmacologic Treatment—Update 2004.” This report states that it is better to treat the pregnant asthmatic than to have her suffer with asthma symptoms and exacerbations. Asthma during pregnancy calls for the same assessment, monitoring, and education as during nonpregnant conditions. The goal is to provide the optimal care for keeping asthma under control using the right medications in order to have the best quality of life for the mother and the optimal conditions for the fetus/neonate.
As described in the EPR-3 guidelines and in the Working Group Report 2004, albuterol is the preferred drug for controlling intermittent asthma, with the addition of an inhaled corticosteroid for persistent conditions (including mild, moderate, and severe persistent asthma). Budesonide (also known as Pulmicort by AstraZeneca) is the preferred inhaled corticosteroid due to the amount of data regarding the drug’s safety and efficacy during pregnancy.[2,6]
Hypoxemia (and hypotension) should be treated early and effectively to avoid complications with the fetus, which may be compromised prior these two problems becoming an issue to the mother.[2,5] Close fetal surveillance is needed whenever the mother has any loss of asthma control, particularly in an acute asthma attack, as the fetus will suffer from oxygen desaturation with the slightest drop in maternal PaO2.
Pregnant women are encouraged to follow a comprehensive approach to asthma control: avoidance of triggers, smoking cessation, immunotherapy, commitment to self-monitoring, following an asthma action plan, proper self-administration of medications, and early intervention if symptoms do not improve with self-management. These issues are no different than for those not pregnant.
The life expectancy has been increasing for patients with cystic fibrosis (CF), to the point where, for those born in the 1990s, the predicted median age of survival has moved well into adulthood (over 40 years of age). With this increase in life expectancy, pregnancy is becoming more frequent. While almost all males with CF are infertile due to closure or absence of the vas deferens, females with CF often have normal reproductive organs and normal menses, and are able to become pregnant. Recommendations call for bimonthly visits to a CF center during pregnancy and assessment, monitoring (including lung function tests), education, and adjustment of medications carried out with care.
When comparing CF patients to non-CF patients 1 year after pregnancy, the CF National Patient Registry database showed no difference in the rate of hospital admissions, use of home IV antibiotics, use of supplemental oxygen, or use of supplemental nutrition. Premature delivery is the most common complication of pregnancy in the CF patient population—occurring in some 24% of those with severe CF. Otherwise, those with CF are comparable to those without CF when looking for obstetric complications. Note that all infants from a CF mother will be carriers of the gene for CF, and in adulthood, if this person mates with another CF carrier, the offspring will have a 1–in-4 chance of having CF.[7,8]
Preeclampsia is a major issue in pregnancy. The worldwide incidence of preeclampsia ranges between 2% and 10%,14 and it is one of the leading causes of morbidity and mortality.[9,10] Of the admissions to the ICU for pregnant women, preeclampsia accounts for 20% to 50% of the cases and is the cause of 12% to 17% of all maternal deaths in the United States.
Preeclampsia is generally defined as hypertension that appears after week 20, with involvement of one or more organ systems. The systolic/diastolic blood pressure thresholds are 140/90 mm Hg, and the organ systems include the central nervous system, cardiorespiratory system, gastrointestinal system, hematological system, renal system, or the uteroplacental/fetal circulation.
Severe preeclampsia is defined as the blood pressure threshold levels climbing above 160/110 mm Hg, coupled with a severe disruption of organ function. With severe preeclampsia, central nervous system dysfunction includes headache, seizures (eclampsia), impaired conscious state, and visual disruptions. Renal problems are reflected in proteinuria with protein spillage in the urine of ≥5 g in 24 hours. Acute pulmonary edema is the major issue with the pulmonary system. Pulmonary edema most often happens in the early postpartum period.[4,9] Various pharmacologic strategies are given to reduce the hypertension. Oral labetalol is the drug of choice for both nonsevere and severe hypertension. This drug is both a selective alpha1-adrenergic and a nonselective beta-adrenergic receptor blocker, so it is not recommended for pregnant females who also have severe asthma. Magnesium sulfate is the drug of choice for treatment of seizures but should not be used as an antihypertensive agent. The only cure for preeclampsia is delivery of the baby and removal of the placenta.
Acute pulmonary edema has been recently reported as the fourth leading form of maternal morbidity. When pulmonary edema presents as a problem, the patient will have a sudden onset of breathlessness, may become agitated, has coughing, and often has orthopnea. Signs include tachycardia and tachypnea, crackles and wheezes detected via auscultation, decreased oxygen saturation, and changes in the chest x-ray (Kerley B lines and pulmonary infiltrates). Transthoracic echocardiography is a key tool for diagnosis and management by providing an excellent noninvasive measure of cardiac function. Risk factors and predisposing factors are divided into five major areas:
- Preexisting cardiac issues, such as hypertension, ischemic heart disease, or arrhythmias;
- Specific diseases in pregnancy, such as preeclampsia, sepsis, cardiomyopathy, pulmonary embolism;
- Pharmacologic agents, such as beta-adrenergic tocolytic agents, corticosteroids, illicit drug use;
- Iatrogenic intravenous (IV) fluid administration (reflected in a positive fluid balance of >2,000 mL); and
- Multiple pregnancies (eg, twins, triplets).
IV fluid administration is frequently a major preventable risk factor and is coupled with another risk factor when pulmonary edema is seen. Acute pulmonary edema may develop as a result of a single, significant cardiovascular event, such as preeclampsia causing an extremely high blood pressure or cardiogenic shock as a complication of myocardial ischemia. On the other hand, pulmonary edema may be the result of inappropriate IV fluid administration combined with other factors, including age, obesity, and preexisting hypertension.
Pulmonary edema in pregnancy should be treated as a medical emergency. Thorough monitoring with careful fluid balance evaluation is needed throughout treatment. IV nitroglycerin is recommended to reduce blood pressure along with IV furosemide to diurese the patient. Noninvasive ventilation with continuous positive airway pressure (CPAP) is used to increase oxygenation, decrease work of breathing, help move fluid out of the alveoli, and help avoid endotracheal intubation. If the patient has to be managed on invasive mechanical ventilation, lung protective strategies (low tidal volumes and low peak pressures) are appropriate and recommended.
The increase of cardiac disease in women prior to conception (and thus during pregnancy) is related to the increase in obesity, hypertension, and diabetes in women of childbearing age. Other factors include delayed conception into the 30s and 40s, as well as increased survival of women who have congenital heart disease. Research shows that some 50% of cardiac disease seen in pregnancy is due to congenital conditions. However, knowledge of any cardiac disorders prior to the pregnancy is often limited; some 15% of women diagnosed with heart disease during the pregnancy have no history of a preexisting cardiac condition. Between 1995 and 2006, the incidence of postpartum hospitalization for heart disease tripled, with most of the admissions due to acute myocardial infarction and cardiac arrest. Certain cardiac conditions carry high risk of maternal death (25% to 50%), and pregnancy is contraindicated in women with these diagnoses. The conditions include pulmonary hypertension, severe systemic ventricular dysfunction, dilation of the aortic root more than 4 cm (often seen in Marfan syndrome), and severe left-sided obstructive lesions (such as aortic or mitral stenosis).
As discussed earlier in this article, cardiovascular changes are a major element of pregnancy, and women unaware of a preexisting cardiac condition may see that condition worsen. Sometimes the diagnosis of a cardiac issue may be delayed due to the common nature of many symptoms: shortness of breath, decreased tolerance to exercise, and peripheral edema. During labor, pain, anxiety, and contractions bring on increases in heart rate, stroke volume, cardiac output, and blood pressure. For the cardiac patient, these stresses may not be tolerated. Moreover, after the baby and placenta are delivered, the mother receives an autotransfusion (up to 500 mL) that may overcome the capacity of her cardiac function.
As a result of all of these issues, careful monitoring of fluid balance and cardiac function is needed. Anticoagulation may be called for if the mother has a mechanical heart valve, atrial fibrillation, or pulmonary hypertension. Warfarin (the usual drug of choice for nonpregnant long-term anticoagulation) carries the risk of causing pathologic changes in the developing fetus. Unfractionated heparin and low-molecular weight heparin have reduced risks but have other complications associated with these products, so at present there is continuing debate as to the best path to take for anticoagulation therapy.
Pregnancy and childbirth are part of the natural human condition and often occur without complications. However, the physiological changes that occur in the mother’s body, combined with potential preexisting (and maybe undiagnosed) conditions, can bring about major issues in the cardiovascular and pulmonary systems. This article has focused on a limited number of problems related to the health of the mother. There are many more health-related topics that have not been mentioned here, including countless topics linked to the health of the neonate. The reader is advised to conduct further study, because many of these issues call for special care from clinicians, including physicians, nurses, and respiratory therapists. The cardiopulmonary issues related to both mother and baby should be well understood by all who work in this realm of healthcare.
Bill Pruitt, MBA, RRT, CPFT, AE-C, FAARC, is a senior instructor and director of clinical education in the department of Cardiorespiratory Sciences, College of Allied Health Sciences, at the University of South Alabama in Mobile. He also works as a PRN therapist at Springhill Medical Center. For further information, contact [email protected]
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- From the NIH website for the National Heart Lung and Blood Institute Guidelines for the Diagnosis and Management of Asthma (EPR-3) released in 2007 http://www.nhlbi.nih.gov/guidelines/asthma/
- Budev MM. Arroliga AC. Emery S. Exacerbation of underlying pulmonary disease in pregnancy. Critical Care Medicine. 2005; 33(10 Suppl):S313-8.
- From the Cystic Fibrosis Foundation website: http://www.cff.org/UploadedFiles/AboutCF/Testing/NewbornScreening/CarriersofCF/My-Baby-is-a-CF-Carrier.pdf.
- Dennis AT. Management of pre-eclampsia: issues for anaesthetists. Anaesthesia. 2012; 67(9):1009-20.
- Gogarten W. Preeclampsia and anaesthesia. Current Opinion in Anaesthesiology. 2009; 22(3):347-51.
- Dennis AT. Solnordal CB. Acute pulmonary oedema in pregnant women. Anaesthesia. 2012; 67(6):646-59.
- Simpson LL. Maternal cardiac disease: update for the clinician. Obstetrics & Gynecology. 2012; 119(2 Pt 1):345-59.
- From the Cystic Fibrosis Foundation website: http://www.cff.org/aboutcf/
- Osungbade, K. Ige, O. Public health perspectives of preeclampsia in developing countries: implication for health system strengthening. J Pregnancy. 2011; 2011: 481095. Published online 2011 April 4. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087154/