INTRODUCTION
Dyspnea is common during pregnancy. The development of dyspnea in the pregnant woman raises the question as to whether she has some form of underlying cardiac or pulmonary disease or whether her dyspnea is due to the pregnancy itself. Making this assessment requires an understanding of the cardiopulmonary changes that occur during normal pregnancy, as well as recognition of the syndrome of dyspnea during normal pregnancy [1-4].
PHYSIOLOGICAL CHANGES IN PREGNANCY POTENTIALLY AFFECTING RESPIRATION
Cardiovascular changes — The most striking cardiovascular changes during pregnancy are increases in blood volume and cardiac output [5-7].
Blood volume — Blood volume starts to rise during the first trimester and eventually reaches a maximum that is 40 to 50 percent above the baseline, nonpregnant blood volume. Because plasma volume increases more than red cell mass, the hematocrit generally falls, resulting in the physiologic "anemia of pregnancy" (figure 1). (See "Hematologic changes in pregnancy".)
Cardiac output — Cardiac output also starts to rise in the first trimester, reaching a peak at 20 to 32 weeks of gestation that is 30 to 50 percent above baseline (figure 2) [7,8]. Although the increase in cardiac output is initially due to a rise in stroke volume, the increase is maintained later in pregnancy by an increase in heart rate, as stroke volume falls during the third trimester. A decrease in systemic vascular resistance accompanies the increase in cardiac output. Blood pressure during pregnancy is often notable for a rise in pulse pressure due to an unchanged systolic pressure accompanied by a decrease in diastolic pressure. (See "Maternal cardiovascular and hemodynamic adaptations to pregnancy".)
Respiratory changes — The normal respiratory tract changes during pregnancy result in a compensated respiratory alkalosis, with a higher PO2 and a lower PCO2 than in the nonpregnant state. The lower PCO2 is thought to provide a diffusion gradient that may facilitate the fetus' ability to eliminate waste from aerobic metabolism. (See "Respiratory tract changes during pregnancy".)
Elevation of the diaphragm — Although the progressively enlarging uterus causes diaphragm position to rise up to 4 cm above its usual resting position, diaphragmatic excursion during respiration is not impaired since chest wall mobility increases and there is flaring of the ribs [9].
Decreased FRC and stable FEV1 — Functional residual capacity (FRC) decreases approximately 20 percent during the latter half of pregnancy, due to a decrease in both expiratory reserve volume (ERV) and residual volume (RV) (figure 3) [10,11]. Variable and generally minor changes in vital capacity (VC) and total lung capacity (TLC) have also been observed, but the magnitude of these changes suggests they are not likely to be clinically significant.
Airway function is preserved during pregnancy, as reflected by an unchanged forced expiratory volume in one second (FEV1) and an unchanged FEV1/FVC ratio. Minor changes, which are of little clinical importance, have been described in diffusing capacity for carbon monoxide (DLCO): an increase during the first trimester followed by a decrease until 24 to 27 weeks of gestation [12].
Increased ventilation and respiratory drive — Perhaps the most striking change in respiratory physiology during pregnancy is an increase in resting minute ventilation, which rises by nearly 50 percent at term. This is primarily due to a larger tidal volume, whereas the respiratory rate remains essentially unchanged [13]. The increase in ventilation is greater than the corresponding elevation in oxygen consumption (approximately 20 percent) (figure 4) [11].
Increased levels of progesterone during pregnancy are thought to be responsible for the rise in ventilation above that explained by the enhanced metabolic requirements. Progesterone is a known stimulant of respiration and respiratory drive, and its levels gradually rise from approximately 25 ng/mL at six weeks to 150 ng/mL at term [14].
Respiratory alkalosis and increased arterial O2 tension — As a result of the progesterone-induced increase in alveolar ventilation, arterial PCO2 falls to a plateau of 27 to 32 mmHg during pregnancy. This respiratory alkalosis is followed by compensatory renal excretion of bicarbonate, so that the resultant arterial pH is normal to slightly alkalotic (usually between 7.40 to 7.45) [15]. (See "Simple and mixed acid-base disorders", section on 'Compensatory respiratory and renal responses'.)
Maternal oxygenation is preserved during pregnancy. In fact, the maternal arterial oxygen tension (PaO2) is generally increased because of hyperventilation, ranging from 106 to 108 mmHg in the first trimester to 101 to 104 mmHg in the third trimester [16,17]. Interpretation of the arterial PO2 must take into account the corresponding level of PCO2, which is generally accomplished most easily by calculation of the alveolar-arterial oxygen difference.
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INTRODUCTION
Dyspnea is common during pregnancy. The development of dyspnea in the pregnant woman raises the question as to whether she has some form of underlying cardiac or pulmonary disease or whether her dyspnea is due to the pregnancy itself. Making this assessment requires an understanding of the cardiopulmonary changes that occur during normal pregnancy, as well as recognition of the syndrome of dyspnea during normal pregnancy [1-4].
PHYSIOLOGICAL CHANGES IN PREGNANCY POTENTIALLY AFFECTING RESPIRATION
Cardiovascular changes — The most striking cardiovascular changes during pregnancy are increases in blood volume and cardiac output [5-7].
Blood volume — Blood volume starts to rise during the first trimester and eventually reaches a maximum that is 40 to 50 percent above the baseline, nonpregnant blood volume. Because plasma volume increases more than red cell mass, the hematocrit generally falls, resulting in the physiologic "anemia of pregnancy" (figure 1). (See "Hematologic changes in pregnancy".)
Cardiac output — Cardiac output also starts to rise in the first trimester, reaching a peak at 20 to 32 weeks of gestation that is 30 to 50 percent above baseline (figure 2) [7,8]. Although the increase in cardiac output is initially due to a rise in stroke volume, the increase is maintained later in pregnancy by an increase in heart rate, as stroke volume falls during the third trimester. A decrease in systemic vascular resistance accompanies the increase in cardiac output. Blood pressure during pregnancy is often notable for a rise in pulse pressure due to an unchanged systolic pressure accompanied by a decrease in diastolic pressure. (See "Maternal cardiovascular and hemodynamic adaptations to pregnancy".)
Respiratory changes — The normal respiratory tract changes during pregnancy result in a compensated respiratory alkalosis, with a higher PO2 and a lower PCO2 than in the nonpregnant state. The lower PCO2 is thought to provide a diffusion gradient that may facilitate the fetus' ability to eliminate waste from aerobic metabolism. (See "Respiratory tract changes during pregnancy".)
Elevation of the diaphragm — Although the progressively enlarging uterus causes diaphragm position to rise up to 4 cm above its usual resting position, diaphragmatic excursion during respiration is not impaired since chest wall mobility increases and there is flaring of the ribs [9].
Decreased FRC and stable FEV1 — Functional residual capacity (FRC) decreases approximately 20 percent during the latter half of pregnancy, due to a decrease in both expiratory reserve volume (ERV) and residual volume (RV) (figure 3) [10,11]. Variable and generally minor changes in vital capacity (VC) and total lung capacity (TLC) have also been observed, but the magnitude of these changes suggests they are not likely to be clinically significant.
Airway function is preserved during pregnancy, as reflected by an unchanged forced expiratory volume in one second (FEV1) and an unchanged FEV1/FVC ratio. Minor changes, which are of little clinical importance, have been described in diffusing capacity for carbon monoxide (DLCO): an increase during the first trimester followed by a decrease until 24 to 27 weeks of gestation [12].
Increased ventilation and respiratory drive — Perhaps the most striking change in respiratory physiology during pregnancy is an increase in resting minute ventilation, which rises by nearly 50 percent at term. This is primarily due to a larger tidal volume, whereas the respiratory rate remains essentially unchanged [13]. The increase in ventilation is greater than the corresponding elevation in oxygen consumption (approximately 20 percent) (figure 4) [11].
Increased levels of progesterone during pregnancy are thought to be responsible for the rise in ventilation above that explained by the enhanced metabolic requirements. Progesterone is a known stimulant of respiration and respiratory drive, and its levels gradually rise from approximately 25 ng/mL at six weeks to 150 ng/mL at term [14].
Respiratory alkalosis and increased arterial O2 tension — As a result of the progesterone-induced increase in alveolar ventilation, arterial PCO2 falls to a plateau of 27 to 32 mmHg during pregnancy. This respiratory alkalosis is followed by compensatory renal excretion of bicarbonate, so that the resultant arterial pH is normal to slightly alkalotic (usually between 7.40 to 7.45) [15]. (See "Simple and mixed acid-base disorders", section on 'Compensatory respiratory and renal responses'.)
Maternal oxygenation is preserved during pregnancy. In fact, the maternal arterial oxygen tension (PaO2) is generally increased because of hyperventilation, ranging from 106 to 108 mmHg in the first trimester to 101 to 104 mmHg in the third trimester [16,17]. Interpretation of the arterial PO2 must take into account the corresponding level of PCO2, which is generally accomplished most easily by calculation of the alveolar-arterial oxygen difference.
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