Respiratory complications during pregnancy are not unusual and can be life threatening. A careful interview and physical examination, a chest x-ray, and an arterial blood analysis are the most useful interventions in the evaluation of these conditions.
Understanding of the cardiorespiratory changes during pregnancy is essential for the diagnosis and treatment of emergencies in normal pregnant women and in women with underlying cardiopulmonary diseases.
Authors of previous edition.
Oxygen is the basis of every aerobic reaction in our organism. The procurement and delivery of oxygen is a vital process that the pregnant woman has to perform for herself and her unborn child. Nature has ensured adequate mechanisms of adaptation in order to exchange oxygen with air and deliver it to her unborn child (and adapting body) through complex anatomic (Table 12-1) and physiologic changes (Table 12-2).
| Upper airways | • Mucosal edema and friability • Capillary engorgement • (A smaller-sized endotracheal tube may be required for intubation because of swelling of the arytenoid region of the vocal cords) |
| Chest wall | • Increases in chest wall circumference (6 cm) • Elevation of the diaphragm (5 cm) • Widening of the costal angles (from 70° to 104°) • Increase in diaphragmatic excursion (1.5 cm) • (All these changes occur before significant increases in uterine size, maternal body weight, or intra-abdominal pressure) |
| Respiratory musculature | • Respiratory muscle function is unchanged • Diaphragm and intercostals accessory muscles contribute equally to tidal volume during pregnancy • Maximum inspiratory and expiratory pressures are unchanged |
| Parameter | Definition | Change in pregnancy |
|---|---|---|
| Respiratory rate | Number of breaths per minute | • No change |
| Tidal volume | Volume of air inspired and expired at each breath | • Increase up to 40% since early breath pregnancy; remains essentially constant for the remainder of gestation (100-200 mL) |
| Minute ventilation (RR × Vt) | Total amount of air (gas) inspired and each minute Sum of the volume of air (gas) participating in gas exchange plus the one filling the airway’s dead space (ie, not participating in gas exchange) | • Increase up to 40% since early pregnancy and remains essentially constant for the remainder of gestation (100-200 mL) |
| Vital capacity | Maximum volume of air that can be forcibly inspired after a maximum expiration | • Unchanged |
| Residual volume | Volume of air remaining in the lungs after a maximum expiration | • Decreases by ~20% due to elevation of the diaphragm |
| Functional residual capacity (FRC) | Volume of air in lungs at resting expiratory level | • Decreases by ~20% due to elevation of the diaphragm |
| Inspiratory capacity | Maximum volume of air that can be inspired from resting expiratory level | • Increases 100-300 mL (5%-10%) as a result of the reduction in FRC |
Respiration involves 2 different but interrelated phenomena: ventilation and oxygenation. The evaluation of these processes lays in the interpretation of arterial blood gases variables: PCO2 and PO2 (Figs. 12-1 and 12-2).
Respiration requires that O2 be obtained from an extracorporeal source (atmosphere or ventilator), then transferred across the alveolar-endothelial barrier, transported to the different organs in the periphery, and subsequently utilized in aerobic metabolism.
At term, there is a small decrease (200-400 mL, 4%) in total lung capacity. Vital capacity (VC) does not change significantly. Functional residual capacity (FRC) consistently decreases 300 to 500 mL (17%-20%). Changing from a sitting to a supine position at term causes a further decrease (25%) in FRC. This may increase closure of small airways, especially in obese patients in the supine or lithotomy positions.
O2 content. The content of oxygen in arterial blood is the sum of that bound to hemoglobin (Hb) and that dissolved in plasma (normally about 1.5%). The main factor that determines the extent of O2 binding to hemoglobin (saturation) is the PaO2 (hemoglobin-oxygen dissociation curve). The shape of the curve indicates that unless the steep part of the curve is reached (a drop of PaO2 to <60 mm Hg), there will not be a significant deleterious effect on Hb saturation and O2 arterial content.
O2 affinity. Several factors can change the affinity of Hb for O2. Acidosis, fever, and increased 2,3-DPG, shift the curve to the right. In the slightly acidic environment of peripheral tissues, a right shift is important to unload O2 to the cells. Alkalosis, hypothermia, and decreased 2,3-DPG, shift the curve to the left. In the slightly alkalotic environment of the pulmonary capillary, a left shift is important to load O2 to the red blood cells. Affinity is also shifted to the left in the fetal hemoglobin.
O2 delivery (DO2). Systemic O2 delivery is the product of arterial O2 content (mL/L of blood) and cardiac output (mL/min).
O2 consumption (VO2). In a normal adult at rest, it is approximately 250 mL/min. During exercise, it can rise to 3000 mL/min. When delivery cannot meet tissue demands, anaerobic metabolism occurs, leading to lactic acidosis.
Pregnancy increases O2 consumption by 15% to 20% (Table 12-3). Half of this increase is associated with the requirements of the feto-placental unit, and the remaining half is secondary to the increased work by the maternal organs (heart, lungs, and kidneys). Increased cardiac output and minute ventilation explain how O2 consumption increases despite no change in PaO2 and a decrease in the arteriovenous O2 difference (a-VO2 difference) as a result of an increase in oxygen delivery.
Despite the favorable effects of pregnancy (progesterone is a central stimulant) on ventilation, at least half of pregnant women complain of shortness of breath (dyspnea), fatigue, and decreased exercise tolerance during gestation.
Pregnancy is characterized by a chronically compensated respiratory alkalosis due to the hyperventilation (rather than tachypnea) state of pregnancy. Pregnancy’s increase in minute ventilation (progesterone-induced hyperventilation of pregnancy) results in a decrease in PaCO2 to around 30 mm Hg. Maternal pH reflects the chronic compensated mild respiratory alkalosis. Compensation is secondary to the decline in bicarbonate concentration (secondary to increased renal excretion). The net result of these changes is facilitation of CO2 exchange from fetus to the mother.
Oxygenation is affected in at least one-fourth of pregnant women while in a supine position (lower PaO2 and larger A-a gradient). These changes are reversed when the maternal position changes to the upright state (Table 12-4).
| ABG variable | Nonpregnant adult | Pregnant |
|---|---|---|
| pH | 7.35-7.43 | 7.40-7.47 |
| PCO2 (mm Hg) | 37-40 | 27-34 (there is a compensatory increase in renal bicarbonate excretion) |
| PO2 (mm Hg) | 103 |
|
| P(A-a)O2 (mm Hg) | 14 |
|
| Bicarbonate (mEq/L) | 22-26 | 18-22 |
| Base deficit (mEq/L) | 1 | 3 |
It is not surprising that pregnant women complain of symptoms suggestive of pulmonary or cardiac disease. In most instances, a careful interrogation and physical examination can establish whether these symptoms are physiologic or a possibility of a specific condition that needs to be addressed and evaluated (Fig. 12-3).
Pregnant patients are prone to
Hypoxemia (due to decreased FRC, increased alveolar ventilation, and increased O2 consumption)
Aspiration (slow gastric emptying, functional displacement of lower esophagus)
Anesthetic overdose (decreased minimal alveolar concentration of anesthetics, decreased functional residual capacity, and increased alveolar ventilation). Induction and emergence of and from general anesthesia occurs more rapidly in pregnant women.
The anatomic and physiologic changes of the cardiac (see Chap. 8) and respiratory systems explain why respiratory symptoms are common during pregnancy. The most frequent respiratory complaint is shortness of breath (dyspnea). Other symptoms include cough and hemoptysis. Unfortunately both benign and life-threatening conditions present with similar complaints. A careful evaluation of these symptoms will allow the practitioner to discern between pregnancy-related complaints and a more severe condition. Even when deemed benign, cardiorespiratory symptoms should be noted and evaluated prospectively in subsequent visits of the patient. Some of the conditions that can be suggested by history or physical examination are included in Fig. 12-3. Specific algorithms addressing the evaluation of dyspnea, cough, and hemoptysis (Figs. 12-4, 12-5, and 12-6) are suggested.
The most frequent indications for mechanical ventilation among obstetric patients admitted to an ICU are acute respiratory failure (39%) and hemodynamic failure (38%), followed by impaired consciousness (17%) and postoperative ventilation (6%).
Leading causes of acute respiratory distress syndrome (ARDS) during pregnancy are infection, preeclampsia or eclampsia, and aspiration.
The two most helpful clinical adjuncts in the evaluation of respiratory conditions during pregnancy are:
Arterial blood gas interpretation. The changes induced by the pregnant state are summarized in Table 12-4. Figures 12-1 and 12-2 illustrate the evaluation of ventilation and oxygenation through the laboratory analysis of an arterial blood sample.
Chest x-ray interpretation. Table 12-5 summarizes the changes described for pregnancy. Aside from heart enlargement secondary to hypervolemia and cardiac remodeling and some cephalad flow redistribution, all other criteria used to interpret chest radiograms remain the same as in the nonpregnant state. Figure 12-7 provides a guideline for evaluation of chest x-rays and the most common pathologic processes encountered by the site of affliction. As was the case with the arterial blood gases, more than one process may coexist and affect the patient.
Multiple intercurrent diseases in the pregnant woman and several conditions specific to pregnancy may compromise the processes of oxygenation or ventilation. While the specific treatment of these conditions may differ, the recognition of the need for supportive respiratory therapy and the prompt institution of adequate ventilation and oxygenation support may be the difference between life and death.
Clinical guidelines for the recognition of respiratory failure (Table 12-6), means to provide noninvasive oxygen (Table 12-7), indications for mechanical ventilation (Table 12-8), indications for endotracheal intubation (Table 12-9), and guidelines for the initiation (Table 12-10) and discontinuation of mechanical ventilation (Table 12-11) are provided. In these situations, the processes of evaluation and treatment are frequently simultaneous (Figs. 12-4 and 12-8).
Mnemonic: MOVE
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