Abstract
Dyspnoea is a common complaint in pregnant women, and may occur as a result of the physiological changes in pregnancy or due to cardio-respiratory disease. A prospective observational study of 62 pregnant women identified that 76% experienced dyspnoea at some point during their pregnancy. Approximately half became symptomatic before 20 weeks’ gestation and the incidence increased until about 30 weeks’ gestation. It is important to be aware that some complications of pregnancy may produce dyspnoea in the previously well patient, so it is important to differentiate pathological conditions from this physiological dyspnoea. This chapter reviews the mechanisms of dyspnoea of pregnancy and the differentiation from pathological conditions.
Dyspnoea is a common complaint in pregnant women, and may occur as a result of the physiological changes in pregnancy or due to cardio-respiratory disease. A prospective observational study of 62 pregnant women identified that 76% experienced dyspnoea at some point during their pregnancy.1 Approximately half became symptomatic before 20 weeks’ gestation and the incidence increased until about 30 weeks’ gestation. It is important to be aware that some complications of pregnancy may produce dyspnoea in the previously well patient, so it is important to differentiate pathological conditions from this physiological dyspnoea. This chapter reviews the mechanisms of dyspnoea of pregnancy and the differentiation from pathological conditions.
Ventilatory Changes in Pregnancy
The cardiopulmonary physiological changes that occur in pregnancy are discussed in detail in Chapter 4 of this book. A very brief review of some of these changes follows. The enlarging uterus causes elevation of the diaphragm and some loss of lung volume, accommodated by widening of the thoracic cage. The effect on total lung capacity is small, vital capacity remains unchanged and the major effect is a reduction in the functional residual capacity (the amount of air left in the lungs at the end of a normal breath).2 However, more significant changes occur in the degree of ventilation that occurs during pregnancy.
An increase in oxygen consumption and carbon dioxide production occurs during pregnancy due to fetal demands and increased maternal metabolic processes, beginning in the first trimester and increasing during pregnancy to about 20–33% above baseline by term.3 Minute ventilation increases in excess of these demands, reaching a level 20–40% above baseline.4 This increase in ventilation is mediated in part by hormonal changes. Progesterone stimulates the respiratory centre while oestrogen increases the number and sensitivity of progesterone receptors in the respiratory-related centres in the brain,5 although the mechanism may be far more complex.6,7 The increased ventilation occurs via an increase in tidal volume (rather than respiratory rate) and produces a mild respiratory alkalosis, with renal compensation.4
It is important to point out aspects of respiratory physiology that are not altered by the pregnant state. As mentioned above, respiratory rate increases minimally as a result of pregnancy. Vital capacity and the forced expiratory volume in 1 second (FEV1) are not affected by pregnancy. The diffusing capacity for carbon monoxide (DLCO or transfer factor) is not significantly affected by pregnancy,8 although some studies have noted variations, possibly related to changes in cardiac output and haemoglobin concentration.
Control of Breathing and Mechanisms of Dyspnoea
Dyspnoea or shortness of breath has been described as ‘a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity’.9 The mechanisms of dyspnoea are complex and not fully understood. The different sensory qualities experienced (e.g. air hunger, chest tightness, increased effort of breathing and unsatisfied inspiration) may occur by different neurological mechanisms.10 The neurological control of breathing and perception of dyspnoea involves central respiratory neurons within the medulla oblongata and pons, which drive motor neurons controlling muscles of the upper airways, the diaphragm, and other thoracic and abdominal muscles. Simultaneous with this motor output, an ascending copy of this activity is sent to the perceptual areas of the brain (corollary discharge). Afferent information related to breathing is received by the brain from a variety of sources, namely chemoreceptors (carotid, aortic, medullary) and vagal pulmonary receptors (stretch, chemical and mechanical receptors), as well as skeletal muscle mechanoreceptors. Adding to the complexity are vagally mediated cold receptors in the upper airways which likely detect changes in airflow.
The different mechanisms of dyspnoea may include imbalances between muscle afferents and the respiratory centre efferents (corollary discharge) for increased sensations of effort of breathing; stimulation of airway receptors for sensations of chest tightness, and imbalances between lung feedback afferents, corollary discharge and inspiratory drive for air hunger (Table 16.1).
Table 16.1 Examples of physiological mechanisms of dyspnoea
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Dyspnoea of Pregnancy: Mechanisms
Many theories have been advanced to explain the dyspnoea experienced by pregnant women who have no evidence of cardiopulmonary disease (Table 16.2). These include (one or a combination of): (i) a normal awareness of the hyperventilation induced by pregnancy, (ii) altered mechanics due to the enlarged uterus and altered chest wall anatomy and (iii) an exaggerated perception of respiratory discomfort for a given minute ventilation. Several studies have addressed these mechanisms.
Table 16.2 Potential mechanisms, features and differential diagnosis of pregnancy-related dyspnoea
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