Changes within the respiratory system are of great significance to the anaesthetist.

Respiratory Tract. Hormonal changes to the mucosal vasculature of the respiratory tract lead to capillary engorgement and swelling of the lining in the nose, oropharynx, larynx, and trachea. Symptoms of nasal congestion, voice change and upper respiratory tract infection may prevail throughout gestation. These symptoms can be exacerbated by fluid overload or oedema associated with pregnancy-induced hypertension (PIH) or pre-eclampsia. In such cases, manipulation of the airway can result in profuse bleeding from the nose or oropharynx; endotracheal intubation can be difficult; and only a smaller than usual endotracheal tube may fit through the larynx. Airway resistance is reduced, probably due to the progesterone-mediated relaxation of the bronchial musculature.

From the middle of the second trimester, expiratory reserve volume, residual volume and functional residual volume are progressively decreased, by approximately 20% at term. Lung compliance is relatively unaffected, but chest wall compliance is reduced, especially in the lithotomy position.

Ventilation and Respiratory Gases. A progressive increase in minute ventilation starts soon after conception and peaks at 50% above normal levels around the second trimester. This increase is effected by a 40% rise in tidal volume and a 15% rise in respiratory rate (2-3 breaths/minute). Since dead space remains unchanged, alveolar ventilation is about 70% higher at the end of gestation. Arterial and alveolar carbon dioxide tensions are decreased by the increased ventilation. An average PaCO₂ of 32 mmHg (4.3 kPa) and arterial oxygen tension of 105 mmHg (13.7 kPa) persist during most of gestation. The development of alkalosis is forestalled by compensatory decreases in serum bicarbonate. Only carbon dioxide tensions below 28 mmHg (3.73 kPa) will lead to a respiratory alkalosis.

During labour, ventilation may be further accentuated, either voluntarily (Lamaze method of pain control and relaxation) or involuntarily in response to pain and anxiety. Such excessive hyperventilation results in marked hypocarbia and severe alkalosis, which can lead to cerebral and uteroplacental vasoconstricton and a left shift of the oxygen dissociation curve. The latter reduces the release of oxygen from haemoglobin with consequent decreased maternal tissue oxygenation as well as reduced oxygen transfer to the fetus. Furthermore, episodes of hyperventilation may be followed by periods of hypoventilation as the blood carbon dioxide tension (PaCO₂) returns to normal. This may lead to both maternal and fetal hypoxia.

Oxygen consumption increases gradually in response to the needs of the growing fetus, culminating in a rise of at least 20% at term. During labour, oxygen consumption is further increased (up to and over 60%) as a result of the exaggerated cardiac and respiratory work load.

Clinical Implications. The changes in respiratory function have clinical relevance for the anesthesiologist. Most importantly, increased oxygen consumption and the decreased reserve due to the reduced functional residual capacity, may result in rapid falls in arterial oxygen tension despite careful maternal positioning and preoxygenation. Even with short periods of apnea, whether from obstruction of the airway or inhalation of a hypoxic mixture of gas, the gravida has little defense against the development of hypoxia. The increased minute ventilation combined with decreased functional residual capacity hastens inhalation induction or changes in depth of anaesthesia when breathing spontaneously. 
 
Gastrointestinal System

Since aspiration of gastric contents is an important cause of maternal morbidity and mortality in association with anesthesia, an examination of the controversy surrounding gastrointestinal changes in pregnancy is justified.

Mechanical Changes. The enlarging uterus causes a gradual cephalad displacement of stomach and intestines. At term the stomach has attained a vertical position rather than its normal horizontal one. These mechanical forces lead to increased intragastric pressures as well as a change in the angle of the gastroesophageal junction, which in turn tends toward greater oesophageal reflux.

Physiological Changes. The hormonal effects on the gastrointestinal tract are an issue of debate among anaesthetists. Relaxation of the lower oesophageal sphincter has been described, but there have been differing views about the effect on motility of the gastrointestinal tract and the times at which it is most prominent. Many believe that there is also retardation of gastrointestinal motility and gastric emptying, producing increased gastric volume with decreased pH, beginning as early as 8-10 weeks of gestation. Recent studies, however, have shed a different light on the subject. Measuring peak plasma concentrations of drugs absorbed exclusively in the duodenum in both non-pregnant and pregnant volunteers, at different times of gestation, it was shown that peak absorption occurred at the same interval in all women with the exception those in labour. This suggests that gastric emptying is delayed only at the time of delivery.

Thus, the raised risk of aspiration is due to an increase of oesophageal reflux and decreased pH of gastric contents. The heightened incidence of difficult endotracheal intubations worsens the situation.

Teaching Point. The gravida should be considered a to be a "full stomach" patient with increased risk of aspiration during most of gestation.

Pulmonary Aspiration of gastric contents can occur either following vomiting (active) or regurgitation (passive). Aspiration of solid material causes atelectasis, obstructive pneumonitis or lung abscess, while aspiration of acidic gastric contents results in chemical pneumonitis (Mendelson's syndrome). The most serious consequences follow aspiration of acidic materials containing particulate matter as may follow swallowing certain antacids such as magnesium trisilicate. Clear antacids such as sodium citrate (0.3 Mol) or bicarbonate should be used. While the incidence of pulmonary aspiration of solid food has decreased due to patient education, that of gastric acid has remained constant.

Clinical Implications. The danger of aspiration is almost eliminated when regional anaesthesia or inhalational analgesia is used. During general anaesthesia airway protection by means of a cuffed endotracheal tube is mandatory. Although awake intubation is safest, discomfort and the lack of patient cooperation and discomfort prevent it being the routine method for securing the airway. The endotracheal tube is placed immediately following loss of consciousness after induction of general anesthesia.

Teaching Point. Special precautions should be heeded, even when induction to intubation time is expected to be brief, to prevent the regurgitation:

1. Supine position with lateral tilt to minimise any increase in intragastric pressure

2. Preoxygenation prior to induction then no positive pressure ventilation prior to insertion of the endotracheal tube to prevent distention of the stomach with gas (rapid sequence induction)

3. Cricoid pressure (Sellick's maneouvre) during induction which is maintained until endotracheal tube placement in the trachea has been confimed. Cricoid pressure should be applied to the cricoid cartilage whilst supporting the back of the neck. This occludes the oesophagus, thus obstructing the path of regurgitation.

(Continued ...)

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