Anesthetics and associated surgical procedures impair pulmonary function through direct impact on the lungs and indirect action on associated systems.
Alveolar ventilation decreases with exposure to volatile inhaled anesthetics, opiates, and intravenous sedatives in a dose-dependent manner through the disruption of different aspects of ventilatory control and ventilation-perfusion (V/Q) mismatch. Volatile anesthetics reduce tidal volumes (Vt) at concentrations greater than 1 minimum alveolar concentration (MAC) yet can stimulate respiratory centers and preserve respiratory drive. Propofol and barbiturates decrease Vt and respiratory drive in a dose dependent manner. Ketamine, etomidate, and dexmedetomidine cause less pronounced effects on respiratory drive and muscle tone, however, concurrent use of other sedatives and anesthetic drugs can result in clinically significant respiratory depression. Opiates reduce respiratory rate and increase tidal volume variability.
Functional residual capacity (FRC) universally decreases with anesthetic administration. FRC is a critical determinant of oxygen reserves and the propensity for ventilator-induced lung injury. FRC decreases primarily due to an increase in external forces on the lung parenchyma and a decrease in respiratory muscle tone (eg, intercostal muscles). This results in lung collapse, or atelectasis. In the supine position, a greater amount of pressure is transmitted from the abdomen to the thorax and the diaphragm shifts cephalad. FRC can decrease by more than one-third in the supine position. The decrease in respiratory muscle tone from anesthetics and/or neuromuscular blocking agents decreases the overall cross-sectional area of the chest wall and further contributes to decreased FRC. Dependent parts of the lung are the most susceptible to collapse. As the lung is tethered together in a network of bronchioles and alveoli, lung collapse compresses adjacent small airways and further impairs gas-exchange. Conditions that decrease the airway tone (eg, COPD, older age) or increase external pressure (eg, obesity) increase the risk of airway collapse. Restoring FRC is feasible through application of positive end-expiratory pressure (PEEP) in spontaneous and controlled breathing, recruitment maneuvers, and upright positioning. In some cases, FRC can be increased through prone positioning.
Gas exchange
Anesthesia increases V/Q mismatch across the lung. Shunt, or the absence of ventilation, is the primary type of mismatch resulting from atelectasis
and reduces arterial oxygenation. Dead-space, or the absence of perfusion, also occurs under anesthesia due to the addition of instrumental dead space (eg, tracheal tube, heat and moisture exchanger), disruption of global (eg, decreased cardiac output) or local (eg, pulmonary thrombus, venous air emboli) perfusion, or alveolar overdistention (eg, excessive PEEP). In response to decreases in alveolar oxygen content, the pulmonary vasculature vasoconstricts, termed hypoxic pulmonary vasoconstriction (HPV), and diverts blood flow away from alveoli with reduced or absent ventilation. Anesthetic gases inhibit HPV, while intravenous anesthetics have a less pronounced effect. Antihypertensive drugs (eg, sodium nitroprusside, nitroglycerin, nicardipine) cause nonselective pulmonary vasodilation and may worsen shunt in the presence of atelectasis.Respiratory reflexes
Minute ventilation increases linearly with arterial carbon dioxide content (PaCO2). Inhaled and intravenous anesthetics diminish this ventilatory response to hypercapnia and hypoxemia in a dose-dependent manner by decreasing the sensitivity of chemoreceptors at the carotid and aortic bodies. Opiates result in a right-shift of the PaCO2–ventilation response curve and a higher resting PaCO2.
Volatile anesthetics reduce airway resistance through bronchodilation and are a treatment for refractory cases of reactive airway disease in the intensive care unit. Pungent volatile agents (eg, desflurane, isoflurane) can result in increased airway irritability, breath-holding, and coughing when administered during spontaneous breathing. They should be avoided for inhalational inductions due to the risk of laryngospasm and bronchospasm. At high doses, desflurane can increase airway tone.
Intravenous anesthetics, especially propofol and ketamine blunt airway reflex bronchoconstriction, although to a lesser degree than volatile anesthetics. Upper airway reflexes are also reduced, facilitating laryngoscopy when used for induction but increase the risk of upper airway obstruction and aspiration.
Ciliary function. Volatile anesthetics and nitrous oxide reduce ciliary beat frequency, slowing the rate of mucous clearance from the airways. Likewise, barbiturates, dexmedetomidine, and benzodiazepines reduce ciliary beat frequency. In contrast propofol and ketamine can stimulate this process. Data examining the effect of opioids on ciliary beat frequency is conflicted. During mechanical ventilation, nonhumidified gasses are often delivered at high flow rates that dry secretions and damage the respiratory epithelium. Artificial airways bypass the nasopharynx that plays a critical role in airway humidification. Passive humidification can occur with use of a heat and moisture exchanger.
Coughing. Effective coughing for airway clearance requires adequate inspiratory and forced expiratory effort and the engagement of accessory muscles. Certain procedures (abdominal, thoracic, and spine surgeries) restrict adequate coughing due to splinting from pain. In high-risk patients, ineffective coughing leads to further atelectasis and mucous plugging. Strategies to provide adequate analgesia and avoid oversedation, including regional and neuraxial techniques, should be used when possible. Respiratory devices such as incentive spirometry or positive expiratory pressure devices can augment effort in inspiration yet require patient compliance and coordination.