2.2 Effects of anesthesia on respiratory system: 

• General anesthesia, with or without the use of neuromuscular blocking drugs, results in the loss of airway patency due to the relaxation of the pharyngeal muscles and posterior displacement of the tongue. The ability to manage secretions is lost, and saliva and mucous can obstruct the oropharynx. 
• The loss of the cough reflex allows secretions (or refluxed gastric contents) onto the vocal cords, causing laryngospasm, or to enter the trachea and lungs causing bronchospasm and ultimately infection. These effects result in airway obstruction and prevent the passage of gases into and out of the lungs resulting in hypoxia and hypercapnia. 
• Most anesthetic drugs cause a dose- dependent reduction in ventilatory minute volume. This can be due to either a reduction in the respiratory rate (e.g. opioids), a reduction in the tidal volume (e.g. volatile anesthetics) or both (e.g. propofol). As alveolar ventilation decreases the PaCO2 increases. Hypercapnia (increase PaCO2) causes vasodilation, tachycardia, arrhythmias, hypertension and in an awake patient, headache, confusion, tremor, sedation and eventually coma (CO2 narcosis). Of equal importance is that the increased PACO2 displaces oxygen from the alveoli and can exacerbate hypoxia. 
• The most important effect of most general anesthetics on breathing is a tendency to promote hypoventilation. The mechanism is probably dual: central depression of the chemoreceptor and depression of external intercostal muscle activity. 
• Regardless of the agent used, light anesthesia often results in irregular breathing patterns; breath holding is common. Breaths become regular with deeper levels of anesthesia. Inhalation agents generally produce rapid and shallow breaths. 
• At deeper levels of anesthesia, muscle activity is depressed, but if there is any rebreathing of CO2, muscle activity in all muscle groups is increased. 
• Induction of anesthesia consistently produces 15–20% reduction in functional residual capacity (FRC) about 400 mL in most patients beyond what occurs with the supine position alone. This decrease in FRC has commonly been thought to be due to a cephalad shift of the diaphragm secondary to loss of muscle tone. This decrease in FRC is not related to anesthetic depth and may persist for several hours after anesthesia. 
• Steep head-down (Trendelenburg) position (> 30°) may reduce FRC even further as intrathoracic blood volume increases. In contrast, induction of anesthesia in the sitting position appears to have little effect on FRC. Muscle paralysis does not appear to change FRC significantly when the patient is already anesthetized. 
• The reduction in FRC associated with general anesthesia would be expected to increase airway resistance. Increases in resistance are not usually observed because of the bronchodilation properties of the volatile inhalation anesthetics. Increased airway resistance is more common due to pathological factors (posterior displacement of the tongue; laryngospasm; bronchoconstriction; or secretions, blood, or tumor in the airway) or equipment problems (small tracheal tubes or connectors, malfunction of valves, or obstruction of the breathing circuit).