A 45 year old male with h/o smoking is scheduled for elective surgery. All are true except
B i.e. Carbon monoxide shift 02-Hb dissociation curve to right Smoking increases airway irritability & secretions, decreases surfactant mucopulmonary transpo and increases the incidence of postoperative pulmonary complications. - Cessation of smoking for 12 to 24 hrs before operation decreases the level of carbon monoxide and carboxyhemoglobin, which shift oxy-hemoglobin dissociation curve to the rightQ and increases the 02 available to tissue. (CO shift oxyHb dissociation curve to left). - Improvement in mucociliary transpo and small airway function and decrease in sputum production require prolonged abstinence (8-12 weeks) from smoking. So the incidence of postoperative pulmonary complications decrease with abstinence from cigarette smoking for > 8 weeks in patients undergoing cardiac (coronary aery bypass) surgery and > 4 weeks in patients underging pulmonary surgery. - Smoking sholy before surgery may be a/w an increased incidence ST segment depression on ECG. Major action of nicotine consists initially of transient stimulation (at small doses) and subsequently of a more persistent depression of all autonomic (sympathetic and parasympathetic) ganglia (at larger doses). Nicotine also possess a biphasic action on adrenal medulla i.e. small doses evoke whereas larger doses prevent the discharge of catecholamines in response to splanchnic nerve stimulation. The effect of nicotine on neuromuscular junction are similar to those on ganglia i.e. initial stimulant phase (contractions) f/b blockade by receptor desensitization (IA rapidly developing paralysis). Nicotine, like Ach, stimulates number of sensory receptors such as mechanoreceptors (to stretch or pressure) of skin, mesentry, tongue, lung and stomach; chemoreceptors of carotid and aoic body, thermal receptors of skin and tongue; pain receptors; and emetic chemorecepto trigger zone (CTZ) in the area postrema of medulle oblongata (causing vomiting). Nicotine markedly stimulates CNS i.e. weak analgesia at low doses; tremors and convulsion at higher doses followed by CNS depression and death from respiratory failure. So it can be assumed for the above description that smoking (low nicotine) can stimulate aoic and carotid body, increase sympathetic tone and stimulate NMJ thereby increasing the muscle relaxant dose requirements.
Effect of nicotine on aoic and carotid bodies can increase sympathetic tone
Carbon monoxide shift 02-lib dissociation curve to right
Muscle relaxant dose requirements are increased
Smoking dereases surfactant levels