Smoking and P50
Smoking is a major risk factor associated with perioperative respiratory and cardiovascular complications. Evidence also suggests that cigarette smoking causes imbalance in the prostaglandins and promotes vasoconstriction and excessive platelet aggregation. Two of the constituents of cigarette smoke, nicotine and carbon monoxide, have adverse cardiovascular effects. Carbon monoxide increases the incidence of arrhythmias and has a negative ionotropic effect both in animals and humans. Smoking causes an increase in carboxyhemoglobin levels, resulting in a leftward shift in which appears to represent a risk factor for some of these cardiovascular complications. There are two mechanisms responsible for the leftward shift of oxyhemoglobin dissociation curve when carbon monoxide is present in the blood. Carbon monoxide has a direct effect on oxyhemoglobin, causing a leftward shift of the oxygen dissociation curve, and carbon monoxide also reduces the formation of 2,3-DPG by inhibiting glycolysis in the erythrocyte. Nicotine, on the other hand, has a stimulatory effect on the autonomic nervous system. The effects of nicotine on the cardiovascular system last less than 30 min.
Smoking Cessation and P50 effect
Smoking increases carboxyhemoglobin concentration in the blood that results in a decrease in available hemoglobin for oxygen transport. Carboxyhemoglobin also shifted P50 to the left. After smoking is stopped for 12 hr, there is a significant decrease in carboxyhemoglobin levels and an increase in P50 of the oxyhemoglobin. Preoperative smoking halt for as little as 12 hr is enough to shift towards normal in patients who smoke one to two packs of cigarettes per day.
- Smoking cessation – acute physiology
- Smoking cessation – Acute effects
- Smoking Cessation and Anesthesia