In: Anesthesia19 Feb 2010
Despite the warnings of health hazards of cigarette smoking, still one third of the population in industrial countries smoke. Cigarette smoke contains over 4000 substances, some of which are pharmacologically active, some antigenic, some cytotoxic, some mutagenic, and some others carcinogenic. It consists of a gaseous phase and a particulate phase. Eighty to 90% of cigarette smoke is gaseous, consisting of mainly nitrogen, oxygen, and carbon dioxide. The gaseous phase also contains carcinogens such as hydrocyanic acid and hydrazine, ciliotoxins, and irritants such as hydrocyanic acid, acetal-dehyde, ammonia, acrolein, and formaldehyde, and an agent impairing oxygen transport, namely carbon monoxide. In the particulate phase, the main toxic ingredient is nicotine. It also contains carcinogens such as tar and polynuclear aromatic hydrocarbons and tumor accelerators such as indole and carbazole.
EFFECT ON THE CARDIOVASCULAR SYSTEM
Nicotine in smoke stimulates the adrenal medulla to secrete adrenaline, resets the carotid body and aortic receptors to maintain a higher blood pressure, and stimulates autonomic ganglia, increasing sympathetic tone. The result is an increase in systolic and diastolic blood pressure, an increase in heart rate, and an increase in peripheral vascular resistance. These increase the myocardial contractility, leading to an increase in oxygen consumption by the cardiac muscle. Increase in excitability leads to more frequent contractions and again an increase in oxygen consumption. Thus, the demand for oxygen is increased. An increase in coronary vascular resistance leads to a decrease in the coronary blood flow, resulting in a decrease in the supply of oxygen. These lead to a decrease in the myocardial oxygen supply : demand ratio. Nicotine also increases intracellular calcium during ischemia. This may exacerbate myocardial cell damage. In smokers, the plasma concentration of nicotine reaches 15-50 ng/mL. The half life of nicotine is 30-60 minutes. Following the smoking of 1 cigarette, the pressor response lasts for about 30 minutes. Three to four hours of abstinence results in insignificant side effects due to nicotine and a significant improvement of the myocardial oxygen supply: demand ratio. canada drugs online
The other constituent of smoke that affects the cardiovascular system is carbon monoxide. Cigarette smoke contains 400 parts per million. In the blood, carbon monoxide combines with hemoglobin to form car-boxyhemoglobin (COHb). In smokers, the amount of COHb in the blood ranges from 5 to 15%. In non-smokers, it is only about 0.3 to 1.6%. Even with environmental pollution, the COHb detected in nonsmokers does not exceed 1.9%. The amount of COHb present in the blood of smokers depends on the type of cigarette smoked, the frequency, and the method of smoking. The concentration is said to be constant throughout the day. The affinity of carbon monoxide for hemoglobin (Hb) is 200 times that of oxygen. Thus, the amount of Hb available for combining with oxygen is drastically reduced. It also shifts the oxyhemoglobin curve to the left due to (i) its high affinity for Hb, (ii) a change in shape of the oxyhemoglobin curve from a sigmoidal to a more hyperbolic curve by carboxyhemoglobin, and (iii) depletion of 2,3-diphosphoglycerate by carbon monoxide. The left shift of the oxyhemoglobin curve makes it difficult for tissues to extract oxygen from the hemoglobin. The result is a decrease in the oxygen available to the tissues. Carbon monoxide also binds with cytochrome oxidase and myoglobin and inactivates mitochondrial enzymes in the cardiac muscle. The result is a decrease in the intracellular oxygen transport and usage and a negative inotropic effect. These mechanisms lead to chronic tissue hypoxia. The body compensates with an increase in red blood cells. The result is an improvement of the oxygen availability at the expense of increased plasma viscosity.
Carbon monoxide also affects the cardiac rhythm. Patients with coronary artery disease having 6% of COHb in their blood have exhibited ventricular arrhythmias during anesthesia. At a concentration of COHb of 4%, no arrhythmias have been detected.
The half life of carboxyhemoglobin depends chiefly on pulmonary ventilation. At rest, the half life is about 4-6 hours. With strenuous exercise, due to rapid breathing, it is decreased to 1 hour. During sleep, when the breathing is slow, its half life is prolonged to about 1012 hours. If one breathes 100% oxygen, its half life is reduced to 40-80 minutes, and with hyperbaric oxygen, it is even further reduced to 23 minutes. Recently, it has been found that its half life is longer in males than females. Thus, on advising patients before anesthesia, these variations should be noted. During the day time, abstinence for 12 hours is sufficient to get rid of carbon monoxide. If an operation is scheduled for the next morning, the patient should not smoke the previous evening. Males should abstain for even a longer period.
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