In: Anesthesia20 Feb 2010
Smoking increases the production of Hb, red blood cells, white blood cells, and platelets and increases plate let reactivity. There is also an increase in fibrinogen. These result in an increase in the hematocrit and the blood viscosity, leading to an increased thrombotic tendency. The result is an increased incidence of arterial thromboembolic disease in smokers. However, there is no increase in the incidence of deep vein thrombosis. In fact, a decreased incidence in comparison with non-smokers has been reported in some studies.
Chronic hypoxia to the cardiac muscle and the increase in incidence of thromboembolic disease causes smokers to be at a 70% greater risk of coronary artery disease compared with nonsmokers, and the postoperative mortality in smokers is higher than in nonsmokers. Of 38% of vascular patients with cardiovascular problems, 80% are smokers. pharmacy united kingdom
EFFECT ON THE RESPIRATORY SYSTEM
As stated earlier, smoking affects oxygen transport and delivery. Irritants in smoke increase mucus secretions. The mucus becomes hyperviscous, with altered elasticity. Cilia become inactive and are destroyed by ciliotox-ins. The result is impaired tracheobronchial clearence. Laryngeal and bronchial reactivity is increased. Cigarette smoke is known to disrupt the epithelial lining of the lung, causing an increase in pulmonary epithelial permeability. This loss of epithelial integrity allows irritants to penetrate the epithelium more easily and stimulate the subepithelial irritant receptors, resulting in increased reactivity. Smoking leads to small-airway narrowing, causing an increased closing volume. Pulmonary surfactant is also decreased. These lead to small-airway disease. An increase in pulmonary proteolytic enzymes or elastolytic enzymes causes loss of elastic lung recoil and emphysema. Lung infection is increased. Twenty-five percent of smokers suffer from chronic bronchitis, occurring five times more often than in nonsmokers. The incidence of chronic obstructive airway disease is also higher than in nonsmokers. When pulmonary function tests are done, chronic smokers with chronic obstructive airway disease show an obstructive pattern. In asymptomatic smokers, the spirometry pulmonary function tests are normal. However, in asymptomatic smokers, closing volumes are significantly increased, exhibiting small-airway disease. Following smoking cessation, ciliary activity starts to recover within 4-6 days. The sputum volume takes 2-6 weeks to return to normal. There is some improvement in tracheobronchial clearance after 3 months. It takes 5-10 days for laryngeal and bronchial reactivity to settle. There is improvement in small-airway narrowing after 4 weeks, and marked improvement is seen after 6 months. One must be careful in stopping smoking in asthmatics as the asthma may worsen.
THE EFFECT ON PERIOPERATIVE EVENTS
Schwilk et al, in a large survey, compared specific respiratory events such as reintubation, laryngospasm, bronchospasm, aspiration, hypoventilation, hypoxemia, and others during anesthesia in smokers and nonsmokers. The incidence was found to be 5.5% in smokers, compared with 3.3% in nonsmokers. They calculated the relative risk of these events occurring during anesthesia and found that the risk in all smokers was 1.8 times than in nonsmokers. In young smokers, it was 2.3 times, and in obese smokers, it was 6.3 times the normal. Thus, obese smokers are at a high risk of having respiratory problems during anesthesia. It was found that smokers have a significantly high risk of having bronchospasms during anesthesia. The risk was higher in female smokers, and the risk was 25.7 times normal in young smokers with chronic bronchitis.
The currently available pulse oximeters measure light absorbance at only 2 wavelengths and cannot distinguish between more than 2 species of hemoglobin. Therefore, they cannot distinguish oxyhemoglobin (Hb02) from carboxyhemoglobin. As a result, the oxygen saturation exhibited by pulse oximeters in chronic smokers will be a gross overestimation of the oxygen saturation. It combines the saturation of Hb02 and COHb as the result. If 10% of COHb is present in the blood and the oximeter reads 100%, the actual reading is less than 90%. To get a correct reading, the oxygen saturation should be measured using a CO oximeter.
Fletcher found that the difference between the partial pressure of arterial carbon dioxide and end tidal carbon dioxide (PaC02 – EtC02) in nonsmokers was 0.3 kPa while in smokers it was 0.9 kPa. They also found that this difference increased with age in smokers but not in nonsmokers. It increased by 0.2 kPa per decade. Thus, a 60-year-old smoker will need 25% more minute ventilation than a nonsmoker to maintain a given partial pressure of arterial carbon dioxide. canadian pharmacy cialis
Blog invites submissions of review articles, reports on clinical techniques, case reports, conference summaries, and articles of opinion pertinent to the control of pain and anxiety in dentistry.