Cigarette Smoking

Smoking is the most common cause of preventable death. Half of cigarette smokers die of a smoking-related disease; on average, smokers lose at least 10 y of life expectancy.

In USA, incidence of smoking is 17.8%: 42.1 million smokers (2013). Consumption in USA peaked in 1965 at 42%. Worldwide consumption still rising, with 5.8 trillion cigarettes smoked per y; fastest consumption growth is in China.

Native Americans/Alaskan Natives have highest rate of smoking in USA at 26% followed by African Americans at 25.5%.

Frequency increased with a lower level of educational attainment (24.2% without high school diploma; 41.4% with GED; 5.6% of those with a graduate degree) and poverty; true even in low- to middle-income countries.

Male:female ratio: 4:3, with young women the fastest-growing group.

Increased risk of CAD × 2 that of nonsmokers of the same age

Postop pulm complications up to × 6 that of nonsmokers

COHb increased (up to 15%)

Hyperreactive airway

No increased risk of pulm aspiration

Reduced risk of postop N/V

Increased rate of death (odds ratio 1.63) and postop complications in elective surgery and major joint, spine, and neurosurgery

CAD, COPD, PVD, productive cough, and reactive airways

Increases physiologic age by 8 y (30 packs per y) relative to nonsmokers

Decreased tolerance to pain, requiring increased doses of analgesics

Increased rate of postoperative delirium

Pediatric passive smoking and reactive airways and increased rate of SIDS

Addictive habit: Cigarette smoke contains >4000 identifiable constituents, many of which are pharmacologically active, toxic, or have tumorigenic effects. Acute effects relate to CO and nicotine.

90% of tobacco smoke is gaseous, consisting of nitrogen, O ₂ , and carbon monoxide along with gaseous irritants and carbon monoxide. Particulate matter consists of nicotine, tar, and other volatile organics.

Nicotine stimulates the sympathetic ganglia, causing release of catecholamines from the adrenal medulla and sympathetic nerve endings, increasing BP, HR, and SVR, that persists for 30 min after one cigarette.

Associated with decreased MAO and increased dopamine levels in the brain.

Inhaled CO produces up to 5–15% COHb, compared with 0.3–1.6% in nonsmokers. Combined effects of nicotine and COHb put diseased myocardium at risk.

Irritates the pulm system, increasing mucus production while decreasing ciliary activity and mucus flow, markedly impairing tracheobronchial secretion clearance.

Chronic use associated with CAD, Htn, COPD, peripheral vascular disease, and numerous cancers.

Smoking also increases all blood cell lines, platelet reactivity, and fibrinogen.

Cessation for 3–4 hours results in insignificant hemodynamic side effects from nicotine, and it improves myocardial O ₂ supply to demand.

Cessation of smoking the night before surgery will reduce the COHb and nicotine levels to that of nonsmokers. Cessation 4–6 d will result in a return of ciliary activity.

Cessation for less than 4 wk has same rate of respiratory and wound healing complications as found in active smokers (OR 1.2); smokers should stop at least 4 wk before surgery.

Cessation for 2 y reduces risk of MI to that of the nonsmoking population.

Smoking is the cause of 1 of every 5 deaths in USA and is the leading cause of preventable mortality (480,000 preventable deaths/y).

Habituation and addiction