Print version ISSN 0034-7094
Rev. Bras. Anestesiol. vol.52 no.3 Campinas May/June 2002
Smoking and anesthetic implications *
Implicaciones anestésicas del tabagismo
Ricardo Dorneles Furtado, M.D.
Anestesiologista do Hospital Santa Rita, Porto Alegre, RS
BACKGROUND AND OBJECTIVES: Smoking is
becoming very important for anesthetic morbidity. In spite of its widespread
noxious effects on health, developing countries have increasing statistics on
smoking population. This review aimed at showing action mechanisms and effects
of cigarettes on different organs and systems, and their impact on physiology,
preoperative risk and management of smokers during preanesthetic preparation,
in addition to postoperative complications.
CONTENTS: Several action mechanisms of cigarettes and their components on organ and systems, organic consequences and the anesthetic approach to decrease perioperative morbidity in those patients are presented.
CONCLUSIONS: Smoking history in preanesthetic evaluation should be highly valued and preventive measures should be taken with regard to systemic effects, thus minimizing surgical and anesthetic risks.
Key words: COMPLICATIONS, Respiratory: smoking; PREOPERATIVE EVALUATION: smoking
JUSTIFICATIVA Y OBJETIVOS: El humo ha
asumido grande importancia en relación a la morbidez anestésica. A
pesar de la divulgación acerca de los prejuízos a la salud, países
reconocidos como en desenvolvimiento presentan estadísticas crecientes
cuanto a la población usuaria de cigarros. El objetivo de esta revisión
es mostrar el modo de acción y efectos del cigarro sobre los diversos órganos
y sistemas y el impacto de éstos sobre la fisiología del organismo,
riesgo pré-operatorio y el manoseo de pacientes fumantes durante la preparación
pré-anestésica y complicaciones pós-operatorias.
CONTENIDO: En esta revisión son presentadas las diversas formas de acción del cigarro y sus componentes sobre órganos y sistemas, repercusiones orgánicas y la conducta anestésica para que haga reducción de la morbidad perioperatoria en estos pacientes.
CONCLUSIONES: La historia del tabagismo en la evaluación pré-anestésica debe ser enfáticamente valorizada y medidas preventivas en relación a los efectos sistemicos deben ser tomadas, minimizando así los riesgos de los procedimientos.
Smoking is becoming very important for anesthetic morbidity. In spite of its widespread noxious effects on health, developing countries have increasing statistics on smoking population. Postoperative pulmonary complications are 2 to 6 times more frequent in smokers as compared to nonsmokers. Smokers have a 70% higher risk for cancer, cardiovascular or pulmonary disease, as compared to nonsmokers 1. In industrialized countries, approximately 1/3 of the adult population smoke and around 20% of natural deaths are attributed to tobacco consumption 2,3. In Brazil, 80 to 100 thousand people die every year from smoking-related diseases 4; in the world, approximately 3.7 million people die, being 1/3 in developing countries. This study aimed at reviewing cigarettes action and effects on several organs and systems, considering their impact on physiology, preoperative risk and management of smokers during preanesthetic preparation, in addition to postoperative complications.
Nicotine is known by men since 1828 and was isolated by Posselt and Reiman; posteriorly, its pharmacology was studied by Orfila in 1843 5. Several organs and systems are damaged by the continuous use of tobacco, which has more than 4000 substances in the smoke, some of them with active pharmacological cytotoxic, antigenic and mutagenic action, including at least 43 carcinogens, and are responsible for a wide range of noxious effects 1,6. Most affected organs and systems are heart, GI tract, lungs, blood and immune and nervous systems. Special attention must be given to the respiratory system which directly receives inhaled gases. One may also mention effects on homeostasis, drug metabolism and patients psychism. Undoubtedly, nicotine is today the most widespread dependence-producing substance 7.
From the total smoke produced by a cigarette, approximately 92% to 95% are in the gaseous phase; from these, 85% are nitrogen, oxygen and carbon dioxide; the remaining gases, presented as non-condensed vapors and material particles determine most clinical manifestations of medical importance. Some compounds of those gases act directly on mouth, nose, pharynx and tracheobronchic tree mucosa, while others are absorbed by the blood or dissolved in the saliva and swallowed 1.
NICOTINE PHARMACOLOGICAL PARTICULARITIES
Nicotine is an alkaloid with dose-dependent ganglionary stimulating and depressing action. Smokers have, in general, 15 to 50 ng.ml-1 nicotine levels. This substance acts on different areas: carotid body and aorta chemoreceptors, in autonomic ganglia through catecholamine release by the adrenal medulla and other chromaffin tissues. Major acute effects include increase in systolic and diastolic blood pressure, heart rate, inotropism and peripheral vasoconstriction. Direct nicotine vasoconstriction may increase coronary vascular resistance impairing blood flow, especially in patients with stenotic coronary lesions. All those effects result in an unfavorable environment for myocardial oxygenation in terms of supply/demand ratio. There is an increase in norepinephrine, epinephrine, growth hormone, cortisol and vasopressin plasma levels 1,8.
Nicotine is absorbed by the skin, mucosa (stomach and intestines) and lungs, being transported by blood flow, reaching the central nervous system (CNS) and acting in approximately 7 seconds by the release of endogen opioids and glucocorticoids 5,7.
It is metabolized by liver (80% to 90%), lung and kidneys (in a lower ratio). Nicotine and its major metabolites - cotinine and nicotine-n-oxide - are promptly excreted by the kidneys, especially in acidified urine. Nicotine plasma half-life after inhalation is 30 to 60 minutes. Although being highly toxic, nicotine is eliminated after one night abstinence. After this period, there is a decrease in heart rate, blood pressure and catecholamine levels. After preanesthetic medication administered at night, patients should be advised not to smoke before sleeping. Cotinine may be measured in urine, blood and saliva and is largely used as a smoking habit determinant 6; since it has a long elimination half-life (more than 20 hours), it may be used to evaluate patients adherence to preoperative abstinence recommendations. Cigarettes themselves represent 8 to 9 mg of nicotine and only 1 mg is systemically made available to smokers because smoked tobacco has 1% to 2% nicotine 5.
Carbon monoxide (CO) is a toxic gas interfering with oxygen transportation and utilization. It is important to remind that hemoglobin (Hb) affinity for CO is approximately 200 times higher than for oxygen; even in low CO alveolar concentrations, smokers have significant amounts of carboxyhemoglobin (COHb) (5-15% in smokers; 0.5 to 3% in nonsmokers), due to Hb metabolism and air pollution 1. CO is only excreted by breathing and has a rather stable binding to Hb, which may be detected even after death 9.
Cigarette smoke inhalation increases pulmonary microvascular patency with the production of free radicals allowing the assumption that these substances may be important in the pathogenesis of tobacco-induced diseases such as emphysema 10.
Among major carcinogens, one may mention polinuclear aromatic hydrocarbons, aromatic amines and nitrosamines. Some mutagenicity indicators are increased in smokers lymphocytes as compared to nonsmokers. Carcinogenesis-related substances, such as catechol, phenol and cresol groups are also found in the smoke 1.
Nicotine is classified as an insecticide with potential toxicity. Clinical symptoms are salivation and vomiting, followed by muscle weakness and prostration, with blood pressure decrease and weak pulse and culminating with chlonic seizures and respiratory arrest 9. There may also be visual or auditory changes, abdominal pain, mental confusion and cold sweating. It is estimated that 60 mg is the nicotine dose needed to cause death. Intoxication treatment includes, gastric lavage, ipecac emetic syrup, in addition to support therapy for hemodynamic and respiratory changes 5.
TOBACCO ACTIONS ON DIFFERENT ORGANS AND SYSTEMS
There is a cardiovascular system theft since there is a higher oxygen consumption through the sympathetic-adrenergic system activation. At the same time, there is an oxygen supply decrease by increased COHb levels and coronary vascular resistance increase. Smoking is the major risk factor for arterial thromboembolism and coronary vasospasm through multiple ways, including direct endothelial and hematological damage and metabolic and biochemical abnormalities 3,6. This substance may increase and even decrease heart rate by acting on sympathetic and parasympathetic systems, in addition to aortic and carotid chemoreceptors 5.
Clinical correlations have not been shown for all those pathophysiological events in terms of anesthesia. Especially, an increase in acute myocardial infarction and unstable angina has not been significantly observed in smokers, in spite of severe cardiovascular physiological changes. Short abstinence periods may influence results due to the relatively short nicotine (30 to 60 minutes) and COHb (4 hours) elimination half-life.
Nicotine action has a two-phase pattern on autonomic ganglia and adrenal medulla, with an initial stimulating effect in low doses and posterior stimulation decrease with higher doses. Increased nicotine concentration causes hypotension and neuromuscular flaccidity because the drug has a ganglionic blocking effect 16. The association of its sympatheticomimetic effects may produce coronary vasospasm and cardiac arrhythmias, even when the patient is a user of slow release nicotine patches, as observed by Williams and Tempelhoff 5,11. These effects contribute to increase cardiovascular morbidity, associated to coronary vasoconstriction and increased myocardial O2 consumption.
Respiratory system changes include mucous hypersecretion and tracheobronchic tree damage by long-term obstruction, as well as restriction of small airways with increased closing ability and trend to changes in the perfusion-ventilation rate. There is also an increase in reflex sensitivity of both conduction ways (high and low), in respiratory epithelium patency and evidences of surfactant factor loss. Further events with anesthetic implications are cell-mediated humoral immunity impairment, in addition to microsomal enzymes induction with the increase in several drugs metabolism 6.
Inveterate smokers have COHb levels of 5% to 15%, which may mean oxygen saturation below 15% indicated by pulse oximetry (oxygen combined to Hb / oxygen transportation ability X 100). In practice, available oxygen would be even lower since COHb shifts Hb dissociation curve to the left. Inherent damage could be measured through increased sympathetic activity and airway hyper-reflex 3,6,12,13.
Hb saturation decrease and hypoxemia (SaO2 < 84%) should also be considered both in inveterate smokers and youngsters. This hypoxemia is often attributed to an increase in closing volume and decreased functional residual capacity. So, O2 should always be offered to those patients during PACU transfer and stay where pulse oximetry is mandatory 1.
With age, excitation threshold tends to be naturally increased due to a decrease in nervous terminations which, combined with upper airway mucosa thickening, decreases the penetration of noxious chemical agents and increases aspiration risk 13. This finding justifies more attention during anesthesia or sedation recovery of geriatric patients.
Major smoking-induced enzymatic changes are concentrated on system P-448. There is no action on liver blood flow. In spite of thiocyanate, substance produced by tobacco smoke, be increased in serum levels of smokers, this is not an indicator of plasma nicotine, cotinine and COHb importance 1.
Approximately ¼ of smokers have chronic bronchitis, which is five times lower in nonsmokers 2. There are evidences that smokers are more vulnerable to upper airway problems, including laryngospasm during anesthetic sedation and emergence. Indirect evidences show that the same problems are reflected in lower airways. However, a clearer demonstration of increased morbidity has been related to preoperative lung complications, such as atelectasy and pneumonia, which are two to six times more frequent in smokers 1,6,12,13.
The obstruction by thich mucus in the bronchioli is frequent in pulmonary inflammatory processes, such as asthma and chronic obstructive disease, and sometimes it can be found in larger bronchi 14. Chronic bronchitis and emphysema may determine pulmonary hypotension with right ventricular failure. Chronic smoking decreases ciliary transportation and cough is a major factor to remove tracheobronchic secretions. Many cigarette components (hydrocyanic acid, acetaldehyde, acrolein, formadehyde, nitrogen oxides) are ciliostatic and ciliotoxic. Smoking abstinence decreases sputum in 50% if lasting for more than 6 weeks and with time, ciliary activity returns to normal 1.
Irritating receptors of fast adaptation are found in all airway cartilaginous structures, being more abundant in the trachea and especially the carina. These receptors respond to mechanical or thermal irritation, inhaled particles or gases. Airway edema and histamine release also activate them, resulting in cough reflex, bronchoconstriction and mucus secretion. Conversely, juxtapulmonary receptors are adjacent to pulmonary capillary located in alveoli interstitium. These seem to respond to pulmonary congestion, edema, inflammation and vigorous exercise. They have a major role in the sensation of dyspnea following situations such as pulmonary congestion 18.
All inhaled CO is excreted without changes by the lungs. A major factor for CO excretion is increased pulmonary ventilation (decreasing PACO) and inspired O2 partial pressure 1.
Nitric oxide (NO) bronchodilating properties are well-known. However Hill et al. 25 have evaluated patients with different abstinence periods submitted to cardiac surgeries and have observed that smokers had more nitric oxide synthetase activity, which is an enzyme precursor to NO during cardiopulmonary bypass, and this would explain the increase in pulmonary complications in this population as compared to nonsmokers.
Passive smokers have increased COHb levels as well as more airway reactivity. Warner et al., in a study evaluating the incidence of pulmonary complications after tobacco abstinence, have observed that there was a higher risk for smokers stopping smoking for up to 8 weeks as compared to those continuing smoking or nonsmokers. Beyond this time, the risk was similar to nonsmokers. Pulmonary functionality abnormalities and the presence of secretions could have caused this effect 1.
Long-term smokers (more than 30 years) often have more signs and symptoms of pulmonary function deterioration and prominent signs, such as sputum production. However, in shorter-term smokers and without major symptoms, the possibility of reactive airways should also be considered 18.
Smoking effects on this system are mainly due to a parasympathetic action with increased tone and intestinal motor activity. Some studies have shown a delay in stomach emptying and an increase in baseline gastric acidity in smokers, but such findings have not been confirmed by more recent studies (Chart I) 5,6. Other studies have suggested that smokers could benefit from the use of antacids or H2 receptors antagonist 1.
Smoking is associated to antidiuretic hormone release (ADH) with water retention and dilution hyponatremia, especially if water ingestion is associated, leading to increased blood volume 1.
Gynecological System and Gestation
The increased risk for myocardial infarction, subarachnoid hemorrhage and peripheral vascular diseases when smoking is associated to contraceptives is well known 15. There would be a decrease in high density proteins and an increase in low density proteins, favoring vascular changes through a synergy between contraceptives and smoking.
A two-fold increase in risk for cervical neoplasia is also reported in smoking patients as compared to non-smoking 15.
Schwilk et al. have found a male:female ratio in the incidence of respiratory complications among young adults of 1:1.9 for nonsmokers and 1:1.1 for smokers, indicating that young women would possibly loose this advantage in becoming smokers 2.
Women who smoke during pregnancy have an increased risk for spontaneous abortion, fetal death, neonatal death and sudden fetal death syndrome. Smoking is also related to impaired conception and decreased birth weight (in average 170 g) producing a condition known as tobacco fetal syndrome. For mothers not smoking for 48 hours, there is an increase in available O2 through a decrease in COHb levels, thus benefiting the neonate during birth, especially during labor or when general anesthesia is induced and, moreover, in the presence of maternal anemia 1. Nicotine can also be detected in smoking womens milk.
There are known effects of CO over Hb and myoglobin, shifting Hb dissociation curve to the left, in addition to P50, with decreased O2 tissue supply. Smokers with normal O2 values may present with reversible polycythemia, situation attributed to high COHb concentrations 1.
Nicotine is a CSN stimulator. Low doses may cause minor shiverings; as doses are increased, seizures may be present, ending in CNS depression and death by respiratory failure, both by central paralysis and respiratory muscles peripheral blockade. Action on the bulb may also cause emesis and vomiting 5.
Studies have shown in passive smoking children an increased incidence of respiratory difficulties, such as asthma. Pulmonary functions tend to be abnormal and there is an increased incidence in respiratory tract infections. Evidences from ENT clinics indicate that living with smoking parents determines a higher incidence of tonsillectomies in children 23.
Children with upper respiratory tract infections are more susceptible to adverse effects during anesthesia due to the increase in upper airway reflexes 3,12,23. During general anesthesia, pulmonary gas exchanges are primarily deteriorated by functional residual capacity decrease, resulting in airway closing. Infants and small children are more susceptible than adults to functional residual capacity decrease and airway closing under general anesthesia. So, they may develop postoperative hypoxia. In a study by Motoyama and Glazener, 43 out of 97 patients had 91% or less oxygen saturation (SaO2) in the immediate postoperative period, while Pulleritis et al. have found 28.1% of children with less than 90% saturation during transfer to PACU 23.
Smokers have more postoperative hypoxemia than nonsmokers after similar anesthesia and surgery. There is an increase in airway resistance and higher closing ability. There may be closing capacity during anesthesia close to or beyond functional residual capacity, resulting in inadequate ventilation/perfusion ratio, increased oxygen alveolar-arterial difference and hypoxemia. These pulmonary function changes continue in the postoperative period and may explain the higher hypoxemia level observed in smokers. Passive smoking children have abnormal airway responsiveness and pulmonary function tests. It is possible that the higher incidence of postoperative hypoxemia in those children has a mechanism similar to that observed in smoking adults. Children do not seem to respond to post-anesthetic hypoxemia through increased alveolar ventilation, probably due to depressive anesthetics residual effects on carotid chemoreceptors. So, oxygen supplementation is recommended for all children in the recovery room, especially those with smoking parents 23.
There are evidences that 80% to 90% of smoking adults start smoking during childhood or adolescence 6. In Brazil, most parents smoke in the presence of their children and is frequent the worsening of respiratory problems during weekends, when the contact with parents is more intense. Respiratory problems frequency and intensity in small passive smokers are directly related to the intensity of smoking at home 4.
PHARMACOKINETIC INTERACTION WITH OTHER DRUGS
Several studies have shown the influence of cigarettes on the pharmacokinetics of several drugs. Cigarette smoke has been indicated as the cause of metabolism induction by enzymes, changing the half-life of drugs processed in the liver, such as local anesthetics. Animal studies have concluded that nicotine is enzyme-inducer. There is an acceleration of several substances metabolism, such as ethylmorphine, norcodeine, aniline, benzopirene, indomethacin, morphine, warfarin and bupivacaine, regardless of the route or the dose 19,22 (Chart II). It has been suggested that the acute exposure to cigarette smoke would decrease indomethacin plasma concentration due to the impaired GI tract absorption (since plasma concentrations were not influenced by smoke when intravenously or rectally administered). This may indicate a possible liver microssomal enzymatic induction during the first days of cigarette exposure 22. A 6 to 8-week abstinence is suggested to eliminate all metabolic changes of several drugs 1.
It seems to be a correlation between the number of cigarettes smoked during the day and the effects on drugs. Some findings are associated to tobacco consumption, such as metabolic acceleration (with drug half-life decrease), increase in excretion and possible addition of drug toxic effects 15.
Several drugs require higher doses in smokers than in nonsmokers for adequate therapeutic effects. In spite of cigarette abstinence, effects decrease may last for months, as it is the case with teophylline 15. In other circumstances the interference may be indirect, such as peripheral vasoconstriction, impairing muscle insulin absorption.
Some drugs may be changed by enzymatic induction, such as some opioids and benzodiazepinics 6. Smokers under benzodiazepinics seem to be more resistant to sedative effects than nonsmokers 19.
Tobacco does not act in an isolated manner to change drug pharmacokinetics. Other factors, such as occupational diseases, physiological changes and even age (with decreased enzymatic induction capacity) should also be considered 1.
Nigrovic and Wierda have studied patients exposed to succinylcholine and observed that smokers had a lower incidence of post-anesthetic myalgia. The hypothesis was that nicotinic receptors would respond less vigorously when stimulated by succinylcholine, which is a nicotinic agonist, but such findings lack further confirmations 21.
ANESTHETIC MANAGEMENT OF SMOKING PATIENTS
COHb elimination half-life and patients physical activities should be considered during pre-anesthetic evaluation. COHb elimination half-life varies from 4 hours in a sedentary person to 1 hour in athletes. This half-life is doubled during sleep. Smoking abstinence for 12 hours brings Hb dissociation curve back to normal due to a decrease in COHb, increasing tissue oxygenation. Even the blood of smoking donors has increased COHb levels, which remain unchanged after 3 weeks of storage. Preoperative objectives are based on secretions control, pulmonary function improvement and stopping smoking several weeks before surgery (Chart III) 1.
A risk level has been shown for cardiovascular and respiratory systems. Currently, the passive smoking problem has been expanded to possible anesthetic implications. Dennis et al. have shown that both active and passive smokers suffer more adverse pulmonary events during anesthetic induction than nonsmokers 26. Lyons et al. have shown that children exposed to passive smoking suffer significantly higher postoperative oxygen desaturation 6,23.
Several studies have investigated preoperative respiratory complications in smokers. Smokers have lower preoperative oxygen arterial tension. Several studies suggest that they are more vulnerable to desaturation after induction and sedation during anesthetic recovery, but other studies have not confirmed such findings. This investigation is, in general, based on pulse oximetry; few studies measure COHb values. Pulse oximetry responds to COHb as if it were oxygenated Hb; so, oxygen saturation reported for smokers is probably overestimated by several studies 3,6. Dennis et al., studying 120 patients ASA I and II, aged 18 to 75 years and submitted to elective surgeries have concluded that during anesthetic induction, active and passive smokers had a higher incidence of adverse effects as compared to nonsmokers. Those complications were translated into high COHb concentrations and a higher number of Hb saturation drops 26.
Caranza et al., in an experiment using nebulized lidocaine before anesthetic induction, have observed a significant decrease of procedure-related complications, indicating its use as part of previous management of smoking patients 20.
Preanesthetic benzodiazepinic drugs may be used, such as diazepam and midazolam. Parasympathomimetic agents, such as atropine, glycopyrrolate and ipratropium seem to be useful. Glycopyrrolate is the drug of choice for its long duration, lack of effects on the central nervous system and minimum cardiovascular action 1.
Anesthetic Induction and Maintenance
In a study evaluating airway reflex sensitivity to chemical and mechanical stimulations, Erskine et al. have observed its increase in chronic smoking patients, which would determine a higher incidence of laryngospasms and airway obstruction, with oxygen saturation decrease 27. A 24-hour abstinence in a group of smokers has not produced significant changes but there has been a progressive decrease in reflex sensitivity 24-48 hours after, with consistent changes after 10 days. Other studies report a minimum 12-hour preoperative abstinence, which would be enough to eliminate acute nicotine effects and, in many cases, would decrease COHb to nonsmoker levels 3,6.
Short-term preoperative abstinence primarily benefits the cardiovascular system; the respiratory system, however, needs at least 6 weeks abstinence, according to Jones et al. 6. On the other hand, Hill et al. evaluating heart surgery patients, have concluded that stopping smoking for 8 weeks or longer determines postoperative pulmonary complication levels similar to nonsmokers 14. A minimum 12-hour period could be established as preoperative abstinence. Warner et al., in a prospective study with patients submitted to coronary artery revascularization, have stressed that 8 weeks are needed for morbidity to decrease to nonsmoker levels 6.
In inveterate smokers, the orientation to stop smoking is more important. Stopping smoking is followed by secretions volume and airway reactivity decrease, as well as by the increase in ciliary mucus transportation. Such benefits, however, take 2 to 4 weeks to develop. Short-term effects (48 to 72 hours) are associated to increased secretions and airway hyperactivity. The only apparent advantage of stopping smoking in the immediate preoperative period seems to be a decrease in COHb with a consequent tissue oxygenation improvement 18.
Some studies have observed acute upper airway reflex response to larynx and lungs stimulation with cigarette smoke, but the exact mechanism of this increased responsiveness caused by chronic exposure to cigarettes is still not clear. Two mechanisms are considered to justify such events: 1) acute pharmacological effects of the smoke on irritating receptors; and 2) chronic changes in airway epithelium characteristics allowing the exposure of irritating receptors located on the sub-epithelium to the chemical stimulation. The first mechanism does not seem feasible since acute pharmacological effects of nicotine or any other 4000 or more smoke components should disappear after 24-hours, which is opposed to the results of both studies performed by this author. The second mechanism seems to be more consistent. Several studies have suggested that airway epithelial layer damage or loss is a major factor to increase their responsiveness, having also a role in restricting the access of inhaled solutes to sub-epithelial structures. Chronic smokers develop laryngeal epithelium inflammation, metaplasia and displasia and may break its integrity. In addition, more recent data suggest that chronic smokers have decreased salivary epidermal growth, which protects mucosa against acute injury helping in gastric healing and duodenal ulcer prevention 27.
Postanesthetic Care and Complications
Historically, obesity and smoking are risk factors for postoperative respiratory complications, since both are significant determinants of severe pulmonary complications, as confirmed by Forrest et al. 2,28. Obviously, the combination of obstructive ventilatory problems induced by smoking and decreased functional residual capacity in obese patients leads to more severe problems 2.
Adverse effects on surgical results may also be attributed to tobacco, especially during vascular, plastic and oral surgeries. Poor healing caused by smoke toxins and global tissue hypoxia are attributable to direct vascular damage 3,6 (Chart IV).
In general, postoperative pulmonary complications are seen in 5% to 10% of surgical patients7; those submitted to abdominal surgery have 4% to 22% of respiratory changes. Wong et al., in a study with patients with severe chronic obstrutive pulmonary disease history, have observed an increased long-term mortality when submitted to non-cardiac or chest surgeries 24. Severe DPOC patients exposed to non-chest surgeries had a long-term mortality similar to those with severe coronary disease submitted to non-cardiac surgery. This same author has concluded that patients with EFV1 < 1.2L and submitted to non-cardiac or chest surgeries, had a 37% higher incidence of postoperative pulmonary complications, excluding atelectasis, and 47% mortality in two years. However, isolated preoperative pulmonary abnormalities are not a prognosis for respiratory complications in patients with severe chronic obstrutive pulmonary disease; in those cases, physical status (ASA) evaluation of respiratory and non-respiratory factors should be considered.
Daley et al., studying hypoxemia-related changes in patients admitted to PACU, have not associated previous smoking history to such events 17. It is important to mention that patients with severe pulmonary disease history were excluded from the study.
Long-term smokers should receive additional O2 during PACU transfer and be monitored by pulse oximetry or arterial blood gas analysis. In some cases, there may be an increased need for analgesics due to increased enzymatic induction 1.
Smokers are more dependent on cough to eliminate tracheobronchic secretions. Secretion retention, as a result of the surgery or the use of drugs, increase the possibility of airway obstruction and, as a consequence, atelectasis. Patients should be encouraged to cough and take deep breaths to eliminate tracheobronchic secretions. Physical therapy should be considered in the immediate postoperative period 1.
Immune function decrease has been observed in smokers, with impaired neutrophyls, immunoglobulins and natural defense cells concentration activity 3.
Smoking history should be highly valued during preanesthetic evaluation and preventive measures against systemic effects should be taken to minimize surgical risks.
01. Beckers S, Camu F - The anaesthetic risk of tobacco smoking. Acta Anaesthesiol Belg, 1991;42:45-56. [ Links ]
02. Schwilk B, Bothner U, Schraag S - Perioperative respiratory events in smokers and nonsmokers undergoing general anaesthesia. Acta Anaesthesiol Scan, 1997;41:348-355. [ Links ]
03. Myles PS, Hendrata M, Layher Y - Double-blind, randomized trial of cessation of smoking after audiotape suggestion during anesthesia. Br J Anaesth, 1996;76:694-698. [ Links ]
04. Torres BS, Cruz RCS, Huggins D - Tabagismo na adolescência: fatores determinantes. Rev Bras Med, 1998;55:251-253. [ Links ]
05. Taylor P - Agentes que Atuam na Junção Neuromuscular e nos Gânglios Autônomos, em: Goodman & Gilman - As Bases Farmacológicas da Terapêutica, 9ª Ed, Rio de Janeiro, McGraw Hill, 1996;131-145. [ Links ]
06. Nel MR, Morgan M - Smoking and anaesthesia revisited. Anaesthesia, 1996;51:309-311. [ Links ]
07. OBrien CP - Dependência e Uso Abusivo de Drogas, em: Goodman & Gilman - As Bases Farmacológicas da Terapêutica, 9ª Ed, Rio de Janeiro, McGraw Hill, 1996;405-420. [ Links ]
08. Jackson EK - Vasopressina e Outros Agentes que Afetam a Conservação Renal de Água, em: Goodman & Gilman - As Bases Farmacológicas da Terapêutica, 9ª Ed, Rio de Janeiro, McGraw Hill, 1996;523-535. [ Links ]
09. Klaassen CD - Agentes Tóxicos Ambientais Não-Metálicos, em: Goodman & Gilman - As Bases Farmacológicas da Terapêutica, 9ª Ed, Rio de Janeiro, McGraw Hill, 1996;1240-1258. [ Links ]
10. Bacon PJ, Pickwoth AJ, Jones JG - Plasma antioxidant activity in smokers. Br J Anaesth, 1994;73:721-722. [ Links ]
11. Williams EL, Anaes FRC, Tempelhoff R - Transdermal nicotine patch and general anesthesia. Anesth Analg, 1993;76:907. [ Links ]
12. Erskine RJ, Murphy PJ, Langton JA - Effect of stopping smoking on upper airway reflexes. Br J Anaesth, 1993;70:478. [ Links ]
13. Erskine RJ, Murphy PJ, Langton JA - Effect of age on the sensitivity of upper airway reflexes. Br J Anaesth, 1993;70:574-575. [ Links ]
14. Hill GE, Ruggeroli A, Pohorecki R - Cigarette smoking reduces endogenous airway nitric oxide production during cardiopulmonary bypass in humans. Anesth Analg, 1995;81: 170-172. [ Links ]
15. Rosemberg J - Interações medicamentosas do tabaco. Rev Bras Anestesiol, 1989;39:160-162. [ Links ]
16. Durrett LR, Lawson NW - Farmacologia e Fisiologia do Sistema Nervoso Autônomo, em: Barash PG, Cullen BF, Stoelting RK - Tratado de Anestesiologia Clínica, 1ª Ed, São Paulo, Manole, 1993;207-282. [ Links ]
17. Daley M, Norman PH, Colmenares ME et al - Hypoxaemia in adults in the post-anaesthesia care unit. Can J Anaesth, 1991;38:740-746. [ Links ]
18. Gal TJ - Bronchial hyperresponsiveness and anesthesia: physiologic and therapeutic perspectives. Anesth Analg, 1994;78: 559-573. [ Links ]
19. Teiria H, Yli-Hankala A, Neuvonen PJ et al - Cigarette smoking does not affect thiopentone pharmacodynamic of pharmacokinetic behaviour. Can J Anaesth, 1997;44: 1269-1274. [ Links ]
20. Caranza R, Raphael JH, Nandwani N et al - Effect of nebulised lignocaine on the quality of induction of anaesthesia in cigarette smokers. Anaesthesia, 1997;52:849-852. [ Links ]
21. Nigrovic V, Wierda JM - Post-succynilcholine muscle pain and smoking. Can J Anaesth, 1994;41:453-454. [ Links ]
22. Bruguerolle B, Attolini L, Roucoules K et al - Cigarette smoke increases bupivacaine metabolism in rats. Can J Anaesth, 1994;41:733-737. [ Links ]
23. Lyons B, Frizelle H, Kirby F et al - The effect of passive smoking on the incidence of airway complications in children undergoing general anaesthesia. Anaesthesia, 1996;51:324-326. [ Links ]
24. Wong DH, Weber EC, Schell MJ et al - Factors associated with postoperative pulmonary complications in patients with severe chronic obstructive pulmonary disease. Anesth Analg, 1995;80:276-284. [ Links ]
25. Ding Y, White PF - Lung collapse after induction of anesthesia in a healthy outpatient. Anesthesiology, 1994;80:689-690. [ Links ]
26. Dennis A, Curran J, Sherrif J et al - Effects of passive and active smoking on induction of anaesthesia. Br J Anaesth, 1994;73: 450-452. [ Links ]
27. Erskine RJ, Murphy PJ, Langton JA - Sensitivity of upper airway reflexes in cigarette smokers: effect of abstinence. Br J Anaesth, 1994;73:298-302. [ Links ]
28. Forrest JB, Rehder K, Cahalan MK et al - Multicenter study of general anaesthesia. Predictors of severe perioperative adverse outcomes. Anesthesiology, 1992;76:3-15. [ Links ]
Dr. Ricardo Dorneles Furtado
Address: Rua Duque de Caxias, 955/1402 B
ZIP: 90010-282 City: Porto Alegre, Brazil
Submitted for publication July 17, 2001
Accepted for publication November 6, 2001
* Received from Serviço de Medicina Paliativa e Tratamento da Dor, Hospital Santa Rita (Irmandade da Santa Casa de Misericórdia), Porto Alegre, RS