Substance Abuse – Nicotine/Smoking

Anesthesia Implications

Anesthesia Implications

Nicotine’s most common method of use is by smoking. For that reason, the primary anesthesia implications will be based on that method of use.

Airway – A reactive airway is typically the primary consideration when dealing with a patient smoking cigarettes. This can lead to cough, breath holding, laryngospasm, and bronchospasm. In addition, incidence of pulmonary edema, aspiration, hypoxemia, and hypoventilation are increased in smokers. Incidence of these intraoperatively are the highest among the young (16-39 years of age) and obese.

GI – smoking causes relaxation of the Lower Esophageal Sphincter (LES), which increases incidence intraoperative reflux and aspiration. Chronic use of cigarettes leads to GERD. Interestingly, smokers have a reduced incidence of PONV.

Hemodynamics – lower doses have a stimulating effect. This increases heart rate and risk of tachydysrhythmias. Higher doses have a sedative/depressant affect.

Central Nervous System – lower doses have a stimulating effect. high doses have a sedative/depressant affect.

8 weeks – Cessation of smoking 8 weeks prior to surgery is one of the most effective methods to optimize the patient and prevent postoperative respiratory complications. Short term abstinence, however, has not been shown to be effective at reducing postoperative risk. Furthermore, evidence shows that the more time placed between cessation of smoking and surgery, the better.

Substance abuse (general considerations) – If necessary, get your urine/blood screen early. The urine screen will take 30 minutes and a serum screen will be closer to an hour. Almost all drug screens will return results for marijuana, amphetamines/methamphetamines, phencyclidine (PCP), cocaine, opioids, barbiturates, and benzodiazepines. Generally speaking, if the patient is acutely intoxicated, the case should be cancelled/delayed. Refer to your facility to get policies on cancellations/delays.

Pathophysiology

Smoking is the primary preventable cause of cardiovascular morbidity and mortality.

Smokers have a risk for coronary heart disease that is 3-4 times that of a person that does not smoke. This is due to the content of cigarettes (primarily nicotine and carbon monoxide). Nicotine with its sympathomimetic effects combined with a reduction in oxyhemoglobin caused by carbon monoxide respectively create greater demand and reduced supply of oxygen to the heart. Adverse affects are also seen in lipid profiles, endothelial lining, and development of atherosclerotic plaques. So, in addition to coronary heart disease, smoking is an independent risk factor for peripheral vascular disease, thromboembolic disease, and stroke.

Respiratory – Reduced airway diameter. A bronchoconstrictive reflex to inhaled particles results in an acute reduction of airway diameter. In addition, small airways prematurely close during expiration, which increases closing volumes and adversely alters ventilation/perfusion ratios. Mucous production and viscosity is increased while mucous clearance is decreased. This can contribute to the formation of mucous plugs and the later development of pneumonia and respiratory failure. 20% of patients that smoke develop COPD. See COPD implications.

The chemical structure of nicotine is very similar to acetylcholine, and has similar implications

Two phases of smoking – the gaseous phase and the particulate phase. The primary component of the gaseous phase is carbon monoxide. The primary component of the particulate phase is nicotine.

Carbon monoxide (CO) has around a 300-fold greater affinity for hemoglobin than the affinity of oxygen. Essentially, CO takes MOST of the seats on the bus. There is also a reduction in 2,3-di-phosphoglycerate (2,3-DPG) levels, which makes it difficult for oxygen unload or ‘step off the bus’. Oxygen delivery to the tissues is therefore greatly reduced.

Metabolism – hepatic (cytochrome P450). Half life is 30 minutes. Active metabolite is called cotinine, which can stay in the blood for as long as 20 hours.

Blood-brain barrier – crosses within 20 seconds of smoking. There it stimulates the release of noradrenaline, adrenaline, vasopressin, serotonin, dopamine, and b-endorphin.

Cancer – smoking is responsible for 90% of the world’s lung cancer.

Reduced Immunity – infection is increased and wound healing is adversely affected.

The WHO has described tobacco as, ‘the only legal drug that kills many of its users when used exactly as intended by manufacturers’.

References

Hines. Stoelting’s anesthesia and co-existing disease. 7th edition. 2018.
Carrick. Smoking and anaesthesia. British Journal of Anaesthesia. 2018 link