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Smoking and Anaesthesia
Dhananjay Sanjekar*
Cigarette smoking is an addiction, a
serious health hazard. Smoking has become fashion particularly in young generation despite the knowledge of its extensive adverse effects. The hazards of smoking including risk of malignancy are directly related to the duration of exposure and intensity of smoking.
Smoking is a :-
Major cause of acceleration of atherosclerotic disease.
Major Precancerous condition.
It has detrimental effects on lung function and structure.
Has tremendous addiction potential because of its nicotine content.
Physiological Properties of Smoke (a heterogeneous aerosol)
1) Gas Phase
Carbon monoxide which impairs O2 transport
Hydrocyanic acid which Gliotoxin and irritant
Acetaldehyde - Vinyl chloride
Ammonia - Formaldehyde
Nitrosamine - Hydrazine
2) Particulate Phase
Nicotine - Addicting drug
Neuroendocrine stimulant
Tar - Carcinogen
Polynuclear aromatic hydrocarbons, phenol/cresol - Carcinogens
b - naphthylamine
Pharmacology of Smoke
- Cigarette smoke has got more than 4000 harmful substances.
- Main ingredients are nicotine and carbon monoxide
Nicotine
It is a highly toxic alkaloid and sympathetic ganglionic stimulant.
Its adverse effects includes:
Profound sympathetic stimulation causing tachycardia and increased cardiac output.
increased BP and increased peripheral vascular resistance
increased myocardial O2 consumption.
decreased threshold for ventricular fibrillation
increased Serum levels of vasopressin, growth hormone and cortisol
Sites of action of nicotine are
Pressor response through carotid body and aortic chemoreceptor.
Release of catecholamines - adrenal medulla and other chromaffin tissues.
Half Life of nicotine is 30 min to 60 min
Carbon monoxide
It is a toxic gas which combines with Hb to form carboxy-Hb. The level of Co-Hb is 3-15% in smoker compared to 1-2% in nonsmoker. Carboxy Hb has - ve inotropic effect on heart. It alters myocardial electrophysiology, decreases O2 content and O2 supply at tissue level. Oxy-Hb dissociation curve is shifted to left. Half life of carbon monoxide is 4-6 hrs at rest and 40 - 80 min after breathing 100% O2..
Body Systems affected by smoking
Effects on cardiovascular system - smoking causes vascular intimal injury, initiation and progression of atherosclerosis, cardiomyopathy. In addition to this there are nicotine mediated increased HR, BP arrhythmia, etc.
Effects on Respiratory System
Anatomical architecture of airways is totally altered. In central airway there is loss of cilia, mucus glands and goblet cell hyperplasia. Similarly metaplasia and mucus plugging occurs at peripheral airways. As a result of which there is mucus hyper secretion, impaired tracheobronchial clearance. Narrowed small airways are more susceptible to bronchospasm leading to increased respiratory morbidity postoperatively.
Central Nervous System
Smoking induced atherosclerosis causes thromoembolic stroke, decreases cerebral blood flow thereby increases the incidence of stroke 2-3 times.
Immune System
Immunity is grossly impaired. Decreased neutrophil chemotaxis, decreased natural killer cells are the final consequences of smoking.
Coagulation
Haemostatic activity is hampered resulting in increased platelet aggregetion, increased plasma viscosity, thromboxane release, decreased platelet survival, bleeding time etc.
Passive Smoking
Your smoking is injurious to our health is a well known comment. Passive smoking by whichever means such as from burning end of cigar or exhaled smoke causes eye irritation, headache, nasal stuffiness, cough etc. Changes in all body system are identical to that of active smokers after long term exposure.
Anaesthesia consideration of Chronic Smokers
Preoperative Evaluation
I) History - Smoking is calculated in the terms of pack years i.e. no. of cigarette packets smoked per day x years of smoking. More than 10 pack/year is associated with all possible intraoperative and postoperative complications. Similarly patient should be evaluated in view of evidence of chronic bronchitis, acute infection, asthma, angina and myocardial infarction.
II) Investigation:
Polycythaemia and leucocytosis
CXR in favour of increased bronchiovascular margins classical of chronic bronchitis.
PET shows decline in FEV1 in the range of 35 - 80 ml per year.
Preoperative respiratory preparation regimen
It involves a five - pronged attack on any airway disease
1) Stop Smoking - Cessation for more than 4-6 weeks is essential. Stopping smoking for only 24 hours has shown to decrease carboxy - Hb levels significantly and decreases Hb available for O2 transport, shift O2 -Hb dissociation curve to right and reduces nicotine induced tachycardia.
2) Dilate the airways with - B2 - stimulants, theophylline, steroids which help by decreasing mucosal oedema thereby preventing release of bronchoconstricting substances.
3) Loosen secretion by local and systemic hydration chest physiotherapy, mucolytic and expectorants.
4) Accumulated secretions should be removed by postural drainage, cough and deep breathing techniques.
5) Lastly increased education and motivation of patient which includes :
Psychological preparation about respiratory care
Incentive spirometry
Secretions removal manoevres.
Exercise - weight reduction.
Intraoperative and Postoperative factors
Smokers are more susceptible to intraoperative and postoperative bronchospasm, laryngospasm, aspiration, hypoxaemia and pulmonary oedema. Induction of general anaesthesia should be smooth with proper bronchodilatation prior to induction. Minimum laryngoscopy time and prevention of lighter plane of anaesthesia with adaquate analgesia is very important. Similar extubation should be done after return of all protective airway reflexes.
Postoperative complications
High incidence of postoperative hypoxaemia in immediate recovery phase.
Atelectasis - bronchitis - lung collapse and pneumonia.
Management of complications
Oxygen therapy by mask or nasal cannula postoperatively.
Adequate postoperative analgesia such as epidural analgesia.
Deep breathing, coughing exercises.
Incentive spirometry
Judicious use of bronchodilators, antibiotics.
High incidence of postoperative myocardial infarction, cerebrovascular events, deep venous thrombosis.
Drug metabolism is also altered causing increased analgesic requirement.
Cessation of Smoking
Primary care physician can play a vital role in motivation towards decision to quit, attempting to quit and maintaining the ex-smoker state of the patient. Explaining all the hazards of smoking and motivating the patients to stop the smoking in the preoperative period can enable the patient to withstand the surgical stress. Similarly general practitioners can play an important role in the implementation of preoperative respiratory care region. Likewise educating the patient about different respiratory exercises can improve the postoperative outcome
Steps to escape smoking are
Self help
Group therapy
Counselling
Behavioural training,
Use of medications or substitutes. |
