3. Smoking and Anaesthesia

Question 1

list of conditions that may require surgery

Answer 1

surgery. These include pulmonary, bladder and
gastrointestinal malignancy as well as peripheral vascular and coronary heart disease

postoperative morbidity and worsens surgical outcomes. Anaesthetists
are unlikely to influence those factors significantly, but they do need to be aware
of the chronic and acute effects, and to mitigate these where possible.

Question 2

Diseases associated with smoking:

Answer 2

chronic problems are well known and include obstructive pulmonary disease,
coronary heart disease, hypertension, cerebrovascular
disease and an increased risk of malignancies in several systems.

Its only benefits appear to be a reduction in the risk of pre-eclampsia in pregnancy and a
lower incidence in smokers of postoperative nausea and vomiting.

Question 3

Nicotine:

Answer 3

It acts directly on receptors at ganglia, indirectly on chromaffin cells via catecholamine
release and on excitatory nicotinic receptors within the central nervous systems.

Dopaminergic stimulation inputs the ‘reward’ centre in the hypothalamus, elevates
mood and establishes a cycle of dependence.

Question 4

The immediate physical effects are familiar:

Answer 4

sympathetic stimulation leads to tachycardia and hypertension,
decreased cutaneous blood flow and coronary
arterial vasoconstriction.

At a cellular level, nicotine increases the formation of
reactive oxygen species with lipid peroxidation, and accelerates neuronal apoptosis.

Question 5

Carbon monoxide (CO)

Answer 5

cigarette smokers can have carbon monoxide (CO)
concentrations of 10% and sometimes higher (in non-smokers <1.5%) at which
level the physiological effects are significant. CO affinity for haemoglobin is 250 times
that of oxygen, and it also shifts the oxygen–haemoglobin dissociation curve to the
left with direct implications for oxygen delivery to the tissues

It inhibits cytochrome oxidase (required for mitochondrial ATP synthesis) and also forms carboxymyoglobin to the detriment of myocardial performance.

Question 6

Hydrocarbons and toxic metabolites

Answer 6

cigarette smoke contains at least 4,000 compounds, including polycyclic aromatic hydrocarbons, aldehydes, nitrogen oxides, metals and hydrogen cyanide.

This diverse chemical array acts as a potent inducer of
the enzyme cytochrome P450 CYP1A2 which also metabolizes many commonly
prescribed drugs.

s this enzyme induction that is believed to confer some protection
against postoperative nausea and vomiting in smokers

Question 7

Pathophysiology of chronic smoking

Answer 7

: the list of smoking-related health complications is a familiar one.

Patients are at greater risk of numerous forms of malignancy,

including lung (more women in the USA die from lung cancer than from breast cancer),
larynx, oropharynx, oesophagus, bladder and cervix.

Coronary artery disease, peripheral vascular disease and cerebrovascular disease occur much more commonly (fourfold), and
some degree of chronic obstructive pulmonary disease
(COPD) is almost invariably present.

More severe forms of COPD with bullous emphysema denote significant destruction of pulmonary tissue and condemn a patient to a dyspnoeic, hypoxic and premature death.

Cutaneous hypoperfusion gives rise to the typical smoker’s facies in around 10% of individuals

Question 8

Smoking cessation in the immediate pre-operative period

Answer 8

: this allows greater clearance of carbon monoxide,
but it may be at the expense of increased anxiety
and agitation, which in its most extreme form may even manifest as a postoperative
nicotine withdrawal syndrome.

A patient who has just had a cigarette may have a CO
concentration of 10% with all the adverse physiological effects outlined previously.

At rest, the elimination half-life of CO is 4–6 hours, which is reduced to around an
hour if breathing 100% oxygen.

This suggests that even 12–24 hours of abstinence is
of benefit

Question 9

Longer-term cessation:

Answer 9

Longer-term cessation:

If a patient gives up smoking 6 months prior to surgery their
postoperative respiratory complication rate falls to that seen in non-smokers,

although at 1–2 months pulmonary complications increase.

This may be due to a reactive bronchorrhea which occurs before ciliary function has returned to normal.

The hyper-reactivity of the smoker’s airway starts to reduce within about 48 hours of
cessation, but it may take 10–14 days before it disappears completely.

Question 10

Anaesthetic implications:

Answer 10

These are straightforward.

Superimposed on smokingrelated co-morbidity are the

problems of an over-reactive airway which may respond
to inhaled and potentially irritant volatile agents with coughing, breath-holding,
laryngospasm and bronchoconstriction.

The increased FiO2 of normal general anaesthesia
is likely to correct any reduction otherwise in oxygen delivery.

Regional anaesthesia is a suitable alternative, although there are some procedures, such as
trans-urethral and intra-ocular surgery during which persistent coughing may seriously
compromise the surgery.

Nicotine addiction does have the one benefit of promoting early mobilization as some patients are desperate to have a first postoperative cigarette.

Specific postoperative problems are predominantly respiratory,
but smokers may have complications related to any of their chronic conditions.