Specialist Questions and Answers

<< Go back to Main Page  


Question: We are treating a woman with a pulmonary embolus who is a heavy smoker .  Can we give a streptokinase injection to this lady & if so, and what dose and how long?
Yes. But it is only recommended when there is cardiovascular compromise (i.e. low output state, sytemic hypotension). The efficacy of thrombolysis in massive PE has been shown in several controlled trials and is as effective as embolectomy. However, the risks may outweigh the benefits. The current recommended regimen is 250000 IU loading dose over 20-30min followed by 100000 IU/hr for 24 hours. Alternatively, 1.5 million units may be used as a single dose. These regimens need not be given directly into the pulmonary artery, but can be given via a peripheral vein.

A more expensive option is to use rtPA (recombinant tissue plasminogen activator). A dose of 0.6mg/kg over 15min followed by 100mg over 2 hours and then full heparinisation until warfarinised. rtPA has the advantage of less risk of anaphylaxis, systemic hypotension and and fewer systemic symptoms. This may be used in haemodynamically stable patients and is better than heparin alone.

For further information and detailed reference list, please see:

BTS Standards of Care Committee. Suspected acute pulmonary embolism: a
practical approach. Thorax 1997; 52 (suppl 4).

Dr Vince Mak, Consultant Physician.


What is the incidence of Pulmonary Embolus in women between the ages of 20 and 30 who are cigarette smokers and who are taking Oral Contraceptives?

There is a slight increased risk (2-4x) in women taking high dose
oestrogen oral contraceptives developing deep vein thrombosis, and thus
by extrapolation, they are at increased risk of PE. However, the
overall risk is still tiny when compared with other aetiologies such as
pregnancy, immobility and pelvic surgery. The combined effect of
smoking is not known but is unlikely to be much more. More frequently
recognised as a predisposing risk factor is the presence of Factor V
Leiden genetic mutation, and there is an additive risk here in young
women on the oral contraceptive pill.

Vince Mak

Further information:


Do you know of any relationship between smoking and
insomnia in otherwise "healthy" people.?

This is an interesting question. Smoking has been associated with snoring, (Schmidt-Nomara et al, 1990). Wetter and Young (1994) remarked that there was little epidemiological or clinical information on the relationship between smoking and sleep disturbance. They looked at 3,516 adults  as part of a longitudinal, epidemiologic study of sleep-disordered breathing. Symptoms of insomnia, hypersomnia, and parasomnia were assessed using diagnostic criteria from the Diagnostic and Statistical Manual of Mental Disorders (3rd ed., revised). Smoking was associated with difficulty initiating sleep (initial insomnia), and difficulty waking up. Excessive daytime sleepiness was related to smoking in women whilst nightmares and disturbing dreams were related to smoking in men. They concluded that smoking was associated with 'sleep fragmentation'. Sleep disturbance may be more prevalent among smokers due to the stimulant effects of nicotine, nightly withdrawal, an increased prevalence of sleep disordered breathing relative to nonsmokers, and/or an association with psychological disturbance. Pullen et al (1994) found that  nicotine patches had the side effect of sleep disturbance.

On the other hand, Prosise et al (1994) examined the effect of smoking withdrawal on sleep quality, daytime sleepiness, and mood in 18 subjects Overnight studies showed a significant increase in the number of relative arousals (a change in sleep stage to wake, stage 1 sleep, or movement), stage changes, and awakenings during smoking cessation.   Also during abstinence, the subjects reported that they felt more irritable, had increased feelings of anxiety, felt greater tension, and had more cravings for cigarettes.

The biochemical effects of smoking nicotine involve dose-dependent neurotransmitter and neuroendocrine effects.  Circulating levels of norepinephrine and epinephrine increase, and the bioavailability of dopamine is altered as well. Neuroendocrine effects include the release of arginine vasopressin, beta-endorphin, adrenocorticotropic hormone, and cortisol.

Ben Green

Further information:

Index of Questions

<< Go back to Main Page

©Priory Lodge Education Limited 1998

Last Amended: 23/03/99

Home • Journals • Search • Rules for Authors • Submit a Paper • Sponsor us   

Rules for Authors
Submit a Paper
Sponsor Us



Default text | Increase text size