Download Fitness to fly for passengers with cardiovascular disease

heartjnl_96_11S1_titlepage.qxd
6/26/10
7:49 PM
Page 1
Fitness to fly for passengers with
cardiovascular disease
The report of a working group of the British
Cardiovascular Society
Fitness to fly
Guidance at a glance
Condition
Functional status
Lay explanation
Restriction/guidance
Angina
CCS angina IeII
Chest pain on considerable exertion with
no recent change in symptoms or
medication
Chest pain on minimal exertion with no
recent change of symptoms or medication
Chest pain at rest or a change in
symptoms and/or medication
No restriction
CCS angina III
CCS angina IV
Post-STEMI and NSTEMI
Low risk: age <65, first event, successful
reperfusion, EF >45%, no complications,
no planned investigations or interventions
Medium risk: EF >40%, no symptoms of
heart failure, no evidence of inducible
ischaemia or arrhythmia, no planned
investigations or interventions
High risk: EF <40%, signs and symptoms
of heart failure, those pending further
investigation, revascularisation or device
therapy
Elective PCI uncomplicated
Elective CABG uncomplicated
Allow for intrathoracic gas resorption. If
complicated or symptomatic, see heart
failure
Acute heart failure
Chronic heart failure
NYHA I and II
NYHA III
NYHA IV
Cyanotic congenital heart disease
NYHA I and II
NYHA III
NYHA IV
Valve disease (see heart failure)
Following pacemaker inplantation
Following ICD implantation
Arrhythmia
Stable
If you have had a heart attack but you are
aged <65 years, the blocked artery has
been opened, the heart pump is not badly
damaged and no further tests or treatment
are planned
If you have had a heart attack, your heart
pump is quite good and you have no
symptoms of breathlessness or chest pain
and no other tests or treatments are
planned
If you have had a heart attack, the heart
pump is significantly damaged and you
have symptoms of breathlessness or you
are waiting for further tests or treatment
You have had the heart arteries treated
with a balloon and stent and there are no
complications
You have had heart bypass surgery and
time must be allowed for any air in the
chest to be absorbed
You have been in hospital or treated at
home because of ‘water in the lungs’
which made you very breathless
You get breathless on mild to moderate
exercise but no recent (within 6 weeks)
change of symptoms or medication
You get breathless on walking 20e100
yards/metres at your own pace but no
recent (within 6 weeks) change of
symptoms or medication
You are breathless at rest and mainly
bedbound
You have congenital heart disease with
blue blood and get breathless on mild to
moderate exertion but no recent (within
6 weeks) change of symptoms or
medication
You have congenital heart disease with
blue blood and get breathless on walking
20e100 yards/metres but no recent
(within 6 weeks) change of symptoms or
medication
You have congenital heart disease with
blue blood and are breathless at rest and
mainly bedbound but no recent (within
6 weeks) change of symptoms or
medication
If you have had a temporary or permanent
pacemaker there is a risk of the lung being
punctured. If it has not been punctured,
you can fly after 2 days. If it has, then you
should wait until 2 weeks after it has fully
healed
If you have had a defibrillator, the same
advice for pacemakers (above) applies
but, in addition, you should not fly after
the ICD has delivered a shock until your
condition is considered stable
If you get occasional palpitations that do
not cause fainting and have not recently
become more frequent or you have an
irregular pulse which is treated and stable
Consider airport assistance and possible
in-flight oxygen
Defer travel until stable or travel with
medical escort and in-flight oxygen
available
Fly after 3 days
Fly after 10 days
Defer travel until condition stable
Fly after 2 days
Fly after 10 days if no complications. If
symptomatic, follow guidance for specific
symptoms
Fly after 6 weeks if stabilised (see chronic
heart failure)
No restriction
May require in-flight oxygen
Advised not to fly without in-flight oxygen
and medical assistance
May require in-flight oxygen*
Consider airport assistance and may
require in flight oxygen advisable*
Advised not to fly without in-flight oxygen
and airport assistance available*
Fly after 2 days if no pneumothorax. In the
event of a pneumothorax, flying should be
deferred for 2 weeks following complete
resolution
The same advice as for pacemakers
above but, in addition, rhythm instability
should be treated
No restriction
Continued
Fitness to fly
Continued
Condition
Functional status
Ablation therapy
Lay explanation
Restriction/guidance
If you have had an ablation (burn)
procedure to get rid of your palpitations
you can fly after 2 days. If flying within
1 week of the procedure, you should
consider yourself at high risk of forming
blood clots and talk to your doctor
Fly after 2 days*
New York Heart Association (NYHA) grading of heart failure
Canadian Cardiovascular Society (CCS) grading of angina
NYHA
I
CCS
I
Symptom
Angina only during strenuous or prolonged
physical activity
II
Slight limitation, with angina only during
vigorous physical activity
Symptoms with everyday living activities
(ie, moderate limitation)
II
III
IV
Symptom
No limitation of physical activity and no
shortness of breath when walking or
climbing stairs
Mild symptoms of shortness of breath and
slight limitation during ordinary activity
Marked symptoms of shortness of breath
during less than ordinary activity (eg,
walking 20e100 yards). Comfortable only
at rest
Severe limitation of activity with
symptoms at rest
III
IV
Inability to perform any activity without
angina or angina at rest
(ie, severe limitation)
*Consider at high risk of DVT/VTE.
CABG, coronary artery bypass graft; CCS, Canadian Cardiac Society; DVT, deep vein thrombosis; EF, ejection fraction; ICD, implantable cardioverter defibrillator; NSTEMI, non-ST elevation
myocardial infarction; NYHA, New York Heart Association; PCI, percutaneous coronary intervention; STEMI, ST elevation myocardial infarction; VTE, venous thromboembolism.
Guidance for the avoidance of deep vein thrombosis and venous
thromboembolism
Blood clots (DVT
and VTE)
Risk criteria
Low risk
No history of DVT/VTE
No recent surgery (4 weeks)
No other known risk factor
Moderate risk
History of DVT/VTE
Surgery lasting >30 min
4e8 weeks ago
Known clotting tendency
Pregnancy
Obesity (BMI >30 kg/m2)
Previous DVT with known
additional risk including
known cancer
Surgery lasting >30 min
within the last 4 weeks
High risk
Risk reduction advice for
passengers
Keep mobile. Drink plenty of
non-alcoholic drinks. Do not
smoke. Avoid caffeine and
sedative drugs
As for ‘low risk’ with the
addition of compression
stockings
As for moderate risk but
subcutaneous injections of
enoxoparin 40 mg before the
flight and on the following day
BMI, body mass index; DVT, deep vein thrombosis; VTE, venous thromboembolism.
Fitness to fly
Fitness to fly for passengers with cardiovascular
disease
David Smith,1 William Toff,2 Michael Joy,3 Nigel Dowdall,4 Raymond Johnston,5
Liz Clark,6 Simon Gibbs,7 Nick Boon,8 David Hackett,9 Chris Aps,10 Mark Anderson,11
John Cleland12
1
Cardiac Department, Royal
Devon and Exeter NHS
Foundation Trust, Exeter, UK
2
Department of Cardiovascular
Sciences, University of
Leicester, Faculty Member of
the NIHR Leicester
Cardiovascular Biomedical
Research Unit, Leicester, UK
3
Postgraduate Medical School,
Surrey University, UK
4
British Airways, UK
5
UK Civil Aviation Authority, UK
6
Peninsula Heart and Stroke
Network, Plymouth, UK
7
National Heart and Lung
Institute, Imperial College
London and Department of
Cardiology, Hammersmith
Hospital, London, UK
8
Past President, British
Cardiovascular Society, London,
UK
9
British Cardiovascular Society,
West Hertfordshire Hospitals
NHS Trust, Hemel Hempstead
General Hospital, UK
10
Guy’s and St Thomas’ NHS
Foundation Trust, London, UK
11
The Cardiac Centre, Morriston
Hospital, Swansea, UK
12
Department of Cardiovascular
and Respiratory Disease,
University of Hull, Castle Hill
Hospital, Hull, UK
Correspondence to
David Smith, Cardiac
Department, Royal Devon and
Exeter NHS Foundation Trust,
Barrack Road, Exeter EX2 5DW,
UK; [email protected]
Accepted 19 May 2010
SUMMARY
Following this review of evidence and after due consideration, it is clear that there are few cardiovascular
conditions that warrant the denial of fitness to fly as a passenger. Given the right aircraft, on-board
equipment and appropriately qualified and experienced escort personnel, aircraft can act as flying intensive
care units and carry extremely ill passengers.1
For those with cardiovascular disease who are not critically ill but who wish to fly on commercial
aircraft, the aircraft environment does not pose a significant threat to their health. It is only when their
underlying condition is associated with a significant risk of acute deterioration that reasonable restrictions
should apply. For those at the more severe end of the spectrum of their specific cardiovascular condition,
services exist to help make the journey more easily and safely. Most carriers and airport authorities provide
assistance on the ground and in the air. Oxygen is available on most major carriers, although this is
sometimes subject to a charge and at least 7 days notice is normally required.2
Passengers are advised to plan their arrival at the airport in plenty of time to avoid having to rush and to
warn the carrier and/or airport authority of any requirements for assistance, including requirement for
in-flight oxygen, well in advance of the date of departure. They are strongly advised to ensure they have an
appropriate supply of their medication, a clear list of the medications and doses they take and a letter of
explanation from their doctor regarding their condition, drugs, allergies and devices (eg, pacemaker).
Physicians are advised to consider the stability of a passenger’s condition and apply the guidance
herein.
The authors have contributed to this document in good faith and consider it to be an honest conclusion of
the review of evidence and assessment of the risks. It is guidance only and responsibility for declaring a patient
fit to travel rests with the attending physician.
The airline carrier should always be informed if a sick passenger is intending to fly. It has a right to refuse the
carriage of a passenger at its own discretion, even if they technically fulfil these guidelines recommendations
shown overleaf.
1. INTRODUCTION
1.1 This Working Group of the British Cardiovascular Society was established to produce a report on
Passenger Fitness to Fly in response to the House of
Lords Science and Technology Committee report on
Air Travel and Health3 in which it is suggested that
specialist cardiology guidance would be of assistance to general practitioners, passengers and
passenger carrying organisations when determining
the risks of passenger flight for those with cardiovascular disorders.
1.2 There are many existing guidelines on passenger
fitness to fly,4e7 most of which include some
reference to certain cardiovascular disorders, but
there is variation in the recommendations, particularly in the time required to elapse between an
event or medical procedure and the flight.
1.3 There is a lack of clarity over the purpose of
the current guidelines. The suggestion by the
House of Lords Committee on Air Travel and
Health that there be specialist cardiology guidance
is vague about the overall goal of the guidance.
There are widespread concerns among the public
that air travel has the potential to be harmful,
many of which are expressed by the House of Lords
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
committee and are reflected in the following few
paragraphs.
1.3.1 Although passenger flight is commonplace,
the aircraft cabin provides what might be considered a relatively alien, restrictive and hostile environment. Passengers are strapped for long periods in
an upright sitting position and subjected to
continuous noise, low humidity, cosmic radiation
and hypobaric hypoxia, any or all of which may
have a deleterious effect on their health.
1.3.2 Passengers may already have a medical
condition and exposure to the flying environment
may precipitate an acute deterioration or potentially catastrophic event.
1.3.3 The aircraft is an isolated environment with
limited facilities for acute health care and out of
reach of assistance other than that which can be
gained from radio communication. It is not an ideal
place in which to fall ill.
1.3.4 There are now a very large number of
passengers, and a high proportion of them are
elderly. The number of passenger hours in the air is
increasing and with it the chance of spontaneous
events occurring in flight but not actually caused or
precipitated by the flight.
ii1
Fitness to fly
1.3.5 Events in flight may cause disruption for staff and other
passengers and, at worst, may lead to the aircraft being diverted
to where appropriate medical care can be provided. Diversions
are very costly and disruptive for the carrier and it is desirable
that such events are kept to a minimum.
1.4 Guidelines may be directed at any of the above problems, but
the British Cardiovascular Society and this Working Group have
considered the House of Lords requirements and feel this guidance should be directed neither at limiting cost and disruption to
airline carriers nor to avoiding potential dangers of the in-flight
environment to healthy passengers, but solely to providing
advice about the risks of flying for passengers with recognised
cardiovascular disease.
2. TERMS OF REFERENCE
2.1 To review the evidence for safety and risk of air travel for
people with cardiovascular conditions.
2.2 To agree appropriate advice and guidance for air travel which
can be expected to be safe for patients with cardiovascular
conditions.
2.3 To agree appropriate advice and guidance for healthcare
requirements for people undertaking air travel with potentially
unsafe cardiovascular conditions, or suspected cardiovascular
conditions, including ‘medical repatriation’.
2.4 To report and to make recommendations to the Board of
Trustees of the British Cardiovascular Society.
3. MEMBERSHIP
Dr L D R Smith (Chairman), Dr C Aps, Dr N Boon (ex officio
British Cardiovascular Society), Mrs E Clark, Dr N Dowling,
Dr S Gibbs, Dr D Hackett (ex officio British Cardiovascular
Society), Professor M Joy, Dr M Anderson, Dr W Toff,
Dr R Johnston (co-opted) and Professor J Cleland (co-opted).
4. WHAT THIS DOCUMENT DOES NOT COVER
4.1 Cardiovascular disease is a term which may be used to include
any pathological condition of the heart and its components, the
great vessels and the peripheral vasculature. It could therefore
include diabetes mellitus, the idiopathic arteritides, peripheral
arteriosclerosis and abdominal aortic aneurysm. It could include
stroke, multi-infarct dementia, carotid artery disease and cerebral
arteriovenous malformations, phlebitis and varicose veins. The
Working Group considered the scope of the report and agreed
that it would not be appropriate to include all these conditions.
For the purposes of this document, the term ‘cardiovascular ’ will
refer to conditions of the heart and the great vessels.
4.2 This guidance does not refer to cardiovascular fitness of
individuals to take control of an aircraft, nor does it deal with
the risks associated with flight in private aircraft, military
aircraft, aircraft with non-pressurised cabins or other means of
flight such as paragliders or balloons.
5. WHAT THIS DOCUMENT DOES COVER
5.1 This document is solely about the fitness to fly of air travel
passengers who have cardiovascular conditions and covers all
aspects of cardiovascular fitness to fly for commercial passengers. It deals with the common questions and problems that
patients, their relatives and their doctors ask about the advisability of flying, and it reviews the existing evidence in the
formulation of guidelines for passenger fitness to fly.
5.2 The overriding consideration for the Working Group was
that the aim of the guidelines should be, wherever possible, to
allow people to fly and not to be unnecessarily restrictive.
ii2
5.3 This document considers the effects of passenger flight and
provides guidance accordingly for the conditions that come
under the broad headings of ischaemic heart disease, heart
failure, cyanotic congenital heart disease, abnormalities of
cardiac rhythm and cardiac devices.
5.4 It is now widely accepted that guidelines published by
professional societies, national and joint international committees follow a specific style that includes an indication of the level
of importance of a particular guideline and the level of
supporting evidence that justifies it. There is such a paucity of
randomised controlled trials, meta-analyses and registries
regarding the risks of commercial flight for passengers with
cardiovascular disease that the Working Group felt unable to
adopt this style. What evidence there is has been reviewed and
used, but a significant element of the guidance within the
document is based on professional judgement and an understanding of the interaction between the flight environment and
the pathophysiology of the cardiovascular condition.
5.5 There was much discussion about the inclusion of venous
thromboembolism (VTE) since this condition has so clearly been
implicated in long-haul air travel. Much has been written on the
subject of VTE already, but the group considered that a section
on VTE should be included.
6. REVIEW OF EVIDENCE
There are very few direct clinical studies of the pathophysiological
effects of commercial passenger flight on patients with existing
cardiovascular diseases. Concerns that there may be deleterious
effects are based on extrapolation from an understanding of the
physics of altitude, cardiorespiratory physiology and studies that
attempt to simulate the conditions of flight, either by studying
patients adapting to living on land at altitude or by studying the
effects of normobaric hypoxia in a laboratory setting.
We have considered the physics and physiology and formed
a view on whether there is evidence to suggest that being
a passenger in a commercial aircraft has any adverse effects that
may increase the risk of a cardiac event.
We have also considered people who may be considered high risk
by dint of a recent cardiac event or procedure and in whom
restrictions on flying are designed to limit the chance of an in-flight
event where facilities for managing medical emergencies are poor.
6.1 Physics of air travel
6.1.1 Dalton’s law
6.1.1.1 The atmosphere is made up of a mixture of a number of
gases, the main components being nitrogen, oxygen and water
vapour. The atmosphere is not of uniform thickness, being greater
at the poles than at the equator. The pressure it exerts varies
accordingly and also with weather systems, but is considered to
have a mean value at sea level of 100 kPa (760 mm Hg) which
decreases with increasing altitude above sea level (figure 1).
6.1.1.2 Since Dalton’s law states that the pressure exerted by
a mixture of non-reacting gases is equal to the sum of the partial
pressures of the component gases, the partial pressure of oxygen
also falls with increasing altitude (figure 1). Oxygen forms 21%
of dry air, nitrogen forming almost all the rest. At 3000 m
(9842 ft) the partial pressure of inspired oxygen is 13.3 kPa and
at 8900 m (29 200ft, the altitude of the top of Mount Everest)
the partial pressure of oxygen falls to approximately 6.2 kPa.
6.1.1.3 Conventional commercial aircraft fly at altitudes from
6500 m (22 000 ft) to 13 500 m (44 000 ft), and without a pressurised aircraft cabin would be untenable for humans.
6.1.1.4 In the USA the cabins of commercial aircraft are required
to be pressurised to a pressure equivalent to an altitude
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
Fitness to fly
Figure 1 Variation in atmospheric
pressure with altitude. Reproduced with
permission from Committee on Air
Quality in Passenger Cabins of
Commercial Aircraft.172
(‘pressure altitude’) of 2438 m (8000 ft), which should never be
exceeded even at their highest attained flying altitude.8 Similar
regulations apply in the UK and Europe.9 At this pressure altitude the partial pressure of oxygen is approximately 15 kPa.
6.1.1.5 It is assumed that the required cabin pressure is maintained at all times, but it may vary at different stages of the
flight. There are suggestions that, although the aircraft systems
are designed to maintain this pressure altitude requirement,
there are still wide variations of cabin pressure during flight.10
Other studies, however, have not supported these suggestions
and, in modern aircraft, point to consistency of cabin pressures
well above the minimum requirement.11
6.1.2 Boyle’s law
6.1.2.1 Boyle’s law states that, for a given amount of a gas at
a constant temperature, the volume is inversely proportional to
the pressure. This has consequences for those changing altitude
as gas in body cavities expands on increasing altitude and falls
again on descending. This has no effect on the heart and circulation but has implications for those who have had recent
surgical procedures when air that has collected in the thorax or
pericardium may expand.
6.1.2.2 The volume of a gas is also related to its temperature
(Charles’ law), but these effects will not be considered here since
the cabin temperature is artificially controlled.
adults at different altitudes up to the maximum pressure altitude of commercial aircraft. It is important to note that PaO2
falls with age despite alveolar pO2 remaining constant. This is
thought to be due to age-related disparity between ventilation
and perfusion.13
6.2.1.2 Above the age of 40 years a constant progressive fall in
pO2 occurs that can be approximated to a fall of 5 mm Hg
(0.67 kPa) per decade, although the linearity of this equation at
extreme old age is not certain.
6.2.1.3 When the oxygen dissociation curve for oxyhaemoglobin
(figure 2) is applied to table 1 it shows that, at a pressure altitude
of 2438 m (8000 ft), the cabin oxygen partial pressure is
118 mm Hg (15.7 kPa), paO2 is 62e67 mm Hg (8.2e9 kPa) and
oxygen saturation is 90e93%.
6.2.1.4 This estimate of arterial oxygen saturations concurs
with measurements using continuous reading pulse oximeters.
Cottrell and colleagues14 measured oxygen saturation in 38
pilots on 21 flights of about 4 h duration. Maximal and
minimal oxygen saturations were 95e99% (mean 97%) and
80e93% (mean6SD 88.662.9%), respectively. Of the subjects,
53% developed an oxygen saturation of <90% at some time
during the flight. With elderly passengers this value is likely to
be lower.
6.2 Physiology of air travel
6.2.1 Hypobaric hypoxia
6.2.1.1 The most significant physiological change that occurs
during flight is hypobaric hypoxaemia. Because the cabin is
pressurised, the partial pressure of oxygen (pO2) does not fall
below 15.7 kPa. Table 1 shows the relative arterial oxygen pressure (paO2), ambient pO2 and barometric pressure for healthy
Table 1 Relationship of barometric pressure, ambient oxygen partial
pressure (pO2) and arterial pO2 with change in altitude in healthy adults
at rest
Barometric
pressure
Altitude
Ambient pO2
Arterial pO2
Feet
metres
mm Hg
kPa
mm Hg
kPa
mm Hg
kPa
0
6000
8000
0
1828
2438
760
609
564
101.3
81.2
75.2
160
128
118
21.3
17.1
15.7
95e100
66e71
62e67
12.7e13.4
8.8e9.5
8.2e9
Reproduced with permission from Slonim and Hamilton.12
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
Figure 2 Oxygen dissociation curve from Aviation, Space and
Environmental Medicine guidelines.4
ii3
Fitness to fly
6.2.2 Effects of hypoxia on the circulation and potential for
myocardial ischaemia
6.2.2.1 Hypoxia is reported to have many effects on the circulation including local vasodilation of coronary and cerebral
vascular beds, increase in heart rate, increase in systemic blood
pressure,15 increased myocardial contractility, increase in cardiac
output16 17 and increase in pulmonary artery pressure.18 19
Responses to exercise are also altered,20 21 and the effects of
hypoxia change with the duration of exposure.21
6.2.2.2 Hyperventilation can occur which in turn activates
pulmonary stretch receptors which override direct effects of
hypoxia and produce tachycardia.22 23
6.2.2.3 Most of the studies from which the above data are
derived are laboratory-based animal studies or have involved the
study of active (walking, climbing or physical work) human
subjects at moderate to extreme altitude for extended periods.
Most of these reported effects do not become apparent until
marked hypoxia with a paO2 of #40 mm Hg occurs.15 18 23
6.2.2.4 Levels of paO2 of 40 mm Hg would not normally be seen
at modest altitude. Using the nomogram devised by Dillard and
Ewald24 for estimating the paO2 at 2438 m (8000 ft) in patients
with pulmonary disease, it can be estimated that to attain
a paO2 of 40 mm Hg would require the resting paO2 at sea level
to be 60 mm Hg and the forced expiratory volume in 1 s to be
29%din other words, someone with very severe pulmonary
disease.
6.2.2.5 There are few data on the effects of short-term isocapnic
mild hypoxia at rest in the semi-recumbent position which is
the state in which airline passengers find themselves.
6.2.2.6 A study by Phillips et al25 measured the dose-response
curve of isocapnic hypoxia and cardiac output in healthy men in
a recumbent position and found an increase in cardiac output
associated with relatively mild levels of hypoxaemia (table 2).
The increase was entirely accounted for by increasing heart rate
and after a 5 min peak tended to return to base level after 20 min.
There was no increase in blood pressure or ventilation rate.
6.2.2.7 Another study26 exposed normal subjects (age range
6e83 years) to an altitude of 2900 m, slightly above the
maximum pressure altitude of an airline cabin, and analysed
cardiovascular parameters at 1 h and over the following 24 h.
Oxygen saturations fell significantly on arrival at altitude and
there were significant increases in heart rate and systolic blood
pressure across all age groups. All other parameters were normal
and there was no correlation between the degree of hypoxia and
the changes in heart rate and blood pressure.
6.2.2.8 Such an inconsistent relationship between blood pressure
and degree of hypoxia was also shown by Thomson et al27 when
studying the circulatory response to isocapnic hyperoxia and
hypoxia in normal healthy men. They exposed the subjects to
each condition in a semi-recumbent position at normal room
temperature for 1 h with a mean oxygen saturation during
hypoxia of 82.6%. Hypoxia induced significant increases in heart
rate and cardiac index and significant falls in systemic vascular
resistance index and arterial stiffness.
Table 2
Haemodynamic and ventilatory response to hypoxaemia
Oxygen saturation (%)
Cardiac output (l/min)
Heart rate (beats/min)
Systolic BP (mm Hg)
Diastolic BP (mm Hg)
Respiratory rate (breaths/min)
97 (room air)
7.0
63
125.6
72.1
17.1
*p<0.0005 for room air and 90% oxygen saturation.
ii4
90.0
7.1
69.7
127.6
74.5
17.3
85.3
7.9*
72
127.1
74.1
16.6
80.5
8.4*
75*
128.2
73.2
16.8
6.2.2.9 In a paper even more relevant to this guidance, Wyss
et al28 took normal controls and a group of patients with angina
(Canadian Cardiovascular Society functional class IIeIII) and
angiographically documented coronary artery disease and
exposed them to simulated altitudes of 4500 m and 2500 m,
respectively. Haemodynamic parameters, ventilation rate,
myocardial blood flow and coronary flow reserve using adenosine and bicycle ergometry were measured. There was a significant increase in rate pressure product at rest in both groups
when exposed to their respective simulated altitudes and an
increase in myocardial blood flow in both groups. However,
there was a significant reduction in coronary flow reserve on
exercise in the coronary artery disease group at the simulated
altitude of 2500 m. There was no significant increase in ventilation in the coronary artery disease group at 2500 m.
6.2.2.10 It is reasonable to conclude from the above that there is
no extreme change in circulatory parameters at rest with
isocapnic hypoxia, even with oxygen saturations as low as 80%.
Circulatory changes are confined to mild (probably transient)
increases in heart rate, small decreases in systemic resistance
which may result in increased cardiac output and some degree of
increased coronary blood flow. Oxygen saturations of 80%
would be unlikely to occur at pressure altitudes of 2500 m in
commercial aircraft.
6.2.2.11 Conclusion
The mild hypobaric hypoxaemia induced by commercial airline
flight may be expected to have little or no effect in precipitating
myocardial ischaemia in people without critical ischaemia at sea
level.
6.2.3 Effects of hypoxia in heart failure
6.2.3.1 It might be expected that hypoxia would have a deleterious effect on patients suffering with left ventricular dysfunction. However, pulmonary vasoconstriction may help protect
the pulmonary microvasculature from increased pressure and
falls in the systemic vascular resistance caused by hypoxia and
thought to be mediated by nitric oxide29 may limit rises in
pulmonary venous and left ventricular filling pressures.
6.2.3.2 There is a paucity of literature on the effects of hypoxia
on central circulatory variables in humans with heart failure,
although work by Hobkirk et al30 has shown that, in 21
patients with treated New York Heart Association (NYHA)
grades III and IV heart failure with ejection fractions <40%,
lying supine and breathing 15% oxygen caused a fall in arterial
oxygen saturation to 86% but did not cause any significant
symptoms. Blood pressure and pulmonary artery pressure rose
significantly but heart rate did not (19 (90%) were on
b blockers). Indirect measures of ventricular filling pressures
suggested a fall.
6.2.3.3 In the Ideal Cabin Environment (ICE) Study,31 72
volunteers (mean age 54 years) with stable NYHA grade II were
subjected to a simulated 7-h flight. The mean oxygen saturation
of the group at ‘sea level’ was 94% and at 2438 m (8000 ft) cabin
altitude mid ‘flight’ it fell to 91%, but there were no symptoms
of dyspnoea or changes in blood pressure. The equivalent mean
values for the normal volunteers (mean age 43 years) were 96%
at ‘sea level’ and 93% at 2438 m (8000 ft).
6.2.3.4 The effect of hypoxia on workload in patients with heart
failure has also been investigated. Agostoni et al32 showed that
patients with severe but stable heart failure (NYHA grades III
and IV) were able to complete cardiopulmonary exercise
without stopping even when subjected to hypoxia equivalent to
an altitude of 3000 m (9842 ft).
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
Fitness to fly
6.2.3.5 Conclusion
The available evidence suggests that, for patients with stable
heart failure including NYHA grades III and IV, short-term (up
to 1 h) hypoxia at rest produces no significant deleterious effects.
Periods of up to 7 h are tolerated by those with mild to moderate
stable heart failure (NYHA grade II).
6.2.4 Effects of hypoxia on the ECG, arrhythmia and pacing
thresholds
6.2.4.1 It might be anticipated that hypoxia and the associated
increase in a- and b-adrenergic stimulation would increase the
susceptibility to arrhythmia, particularly in the presence of
myocardial ischaemia, but there are surprisingly few data on the
subject. In a study of healthy men aged 50e64 years, increased
atrial and ventricular ectopy was observed during acute ascent in
a cable car to altitudes up to 2632 m (863 4ft) above sea level,
the frequency of ectopy being proportional to the altitude.33
6.2.4.2 In another study healthy volunteers subjected to
a simulated ascent of Mount Everest in a hypobaric chamber34
showed transient changes in mean frontal QRS axis and voltages
and increases in heart rate proportional to the degree of hypoxia.
There were no ECG signs of ischaemia or arrhythmia even with
an oxygen saturation of 49%.
6.2.4.3 It is not known whether hypoxia during air travel results
in an increased predisposition to sustained ventricular
arrhythmia and implantable cardioverter defibrillator (ICD)
activation in susceptible individuals.
6.2.4.4 Profound hypoxaemia induced by inhalation of a gas
mixture containing 10% oxygen has been shown to result in
a significant and reversible increase in pacing threshold.35
However, acute exposure of 13 patients with implanted pacemakers to an altitude equivalent of 4000 m, simulated in a hypobaric chamber, did not result in any alteration of stimulation
thresholds after 30 min.36
6.2.4.5 Conclusion
Hypoxia is unlikely to produce an increase in susceptibility to
arrhythmia or to have any adverse effect on pacing threshold at
cabin altitudes likely to be encountered during air travel.
6.2.5 Effects of hypoxia on thrombogenicity (see also section on
DVT/VTE)
6.2.5.1 Passengers with existing atheromatous coronary disease,
whether diagnosed or not, may be at risk of acute coronary
syndromes if being a passenger on a commercial flight has
a prothrombotic effect which might predispose them to
formation of occlusive coronary thrombus.
6.2.5.2 Hypoxia has been shown not to enhance exercise-induced
activation of clotting factors in healthy athletes37 and, although
short-term and long-term periods at high altitude (>5000 m)
have been shown to produce activation of clotting factors,38 39
well-controlled studies of both normobaric40 and hypobaric41
isocapnic hypoxia simulating an altitude of 3600 m for 8 h
revealed no significant effect.
6.2.5.3 Toff et al42 simulated a long-haul flight by subjecting 73
low-risk ‘passengers’ to 8 h of either sedentary normoxia or
hypoxia in a crossover trial using a hypobaric chamber. A small
proportion of women taking oral contraceptives were included
but subjects with factor V Leiden and prothrombin G20210
mutations were not. Measures of endothelial function, platelet
activation and clotting showed no significant difference between
the hypoxic and normoxic conditions suggesting that, in lowrisk passengers, hypoxia has no prothrombotic effect over and
above prolonged sitting.
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
6.2.5.4 In a study of predominantly high-risk ‘passengers’43 with
a high proportion of participants taking oral contraceptives or
bearing the factor V Leiden mutation, an 8-h flight was
compared with other 8-h periods of sitting in a cinema or light
ambulatory activity. There were increases in clotting factors (Ddimer, thrombin/antithrombin complex and prothrombin fragments 1 and 2). This suggests that, in high-risk individuals, mild
hypoxia alone may have a prothrombotic effect.
6.2.5.5 Conclusion
Commercial airline passengers breathe air with a reduced oxygen
content which results in low blood oxygen saturations. The
levels of blood oxygen saturations attained appear to have little
or no adverse circulatory effects which would make the
passenger more liable to myocardial ischaemia, myocardial
infarction, left ventricular failure or arrhythmia. Passengers
already at high risk may suffer additional risk from hypoxia
during flight. This conclusion is supported by the available
evidence and applies to short or medium length flights. There is
no adequate information to indicate whether extended flying
(>12 h) might have adverse effects.
6.2.6 Effects of pre- and post-flight environment
Taking a flight with a commercial airline involves more than the
time spent in the aircraft during flight, and the potential threats
to the health of passengers with cardiac disease may occur before
and after flight.
6.2.6.1 Anxiety: A significant proportion of the population
(10e40%) report a fear of flying,44 although this prevents few
from completely avoiding it.45 Fear and anxiety may be
heightened at take-off and landing or if turbulence is experienced. The threat of terrorism adds to the fear of flying and can
a have a major impact on passenger willingness to fly. Ito and
Lee assessed the September 11 attacks in New York as having
a major effect on reducing passenger numbers, an effect which
continued at least until 2003.46
6.2.6.2 The security measures which are now in place mean
passengers have to arrive well ahead of their flight time. Concern
about missing the flight, uncertainties about where to check in
and identifying the departure gate all add to the stress and mean
passengers may be hurrying and anxious.
6.2.6.3 Frustration about delays has been shown to result in
anger,47 and anger is one of the more potent of the many mental
stresses that may provoke myocardial ischaemia.48
6.2.6.4 Exercise: After arrival at the airport a considerable amount
of physical activity is involved, much of it carrying, pushing or
pulling bags, which may be well in excess of the passenger ’s
normal exercise limits. Similar stresses apply at the destination
airport and may also be exacerbated by the altitude or temperature
of the destination. Many major destination cities are above
5000 ft, especially in North and South America, Africa and the
East, and many have extremes of temperature. The potential for
the airport stresses to induce a deterioration of a chronic condition
is well recognised and most airports provide excellent services to
assist the disabled passenger. These services can be found on
arrival, but it is better to call ahead and make the arrangements
beforehand.
6.2.7 Sleep deprivation and circadian rhythm disruption
6.2.7.1 Departure times in the early hours of the morning often
mean that, with travel time to the airport and the delay before
boarding, passengers may be awake much of the night before
travel. This may result in sleep deprivation and disruption of
ii5
Fitness to fly
circadian rhythm that can also occur with flights that cross
many time zones.
6.2.7.2 The circadian rhythm of the cardiovascular system
reflects the changing sympathetic-vagal balance and is recognised to result in periods of cardiac vulnerability.49 Studies of
shift workers suggest that sleep deprivation and disruption of
circadian rhythm may increase the risk of coronary events.50
Heart rate variability as a marker of circadian variation may be
altered in patients after infarction and in those with congestive
heart failure, hypertension and diabetes51 and can be modulated
by b blockers.
6.2.7.3 Despite this, one study has shown that, in patients with
heart failure, there is no relationship of circadian rhythm with
sudden cardiac death52 and there is no direct evidence of
increased cardiac vulnerability resulting from occasional shortterm disruptions such as those experienced by airline passengers.
6.2.7.4 Probably the most important effect of disturbed diurnal
patterns for the passenger with cardiovascular disease is the ease
with which the regularity of medications is disrupted. It is very
difficult to adhere to a pattern of tablet-taking when the daily
routine is altered, especially when confusion about the right
time compounds the problem. For passengers with stable heart
failure, angina or arrhythmia, it is very important that they
maintain the regularity of their medication.
7. PASSENGER FLIGHT WITH CHRONIC CONDITIONS AND
AFTER CARDIAC EVENTS OR PROCEDURES
Regardless of any direct deleterious effects that the aircraft cabin
environment may have, it does not provide an ideal environment
in which to manage medical problems and an acute in-flight
event may result in diversion of the flight, poor medical outcomes
or both. Cardiac events or procedures, diagnostic or therapeutic,
may leave people at short-term high risk of a further event or
complication. This acute risk normally reduces in the short to
medium term until a stable situation is reached. If a cardiac event
or procedure carries a significant risk of events or complications
occurring, then consideration must be given to the time interval
before the risk becomes acceptable and the cabin environment no
longer a concern. It is generally the instability of the condition
that predicts risk rather than the severity alone.
Although some considerations are relatively easy to define,
such as the time it takes for post-thoracotomy intrathoracic air to
be reabsorbed, most of the situations are complex. Patients have
a multitude of factors that contribute to the risk of an event and
consequently any guidance is necessarily a generalisation based
on reasonable judgement and should not be considered absolute.
In the following section acute and chronic conditions and
different cardiac procedures are considered and the appropriate
time that should pass between the event and the flight
suggested. The conditions and procedures considered are listed in
table 3.
Table 3
7.1 Acute coronary syndromes (ACS) including ST elevation
myocardial infarction (STEMI) and non-ST elevation myocardial
infarction (NSTEMI) and troponin-negative acute coronary
syndromes
7.1.1 The observations of the limited effects of the cabin environment on cardiac physiology (see above) should be equally
applicable to patients following an acute coronary syndrome,
there being little or no deleterious effect.
However, following an acute coronary syndrome, patients
may be at risk of events as a direct result of their condition. The
early risk following an acute coronary syndrome is multifactorial
and includes age, heart rate, ventricular function/Killip class,
severity of the coronary disease and the degree of
revascularisation.53e58 In existing guidelines on fitness to fly,
only acute myocardial infarction (AMI) is considered without
distinction between different clinical presentations although it is
sometimes separated into complicated and uncomplicated.
7.1.2 There is conflicting advice regarding the delay to flying
following AMI, with varying guidance from professional
bodies4e7 and varying acceptance by passenger carriers. Data on
which to base guidance are relatively sparse.
7.1.3 Retrospective analyses of patients following myocardial
infarction have suggested that flyingdboth short and long
hauldis safe at 2e4 weeks,59 60 but in these studies the elapsed
time between myocardial infarction and the flight was not an
adjustable variable.
7.1.4 Another retrospective study61 analysed 213 aeromedical
repatriation patients after myocardial infarction and concluded
that travel <2 weeks after AMI can be safely undertaken and
that there is a low incidence of transfer-related complications.
The patients were clinically heterogeneous, some having ST
elevation myocardial infarction (STEMI) and some non-ST
elevation myocardial infarction (NSTEMI), with varying
numbers having undergone revascularisation. All the patients in
this study were accompanied by an appropriately trained
medical escort, and it is not clear whether this actively
contributed to the low complication rate.
7.1.5 A small prospective trial62 analysed the effects of flight
2 weeks after AMI in patients who were able to climb a flight of
stairs and who were randomised to receive oxygen (2 l/min) or
no oxygen during the flight. Holter monitoring was performed
for ST shift and arrhythmia and oxygen saturation was
measured throughout the flight. The authors noted some
asymptomatic hypoxia (oxygen saturation <90%), which was
also noted in a few patients in the paper by Thomas et al,61 but
only one episode of ST shift on the Holter tracing which was
asymptomatic. There was no difference in outcome between
patients with supplemental oxygen and those without. The
authors concluded that, in this group of patients, commercial
flight was safe and did not induce myocardial ischaemia, that
supplemental oxygen as routine was not required and that
medical attendants were unnecessary.
Conditions, procedures and events considered in this section
Acute conditions
Chronic conditions
Diagnostic procedures Therapeutic procedures
Acute coronary
syndromes
Acute left ventricular
failure
Stable angina
Stable heart failure
Paroxysmal SVT
Persistent/permanent AF
Cyanotic congenital heart
disease
Anaemia
Cardiac catheterisation
Electrophysiological
studies
Emergency PCI
Elective PCI
Insertion of pacemaker/AICD
CABG
Surgical valve replacement
Percutaneous valvotomy
Ablation flutter, right-sided pathways,
left-sided pathways, AF
AF, atrial fibrillation; AICD, implantable cardioverter defibrillator; CABG, coronary artery bypass grafting; PCI, percutaneous coronary
intervention; SVT, supraventricular tachycardia.
ii6
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
Fitness to fly
7.1.6 Longer distance medical transport is also reported in
a retrospective study by Essebag et al63 in which 51 patients
were transported within 7 days of AMI, half of them high risk
with Killip class IIeIV. This study suggested that transfer was
safe 3e7 days after admission.
7.1.7 These studies do not distinguish between high-risk and
low-risk post-infarction patients. There is a spectrum of risk
which will depend on the success of reperfusion, extent of
myocardial dysfunction, predisposition to arrhythmia and
presence of major complications.
7.1.8 STEMI
7.1.8.1 Figures from the Myocardial Infarction National Audit
Project (MINAP) suggest overall mortality from STEMI is
highest in the acute phase, falling to 2% after 10 days,64 but
these figures include all patients with STEMI and do not
distinguish between high- and low-risk groups.
7.1.8.2 Successful revascularisation during primary angioplasty
for STEMI confers a prognostic benefit in the short and medium
term, especially in low-risk STEMI,65 and in a cohort of 1791
patients treated by primary angioplasty de Luca et al devised
a scoring system to identify the risk of 30-day mortality.66 The
authors’ score card (see table 4) was able to identify patients at
very low risk of early mortality or cardiac arrest (0.1% at 2 days
and 0.2% at 2e10 days). They were able to demonstrate the
stability of the score over the following year. Although patients
with higher scores had higher early and late mortality in all
groups, actuarial survival curves showed that relative stability
of risk had been reached by 10 days. They concluded that a large
proportion of patients following primary percutaneous coronary intervention (PCI) for STEMI may be identified as very
low risk (score #3) with a stable risk from 2 days onwards.
There was a strong correlation between risk score and ejection
fraction (EF), patients with scores of 0e3 having mean6SD EF
of 45610% and those with scores of 4e6 having a mean6SD EF
of 40612%. This suggests that patients with low risk scores
Table 4 Zwolle risk score for ST elevation myocardial infarction
(STEMI)
Killip class
Points
Risk score
RR (95% CI) of
death by 30 days
1
2
3e4
TIMI flow post PCI
3
2
0e1
Age
<60
$60
3 vessel disease
No
Yes
Anterior infarct
No
Yes
Ischaemic time <4 h
No
Yes
0
4
9
0e1
2
0.09 (0.02 to 0.37)
0
1
2
3
1.04 (0.04 to 2.45)
4
1.40 (0.5 to 3.98)
0
2
5
2.48 (0.96 to 6.42)
6
2.52 (0.75 to 8.46)
7
5.99 (1.98 to 18.1)
Total available score
16
0
1
0
1
$8
0.03 (0.008 to 0.13)
32.1 (18.6 to 55.8)
0
1
and EF >40% have a very low chance of events from day 3
onwards.
7.1.8.3 The treatment of STEMI with primary angioplasty is
increasingly widespread but still not the norm. In 2007, MINAP
reported 4228 primary angioplasties in England and Wales out of
a total of 27 199 STEMI (John Birkhead, MINAP, personal
communication, April 2009). The British Cardiovascular Intervention Society (BCIS) audit returns67 reported a slightly higher
figure at 4858 primary angioplasties. Either way, it only represents about 15% of those with STEMI but it is rapidly
increasing. The remainder received fibrinolytic agents or no
reperfusion therapy. In these patients, successful reperfusion,
extent of coronary disease and degree of left ventricular
dysfunction are not known so quickly after hospitalisation and
it is recommended that patients undergo further investigation
and risk stratification using echocardiography within 48 h and
coronary angiography during the same admission.68 If there
remain concerns about possible inducible ischaemia, stress
testing may be undertaken in the following 4e6 weeks and
appropriate revascularisation planned. Revascularisation with
PCI or coronary artery bypass graft (CABG) almost halves the
risk of subsequent unstable angina or death.69
7.1.8.4 Left ventricular EF is a marker of increased risk of
ventricular arrhythmia and sudden cardiac death (SCD). Patients
with an EF $40% and no ventricular tachycardia after day 2 are
at low risk of SCD. Those with EF #30% and prolonged QRS
duration may be considered for an implantable defibrillator
(AICD).70
7.1.8.5 Bradyarrhythmia complications may require temporary
or permanent insertion of a pacemaker. In either case there
is a risk of pneumothorax (see section on pacemaker insertion).
7.1.9 NSTEMI and troponin-negative acute coronary syndromes
Patients with NSTEMI are at increased risk of death or further
myocardial infarction and are recommended to undergo coronary angiography and appropriate revascularisation before
discharge.71
7.1.10 Haemorrhage
Current management of all acute coronary syndromes involves
the use of antithrombotic agents and anticoagulants as well as
invasive strategies for revascularisation. There is a therefore
a risk of haemorrhage related to the arterial access site as well as
a risk of spontaneous bleeding from the gastrointestinal tract or,
rarely, retroperitoneal haemorrhage.
7.1.10.1 Haemorrhagic complications are more likely with
femoral artery than radial artery access,72 but are unlikely to
occur after 1 week. Subacute gastrointestinal haemorrhage is
reported after both primary angioplasty73 and fibrinolytic
therapy74 and may complicate the in-hospital course. Heparin
and the small molecule IIbIIIa receptor antagonists have a short
half life, but abciximab may still have effects at 7e10 days.
Gastrointestinal haemorrhage from the use of the antiplatelet
agents may also occur after discharge, but it is relatively rare at
0.07 per patient-year.75
7.1.10.2 If there are haemorrhagic complications during the inhospital course after an acute coronary syndrome, it may alter
the advisability of flying early after discharge.
7.1.11 Conclusion
Reproduced with permission from de Luca et al.
PCI, percutaneous coronary intervention; TIMI, thrombolysis in myocardial infarction.
66
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
Passengers who have suffered an acute coronary syndrome can
be reasonably divided into those at very low risk who may safely
fly as early as 3 days after the event, those at medium risk who
ii7
Fitness to fly
may fly from 10 days onwards and those at high risk or awaiting
further investigation/treatment in whom flying should be
deferred until a more stable situation is achieved.
Very low risk: age <65 years, first event, successful reperfusion, EF >45%, no complications and no planned investigations
or interventions.
Low risk: EF >40%, no symptoms of heart failure, no evidence
of inducible ischaemia or arrhythmia and no further investigations
or interventions planned.
High risk EF: <40% with signs and symptoms of heart failure,
those pending further investigation with a view to
revascularisation or device therapy.
7.2 Heart failure
7.2.1 Acute left ventricular failure
The risk of hospitalisation for heart failure following AMI is
highest in the few weeks after the infarction but stabilises after
45 days.76 Episodes of acute left ventricular failure may be
caused by an acute coronary syndrome (see above) or provoked
by anaemia or infection on the background of chronic left
ventricular dysfunction. Once any precipitant is identified and
treated, most cases should be stabilised within 6 weeks and
should be safe to fly.
7.2.2 Chronic heart failure
Passengers with stable chronic heart failure without recent
changes in symptoms or medication are likely to be able to
tolerate the mild hypoxia of the aircraft cabin environment even
if they have severe heart failure.30e32 It is advisable that they
take the precautions of avoiding physical exertion at the airport
and making sure that they take their regular medication. It is
probably prudent for passengers who are severely limited
with NYHA class IV symptoms not to fly without special
consideration and the availability of in-flight oxygen.
7.2.3 Conclusion
Following an episode of acute heart failure, most patients should
be stable within 6 weeks and be able to fly. With chronic heart
failure there should be no restriction, although those with
NYHA III and IV should consider airport assistance and request
the availability of in-flight oxygen.
7.3 Stable angina
The available evidence suggests that it is unlikely that flying
would precipitate acute myocardial ischaemia and no restriction
should be applied. Passengers should be advised to allow plenty
of time at either end of their journey to limit anxiety and haste.
Passengers should be advised to seek assistance with personal
transport at the airport if needed. They should also be advised to
remember to take their medication in the usual way and at the
usual times.
7.4 Arrhythmia
7.4.1 Paroxysmal supraventricular arrhythmia
Flight itself does not appear to induce paroxysmal supraventricular tachycardia, atrial fibrillation or atrial flutter, and
providing the passengers are symptomatically stable with a low
frequency of events, there should be no restriction to flying.
7.4.2 Passengers with permanent or persistent atrial fibrillation
should be stable with appropriate rate control and anticoagulation.
7.4.3 Passengers with a history of ventricular arrhythmias
should have these controlled before flying. Ventricular arrhythii8
mias may be treated by implantable defibrillators (see section on
DVT and VTE).
7.4.4 Patients with uncontrolled haemodynamically significant
ventricular arrhythmias should not travel on commercial
aircraft.
7.5 Cyanotic congenital heart disease
7.5.1 Patients with congenital cyanotic heart disease with
Eisenmenger syndrome77 78 are hypoxaemic with a consequent
erythrocytosis and haemoglobin levels of 15e24 g/l. They might
be thought to be at risk when flying owing to the effects of
hypoxia and hyperviscosity.
7.5.2 The circulatory pathology, however, does not impair
alveolar gas transfer and the arterial hypoxia does not result
from low alveolar oxygen tension but from the central right-toleft shunting. As a result, small changes in the alveolar oxygen
concentration have little effect on hypoxaemia. In addition,
a chronic adaptation of a shift in the oxygen dissociation curve
to the right has been suggested by Harinck et al79 and subsequently confirmed in a study by Broberg et al.80
7.5.3 In the study by Broberg et al, 53 patients with Eisenmenger
syndrome were compared with 48 acyanotic patients and
a 10-year record of 1157 flights was studied. One or two of the
patients reported symptoms of breathlessness during flight and
were treated with in-flight oxygen therapy but the authors
reported no serious adverse effects on account of the relative
additional hypoxia experienced in-flight and suggested there was
no justification for limiting air travel in these patients.
7.5.4 The erythrocytosis that occurs may increase the already
existing risk of venous thromboembolic disease but with the
additional possibility of a ‘paradoxical’ embolus. One patient in
the study by Broberg et al was thought to have had a transient
cerebral event.
7.5.5 Conclusion
Passengers with the Eisenmenger syndrome should not be
restricted from flying although they are advised to request inflight oxygen. They are also advised to maintain good levels of
hydration, avoid alcohol and follow the guidance for VTE
prophylaxis for high-risk groups (see section on DVT and VTE).
7.6 Anaemia
7.6.1 Reduced circulating haemoglobin restricts the oxygencarrying capacity of a unit volume of blood and induces
compensatory mechanisms in the circulation that result in
increased cardiac output and ventricular stroke work.81 82
7.6.2 In the normal healthy heart, remarkably low haemoglobin
levels can be tolerated83 although chronic anaemia may precipitate angina in those with normal coronary arteries.84 However,
in an already compromised circulation, anaemia may risk
pulmonary oedema or critical myocardial ischaemia.85
7.6.3 It is well recognised that anaemia commonly complicates
chronic heart failure86 and that treatment significantly improves
the functional class.87 The same applies to those with chronic
angina88 and following either PCI89 or CABG.90
7.6.4 The Canadian Cardiac Society Guidelines on Flying6
recommend that a haemoglobin level of 9 g/l is a threshold value
below which travel is inadvisable in passengers who have
undergone CABG.
7.6.5 Conclusion
When considering passengers with cardiovascular disease wishing
to fly, physicians should consider the additional potential effect of
anaemia on the underlying cardiovascular pathology.
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
Fitness to fly
7.7 Cardiac catheterisation
Uneventful cardiac catheterisation should not restrict flying and
patients may fly the next day. Bleeding from the access site may
be a reason to defer a flight, as may other complications.
7.8 Elective PCI
Elective PCI varies in its complexity from simple single vessel PCI
to complex three vessel treatments and the use of adjunctive
devices and pharmacology. With aggressive anticoagulant and
antiplatelet regimens, bleeding is a more likely event than with
elective cardiac catheterisation and bigger contrast loads are more
likely to cause renal impairment. In an uncomplicated case there is
no reason to restrict flying for more than 2 days, but there should
be discretion in the advice given by the physician and account
taken of the degree of ventricular and renal dysfunction.
7.9 Pacemaker insertion including temporary systems,
implantable cardioverter defibrillators (ICD) and biventricular
devices
7.9.1 The insertion of any type of pacemaker including temporary wires, permanent pacemakers, biventricular pacemaker and
implantable cardio-defibrillators (ICD) may involve subclavian
vein puncture. Pneumothorax is a recognised complication.
Before discharge an anteroposterior chest x-ray is routinely
obtained to check the lead positions and to exclude pneumothorax, although it is possible that very small pneumothoraces
may not be evident on the x-ray. In the absence of complications, patients are typically discharged from hospital within 24 h
of implantation of the device.
7.9.2 Pneumothorax requiring intervention (aspiration or chest
drain insertion) occurs in 0.6e0.8% of cases with less significant
pneumothoraces (occupying <10% of the lung field) in a further
1%.91 92
7.9.3 Passengers should not fly with a pneumothorax because of
the risk of gaseous expansion at altitude which may compromise
respiratory function and the possible development of tension
pneumothorax. If implantation has been complicated by pneumothorax, travel should be deferred for 2 weeks after full
radiographic resolution.93
7.9.4 In the context of aeromedical repatriation with a medical
escort, a stable patient with a persistent bronchopleural fistula
may be able to fly safely with a chest drain attached to
a one-way Heimlich valve.
7.9.5 In the absence of pneumothorax or other complications
such as bleeding or electrode problems, there is no absolute
contraindication to air travel within a 1e2 days of implantation.
However, travel with a fresh surgical wound might be associated
with discomfort and an increased risk of mechanical or infective
complications. A small pneumothorax might not be evident or
detected on the initial postoperative x-ray and a delay of a few
days might allow an undetected pneumothorax to resolve. In
the early weeks after pacemaker implantation, patients are
generally advised to restrict arm movements on the ipsilateral
side, to avoid raising the elbow above the shoulder and to avoid
heavy lifting in order to minimise the risk of lead displacement.
This may limit their ability to carry luggage and use the
overhead lockers in the aircraft cabin.
7.10 Ablation
7.10.1 Electrophysiological studies with or without ablation
therapy involve the often prolonged insertion of a number of
catheters into the systemic veins. The clotting cascade is activated by the presence of the catheters and increases with the
duration of the procedure.94 Femoral vein thrombosis is a wellHeart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
recognised complication and, although relatively rare as clinical
complication, can be found subclinically much more frequently.
In a study of 52 cases (68 femoral veins), non-occlusive
thrombus was found in 17% but had disappeared after 1 week.95
7.10.2 Clinically evident thromboembolic complications
including femoral vein thrombosis and pulmonary embolus have
been reported in 0.14%,96 0.8%97 and 1.04%98 of right-sided
procedures. This rate is sufficiently low and the benefit of aspirin
as prophylaxis for systemic venous thrombosis insufficiently
high99 that use of routine aspirin after right-sided ablation is not
a recommendation in the consensus document of the European
Heart Rhythm Association.100
7.10.3 It is recommended that patients undergoing left heart
electrophysiological studies and ablation involving transeptal
puncture for atrial fibrillation or ventricular tachycardia should
be given warfarin for at least 3 months and 1 month, respectively.100
7.10.4 Given the small additional risk of thromboembolism
during or following flight, it is advisable for any passenger
wishing to fly within 1 week after left- or right-sided ablation
therapy for arrhythmia to be considered to be in a high-risk
group and follow the advice for high-risk passengers with DVT/
VTE (see below).
7.11 Open chest heart surgery including coronary artery bypass
grafting and valve replacement
After the chest has been opened to perform cardiac surgery it is
inevitable that some air will remain once the chest wound is
closed. It takes 3e10 days for air to be reabsorbed. If any
significant amounts of air remain in the pericardial space or in
the thoracic cavity it may expand by up to 60% (see section on
physics of flight) and this may be painful or dangerous.
Fast-track postoperative care and early extubation are leading
to earlier discharge for patients following surgery101 but without
an impact on readmission to hospital.102 Patients undergoing
cardiac surgery which is without complication are mobile and at
home in less than 10 days. Cardiac function should be improved
following the surgery, but there may be complications of
arrhythmia, pleural effusion, wound infection, anaemia, rhythm
disturbances and left ventricular dysfunction. In patients
without any of these complications, flying should be safe at
10 days. If complications do occur or there are symptoms of
angina, heart failure or arrhythmia, patients should be advised
about flying according to the guidance for those specific conditions (see appropriate section).
Patients may be in discomfort after cardiac surgery and should
be advised not to carry heavy bags or hurry. If travelling between
10 days and 6 weeks after surgery, ground assistance may be
required.
8. PACEMAKERS AND ICDS
8.1 Background
8.1.1 In the UK over 40 000 new patients receive an implanted
pacemaker or ICD each year.103 The majority of these devices are
conventional pacemakers, but there are an increasing number of
cardiac resynchronisation therapy (CRT) pacemakers and ICDs,
with or without CRT capability.
8.1.2 It is estimated that there are currently 380 000 patients
with pacemakers, 6000 patients with CRT pacemakers and
33 000 patients with ICDs (including 7000 with CRT capability)
in the UK (D Cunningham, personal communication, 2009).
The majority of pacemaker recipients are elderly (mean age at
implant 75.5 years), but patients may receive a pacemaker at any
age from infancy to adult life.
ii9
Fitness to fly
8.1.3 The main indications for pacing are atrioventricular block
or sinus node disease, the predominant aetiologies being agerelated fibrosis or ischaemic heart disease. Patients with pacemakers have a comparable survival to those without, and most
return to a full and active life with little limitation of work and
leisure activities in relation to the device.
8.1.4 Patients receiving CRT and ICDs tend to be younger (mean
age at implant 69.9 and 62.5 years, respectively) and more often
have significant underlying cardiac disease such as previous
myocardial infarction, cardiomyopathy, impaired left ventricular
function and heart failure. When assessing the patient’s fitness
to fly, the nature and stability of these underlying conditions
require careful consideration and may be of greater significance
than the presence of the device.
8.1.5 Although the majority of patients with an implanted
device may travel safely by air, there are a few specific issues that
should be considered before travel and a number of concerns for
which the patient may require guidance or reassurance.
8.2 Electromagnetic interference (EMI)
8.2.1 Pacemakers and ICDs are inherently susceptible to electromagnetic interference (EMI) in the presence of strong electric
or magnetic fields. Modern devices are well shielded against
electromagnetic radiation and interference signals predominantly enter the devices via the lead which effectively acts as
a loop aerial. Unipolar systems are more susceptible than bipolar
systems owing to the larger electrode separation and greater
effective area for inductive coupling.104
8.2.2 Most pacing systems are now implanted using bipolar
leads which markedly reduce the risk of EMI. The devices
incorporate specific design features to detect and reject EMI, and
also a noise reversion mode (typically fixed-rate pacing) to which
pacemakers will switch in the presence of EMI that is recognised
as such by the device.
8.2.3 The possible effects of undetected EMI on pacemaker
function include inappropriate inhibition of output (missed
pulses or complete cessation of pacing) due to the input signal
being falsely interpreted to be of cardiac origin and triggering,
according to the operating mode. Alteration of the programmed
settings may occasionally occur. The clinical consequences of
EMI will be influenced by its duration and by the extent to
which the patient is pacemaker-dependent. Fewer than one-fifth
of patients have symptoms or fail to develop an adequate escape
rhythm in response to abrupt inhibition.105
8.2.4 In an ICD, EMI may be falsely interpreted as tachyarrhythmia and trigger inappropriate therapies (antitachycardia
pacing or shocks). Interference protection has improved
substantially since the introduction in recent years of feedthrough capacitors which are now incorporated into the
majority of modern pacemakers and ICDs. These filters effectively attenuate most EMI in the frequency range from 30 MHz
to 10 GHz.106
8.3 Airport security
8.3.1 Before boarding the aircraft passengers are normally
required to pass through a metal detector gate. These gates
typically incorporate one or more coils through which alternating
current is passed to induce a primary magnetic flux. Movement
of metallic objects within the coils results in a secondary
magnetic flux which causes voltage changes in the coils that are
used for detection. Studies of typical installations showed
magnetic field frequencies between 0.1 kHz and 3.5 kHz with
predominantly saw-toothed or pulsed waveforms and relatively
high field strengths of up to 299 A/m (3741 mG) peak to peak.107
ii10
8.3.2 Nonetheless, clinical experience and experimental data
suggest that clinically significant EMI is highly unlikely if
patients walk briskly through the gate. In an early experimental
study reported 20 years ago, 103 patients with implanted pacemakers were monitored as they walked through a typical airport
metal detector gate.108 No EMI or adverse effect on pacemaker
function was detected. In a more recent study, 348 patients (200
with a pacemaker and 148 with an ICD) were monitored during
passage through a security gate with no evident interference to
device function.109 Patients should be advised to walk through
the gate at a normal pace if requested to do so and not to linger
in the vicinity. They should, however, alert the security staff to
the presence of the device as the metal casing of the device may
activate the alarm.
8.3.3 In some instances, passengers may also be asked to submit
to scanning using a hand-held metal detector. These typically
operate at a higher frequency than the walk-through gates
(89e133 kHz) with sinusoidal waveforms and substantially
lower field strengths of up to 6 A/m (76 mG) peak to peak.107
There has been at least one report of a spurious ICD shock
triggered by a hand-held metal detector.110 Consequently, some
reviewers have suggested that patients with ICDs request
a hand search as an alternative to use of the hand-held
detector.111 If a hand-held detector is used in a passenger with an
implanted device, it should not be held close to the implant for
longer than absolutely necessary and repeated sweeps to and fro
should be avoided.
8.3.4 Notwithstanding the remoteness of the risk of clinically
significant EMI, the US Transportation Security Administration
and some other airport authorities permit or may even recommend that patients with an implanted device who have been so
advised by their physician request a pat-down search rather than
passing through the metal detector gate or being handwanded.112 113 Bearing in mind the possibility that unadvertised
changes in screening technology might be introduced, a reasonable approach might be to reassure patients that the risk of EMI
from metal detectors is remote and suggest that they inform the
security staff of the presence of an implanted device and be
guided by them.
8.4 EMI during flight
8.4.1 The risk of EMI affecting pacemaker function in
commercial aircraft has been comprehensively assessed in the
context of pilots with pacemakers seeking recertification to
fly.114e117
8.4.2 The aircraft environment has many sources of broadband
radiation which may give rise to transients of relatively high
field strength associated with activation of aircraft equipment.
While these are a potential source of EMI, their brief duration
makes it unlikely that they would cause clinically significant
effects. Aircraft systems also include a wide variety of radiofrequency emitters in the HF, VHF and microwave bands which
present a greater theoretical hazard. Several investigators have
empirically assessed the effect of the environment in different
types of aeroplane on the function of explanted pacemakers in
a variety of test rigs. These either showed no effects or, at worst,
one or two missed pacing pulses.115 117e120
8.4.3 Experimental studies in the 1980s showed that explanted
unipolar pacemakers were susceptible to EMI at field strengths
and frequencies that might be encountered in commercial
aircraft.114 115 117 Susceptibility was greatest in the HF and VHF
bands and increased by modulation and pulsing of the radiated
signal. However, exposure of similar implanted devices showed
them to be unaffected at field strengths at which the explants
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
Fitness to fly
showed interference and failure. This provided support for the
hypothesis that shielding by body tissues offers at least some
protection against the effects of EMI. Explanted bipolar devices
were also shown to be less susceptible to EMI.
8.4.4 Since these studies were conducted, there have been
significant improvements in EMI protection of pacemakers and
ICDs, notably the widespread use of feed-through capacitors
which are most effective in the VHF and microwave bands.
8.4.5 The potential for portable electronic devices to interfere
with aircraft systems is well recognised and the potential risks
associated with the use of implanted devices in commercial
aircraft have been considered by the aviation authorities. The
risk of significant interference arising from implanted devices is
likely to be negligible and both the US Federal Aviation
Administration and the UK Civil Aviation Authority suggest
that they should be exempted from the general restriction on the
use of portable electronic devices, although policy is ultimately
determined by the individual airlines.121 122
8.4.6 Conclusion
The accumulated data suggest that the risk of clinically significant EMI affecting pacemakers or ICDs in the aeroplane environment is minimal.
8.5 Cosmic radiation
8.5.1 It has been recognised for many years that cosmic radiation
can disrupt the function of electronic devices, even at sea
level.123 The interaction of high-energy neutrons with the silicon
nuclei in the static random access memory integrated circuit of
an ICD can result in a ‘single-event upset’ that may affect the
critical software control of the device.124 The ICD architecture
incorporates internal checks that routinely screen for such
events and either correct them or, when a manufacturer-defined
threshold is reached, trigger an automated software reset. These
resets typically result in reversion from the programmed settings
to the manufacturer ’s nominal settings for the device and they
do not usually result in any significant hazard.
8.5.2 Events of this type are distinct from the very rare but more
serious disruption of ICD function due to ‘latch-up’. This causes
battery depletion, transient loss of output and hardware reset
which suspend tachycardia detection and therapy and has been
reported in relation to the effects of cosmic radiation on
a particular chip used in some specific older devices.125
8.5.3 The estimated overall frequency of ICD software resets
induced by cosmic radiation is approximately 1 in 100 over
5e6 years (V Ivans, personal communication, 2009).
8.5.4 Experimental studies have shown that single-event upsets
due to cosmic radiation are more frequent at higher altitude and
it is likely that the risk will be increased several fold during air
travel.123 The radiation exposure at typical cruising altitude is
about 100 times that on the ground.126
8.5.5 A single centre conducting ICD follow-up recently reported
three cases of single-event upsets resulting in device electrical
resets in three patients with an ICD during air travel.127 128 In
each case, time and date stamping of the event confirmed its
occurrence during a flight.
8.5.6 In the absence of other reports, this is likely to be a relatively rare phenomenon but the observation of three events in
a single follow-up clinic in as many years suggests that it may
simply be unrecognised or under-reported. Software resets often
trigger an audible patient alert, but this was overlooked by the
patient in one of the three reported cases and the reset only
came to light at a routine follow-up visit.
8.5.7 It may be prudent to alert patients with an ICD to the
possible effects of cosmic radiation, particularly when
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
a prolonged flight is planned. They may, however, be reassured
that such interactions are unlikely to have a significant effect on
the ability of the device to detect and treat life-threatening
arrhythmia.128
8.6 Vibration
8.6.1 Activity-sensing rate-adaptive pacemakers and ICDs
commonly incorporate a piezoelectric crystal or accelerometer to
detect vibration from heel strike during walking or body motion,
which is used to match the pacing rate to the user’s perceived
level of activity. These sensors may be sensitive to the effects of
external vibration during vehicular transport of any sort. The
extent and impact on pacemaker function of vibration during air
travel have been extensively investigated in devices incorporating a piezoelectric crystal sensor.117 129e131
8.6.2 A more recent study has also assessed the function of two
accelerometer-based rate-adaptive pacemakers in single-engine
fixed-wing aircraft.120 In fixed-wing aircraft, vibration levels are
generally low and unlikely to cause significant rate rises except
during take off, landing and turbulence when modest increases
in pacing rate may occur.
8.6.3 In helicopters, however, vibration levels are high
throughout the flight and sustained rises in pacing rate are seen
which might be problematic for some patients.117 129e131 The
problem may be avoided by reprogramming the device to
attenuate or disable the rate-response function prior to the
flight. In the absence of a programmer, application of a magnet
will usually disable the rate-adaptive function of a pacemaker
and cause it to switch to asynchronous pacing at an increased
rate.
8.6.4 Magnet application over an ICD will cause temporary
suspension of tachyarrhythmia detection and therapy but does
not usually affect bradycardia pacing functions.
9. DEEP VEIN THROMBOSIS (DVT) AND VENOUS
THROMBOEMBOLISM (VTE)
9.1 World scheduled airlines carried some 2.1 billion passengers
in 2006 on flights with an average duration of 2 h. This mean
value has doubled over the last 30 years due to increasingly
lengthy international sectors now spanning 12e14 h or more.
Prolonged immobility, discomfort and dehydration may
contribute to an increased risk of deep venous thrombosis (DVT)
and its significant complication venous thromboembolism
(VTE). These pathologies have a substantial morbidity and
mortality. The Olmsted County Study132 indicated an age- and
sex-corrected annual incidence of 117 per 100 000 population
while the Clinical Outcomes in the International Cooperative
Pulmonary Embolism Registry133 recorded a 3-month adjusted
mortality of 15.3%.
9.2 In 1940 Simpson134 recorded an increased incidence of
pulmonary embolism in subjects confined in air raid shelters, but
it was Homans135 who first recorded a relationship between air
travel and VTE. Symington and Stack later labelled this the
‘economy class’ syndrome.136
9.3 One and half centuries ago Virchow suggested that the
triadevenous stasis, vessel wall trauma and altered coagulationdwere implicated in venous thrombosis. Inherited
increased susceptibility to venous thrombosiseethe thrombophilic syndromesdinclude antithrombin III deficiency, protein S
deficiency, protein C mutation, hyperhomocysteinaemia, factor
V Leiden mutation and antiphospholipid antibodies. ‘Idiopathic’
venous thrombosis is associated with a 2e3-fold increased risk of
neoplasm over the succeeding 12e24 months, affecting 13.0% of
854 patients followed for 8.1 years.137
ii11
Fitness to fly
9.4 Strongly age-skewed in terms of risk, the most common
acquired comorbidities of DVT in the DVT FREE study138
included hypertension, recent surgery, immobilisation, neoplasm
and obesity. The Sirius study139 (which excluded patients
undergoing surgery within the preceding 3 weeks) found that
additional risk factors such as previous VTE, venous insufficiency, chronic heart failure, immobile standing position, pregnancy, violent effort, muscular trauma, infectious disease,
cigarette smoking and long-distance travel were significantly
more frequent in the study group than in the control group.
9.5 Seat pitch in aircraft has been an object of concern. The
House of Lords Science and Technology Committee140 recommended that the United Kingdom Civil Aviation Authority
should implement the recommendations of the Joint Aviation
Authority and require a minimum seat pitch of 28.2 in (72 cm).
This issue is now with the European Aviation Safety Agency. It
was also recommended that it worked with its Aviation Health
Unit to provide advice on the risks of travellers’ VTE.141 The
emergence of the ‘economy class’ syndrome has been the focus
of attention for worried travellers and potential litigants for
some years. In a French study,142 135.29 million passengers from
145 countries arrived at Charles de Gaulle Airport over a 7-year
period; 56 suffered confirmed pulmonary embolism. The incidence of VTE was higher in passengers who had travelled
>5000 km than in those who had travelled <5000 km (1.5 cases
per million vs 0.01 cases per million), with >4.8 cases per million
for those travelling >10 000 km (see figure 3). Similar results
were obtained by Perez-Rodriguez.143
9.6 Schwarz et al144 and Scurr et al145 both identified a significantly increased risk of isolated calf muscle thrombosis
following a long-haul flight. Thus, although there was the
persisting impression of a problem,146 there was little evidence
that the risk of such a complication is greater than when travelling in business class, first class or after prolonged travel by rail
or road. For this reason, the term ‘travellers’ thrombosis’ was
proposed by the Aerospace Medical Association.147
9.7 The WHO Research Into Global Hazards of Travel
(WRIGHT) report148: In 2001 the World Health Organization
(WHO) convened a meeting to review the scientific evidence
relating to air travel and VTE. It proposed areas for research and
further review. Participants included the International Civil
Aviation Organisation, the International Air Transport Association, the European Commission, representatives of the airlines
and other interested groups. It was felt that a link probably
existed between air travel and VTE but that this risk was not
confined to aviation. It was concluded that data were too scant
to make secure recommendations, and a number of epidemiological studies with hard end points was proposed. These, it was
hoped, would determine the absolute risk of DVT/VTE any one
flight/time-distance flown. Intermediate end points using
volunteers to review environmental and behavioural factors
were planned. The studies were funded by the UK Departments
of Transport and Health and the European Commission. A
number of associated papers have been published149e160 and the
following paragraphs summarise the principal conclusions.
9.8 The epidemiological population-based caseecontrol arm of
the MEGA study involved 1906 attendees and a similar number of
control subjects at six Dutch anticoagulant clinics. The combined
effect for travelling and the risk factors for DVT (factor V Leiden,
prothrombin 20210A mutation, body mass index (BMI) and
height) was assessed. Travelling for >4 h doubled the risk of VTE
(odds ratio 2.1, 95% CI 1.5 to 3.0) compared with not travelling,
the risk being highest in the first week after travel but persisting
for 2 months. The risk of VTE was similar to that incurred by
travelling by car, bus or train. Factor V Leiden mutation (odds ratio
8.1, 95% CI 2.7 to 24.7), height >1.90 m (odds ratio 4.7, 95% CI 1.4
to 15.4) and oral contraceptive use increased the VTE risk (estimated odds ratio >20) most notably with air travel. Short people
(<1.6 m) had an increased risk following air travel only (odds ratio
4.9, 95% CI 0.9 to 25.6). Obese subjects (BMI >30 kg/m2) were at
increased risk.
9.9 Incidence studies among a group of international employees
suggested a risk of VTE of 4.0/1000 persons/year compared with
1.2/1000 non-flying persons/year. This gave a relative risk of
VTE of 3.45 (95% CI 2.3 to 5.1) for a flight of 4 h. The risk was
increased for multiple flights and for prolonged flights. The
absolute risk of VTE in a fit person was calculated at 1/6000 for
a flight of 4 h.
9.10 A group of 2499 Dutch pilots of mean age 35.8 years did not
appear to be at higher risk of VTE than the general population.
Likewise, a hypobaric hypoxia study provided no evidence of
a prothrombotic effect in fit young volunteers following an
flight of 8 h. Coagulation and the fibrinolytic system was activated in susceptible individuals (factor V Leiden, contraceptive
use) in the travel part of the travel/non-travel immobility arm of
the study, raising the possibility of some unidentified flightspecific factor, an effect which was not reproducible following
a similar period of immobility on the ground.
Summary
Figure 3 Incidence of pulmonary embolism expressed as the number
of cases per million passengers per 2500 km travelled.142
ii12
1. Travelling for >4 h doubles the risk of VTE compared with
not travelling.
2. The risk is highest in the first week following travel but
persists for 2 months.
3. The risk is similar to that incurred by travelling by car, bus or
train over a similar period.
4. Factor V Leiden mutation, height (>1.90 m and <1.6 m) and
oral contraceptive use increase the risk of VTE, notably with
air travel. Likewise, obesity (BMI >30 kg/m2) is associated
with increased risk.
5. The relative risk of VTE is 3.45 for a flight of 4 h. This risk is
increased for multiple and for prolonged flights. The absolute
risk of VTE in a fit person is of the order of 1/6000 for a flight
of >4 h.
6. Pilots (mean age 35.8 years) do not appear to be at higher risk
of VTE than the general population.
7. Hypobaric hypoxia appears to have no prothrombotic effect
in fit young volunteers following a flight of 8 h.
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
Fitness to fly
8. Coagulation and the fibrinolytic system are activated in
susceptible individuals (factor V Leiden, contraceptive use),
with the possibility that some unidentified flight-specific
factor may contribute to an effect which is not reproduced by
a similar period of immobility on the ground.
Advice to long-distance (air) travellers (>6 h)
1. Low risk
< No history of DVT/VTE.
< No recent surgery (4 weeks).
< No other known risk factor.
It is common sense, given the foregoing, that encouragement be
given to keep mobile in so far as is possible, adopt regular flexion
and extension exercises of the lower limbs and extremities with
the avoidance of dehydration. The passenger should be wellhydrated the day before as well as on the day of the flight.
Smoking (now generally banned on aircraft) should be avoided.
Also to be avoided are alcohol and/or caffeine, which contribute
to dehydration, and hypnotics, particularly in a cramped
environment.
2. Moderate risk
< Previous history of DVT/VTE.
< Recent surgery lasting >30 min in the past 2 months but not
in the last 4 weeks.
< Known thrombophilia.
< Pregnancy.
< Obesity (BMI >30 kg/m2).
The guidance for low risk should be adopted with the addition
of compression stockings which have been shown to reduce
risk,161 although their use has given rise to adverse comment.162
3. High risk
< Recent (within 4 weeks) surgery under general anaesthesia
lasting >30 min.
< Previous DVT with known additional risk factor(s) including
known cancer.
The guidance for low and moderate risk should be adopted and
low molecular weight heparin considered (ie, subcutaneous
enoxoparin 40 mg on the morning of the flight and on the
following day).163 Although rare compared with unfractionated
heparin, complications including bleeding and thrombocytopenia can occur so it is only recommended in those at high risk.
Co-existent treatment with warfarin is protective and should
be continued. Advice should be sought for patients with
a plaster cast and consideration given towards a split cast to
relieve limb compression. Similarly, advice is needed following
recent (<2 weeks) DVT/VTE. Aspirin had no effect in one study
of the prevention of DVT during air travel146 and its use was
associated with gastrointestinal symptoms in 13% of those who
used it. It is not currently recommended in this context for
DVT/VTE prophylaxis.
required. There are many organisations that provide these
services using air ambulances which are designed specifically for
this purpose. The Association of Air Ambulances UK164 and the
Association of Air Medical Services165 represent these organisations in the UK and USA, respectively, and the Assistance
Services Medical Directors Forum166 exists in the UK to help
develop assistance and retrieval medicine.
10.3 The majority of air ambulances are helicopters which are
used predominantly for short distances, but fixed wing aircraft
including turbo prop and jet are commonly used for longer
distance flights. Air ambulances are used predominantly for
emergency transport and not for elective repatriation which is
normally done using commercial aircraft.
10.4 Successful emergency transport of acutely ill cardiac
patients is well reported for relatively short distances using helicopters167 168 and, in the Air-PAMI study,169 was shown to carry no
increased risk compared with road transport in patients with acute
myocardial infarction. Long distance transport of acutely ill
patients has also been described. Thirty years ago Incenogle170
described the successful transport of six patients in cardiogenic
shock with inotropes or intra-aortic balloon pump support for
>1000 miles.
10.5 The most common complications that occur during transport are hypotension and tachyarrhythmia and bradyarrhythmia which can be treated in the usual way providing the
appropriate equipment is on board.
10.6 This includes continuous cardiac rhythm and arterial
oxygen saturation monitoring, intravenous cannulae, fluids,
inotropes, anti-arrhythmic drugs and atropine, oxygen therapy
and the facility to intubate and ventilate as well as some form of
pacemaker device. Internal transvenous flotation-guided
temporary pacemakers require appropriate expertise for placement whereas external pacemakers do not and are probably
more suitable for standby in these circumstances. It is possible
(although unusual) for pacemakers to pace inappropriately,
especially with rotary wing aircraft (see section on pacemakers).
10.7 If an intra-aortic balloon pump is in situ it can continue to
be used in the air, but it has been noted that balloon size may
increase as a result of increasing altitude and it has been
recommended that the aortic pressure is equalised every 1000 ft
ascent to prevent overexpansion of the balloon,171 although
more modern machines may do this automatically.
10.8 Repatriation on commercial aircraft after hospitalisation for
an acute cardiac event should follow the same guidance as for
any passenger wishing to take a commercial flight.
Provenance and peer review Not commissioned; externally peer reviewed.
REFERENCES
1.
2.
10. REPATRIATION AND EMERGENCY AIR TRANSPORT OF
PATIENTS WITH ACUTE CARDIAC DISEASE
10.1 Passengers may fall ill while abroad and require air transport
home or they may be in a critical condition and require transfer
to a more suitable or better-equipped facility to continue treatment of their condition. There are concerns about the timing of
such travel after cardiac events and about the requirements for
appropriately-trained escorts and in-flight medical facilities.
10.2 It is common for patients who are very unwell or critically
ill to be transported by air from where they fall ill to a hospital
or between hospitals if urgent treatments unavailable locally are
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
3.
4.
5.
6.
7.
8.
9.
10.
Kramer MR, Jokobsen DJ, Springer C, et al. The safety of air transportation of
patients with advanced lung disease experience with 21 patients requiring
lung transplantation or pulmonary thromboendarterectomy. Chest
1995;108:1292e6.
Stoller JK, Hoisington E, Auger G. A comparative analysis of arranging in-flight
oxygen aboard commercial air carriers. Chest 1999;115:991e5.
Anon. Air travel and health: an update. House of Lords Science and Technology
Committee Report, 2007: p38.
Anon. Medical guidelines for air travel. Aviat Space Environ Med 2003;74:5.
UK Civil Aviation Authority. Assessing fitness to fly. Guidelines for medical
professionals from the Aviation Health Unit. UK Civil Aviation Authority, 2007.
Simpson C, Ross D, Dorian P, et al. CCS Consensus Conference 2003: Assessment
of the cardiac patient for fitness to drive and fly e executive summary. Can J
Cardiol 2004;20:1313e23.
Aerospace Medical Association. Medical guidelines for airline passengers.
Aerospace Medical Association, 2002.
Code of Federal Regulations Title 14 part 25.841 Washington, DC: US Government
Printing Office 1986.
European Aviation Safety Agency (EASA). Doc CS25 amendment 2 para 25.841
Cottrell JJ. Altitude exposure during aircraft flight. Chest 1988;93:81e4.
ii13
Fitness to fly
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
ii14
Kelly PT, Seccombe LM, Rogers PG, et al. Directly measured cabin pressure
conditions during Boeing 747-400 commercial aircraft flights. Respirology
2007;12:511e15.
Slonim NB, Hamilton LH. Respiratory physiology. 2nd edn. St Louis, Missouri, USA:
C V Mosby, 1971.
Sorbini CA, Grassi V, Solinas E, et al. Arterial oxygen tension in relation to age in
healthy adults. Respiration 1968;25:3e13.
Cottrell JJ, Lebovitz B, Fennell RG, et al. In flight arterial saturation: continuous
monitoring by pulse oximetry. Aviat Space Environ Med 1995;66:126e30.
Heistad DD, Abboud FM. Circulatory adjustments to hypoxia. Circulation
1980;61:463e70.
Vatner SF, Rutherfor JD. Control of the myocardial contractile state by carotid
chemo-and baroreceptor and pulmonary inflation reflexes in conscious dogs. J Clin
Invest 1978;61:1593e601.
Lugliani F, Whipp BJ, Wasserman K. A role for the carotid body in cardiovascular
control in man. Chest 1973;63:744e50.
Pelletier CL. Circulatory responses to graded stimulation of the carotid
chemoreceptors in dogs. Circ Res 1972;31:431.
Von Euler US, Liljestrand G. Observations on the pulmonary arterial blood pressure
in the cat. Acta Physiol Scand 1946;12:301e20.
Hultgren HN. Effects of altitude upon cardiovascular diseases. J Wilderness Med
1992;3:301e8.
Bartsch P, Gibbs SR. Effect of altitude on the heart and lung. Circulation
2007;116:2191e202.
De Burgh Daly M, Scott MJ. An analysis of the primary cardiovascular reflex
effects of stimulation of the carotid body chemoreceptors in the dog. J Physiol
1962;162:555e73.
Cutaia M, Rounds S. Hypoxic pulmonary vasoconstriction: physiologic significance,
mechanism and clinical relevance. Chest 1990;97:706e18.
Dillard Ewald F. The use of pulmonary function testing in piloting, air travel,
mountain climbing, and diving. Clin Chest Med 2001;22:803.
Phillips BA, McConnell JW, Smith MD. The effects of hypoxaemia on cardiac
output. A dose response curve. Chest 1988;93:471e5.
Veglio M, Maule S, Cametti G. The effects of exposure to moderate altitude
on cardiovascular autonomic function in normal adults. Clin Auton Res
1999;9:123e7.
Thomson AJ, Drummond GB, Waring WS, et al. Effects of short-term isocapnic
hyperoxia and hypoxia on cardiovascular function. J Appl Physiol 2006;101:809e16.
Wyss CA, Koepfli P, Fretz G, et al. Influence of altitude exposure on coronary flow
reserve. Circulation 2003;108:1202.
Pohl U, Busse R. Hypoxia stimulates release of endothelium derived relaxant factor.
Am J Physiol 1989;256:H1595e600.
Hobkirk J, Damy T, Bennett A, et al. Effects of reduced inspired oxygen
concentration in patients with chronic heart failure (abstract). Proceedings of ESC
2009.
Ideal Cabin Environment study.
Agostini P, Cattadori G, Guazzi M, et al. Effects of simulated altitude-induced
hypoxia on exercise in patients in chronic heart failure. Am J Med
2000;109:450e5.
Kujanik S, Snincak M, Galajdova K, et al. Cardiovascular changes during sudden
ascent in a cable cabin to moderate altitude. Physiol Res 2000;49:729e31.
Malconian M, Rock P, Hultgren H, et al. The electrocardiogram at rest and
exercise during a simulated ascent of Mt Everest (Operation Everest II). Am J
Cardiol 1990;65:1475e80.
Westerholm CJ. Threshold studies in transvenous cardiac pacemaker treatment.
Direct measurement with special reference to short and long term stimulation and
influence of certain metabolic, respiratory and pharmacological factors. Scand J
Thorac Cardiovasc Surg Suppl 1971;8:1e35.
Weilenmann D, Duru F, Schönbeck M, et al. Influence of acute exposure to high
altitude and hypoxemia on ventricular stimulation thresholds in pacemaker patients.
PACE 2000;23:512e15.
Siedler K, Kreutzberger R, Menold E, et al. Acute normobaric hypoxia (FIO2¼0.12)
does not enhance exercise-induced thrombin and fibrin formation. Int J Sports Med
2002;23:S120.
Le Roux G, Larmignat P, Marchal M, et al. Haemostasis at high altitude. Int J
Sports Med 1992;13:S49e51.
Mannucci PM, Gringeri A, Peyvandi F, et al. Short-term exposure to high altitude
causes coagulation activation and inhibits fibrinolysis. Thromb Haemost
2002;87:342e3.
Crosby A, Talbot NP, Harrison P, et al. Relation between acute hypoxia and
activation of coagulation in human beings. Lancet 2003;361:2207e8.
Hodkinson PD, Hunt BJ, Parmar K, et al. Is mild normobaric hypoxia a risk factor
for venous thromboembolism? J Thromb Haemost 2003;1:2131e3.
Toff WD, Jones CI, Ford I, et al. Effect of hypobaric hypoxia, simulating conditions
during long-haul air travel, on coagulation, fibrinolysis, platelet function, and
endothelial activation. JAMA 2006;295:2251e61.
Schreijer AJM, Cannegieter SC, Meijers JCM, et al. Activation of coagulation
system during air travel: a cross over study. Lancet 2006;367:832e8.
Dowdall N. Customer health: a new role for occupational physicians. Occup Med
2003;53:19e23.
Van Gerwen LJ, Diekstra RF. Fear of flying treatment programs for passengers: an
international review. Aviat Space Environ Med 2000;71:430e7.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
70.
71.
72.
73.
74.
75.
76.
Ito H, Lee D. Assessing the effect of September 11th terrorist attacks on US airline
demand. J Econ Business 2005;57:75e95.
Folkes VS, Kaletsky S, Graham JL. A field study of causal inferences and consumer
reaction: the view from the airport. J Consumer Res 1987;13:534e9.
Strike PC, Steptoe A. A systematic review of mental stress-induced myocardial
ischaemia. Eur Heart J 2003;24:690e703.
Hu K, Ivanov PCh, Hilton MF, et al. Endogenous circadian rhythm in an index of
cardiac vulnerability independent of changes in behavior. Proc Natl Acad Sci USA
2004;101:18223e7.
Knutson A. Health disorders of shift workers. Occup Med 2003;53:103e8.
Kerut EK, Winterton J, Roffidal L, et al. Congestive heart failure: influence of
hypertension with or without diabetes mellitus on circadian variation in autonomic
balance. Am J Hypertens 1995;8:174A.
Carson PM, O’Connor CM, Miller AB, et al. Circadian rhythm and sudden death in
heart failure: results from prospective randomised amplodipine survival trial. J Am
Coll Cardiol 2000;36:541e6.
Boersma E, Pieper KS, Steyerberg EW, et al. Predictors of outcome in patients
with acute coronary syndromes without persistent ST-segment elevation. Results
from an international trial of 9461 patients. The PURSUIT Investigators. Circulation
2000;101:2557e67.
Califf RM, Pieper KS, Lee KL, et al. Prediction of 1-year survival after thrombolysis
for acute myocardial infarction in the global utilization of streptokinase and TPA for
occluded coronary arteries trial. Circulation 2000;101:2231e8.
Granger CB, Goldberg RJ, Dabbous O, et al. Predictors of hospital mortality
in the global registry of acute coronary events. Arch Intern Med
2003;163:2345e53.
Morrow DA, Antman EM, Giugliano RP, et al. A simple risk index for rapid initial
triage of patients with ST-elevation myocardial infarction: an InTIME II substudy.
Lancet 2001;358:1571e5.
Dorsch MF, Lawrance RA, Sapsford RJ, et al. A simple benchmark for evaluating
quality of care of patients following acute myocardial infarction. Heart 2001;86:150e4.
Kurz DJ, Bernstein A, Hunt K, et al. Simple point-of-care risk stratification in acute
coronary syndromes: the AMIS model. Heart 2009;95:662e8.
Zahger D, Leibowitz D, Tabb IK, et al. Long-distance air travel soon after an acute
coronary syndrome: a prospective evaluation of a triage protocol. Am Heart J
2000;140:241e2.
Cox GR, Peterson T, Bouchel L, et al. Safety of commercial air travel following
myocardial infarction. Aviat Space Environ Med 1996;67:976e82.
Thomas MD, Hinds R, Walker C, et al. Safety of aeronautical repatriation after
myocardial infarction: a retrospective study. Heart 2006;92:1864e5.
Roby H, Lee A, Hopkins A. Safety of air travel following acute myocardial infarction
Aviat Space Environ Med 2002;73:91e6.
Essebag V, Lutchmedial S, Churchill-Smith M. Safety of long distance aeromedical
transport of the cardiac patient: a retrospective study. Aviat Space Environ Med
2001;72:182e7.
Myocardial Infarction National Audit Project (MINAP). 2004.
Heggunje PS, Harjal KJ, Stone GW, et al. Procedural success versus clinical risk
status in determining discharge of patients after primary angioplasty for acute
myocardial infarction. J Am Coll Cardiol 2004;44:1400e7.
deLuca G, Suryapranata H, van’t Hof AWJ, et al. Prognostic assessment of
patients with acute myocardial infarction treated with primary angioplasty.
Implications for early discharge. Circulation 2004;109:2737e43.
Ludman PF. British Cardiovascular Intervention Society (BCIS) audit returns for
2007. http://www.bcis.org.uk/resources/documents/BCIS%20Audit%20web.pdf.
Van de Verf F, Bax J, Betriu A, et al. for the Task Force of the European Society of
Cardiology. Management of acute myocardial infarction for patients presenting with
persistent ST segment elevation. Eur Heart J 2008;29:2909e45.
Jan K, Madsen JK, Peer G, Saunamäki K, et al. Danish multicenter randomized
study of invasive versus conservative treatment in patients with inducible ischemia
after thrombolysis in acute myocardial infarction (DANAMI). Circulation
1997;96:748e55.
National Institute for Health and Clinical Excellence (NICE). Guidance on
implantable defibrillator and arrhythmia. London: NICE, 2006.
Task Force of the European Society of Cardiology. Guideline for the diagnosis
and treatment of non ST elevation acute coronary syndromes. Eur Heart J
2007;28:1598e660.
Ludman PF. British Cardiovascular Intervention Society audit returns 2007 and
2008. http://www.bcis.org.uk/resources/audit.
Abbas AE, Brodie B, Dixon S, et al. Incidence and prognostic impact of
gastrointestinal bleeding after percutaneous coronary intervention for acute
myocardial infarction. Am J Cardiol 2005;96:173e6.
Berkowitz SD, Granger CB, Pieper KS, et al. for the Global Utilization of Streptokinase
and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) I
Investigators. Incidence and predictors of bleeding after contemporary thrombolytic
therapy for myocardial infarction. Circulation 1997;95:2508e16.
Buresly K, Eisenberg MJ, Zhang X, et al. Bleeding complications associated with
combinations of aspirin, thienopyridine derivatives, and warfarin in elderly patients
following acute myocardial infarction. Arch Intern Med 2005;165:784e9.
Lewis EF, Velazquez EJ, Solomon SD, et al. Predictors of the first heart failure
hospitalization in patients who are stable survivors of myocardial infarction
complicated by pulmonary congestion or left ventricular dysfunction: a VALIANT
study. Eur Heart J 2008;29:748e56.
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
Fitness to fly
77.
78.
79.
80.
81.
82.
83.
84.
85.
86.
87.
88.
89.
90.
91.
92.
93.
94.
95.
96.
97.
98.
99.
100.
101.
102.
103.
104.
105.
106.
Eisenmenger V. Die angeborenen Defekte der Kammerscheidewande des
Herzens. Zeitschr. Klin Med 1897;32:1e28.
Partin C. The evolution of Eisenmenger’s eponymic enshrinement. Am J Cardiol
2003;92:1187e91.
Harinck E, Hutter PA, Hoorntje TM, et al. Air travel and adults with cyanotic
congenital heart disease. Circulation 1996;93:272e6.
Broberg CS, Uebing A, Cuomo L, et al. Adult patients with Eisenmenger syndrome
report flying safely on commercial aircraft. Heart 2007;93:1599e603.
Duke M, Abelmann WH. The hemodynamic response to chronic anemia. Circulation
1969;39:503e13.
Roy SB, Bhatia ML, Mathur VS, et al. Hemodynamic effects of chronic severe
anemia. Circulation 1963;28:346e56.
Weiskopf RB, Viele MK, Feiner J, et al. Human cardiovascular and metabolic
response to acute, severe isovolemic anemia. JAMA 1998;279:217e21.
Roig E, Betriu A, Castaner A, et al. Disabling angina pectoris with normal coronary
arteries in patients undergoing long-term hemodialysis. Am J Med 1981;71:431e4.
Case RB, Berglund E, Sarnoff SJ. Ventricular function. Changes in coronary
resistance and ventricular function resulting from acutely induced anemia and the
effect thereon of coronary stenosis. Am J Med 1955;18:397e405.
Cromie N, Lee C, Struthers AD. Anaemia in chronic heart failure: what is its
frequency in the UK and its underlying causes? Heart 2002;87:377e8.
Silverberg DS, Wexler D, Sheps D, et al. The effect of correction of mild anemia in
severe, resistant congestive heart failure using subcutaneous erythropoietin and
intravenous iron: a randomized controlled study. J Am Coll Cardiol
2001;37:1775e80.
Levy PS, Kim SJ, Eckel PK, et al. Limit to cardiac compensation during acute
isovolemic hemodilution: Influence of coronary stenosis. Am J Physiol
1993;265:H340e9.
Lee PC, Kini AS, Chowdhury A, et al. Anemia is an independent predictor of
mortality after percutaneous coronary intervention. J Am Coll Cardiol
2004;44:541e6.
Koch CG, Weng Y, Zhou SX, et al. Prevalence of risk factors, and not gender per
se, determines short- and long-term survival after coronary artery bypass surgery.
J Cardiothorac Vasc Anesth 2003;17:585e93.
Chauhan A, Grace AA, Newell SA, et al. Early complications after dual chamber
versus single chamber pacemaker implantation. PACE 1994;17:2012e15.
Aggarwal RK, Connelly DT, Ray SG, et al. Early complications of permanent
pacemaker implantation: no difference between dual and single chamber systems.
Heart 1995;73:571e5.
British Thoracic Society Standards of Care Committee. Managing passengers
with respiratory disease planning air travel. British Thoracic Society
recommendations. http://www.brit-thoracic.org.uk/Portals/0/Clinical%
20Information/Air%20Travel/Guidelines/FlightRevision04.pdf (accessed
2 Jan 2009).
Dorbala S, Cohen AJ, Hutchinson LA, et al. Does radiofrequency ablation induce
a prethrombotic state? Analysis of coagulation system activation and comparison to
electrophysiologic study. J Cardiovasc Electrophysiol 1998;9:1152e60.
Chen JY, Chang KC, Lin YC, et al. Safety and outcomes of short-term multiple
femoral venous sheath placement in cardiac electrophysiological study and
radiofrequency catheter ablation. Jpn Heart J 2004;45:257e64.
Scheinman MM, Huang S. The 1998 NASPE prospective catheter ablation
registry. PACE 2000;23:1020e8.
Greene T, Huang S, Wagshal A, et al. Cardiovascular complications after RF
catheter ablation of supraventricualr tachyarrhythmias. Am J Cardiol
1994;74:615e17.
Hindricks G. The Multicentre European RF Survey (MERFS): complications of RF
catheter ablation of arrhythmias. The Multicentre European RF Survey (MERFS)
investigators of the Working Group on Arrhythmias of the European Society of
Cardiology. Eur Heart J 1993;14:1644e53.
Antiplatelet Trialists’ Collaboration. Collaborative overview of randomised trials
of antiplatelet therapy III. Reduction in venous thrombosis and pulmonary embolism
by antiplatelet prophylaxis among surgical and medical patients. BMJ
1994;308:235e46.
Blanc JJ, Almendral J, Brignole M, et al. Scientific Initiatives Committee of the
European Heart Rhythm Association. Consensus document on antithrombotic
therapy in the setting of electrophysiological procedures. Europace
2008;10:513e27.
Harold L, Lazar HL, Fitzgerald CA, et al. Early discharge after coronary artery bypass
graft surgery: are patients really going home earlier? J Thorac Cardiovasc Surg
2001;121:943e50.
Beggs VL, Birkemeyer NJ, Nugent WC, et al. Factors related to rehospitalization
within thirty days of discharge after coronary artery bypass grafting. Best Pract
Benchmarking Healthc 1996;1:180e6.
Network Devices Survey Group. Pacemakers and implantable defibrillators:
UK National Survey 2006 (version 2.1). London: Department of Health, 2008.
http://www.devicesurvey.com (accessed 2 Jan 2009).
Irnich W. Electronic security systems and active implantable medical devices.
Pacing Clin Electrophysiol 2002;25:1235e58.
Rokas S, Crick JCP, Sowton E. Does pacemaker dependence exist? Br Heart J
1981;45:340.
Stevenson RA. Design and application of broadband ceramic feedthrough
capacitor EMI filters to cardiac pacemakers and implantable defibrillators.
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091
107.
108.
109.
110.
111.
112.
113.
114.
115.
116.
117.
118.
119.
120.
121.
122.
123.
124.
125.
126.
127.
128.
129.
130.
131.
132.
133.
134.
135.
136.
137.
138.
139.
Proceedings 19th International Conference, IEEE Engineering in Medicine and
Biology Society 1997;6:2558e62.
Boivin W, Coletta J, Kerr L. Characterization of the magnetic fields around walkthrough and hand-held metal detectors. Health Phys 2003;84:582e93.
Copperman Y, Zarfati D, Laniado S. The effect of metal detector gates on
implanted permanent pacemakers. Pacing Clin Electrophysiol 1988;11:1386e7.
Kolb C, Schmieder S, Lehmann G, et al. Do airport metal detectors interfere with
implantable pacemakers or cardioverter-defibrillators? J Am Coll Cardiol
2003;41:2054e9.
Pinski SL, Trohman RG. Interference in implanted cardiac devices, Part I. Pacing
Clin Electrophysiol 2002;25:1367e81.
Possick SE, Barry M. Evaluation and management of the cardiovascular patient
embarking on air travel. Ann Intern Med 2004;141:148e54.
Transportation Security Administration (TSA). Travelers with Disabilities and
Medical Conditions: Pacemakers, Defibrillators, Other Implanted Medical Devices,
and Metal Implants. http://www.tsa.gov/travelers/airtravel/specialneeds/
editorial_1374.shtm (accessed 2 Jan 2009).
BAA. http://www.baa.com/portal/controller/dispatcher.jsp?ChPath¼Global%
5EMisc%5ESearch&searchChannel¼Global&queryString¼pacemaker (accessed 2
Jan 2009).
Toff WD, Deller AGMcC, Hobbs RA, et al. Radiofrequency interference with
pacemaker function in the aircraft environment. New Trends in Arrhythmias
1988;III/IV:777e80.
Toff WD, Camm AJ. Implanted devices and aviation. Eur Heart J
1988;9(Suppl G):133e8.
Deller AGMcC, Toff WD, Hobbs RA, et al. The development of a system for the
evaluation of electromagnetic interference with pacemaker function: hazards in the
aircraft environment. J Med Eng Technol 1989;13:161e5.
Toff WD. Cardiac pacemaker function in the aviation environment. MD thesis.
London: University of London, 1994.
Carleton RA, Sessions RW, Graettinger JS. Environmental influence on implantable
cardiac pacemakers. JAMA 1964;190:938e40.
Brown JH, Carter ET, Silverstein MN, et al. Would you fly with these pilots?
Aerospace Med 1973;44:786e93.
De Rotte AA, Van Der Kemp P. Electromagnetic interference in pacemakers in
single-engine fixed-wing aircraft: a European perspective. Aviat Space Environ Med
2002;73:179e83.
Federal Aviation Administration. Use of portable electronic devices aboard
aircraft. Advisory Circular AC 91e21.1B. 8/25/06. http://rgl.faa.gov/
Regulatory_and_Guidance_Library/rgAdvisoryCircular.nsf/list/AC%2091.21-1B/
$FILE/AC%2091.21-1B.pdf (accessed 2 Jan 2009).
Civil Aviation Authority. Portable electronic devices. 2009. http://www.caa.co.uk/
default.aspx?catid¼1770&pagetype¼90&pageid¼9853 (accessed 2 Jan 2009).
Ziegler JF, Curtis HW, Muhlfeld HP, et al. IBM experiments in soft fails in computer
electronics 1978e1994. IBM J Res Develop 1996;40:3e18.
Bradley PD, Normand E. Single event upsets in implantable cardioverter
defibrillators. IEEE Trans Nucl Sci 1998;45:2929e40.
St Jude Medical Inc. Physician communication: important physician advisory. 2005.
http://www.sjm.com/companyinformation/physicianletter.html (accessed 2 Jan 2009).
World Health Organization. Information sheet Nov. 2005: Cosmic radiation and
air travel. http://who.int/ionizing_radiation/env/cosmic/en/print.html (accessed 2
Jan 2009).
Ferrick AM, Bernstein N, Aizer A, et al. Cosmic radiation induced software
electrical resets in ICDs during air travel. Heart Rhythm 2008;5:1201e3.
Bhakta D, Foreman LD. Cosmic radiation: not science fiction but clinical reality.
Heart Rhythm 2008;5:1204e5.
French RS, Tillman JG. Pacemaker function during helicopter transport. Ann Emerg
Med 1989;18:305e7.
Gordon RS, O’Dell KB. Activity-sensing permanent internal pacemaker dysfunction
during helicopter aeromedical transport. Ann Emerg Med 1990;19:1260e3.
Toff WD, Leeks C, Joy M, et al. The effect of aircraft vibration on the function of an
activity-sensing pacemaker. Br Heart J 1987;57:573e4.
Silverstein MD, Heit JA, Mohr DN, et al. Trends in the incidence of deep vein
thrombosis and pulmonary embolism.A 25-year population-based study. Arch Intern
Med 1998;158:585e93.
Goldhaber SZ, Visani L, De Rosa M. Pulmonary embolism: clinical outcomes in the
International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet
1999;353:1386e9.
Simpson K. Shelter deaths from pulmonary embolism. Lancet 1940;2:744.
Homans J. Thrombosis of the deep leg veins due to prolonged sitting. N Engl J
Med 1954;250:148e9.
Symington IS, Stack BHR. Pulmonary thromboembolism after travel. Br J Dis Chest
1977;71:138e40.
Schulman S, Lindmarker P. Incidence of cancer after prophylaxis with warfarin
against recurrent venous thromboembolism for the Duration of Anticoagulation Trial.
N Engl J Med 2000;342;1953e8.
Goldhaber SZ, Tapson VF. DVT FREE Steering Committee. A prospective registry of
5,451 patients with ultrasound-confirmed deep vein thrombosis. Am J Cardiol
2004;93:259e62.
Meyer-Michel S. for the Sirius Study Group. Epidemiologic study of risk factors for
deep vein thrombosis in medical outpatients. The Sirius Study. Arch Intern Med
2000;160:3415e20.
ii15
Fitness to fly
140.
141.
142.
143.
144.
145.
146.
147.
148.
149.
150.
151.
152.
153.
154.
155.
ii16
Anon. Air travel and health: an update. HL 7, House of Lords Science and
Technology Committee. London: The Stationery Office, 2008.
Civil Aviation Authority. http://www.caa.co.uk/docs/923/FitnessToFlyPDF_
FitnesstoFlyPDF%20Feb%2009.pdf.
Lapostolle F, Surget V, Borron SW, et al. Severe pulmonary embolism associated
with air travel. N Engl J Med 2001;345:779e83.
Perez-Rodriguez E, Jimenez SJ, Diaz G, et al. Incidence of air travel-related
pulmonary embolism at the Madrid-Barajas airport. Arch Intern Med
2003;163:2766e70.
Schwarz T, Siegert G, Oettler W, et al. Venous thrombosis after long haul flights.
Arch Intern Med 2003;163:2759e64.
Scurr JH, Machin SJ, Bailey-King S, et al. Frequency and prevention of
symptomless deep venous thrombosis in long haul flights: a randomised trial. Lancet
2001;357:1485e9.
Hughes R, Heuser T, Hill S, et al. Recent air travel and venous thrombo-embolism
resulting in hospital admission. Respirology 2006;111:75e9.
Aerospace Medical Association Medical Guideline Task Force. Medical
guidelines for airline travel, 2nd ed. Aviat Space Environ Med 2003;74 Section II:
A1eA12.
The WRIGHT Project Study Group. WHO Research Into Global Hazards of Travel
(WRIGHT) Project: final report of phase 1. World Health Organization, 2007. http://
www.who.int/cardiovascular_diseases/wright_project/phase1_report/WRIGHT%
20REPORT.pdf.
Cannegieter SC, Doggen CJ, van Houwelingen HC, et al. Travel-related venous
thrombosis: results from a large population-based case control study (MEGA Study).
PLoS Med 2006;3:e307.
Coppens M, van Doormaal FF, Schreijer AJ, et al. Intermittent mechanical
compression for prevention of travellers’ thrombosis. J Thromb Haemost
2006;4:1836e8.
Kuipers S, Cannegieter SC, Middeldorp S, et al. Use of preventive measures for air
travel-related venous thrombosis in professionals who attend medical conferences.
J Thromb Haemost 2006;4:2373e6.
Levi M, Rosendaal FR, Büller HR. Deep vein thrombosis and pulmonary embolism
due to air travel. Ned Tijdschr Geneeskd 2006;150:2474e8.
Rosendaal FR, Cannegieter SC. Vliegen entrombose. In: Keeman JN, de Leeuw
PW, Mazel JA, Zitman FG (eds). Het medisch jaar. Bohn Stafleu van Lughum,
Houten, 2004:224e32.
Rosendaal FR. Venous thrombosis: the role of genes, environment, and behavior.
Hematology Am Soc Hematol Educ Program 2005;1e12.
Rosendaal FR. Interventions to prevent venous thrombosis after air travel: are they
necessary? J Thromb Haemost 2006;4:2306e7.
156.
157.
158.
159.
160.
161.
162.
163.
164.
165.
166.
167.
168.
169.
170.
171.
172.
Schreijer AJ, Cannegieter SC, Rosendaal FR. Effect of prolonged sitting on
thrombin generation: not evidenced yet: rebuttal. J Thromb Haemost 2003;1:2700.
Schreijer AJ, Cannegieter SC, Rosendaal FR, et al. A case of thrombosis at high
altitude. Thromb Haemost 2005;94:1104e5.
Schreijer AJ, Cannegieter SC, Meijers JC, et al. Activation of coagulation system
during air travel: a crossover study. Lancet 2006;367:832e8.
Schreijer A, Cannegieter SC, Büller HR, et al. Activation of coagulation system
during air travel (authors’ reply). Lancet 2006;368:26.
Toff WD, Jones CI, Ford I, et al. Effect of hypobaric hypoxia, simulating conditions
during long-haul air travel, on coagulation, fibrinolysis, platelet function, and
endothelial activation. JAMA 2006;295:2251e61. Erratum in: JAMA 2006;
296:46
Belcaro G, Geroulakos G, Nicolaides AN, et al. Venous thromboembolism from air
travel: the LONFLIT study. Angiology 2001;52:369e74.
Campbell C, Rayner CFJ. Guidelines on prevention of venous thrombo-embolism on
long haul flights. Thorax 2003;58:91e2.
Cesarone MR, Belcaro G, Nicolaides AN, et al. Venous thrombosis from air
travel: the LONFLIT3 study - prevention with aspirin vs. low-molecular-weight
heparin (LMWH) in high-risk subjects: a randomized trial. Angiology
2002;53:1e6.
Association of Air Ambulances UK. http://www.airambulanceassociation.co.uk.
Association of Air Medical Services (AAMS). http://www.aams.org.
Assistance Services Medical Directors Forum (ASMDF). http://www.ASMDF.org.
Bellinger R, Califf R, Mark D, et al. Helicopter transport of patients during acute
myocardial infarction. Am J Cardiol 1988;61:718e22.
Topol E, Fung A, Kline E. Safety of helicopter transport and out-of-hospital
intravenous fibrinolytic therapy in patients with evolving myocardial infarction.
Catheter Cardiovasc Diag 1986;12:151e5.
Grines CL, Westerhausen DR, Grines LL, et al. A randomized trial of transfer for
primary angioplasty versus on-site thrombolysis in patients with high-risk myocardial
infarction: the air primary angioplasty in myocardial infarction study. J Am Coll
Cardiol 2002;39:1713e19.
Incenogle T. Long distance transport of cardiac patients in extremis: the Mobile
Intensive care (MOBI) concept. Aviat Space Environ Med 1988;59:571e4.
Mertlich G, Quall S, Borgmeier P, et al. Effect of increased intra-aortic balloon
pressure on catheter volume: relationship to changing altitudes. Crit Care Med
1992;20:297e303.
Committee on Air Quality in Passenger Cabins of Commercial Aircraft. The
airliner cabin environment and the health of passengers and crew. Board on
Environmental Studies and Toxicology Division on Earth and Life Studies, National
Research Council. Washington, DC: National Academy Press, 2002.
Heart 2010;96:ii1eii16. doi:10.1136/hrt.2010.203091