AIR TRAVEL FOR INFANTS WITH CONGENITAL HEART DISEASE

Abstract

INTRODUCTION
:
It
is
well
documented
that,
healthy
person
can
tolerate
the
cabin
environment
of
a
commercial
airline
which
is
pressurized
to
the
level
of
5000
ft.
however
this
environment
brings
profound
physiological
changes
in
patients
with
cardiovascular
dise
a
se.
With
rise
in
number
of
patients
travelling
internationally
for
treatment
of
cardiac
problems
especially
infants
travelling
by
air
for
congenital
heart
disease
treatment
has
increased
in
the
recent
time
and
is
evident
by
the
reports
of
medical
incidents
involving
infants
with
congenital
heart
disease
onboard
.
(1)
Though
the
IATA
medical
manual
mentions
that
adult
patients
with
Esenminger
Syndrome
should
not
undertake
air
travel
.
(2)
This
article
examines
the
case
for
infants
with
congenital
heart
diseases
as
there
have
been
no
previous
studies
reported

Full text

ORIGINAL ARTICLE
J of Evidence Based Med & Hlthcare, pISSN- 2349-2562, eISSN- 2349-2570/ Vol. 2/Issue 5/Feb 02, 2015 Page 522
AIR TRAVEL FOR INFANTS WITH CONGENITAL HEART DISEASE
Adarsh M. Patil1
HOW TO CITE THIS ARTICLE:
Adarsh M. Patil. ”Air travel for infants with congenital heart Disease”. Journal of Evidence based Medicine
and Healthcare; Volume 2, Issue 5, February 02, 2015; Page: 522-527.
ABSTRACT: INTRODUCTION: It is well documented that, healthy person can tolerate the
cabin environment of a commercial airline which is pressurized to the level of 5000 ft. however
this environment brings profound physiological changes in patients with cardiovascular disease.
With rise in number of patients travelling internationally for treatment of cardiac problems
especially infants travelling by air for congenital heart disease treatment has increased in the
recent time and is evident by the reports of medical incidents involving infants with congenital
heart disease onboard.(1) Though the IATA medical manual mentions that adult patients with
Esenminger Syndrome should not undertake air travel.(2) This article examines the case for infants
with congenital heart diseases as there have been no previous studies reported.
KEYWORDS: Air travel for congenital heart disease.
INTRODUCTION: METHOD: A retrospective analysis of data collected from airline Pertaining to
the number of infants with congenital heart disease transported, nature of the congenital heart
disease and the subsequent outcome. Data was collected from 5 major airline operating in India.
PHYSIOLOGICAL ASPECTS OF AIR TIRAVEL: The primary difference between the aircraft
environment and the ground environment relates to the atmosphere. Contrary to popular belief,
modern aircraft are not pressurized to sea level equivalent. Instead, on most flights the cabin
altitude will be between 5000 and 8000 ft. (1524 m and 2438 m). This results in reduced
barometric pressure with a concomitant decrease in partial pressure of oxygen (PO2). While the
barometric pressure is 760 mm Hg at sea level with a corresponding PaO2 (arterial O2 pressure)
of 98 mm Hg, the barometric pressure at 8000 ft. will be 565 mm Hg with PaO2 of about 55 mm
Hg.(3) If these last data are plotted on the oxyhemoglobin dissociation curve, we obtain a blood
oxygen saturation of 90% at. Although most healthy travellers can normally compensate for this
amount of hypoxemia, this may not be true for coronary, pulmonary, cerebrovascular, and
anaemic patients. Because these patients may already have a reduced PaO2 on the ground,
further reduction in aircraft cabin pressure will bring them to the steep part of the oxyhemoglobin
dissociation curve with a resultant very low saturation, which could cause distress and/or
exacerbation of their illness
BREIF OF CONGENITAL HEART DISEASE:
INCIDENCE: Congenital heart disease occurs in approximately 8 of 1,000 live births. The
incidence is higher among stillborns (2%), aborts (10}–25%), and premature infants (about 2%)

ORIGINAL ARTICLE
J of Evidence Based Med & Hlthcare, pISSN- 2349-2562, eISSN- 2349-2570/ Vol. 2/Issue 5/Feb 02, 2015 Page 523
TABLE 1:
Lesions % of All Lesions
-
Ventricular septal defect 25–30
Atrial septal defect (secundum) 6–8
Patent ductus arteriosus 6–8
Coarctation of aorta 5–7
Tetralogy of Fallot 5–7
Pulmonary valve stenosis 5–7
Aortic valve stenosis 4–7
D–Transposition of great arteries 3–5
Hypoplastic left ventricle 1–3
Hypoplastic right ventricle 1–3
Truncus arteriosus 1–2
Total anomalous pulmonary venous return 1–2
Triscuspid atresia 1–2
Single ventricle 2
Double–outlet right ventricle 1–2
Others 5–10
-
*Excluding patent ductus arteriosus in preterm neonate, bicuspid aortic valve, peripheral
pulmonic stenosis, mitral valve prolapse.
CLASSIFICATION: First, congenital cardiac defects can be divided into two major groups based
on the presence or absence of cyanosis,.
CYANOTIC CONGENITAL HEART LESIONS: This group of congenital heart lesions can also
be further divided based on pathophysiology: whether pulmonary blood flow is decreased or
increased
CYANOTIC LESIONS WITH DECREASED PULMONARY BLOOD FLOW: These lesions must
include both an obstruction to pulmonary blood flow (at the tricuspid valve, right ventricular, or
pulmonary valve level) and a pathway by which systemic venous blood can shunt right to left and
enter the systemic circulation (via a patent foramen ovale, ASD, or VSD). Common lesions in this
group include tricuspid atresia, tetralogy of Fallot, and various forms of single ventricle with
pulmonary stenosis. In these lesions, the degree of cyanosis depends on the degree of
obstruction to pulmonary blood flow.
CYANOTIC LESIONS WITH INCREASED PULMONARY BLOOD FLOW: In this group of
lesions, there is no obstruction to pulmonary blood flow. Cyanosis is caused by either abnormal
ventricular-arterial connections or by total mixing of systemic venous and pulmonary venous
blood within the heart. Transposition of the great vessels (TGV) is the most common of the

ORIGINAL ARTICLE
J of Evidence Based Med & Hlthcare, pISSN- 2349-2562, eISSN- 2349-2570/ Vol. 2/Issue 5/Feb 02, 2015 Page 524
former group of lesions. In TGV, the aorta arises from the right ventricle and the pulmonary
artery from the left ventricle. The total mixing lesions include those cardiac defects with a
common atria or ventricle, total anomalous pulmonary venous return, and truncus arteriosus.
ACYANOTIC CONGENITAL HEART LESIONS: Acyanotic congenital heart lesions can be
further classified according to the predominant physiologic load they place on the heart as the
lesion producing increased volume load and lesion producing pressure load.
LESIONS RESULTING IN INCREASED VOLUME LOAD: The most common lesions in this
group are those that cause left-to-right shunts: atrial septal defect (ASD), ventricular septal
defect (VSD), atrioventricular septal defects (AVSD, AV canal), and patent ductus arteriosus
(PDA).
The pathophysiologic common denominator in this group is a communication between the
systemic and pulmonary sides of the circulation, resulting in the shunting of fully oxygenated
blood back into the lungs. The direction and magnitude of the shunt across such a
communication depends on the size of the defect and the relative pulmonary and systemic
pressures and pulmonary and systemic vascular resistances.
LESIONS RESULTING IN INCREASED PRESSURE LOAD: The pathophysiologic common
denominator of these lesions is an obstruction to normal blood flow. The most common are
obstructions to ventricular outflow: valvar pulmonic stenosis, valvar aortic stenosis, and
coarctation of the aorta. Unless the obstruction is severe, cardiac output will be maintained and
symptoms of heart failure will be either subtle or absent.
DISCUSSION: Thought the effects of cabin environment on congenital heart disease are
obvious the reasons many of them travel are lack of awareness among the physicians, Anxiety of
parents for quick treatment and non-availability of published data.
The effect of cabin environment will not only depend on the duration of the exposure but
also severity of the disease.(4) These factors are dynamic and may change dramatically with:
Pressure changes during the assent or descent of the aircraft; physiological changes in a
newborn.
The jet airliner can climb at over 5000 feet per minute, and the cruising altitude is usually
attained within 15 minutes. For this reason, "altitude" has been divided into "cruising", "take-off",
"landing", and "ground". The cabin pressure during various altitudes may vary between 5000 to
8000 ft9.(5)
Age
Nature of
Congenital
Heart
disease
Duration
of flight
In-Flight
Oxygen
supplementation
Outcome
1
51 days
PDA
Short
yes
Completed the journey safely
2
60 days
VSD, PAH,
PDA
Short
yes
Completed the journey safely

ORIGINAL ARTICLE
J of Evidence Based Med & Hlthcare, pISSN- 2349-2562, eISSN- 2349-2570/ Vol. 2/Issue 5/Feb 02, 2015 Page 525
3
30 days
TGA, PDA,
CFO, PPHN
short
yes
Completed the journey safely
4
2 days
Not known
No
Expired
5
-
TOF
long
-
Developed severe hypoxia
with Spo2 50% had to be
resuscitated with defibrillator
completed the journey
6
Not known
Not known
Not known
Not known
Expired
7
Not known
Not known
Not known
Not known
Diverted
Table 2
The basic pathophysiology in congenital heart disease is the altered oxygen capacity
either due to shunting of deoxygenated blood back in to the systemic circulation or the mixing.
This is further affected by the fact that the cabin barometric pressures results in a decrease in the
partial pressure of arterial oxygen from about 95 mm Hg to about 56 mm Hg in healthy
passengers. This represents only a 4 percent reduction in the oxygen carried by the blood, The
important point is that the partial pressure of oxygen of 56 mm Hg lies on the flat part of the
oxyhemoglobin dissociation curve. However Arterial oxygen saturation in children with Cyanotic
congenital heart disease is about 83.9%(6) and lies on the steep portion of the oxyhemoglobin
dissociation curve already, any small changes in the PaO2 are proportional to changes in the
SaO2. At ordinary cabin pressures the oxygen saturation may fall dramatically and increase the
risk of hypobaric hypoxia.
In case of cyanotic lesions with decreased pulmonary blood flow, the degree of cyanosis
depends on the degree of obstruction to pulmonary blood flow. If the obstruction is mild,
cyanosis may be absent at rest. However, these patients may develop hypercyanotic ("tet") spells
during conditions of stress. These hyper cyanotic spells may be exacerbated by the cabin
atmosphere and could be fatal.
In patients with cyanotic lesions with increased pulmonary blood flow. Cyanosis is caused
by either abnormal ventricular-arterial connections or by total mixing of systemic venous and
pulmonary venous blood within the heart. The total mixing, in this group, deoxygenated systemic
venous blood and oxygenated pulmonary venous blood mix completely in the heart, resulting in
equal oxygen saturations in the pulmonary artery and aorta. Thus exposure to hypoxia can cause
steep fall in oxygen saturation.
Transposition of the great vessels (TGV) is the most common of the former group of
lesions. Systemic venous blood returning to the right atrium is pumped directly back to the body,
and oxygenated blood returning from the lungs to the left atrium is pumped back into the lungs.
The persistence of fetal pathways (foramen ovale and ductus arteriosus) allows for a small
degree of mixing in the immediate newborn period; however, when the ductus begins to close,
these infants develop extreme cyanosis.
In case of acyanotic congenital heart lesions though not clinically obvious there is some
amount of compromise in oxygen carrying capacity of the blood. For lesions resulting in increased
volume load, the direction and magnitude of the shunt across such a communication depends on

ORIGINAL ARTICLE
J of Evidence Based Med & Hlthcare, pISSN- 2349-2562, eISSN- 2349-2570/ Vol. 2/Issue 5/Feb 02, 2015 Page 526
the size of the defect and the relative pulmonary and systemic pressures and pulmonary and
systemic vascular resistances. And for lesions resulting in increased pressure load, Unless the
obstruction is severe, cardiac output will be maintained and symptoms of heart failure will be
either subtle or absent. Though the effect of exposure to cabin atmosphere on short routes is
debatable in these cases, effects in case of long haul route are obvious.
CONCLUSION: Even though air travel for adults with cyanotic congenital heart has been
reported to be safe due to acclimatization secondary to exposure to chronic hypoxia(7), this does
not apply for infants with cyanotic congenital heart disease and exposure to hypoxia could lead to
fatal cyanotic spells.
In case of acyanotic congenital heart disease the effect of hypoxia are debatable however
exposure to hypoxia on long haul flights could lead to dangerous fall in oxygen saturation.
We recommend that infants with cyanotic congenital heart disease should not be exposed
to cabin atmosphere without supplemental oxygen.
However retrospective analysis of larger data available with airlines could provide
conclusive evidence as a prospective study of exposing an infant with congenital heart disease
would be impractical.
REFERENCES:
1. Goodwin T. In-flight medical emergencies: an overview. BMJ 2000; 321: 1338-41.
2. Medical Guidelines for Airline Travel, 2nd Edition Aerospace Medical Association Medical
Guidelines Task Force Alexandria, VA Chest 1960; 37; 579-588.
3. Responding to medical events during commercial airline flights mark a. g endreau, m. d.,
and charles d e john d.o., m.p.h. J Med, Vol. 346, No. 14 · April 4, 2002; 1067 – 1073.
4. Air Travel in Cardiorespiratory Disease: Report of the Section on Aviation Medicine
Committee on Physiologic Therapy American College of Chest Physicians Chest. 1960; 37
(5): 579-588.
5. Select Committee on Science and Technology. Air travel and health: fifth report. London:
United Kingdom House of Lords, November 15, 2000.
6. P. J. Stow. Arterial oxygen saturation following premedication in children with cyanotic
congenital heart disease. Can J Anaesth. 1988 Jan; 35 (1): 63-6.
7. Air Travel and Adults With Cyanotic Congenital Heart Disease EricHarinck, MD, PhD; Paul A.
Hutter, MD American Heart Association by 1996; 93: 272-276.

ORIGINAL ARTICLE
J of Evidence Based Med & Hlthcare, pISSN- 2349-2562, eISSN- 2349-2570/ Vol. 2/Issue 5/Feb 02, 2015 Page 527
AUTHORS:
1. Adarsh M. Patil
PARTICULARS OF CONTRIBUTORS:
1. Consultant Surgeon, Department of
Cardiac Surgery, M. V. J. Medical
College.
NAME ADDRESS EMAIL ID OF THE
CORRESPONDING AUTHOR:
Dr. Adarsh M. Patil,
Consultant Surgeon,
Department of Cardiac Surgery,
M. V. J. Medical College.
E-mail: dradarsh008@gmail.com
Date of Submission: 16/12/2014.
Date of Peer Review: 17/12/2014.
Date of Acceptance: 21/01/2015.
Date of Publishing: 28/01/2015.