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the tricuspid valve regurgitant velocity and thereby assessment of the pulmonary peak systolic pressure.
Right heart catheterization may be required.
A period of six months is usually recommended for treatment with warfarin following pulmonary
embolism, and medical certification should not be considered during this time. Certification will require
restriction to multi-crew operations. Pulmonary hypertension (systolic pressure > 30 mm Hg – tricuspid
valve Doppler velocity > 2.5 m/s), whether primary or secondary, should disbar from all forms of
certification to fly.
SYNCOPE
Syncope (Gr. ‘cutting off’) may be defined as transient loss of consciousness, usually associated with
falling. The mechanism is global cerebral hypoperfusion due to a number of causes. As a rule, recovery is
spontaneous and complete but although recovery to consciousness is usually rapid, full return of
intellectual function may be delayed. Depending on cause, syncope may be abrupt and without warning,
or there may be a prodrome (presyncope) of variable length with symptoms such as nausea, weakness,
light-headedness and visual disturbance. Retrograde amnesia occurs in some, particularly older,
individuals. Recovery, although somewhat subjective, may be rapid (seconds/minutes), as in the case of
ICAO Preliminary Unedited Version — October 2008 III-1-45
an Adams-Stokes attack1, or prolonged sometimes, as in vasovagal syncope. If the attack is
complicated by an anoxic epileptic seizure, recovery will inevitably be delayed further.
Differential diagnosis of syncope due to circulatory cause:
• Neurocardiogenic syncope is marked by a variety of autonomic circumstances including
nausea/vomiting and gastrointestinal disturbance. It is associated with systemic hypotension and
cerebral hypoperfusion. It may also be associated with either bradycardia or tachycardia.
• Orthostatic hypotension may be caused by blood loss or impairment of autonomic regulation
from a number of causes. It occurs in severe left (or right) ventricular dysfunction. It is a common
transient experience in normotensive subjects on gaining the erect position.
• Structural heart disease, exemplified by valvar aortic stenosis (or subaortic stenosis as in some
forms of hypertrophic cardiomyopathy), if severe, is associated with syncope. More than one
mechanism is involved.
• Cardiac arrhythmias, including supraventricular and ventricular tachycardias and sinoatrial or
atrioventricular conduction disorders, may be complicated by syncope.
• The “steal” syndromes in which there is competitive demand for cerebral perfusion are rarely
seen in the pilot population.
Consciousness may also be impaired or lost due to hypoglycaemia, hypoxia, hyperventilation,
somatization disorders, and epilepsy.
Vasovagal (neurocardiogenic) syncope
Vaso-vagal (neurocardiogenic) syncope or the common faint was described over 200 years ago and is the
mechanism of what used to be known, in classical literature, as the “drawing-room swoon”. It is a
common phenomenon — it has been suggested that between one-third and two-thirds of the population
experience an attack at least once during their lifetime. The attacks are sporadic and often cluster, the
population being heterogeneous. It often presents in teenage years and disappears, reappearing later in
life, sometimes as clusters of episodes. It contributes to at least 40 per cent of the syncopal events seen in
the outpatient setting. It is difficult to manage, partly because the triggering mechanisms, even after
having been investigated extensively, are imperfectly understood.
The regulation of the circulation involves a number of interacting reflexes. Initially, on change in posture,
baroreflex mechanisms are activated to counteract the effect of gravity on the venous blood pool. The
renin-angiotensin-aldosterone axis is also involved, both interacting with the autonomic nervous system
and influencing salt and water metabolism. Adequate blood pressure is needed to maintain the blood
supply to the vital organs, including the brain, kidneys and gut. If it falls beyond a certain point, cerebral
auto-regulation fails and the subject loses consciousness. With an abrupt fall in blood pressure, this occurs
very rapidly — within five to ten seconds. Provided the pressure is restored rapidly (often brought about
by the patient falling to the ground), recovery of consciousness ensues but, depending on the provocative
circumstances, a minimum period of some 30 minutes is required for effective recovery. This can be
prolonged considerably if there is recurrence of the syncopal episode, if the provocative circumstance is
ongoing, e.g. in the case of nausea or vomiting, or if the period of hypotension was sufficiently prolonged
　
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