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1) Classic simple faint (Vasovagal Syncope)
This is depicted in the figure. Typically
patients easily tolerate the early parts of tilt with little change in
blood pressure or sensorium. Following a variable period of time – on
the order of 7 to 20 minutes, patients develop orthostatic symptoms of
nausea, dizziness, heat, heavy breathing, and sweatiness associated most
commonly with a small initial slow fall in blood pressure (which can be
seen if the figure is inspected closely). In short order there is an
abrupt drop in blood pressure and heart rate. The early fall in blood
pressure is coincident with a decrease in vasoconstriction (the peripheral arteries
vasodilate) which normally occurs as part of the neurovascular compensation
required to maintain blood pressure with orthostasis. Blood pressure and heart
rate may plummet precipitously, and asystole may occur. When this happens there
is a rapid loss of central nervous system activity and often a dysinhibition of
peripheral neurologic responses resulting in muscular movements mimicking a
tonic-clonic seizure. This is denoted "convulsive syncope". That no
true seizure activity is present has been confirmed as early as the 1950’s by
Gastaut and associates and later reconfirmed using HUT methods by Grubb and
coworkers in the 1990’s. Such episodes, while relatively uncommon, are
quite dramatic and such phenomena are periodically "rediscovered" by
beginning practitioners of the HUT art. There are several sidebar observations
on simple faint that stem from the convulsive variant:
a) If the episode occurs rapidly the patients can be injured. It is
estimated that approximately 15% of patients with simple faint are injured
overall during a faint. This can take relatively innocuous forms as a
superficial cut while falling or can be more pernicious when a car is
overturned. In the latter case it is evident that treatment for fainting
is necessary.
b) Fainting usually is short lived; upon assuming recumbence the
patient usually awakes after a few seconds. But some patients do not awake
immediately and prolonged sleep-like states have occurred. These may mimic
post-ictal states.
c) A patient persistently maintained upright in a severe simple faint
(for example proceeding to asystole) can potentially die. Although there
is no reported pediatric death during HUT, the same cannot be said for
adult testing. The figure illustrates one possible scenario for death
which is the rapid onset of asystole. This is often designated
"malignant syncope" or "convulsive syncope" because of
the frequent association with seizure like movements (mostly tonic
posturing without clonus). Gastaut in the 1950's showed that these
'seizures' were not be related to brain seizure activity but rather to
cessation of CNS activity (flat-line) and peripheral nerve escape.
Pacemaker insertion has been advocated in some adults with convulsive/asystolic
syncope but remains controversial. There is no literature on the use of
pacemakers in the pediatric age range. Maintaining such a patient upright
would be fatal.
A corollary is that upright tilt testing is potentially lethal and
should be only performed by experienced personnel. Similar events may also
occur in the real world, so called "telephone booth syncope’. This
has decreased since telephone booths are largely anachronistic. However,
recently one of my patients with known vasovagal syncope managed to prop
herself up with impending faint and nearly required a full resuscitation.
Patients should be placed supine or allowed to fall to a recumbent
position. Recumbence invariably resolves all symptoms and signs.
Until recently most research concerning orthostatic
intolerance was primarily concerned with syncope. Even here there is no
consensus about mechanism. The most popular proposed mechanism holds that
fainting results from a stretch reflex from the left ventricle. The reflex is
presumably activated by an underfilled (due to reduced venous return), overly
contractile (due to sympathetic activation), left ventricle. This results in a
“paradoxical reflex” mediated by unmyelinated C-fibers coursing from the
ventricle to the CNS and causing vagally mediated bradycardia as well as
vasodilation Treatment which increases blood volume would be expected to help relieve underfilling while negative inotropic agents should help to reduce cardiac
contractility. However, just because a reflex is possible, does not make it
probable. Both hypercontractility and decreased ventricular stretch have been
called into question by recent research. Also, patients receiving cardiac transplants retain the ability to faint
, which implies that the ventricular receptor theory cannot explain all simple
faints. Most significantly, animal research performed by Hainsworth and
associates have convincingly demonstrated that once coronary baroreflex function
is separated from ventricular receptor action, little in the way of
Bezold-Jarisch like reflex activity remains under physiologically achievable
conditions. Other theories of fainting include epinephrine or renin surges and
vasopressin decreases. This would rationalize the common use of isoproterenol as adjunctive
provocation
. Such surges have been shown to occur in those who faint and often take many
minutes to develop. However, it remains unclear whether these humoral changes
are the cause of the hemodynamic abnormalities or the result of attempted
compensation for decreased blood pressure and peripheral resistance during
incipient fainting. A decrease in cerebral blood flow has also been shown to
occur in syncopal patients and may precede a large fall in blood pressure
. Cerebral syncope is thought to exist independent of blood
pressure changes. Also, blood flow is similarly impaired in chronic orthostatic
intolerance in which hypotension does not usually occur
. Other proposed mechanisms include changes in CNS neurotransmitters such as
serotonin, norepinephrine, neuropeptide Y and substance P
. In our laboratory, we have recently demonstrated a relation between postural
fainting and excess splanchnic
pooling which in turn produces an unusual degree of thoracic hypovolemia. Causation has not been established. In summary it is fair to say that we still
have no precise understanding of the mechanism or mechanisms of simple faint.
Treatment
Without a clear mechanism there is no clear treatment. Moreover,
many patients with infrequent simple faints, who do not injure themselves and
who do not have convulsive syncope, may require no specific therapy above
training in aversive maneuvers. The simplest of these maneuvers is lying down
although leg crossing, bending at the waist, squatting and other maneuvers may
also be effective. Increased fluid and salt intake is always helpful in
ameliorating the initial thoracic hypovolemia of orthostasis. Lower body
exercise, particularly isometric exercise, can be a genuine help by enhancing
the muscle pump and by increasing venous tone in the lower extremities. Elastic
support hose can be useful at times but are often unacceptable to children.
Other investigators have advocated a regimen of progressively longer quiet
standing as a form of "orthostatic training". In terms of medication,
often beta-1 blockade works well. This may have its basis in reducing putative
hypercontractility but other possible roles for beta-1 blockade include blunting
the release of epinephrine or renin, which are modulated by beta-1 receptors and
central effects. Other possible medications include fludrocortisone (florinef),
which retains sodium and water at the expense of small potassium wasting and has
modest if any corticosteroid side effects. In addition to its other actions,
florinef may aid in sensitizing alpha-receptors and blocking vasodilation. A
new, direct acting alpha-1 agonist, midodrine (proamatine) has been used to good
effect in many patients with assorted forms of orthostatic intolerance. Other
agents have included alpha-2 adrenergic agents (both clonidine and its obverse
yohimbine) which have been used in select patients. Disopyramide has been used
occasionally but controlled studies do not support its efficacy. Recently,
selective serotonin reuptake inhibitors have been used to good effect in a
variety of orthostatic disabilities. These seem to interfere with hypotensive
responses at a central level. Grubb and associates have demonstrated efficacy of
sertraline and fluoxetine in a series of controlled studies. The studies were
performed after careful psychiatric screening had ruled out significant
depression. Personal experience bears this out and the SSRI’s remain a useful
medication for many forms of orthostatic intolerance.
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Vasovagal Syncope
