Syncope (fainting) is a reasonable starting point. In
principle, it is familiar to all of us because it is common. Perhaps 40% of all
people will have one or more faints during their lifetime. However, it
represents a sudden change in well-being that often stimulates fear in families
and discomfort among physicians. Syncope translates from the Greek as “a
cutting short” (1). It is defined as a sudden transient loss of consciousness
with loss of postural tone and spontaneous recovery caused by impaired blood
flow to the central nervous system. Syncope may occur supine or upright and
under a wide variety of conditions. It may be due to medication, cardiac
disease, most commonly arrhythmic disease, or severe impairment of cardiac blood
flow by mechanical pump failure or obstruction. It may be due to transient
impairment of central nervous system function as in a transient ischemic attack
(mild stroke) but this is less common. However, although convulsive-like
movements may occur during syncope, it is distinct from a seizure disorder, and
is distinct from coma in which loss of consciousness is not transient at all.
Cardiac syncope is often quite serious and should be
regarded as life-threatening. Although cardiac syncope is not often closely
associated with orthostasis it may be. Causes of cardiac syncope include the
long QT syndrome, arrhythmogenic right ventricular dysplasia, cardiomyopathies,
left ventricular outflow obstruction, myocardial infarction, primary pulmonary
hypertension, and most commonly ventricular tachycardia (fast heart rate),
bradyarrhythmias (overly slow heart rate) and related arrhythmic events (3). The
first job in evaluating syncope is to evaluate the patient for possible cardiac
syncope. When specific cardiac disease is found, it is treated specifically.
Thus, for example, ventricular tachycardia is treated with antiarrhythmics,
bradyarrhythmias causing syncope are treated with a pacemaker, long QT syndrome
with medication and a defibrillator if needed, and aortic valve disease with
surgery. Cardiac syncope may first manifest during exercise, which is the best
and most physiologic stressor of the myocardial circulation and overall cardiac
function. Exercise related syncope should raise a “red flag” for underlying
heart disease (4). Nevertheless, despite flag-waving, the large majority of
exercise related syncope cases are non-cardiogenic in origin, at least for
children and adolescents. Cardiogenic syncope has been well described in
numerous texts including those already referenced and is not the central topic
for discussion here because it accounts for a small percentage of syncope in
children and of those many have previously known cardiac conditions.
Approximately 90% of syncope in children is either
vasovagal or “unexplained”. Often the unexplained variety is
reclassified as vasovagal once tilt table testing has been performed (5).
"Neurocardiogenic" has also been used in the place of vasovagal.
Fainting is mediated
through a combination of inappropriate vascular (blood vessel) and heart rate
control. It is rarely fatal but it can be injurious. Some patients with VVS may
have cardiac standstill ("asystole") of abrupt onset resulting in
severe injuries. There is little compelling evidence
for a primary role for the heart in neurocardiogenic syncope, once cardiogenic
syncope has been ruled out. The term neurocardiogenic is thus somewhat misleading. Synonyms for
neurocardiogenic include neurally mediated syncope and reflex syncope although
the latter often includes situational syncope as well. Almost
all syncope in children is vasovagal. On the other hand
adult syncope is much more likely to be cardiogenic – about a 50/50 split with
neurocardiogenic syncope. Vasovagal syncope almost always occurs in the upright
position, which may sometimes include sitting. Therefore it is regarded as a
form of orthostatic intolerance.
Defining Characteristics glossary
means standing up. Orthostatic intolerance can be defined by the inability to
tolerate the upright posture because of signs and symptoms relieved by lying
. If symptoms initiate while supine, then there is
no OI. Transient OI is commonly experienced during dehydration or infectious
disease. Typical signs and symptoms include: loss of consciousness or lesser
cognitive deficits (memory loss, decreased reasoning and concentration); visual
headache; fatigue; either increases of BP (hypertension), decreases
(hypotension) of BP; weakness; nausea and abdominal pain; sweating;
tremulousness; and exercise intolerance
. Unless in harm's way (e.g. standing on a cliff)
OI is not lethal. Some OI findings, such as nausea and sweating pertain directly
to autonomic activation. However, loss of consciousness, severe lightheadedness,
and neurocognitive loss relate to central nervous system (CNS) dysfunction and
oblige recumbence. CNS symptoms are produced by altered brain blood flow perhaps
involving the brainstem. Cerebral
autoregulation may be compromised
as in POTS
may be reduced by hyperventilation and hypocapnic cerebral vasoconstriction.
Involuntary postural hyperventilation, mostly hyperpnea, is observed in all VVS
and 50% of POTS patients in my laboratory
. Trigeminal, sympathetic, or parasympathetic nerve
activity may also affect orthostatic CBF
Physiology of Orthostasis
supine, blood volume within the central thoracic vasculature is relatively
large, although a disproportionate amount (25-30%) of blood is stored within the
splanchnic venous reservoir
. Standing transfers >500ml of central blood
caudally, further increasing the volume of the splanchnic pool and filling veins
of the lower extremites An initial period of instability follows, denoted
“initial orthostatic hypotension”
which BP can decrease by 30% or more, reaching its nadir at 10-20 seconds after
standing. Reflex tachycardia occurs. BP is restored within 30-60 seconds. IOH
results from the normal delay of arterial baroreflex detection and response to
gravitational blood volume redistribution. Lightheadedness, postural instability
and occasionally brief loss of consciousness occur and are relieved by
recumbency making IOH a form of orthostatic intolerance. Thereafter, HR
decreases but remains elevated compared to supine, and BP is restored by
arterial vasoconstriction, by elastic recoil of venous blood in dependent veins,
and by active venoconstriction in splanchnic veins
IOH recovery, upright blood volume slowly decreases because of microvascular
. Decreased venous return decreases central blood volume and cardiac output (CO)
by 20% despite baroreflex mediated vasoconstriction, increased cardiac
contractility, and increased HR. Cerebral blood flow velocity (CBFv) decreases
by 3-12% partly because of reduced cerebral perfusion pressure by 20mmHg
. Cerebral autoregulation (unchanged CBF despite changing BP) is blunted during
orthostasis. Unless the muscle pump is evoked, standing still places us at risk
for decreased CO and CBF.
posture (orthostasis) stresses regulatory capabilities of the circulatory system including
an intact heart, intact vascular structure and function, adequate blood volume,
and intact physical pumps comprising the skeletal muscle pump - leg muscles that
compress leg veins - and the respiratory-abdominal muscle pump which enhances
systemic venous return during respiration
. Upright stance causes dependent venous pooling.
Muscle pumps propel blood back to the heart when upright and during exercise
the skeletal muscle pump forms an important class of physical
“countermeasures” against orthostatic intolerance
Apart from muscle pumps, rapid orthostatic circulatory adjustments depend
on the autonomic nervous system (ANS) comprising sympathetic and parasympathetic
arms forming a framework for heart rate (HR) and blood pressure (BP) stability.
The myogenic response
and flow dependent mechanisms
, and co-transmitters neuropeptide Y and ATP
to produce arterial vasoconstriction and
venoconstriction, increase cardiac contractility and HR, stimulate adrenal
epinephrine release, and control the neuroendocrine and vascular function of the
kidney and long term BP control. The parasympathetic arm via vagal nerve
efferents contributes most to heart rate changes at rates less than the
. Recent work indicates strong vagal influences on
and important effects on nitrergic (nitric oxide
containing nerves) vasodilation of the large cerebral arteries
. Endocrine and local systems (e.g. nitric oxide,
local angiotensin) impact the vascular milieu but are slower to develop, often
acting to modulate or set tonic activity of the ANS
. Autonomic control of HR and BP during orthostasis
is provided by subsystems designated “baroreflexes” (pressure reflexes),
loosely grouped as arterial and cardiopulmonary baroreflexes, which maintain BP
under changing conditions such as orthostasis
Patterns of Orthostatic Intolerance-Orthostatic Stress Testing
and Head-up Tilt
Patterns of orthostatic intolerance are best defined by an orthostatic
stress test – i.e. a means by which upright standing stress can be imposed in
a controlled fashion and the physiological response monitored in detail. While
standing can be used, individual differences and patient motion may make this
difficult. Moreover, standing has only recently benn validated against upright
tilt for adults and similar validation has not been performed in the young. Therefore the standard of orthostatic assessment
in the young is the head-up tilt
table test. Although head-up tilt was used to evoke autonomic reflexes in early
NASA experiments, it was first used as a provocative agent in 1986 by Richard
device comprises a table driven by an electrical motor with a supportive
footboard enabling positioning of a patient at varying angles of upright tilt.
Although it would seem that an angle of 90o is most physiologic, this
usually induces too many “false positives” (patients with no history of
orthostatic intolerance who have intolerance induced during testing). Therefore
lesser angles such as 60o or 70o are customarily used. Following a resting period, the patients are placed upright and their
response over a period of tilt assessed – this is usually anywhere between
30-45 minutes. At a minimum, blood pressure
and continuous electrocardiography are assessed. Typically a form of continuous
blood pressure assessment such as a finger plethysmography or an arterial
tonometer is used and respirations are also assessed on a moment to moment
basis. Other researchers have used methods to directly assess sympathetic
activity (microneurograaohy). peripheral, thoracic
(chest), and central nervous system blood flows which are methods still consigned
to the research domain. Many laboratories use medications to enhance the
fainting response, sometimes isoproterenol but more often sublingual
nitroglyceron. The central purpose of a tilt table test is to reproduce
symptoms of orthostatic intolerance in a setting in which hemodynamic variables
(blood pressure, heart rate, blood flow) can be assessed. Most often there is
correlation with changing physiological signs, but the definition of orthostatic
intolerance requires symptoms. Thus for example the incidence of false
positive faints during head-up tilt is high. If the complaining symptoms are not
reproduced but the patient has a simple faint, the test is judged as negative.
For example, my son fainted during his tenure as a HUT control patient. He has
no history of fainting and the episode bore no relation to any prior complaints.
This is a false positive and not a sign of orthostatic intolerance.
Other patterns of hemodynamic disturbance (see below) seem invariably
associated with symptoms and are more reliable indicators of chronic impairment.
normal response to HUT is a modest increase in heart rate (with an increased heart rate by 10-20 beats/min),
a small increase in systolic BP and a larger increase in diastolic pressure.
Systolic blood pressure should not fall. Abnormal tilt test responses can be used to categorize patterns of
orthostatic intolerance. The overall patient assessment of chronicity and
severity of impairment should be combined with these lab data to reach any
conclusion concerning the nature of orthostatic intolerance in a particular
patient. In addition to the normal pattern, three typical patterns of
orthostatic intolerance are depicted in the figure, which
shows the systolic blood pressure and heart rate in-patients during tilt.
with prominent 0.1Hz oscillations
Slow and Steady ↓BP,
↓ CO, ↑HR, ↑MSNA, ↑TPR,
↓ HR, ↓TPR
is depicted in the figure . Typically patients easily
tolerate the early parts of tilt with little change in blood pressure or
sensorium (phase 1). 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 initiated by a slow
fall in blood pressure (phase 2). Later, there is an abrupt drop in blood pressure and
heart rate with loss of consciousness (phase 3). Phase 1 is associated with an
increase of arterial vasoconstriction but reduced cardiac output. Phase 2 with a
slow fall of arterial resistance along with cardiac output. Phase 3 with
arterial vasodilation and variable cardiac output.:
|| 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”, which might be
construed as extremely brief phase 2 with immediate cardioinhibition as
occurs in phase 3. There is no true seizure activity present
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
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
(post seizure) states.
c) A patient persistently maintained upright in a severe
simple faint (for example proceeding to asystole) can potentially die. There is
no reported pediatric death during HUT. A corollary is that such testing is
potentially risky and should be 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.
for Vasovagal Faint
The most popular proposed
mechanism holds that fainting results from an errant stretch reflex (aki to the
Bezold=Jarisch chemoreflex) from the
left ventricle. The reflex is 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-fiber
nerves coursing from the ventricle to the CNS and causing vagally mediated
bradycardia as well as vasodilation. For the most part this explanation has
Reflex is an “an eponym for a triad of responses (apnea, bradycardia, and
hypotension) following intravenous injection of veratrum alkaloids in
experimental animals.” The response to mechanical stimulation is much
weaker. Aviado DM, Guevara AD. The Bezold-Jarisch reflex. A historical
perspective of cardiopulmonary reflexes. Ann N Y Acad Sci. 2001;940:48-58.
This mechanism was proposed despite the fact that any stimulus could only be
short lived and baroreceptors would immediately be unloaded. Hainsworth R.
Syncope: what is the trigger? Heart. 2003;89:123-124.
Relatively few afferent nerves were excited in the original Oberg and Thoren
hemorrhaged cat model. Oberg B, Thoren P. Increased activity in left
ventricular receptors during hemorrhage or occlusion of the caval veins in
the cat. A possible cause of the vasovagal reaction. Acta Physiol Scand
VVS can occur in a ventricular denervated transplant recipient given the SNP.
Scherrer U, Vissing S, Morgan BJ, Hanson P, Victor RG. Vasovagal syncope
after infusion of a vasodilator in a heart-transplant recipient. N Engl J
•The heart before syncope need not be empty nor hypercontractile. Novak V,
Honos G, Schondorf R. Is the heart "empty' at syncope? J Auton Nerv
Syst. 1996 Aug 27;60(1-2):83-92. Liu E et al Left ventricular geometry and
function preceding neurally mediated syncope. Circulation. 2000 Feb
Other theories of fainting include epinephrine or renin surges (which
would rationalize the common use of isoproterenol as adjunctive provocation). Such surges do indeed occur in those who faint and take some minutes to
develop. However, it remains unclear whether these changes are the cause of the
hemodynamic abnormalities or an effect of them acting as compensation for decreased blood
pressure and peripheral resistance during faint. A decrease in cerebral blood
flow has also been shown to occur in syncopal patients and may precede a large
fall in blood pressure. However, blood flow is similarly impaired in
chronic orthostatic intolerance in which hypotension (low blood pressure)
does not usually occur. Other proposed mechanisms include various
changes in CNS neurotransmitters such as serotonin, norepinephrine, neuropeptide
Y and substance P. Causation has not been established. In summary it is fair to
say that we still have no precise understanding of the mechanics or the
mechanism of simple faint.
of Vasovagal Faint
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”.
VVS is not deadly unless in harm’s way.
date, no single pharmacological intervention has been proven effective
above the placebo effect in younger patients in large clinical trials
. Placebo exerts 30-40% benefit
in these studies.
and even ferritin deficiency aggravates VVS
athletes have increased risk of VVS compared to untrained persons
and water supplementation can be helpful but a large amount of salt is needed
compensatory physical countermaneuvers are the recommended treatment
fainting prodrome must be recognized for countermeasures to be effective.
First faints are rarely countered because patients don’t understand what's
Countermeasures: immediate lying down or
squatting cause postural VVS to cease; with prolonged prodrome
counterpressure such as leg-crossing, buttocks clenching, fist clenching, may
supine, the patient should not immediately stand. Instead, I suggest a 16 oz
bottle of water and remaining supine for >20 minutes following the episode.
If there is no prodrome or if there is abrupt onset
with injury, then consider asystolic vasovagal faint or an arrhythmia
and evaluate by loop recording electrocardiography
. Holter monitoring 24-hour is inadequate for
total loss of consciousness is not transient, then it is not a faint, it
is coma. VVS is less than 2 minutes of total loss of consciousness, as a matter
of consensus. Rarely, fainting promotes an underlying seizure disorder via
Very frequent or extremely prolonged syncope can
point to psychogenic syncope or conversion responses. These can be distinguished
from true syncope in the laboratory because there is no hypotension or reduced
CBF. But attacks may be real to the
patient. Some patients may have had bona fide VVS interspersed with more
frequent psychogenic episodes as learned or conditioned responses. One school of
thought suggests that such patients actually experience the symptoms of true VVS
without the sign
in this group are patients with true “neurogenic orthostatic hypotension” defined by
the American Autonomic Society to be a sustained fall in systolic blood
pressure of >25 mmHg within 3 minutes of assuming the upright position . This
is discussed in more detail elsewhere in this website. This group harbors patients with autonomic failure. Autonomic failure includes
primary forms such as primary autonomic failure and multiple system atrophy, and
more common secondary forms occurring with Parkinson’s disease and diabetes.
Dysautonomia may also be drug induced. Pediatric causes are rare and include
familial dysautonomia as the only “relatively” common variants (32). Acute
forms may occur during infectious and inflammatory diseases or be related to
peripheral nerve disease.
Chronic Orthostatic Intolerance and the Postural Tachycardia
orthostatic tachycardia syndrome is a disabling disease state described at least
since 1940 (33) and is the most common reason for referral for orthostatic
intolerance in adults. It is an emerging form of orthostatic intolerance
in children. Patients have day-to-day disability - a feature not shared with
those with simple faint. With some exception, traditional tests of autonomic
function are normal in these patients. Patients are often unable to hold jobs or
attend schools. Dr. David Robertson of the Vanderbilt autonomic laboratories,
has stated that this is the most common form of chronic orthostatic disability,
and is present in virtually every patient with day-to-day orthostatic
intolerance. He has therefore
initially named the illness “Chronic Orthostatic Intolerance” (COI). Our understanding
of its pathophysiology remains incomplete.
The central physical finding is upright tachycardia without concurrent
hypotension. Hypotension can be induced with unusually prolonged standing.
A resting tachycardia may also be present. An operational definition of the
syndrome most often called POTS for the postural tachycardia syndrome includes symptoms of orthostatic intolerance associated with an
increase in heart rate from the supine to upright position of more than 30 beats
per minute or to a heart rate greater than 120 beats per minute within 10
minutes of head-up tilt (HUT). Recent literature indicate that higher increases
in HR are found in younger patients.
Day-to-Day Symptoms of OI
or HR>120bpm within 10min
Adolescent – Δ>43
(IOH a confound)?
Concurrent Symptoms of OI
Improved by Recumbence
Onset of symptoms often follows an infectious
disease and may be related to inflammatory mediators (42). We reported the first
pediatric cases of POTS. Our data showed that POTS physiology underlies
orthostatic intolerance in the large majority of adolescents with the chronic
fatigue syndrome (CFS) . POTS is common, affecting an undisclosed number
of patients mostly in the age range of 12 to 50 years, mostly female
(approximately 80%). There is an as yet undetermined but increasing apparent
prevalence in children and adolescents (43).
is caused by alterations of the autonomic nervous system, although, mild to
moderate all-cause hypovolemia mimics POTS.
Vagal Withdrawal and the Sinus
In some mildly ill individuals, POTS is related to loss of parasympathetic
slowing of the heart with few peripheral circulatory abnormalities. Upright
heart rates rarely exceed 120 bpm. Oten agents that increase cardiac
parasympathetic activity such as beta blockers
, cardiac glycosides
, acetylcholinesterase inhibitors (pyridostigmine)
(not FDA approved) relieve symptoms.
may have excessive beta adrenergic sensitivity of the sinus node. This condition
is denoted "inappropriate sinus tachycardia"
, and is regarded as distinct from POTS but less
common. Supine heart rates >100bpm are observed, symptoms are less severe
than in POTS, and beta blocker therapy can be efficacious.
POTS and Hyperadrenergic POTS
The remainder of patients are often partitioned among "neuropathic
POTS", in which "partial dysautonomic" adrenergic denervation
occurs, and "hyperadrenergic POTS", in which sympathetic overactivity
originally described, decreased adrenergic vasoconstriction in the legs causes
decreased norepinephrine spillover
, and increased blood flow even supine
. When upright, redistributive central hypovolemia
caused by leg blood pooling leads to reflex tachycardia
. In another neuropathic variant decreased
adrenergic vasoconstriction and redistribution of central blood to the
tachycardia. Intense leg vasoconstriction produces acrocyanosis. Autonomic
, presenting as POTS, causes similar reflex
tachycardia. Central hypovolemia produces hyperpnea and hypocapnia in 50% of our
. Treatment with vasoconstrictors (e.g. midodrine)
and pyridostigmine can help.
adrenergic synapse can be altered at pre-synaptic or post-synaptic levels.
Pre-synaptic abnormalities include increased sympathetic nerve activity even
when supine. While this has been reported
, the finding is not consistent
synaptic norepinephrine is observed in the norepinephrine transporter (NET)
, and in more prevalent epigenetic NET
and post-synaptic adrenergic activity may be enhanced by local chemical milieu,
including angiotensin-II excess caused by ACE-2
deficit and nitric oxide deficiency - a
hyperadrenergic variant with tachycardia, pallor, vasoconstriction and absolute
hypovolemia. Angiotensin [type 1] receptor blockers have shown benefit. Beta
blockers may also help.
among POTS Variants, a Matter of Opinion
among POTS variants may be difficult for the pediatrician (and for the OI
expert) despite apparent straight forward differences. Some would say that POTS
with increased upright blood pressure is hyperadrenergic, others would say that
increased plasma catecholamines (or better, increased norepinephrine spillover)
is required. Excessive orthostatic BP is a matter for consensus since both
systolic and diastolic BP normally increase upon standing: how much is too much
is unclear. As a heuristic, POTS patients with high supine HR, cool to touch and
pasty white in appearance when supine, often have hyperadrenergic POTS. Standing
HR is elevated to the 130-180 range during quiet standing indicating
hyperadrenergic drive; vagal withdrawal alone increases HR to the 100-120 range.
Those with upright HR < 120bpms are more likely neuropathic. Recent
(unpublished) work with sympathetic nerve recordings have demonstrated normal
sympathetic activity when supine, and supranormal activity upright. This
supports adrenergic enhancement (NET deficiency, Ang-II excess) in patients with
“hyperadrenergic POTS”. Confusing matters further, neuropathic patients can
have increased upright catecholamines even though spillover is decreased in the
Deconditioning – Caveat Bedrest!
One confounding and alarming issue is the tendency for POTS patients to bedrest.
Prolonged bedrest emulates microgravity and has deleterious effects
, profound reductions in blood volume and cardiac
size, redistribution of blood, osteoporosis, skeletal muscle pump atrophy and
. Vasoconstriction is impaired
. Bedrest causes a self-perpetuating state of OI
which can emulate or intensify POTS. It is paramount for POTS patient to
leave bed and recondition. Well-structured exercise protocols are essential and
must accommodate patients start off bedrested
. Reconditioning invariably improves patient
well-being. Recent work support the idea that POTS patients are also exercise
deconditioned compared to matched volunteers
. While exercise deconditioning may or may not be
causal in POTS, it is clear that exercise reconditioning is beneficial and
should be advocated for all POTS patients.
treatment for chronic orthostatic intolerance is being developed but will depend
on specific etiologies as these are discovered. For the moment we continue to
use some of the medications outlined in the vasovagal section. Of these florinef, midodrine,
beta blockers and pyridostigmine seem to be most effective with an emerging use of SSRI’s.
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