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Blunted
Heart Rate and Blood Pressure Response to Static Handgrip in Low Flow
POTS
Our results show a significantly attenuated change in blood pressure and
heart rate in low flow POTS patients only. These patients have evidence
for sympathetic over-activation at rest with blunted changes observed in
response to sympathetic stimuli particularly affecting the distribution
and redistribution of blood volume (see below). Typically, while low
flow patients are normotensive they share many phenotypic features of
circulatory insufficiency including pallor, baseline tachycardia,
peripheral vasoconstriction and reduced central blood volume with
blunted responses to subsequent sympathetic stimuli.
The Increase
in Central Blood Volume is Blunted in POTS
The normal increase in central blood volume during the exercise pressor
reflex is abolished in low flow POTS patients and attenuated in normal
flow POTS. In general there appears to be an overall reduction in
regional blood volume redistribution in low flow POTS.
Normal flow POTS
patients have blunting of blood volume redistribution that relates to
selective pooling in the splanchnic circulation. This limits the
increases in central blood volume during handgrip. Similar limitation of
central blood volume occurs during orthostatic stress.
Total
Peripheral Resistance rather than Cardiac Output Drives Regional Blood
Volume
The most important
new finding in this study is that the exercise pressor reflex
produces a smaller pressor response in low flow POTS patients and that
the mechanism of the pressor response is shifted from the increased
cardiac output and central blood volume observed in control subjects to
increased vasoconstriction and peripheral resistance. Specifically,
in low flow POTS, the cardiac output component is essentially
abolished and the pressor response is completely driven by increased
peripheral resistance. In normal flow POTS vasoconstriction is more
selective and is deficient within the splanchnic regional circulation.
We have presented evidence for sympathoexcitation in POTS and others
have presented measurements of increased sympathetic nerve activity with
blunting of responses to diverse stimuli. We propose that the data
shown here support the theories that low flow POTS patients have
inappropriate sympathetic and adrenergic activation possibly driven by
central nervous system mechanisms controlling sympathetic outflow,
while normal flow POTS patients have reflex peripheral sympathetic
activation produced by selective splanchnic blood flow deficits.
Baroreflex
regulation of Heart Rate during Handgrip (Cardiovagal
Regulation):
As noted previously, HRV technique alone or combined with measurement of
blood pressure variability primarily estimates parasympathetic control
of heart rate. The difficulty in interpreting sympathetic change
is somewhat improved by using the low frequency to high frequency
ratios. In that regard, it is interesting that overall HRV power and low
frequency power, although decreased compared to control in low flow POTS
patients, is sustained or even increased during exercise. This is
different from results from control patients in whom heart rate
variability and by extension baroreflex gain are reduced by the
metaboreflex with similar findings in animal models. Sustained
sympathetic effects on the heart and are consistent with sustained
sympathetic cardiac contractility. In support, low flow POTS patients
have markedly increased cardiac afterload, no increase in cardiac
preload and sustained cardiac output suggesting increased contractility.
Therefore, it may be reasonable to infer that cardiac sympathetic
innervation remains relatively intact in POTS even though baroreflex
gain may be reduced.
On the other hand,
cardiovagal coherence is inadequate in low flow POTS at all times. This
indicates uncoupling between blood pressure and heart rate regulation
The Exercise
Pressor Reflex in POTS - Central Sympathetic Activation
The shift from a cardiac output driven exercise pressor response to an
arterial resistance-driven pressor response is similar to observations
made in congestive heart failure. In heart failure, baroreflexes are
markedly impaired with reductions in both sympathetic and cardiovagal
baroreflex sensitivities. As a result the ability of the arterial
baroreflex to buffer the muscle metaboreflex is severely attenuated .
In low flow POTS, the baroreflexes are also impaired with reductions in
both sympathetic and cardiovagal baroreflex sensitivities. The arterial
baroreflex buffers the vasoconstriction from the muscle metaboreflex and
mechanoreflex comprising the exercise pressor reflex by reducing this
peripheral vasoconstriction. Arguing by analogy, recent data concerning
heart failure indicate an important role for increased angiotensin II
and decreased neuronal nitric oxide activity in attenuating the
baroreflex. Increased angiotensin II and reduced nitric oxide are
features of low flow POTS.
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Exercise Intolerance- the Exercise Pressor Reflex in POTS
