VOLATILE ANESTHETICS AND NEURAL CONTROL OF THE CIRCULATION
Volatile anesthetics depress baroreceptor reflex control of arterial
pressure in experimental animals to various degrees.[198]
[428]
[429]
[430]
[431]
[432]
[433]
[434]
[435]
This
inhibition of baroreceptor reflex activity occurs as a result of depression of central
nervous system integration of afferent baroreceptor input, attenuation of efferent
autonomic nervous system activity, and reductions in ganglionic transmission and
end-organ response.[198]
[431]
[436]
[437]
Volatile
anesthetics increase resting afferent nerve traffic and enhance the sensitivity of
arterial baroreceptors by a Ca2+
-dependent mechanism.[431]
[436]
[438]
These anesthetic-induced increases in baroreceptor sensitivity and discharge frequency
tonically reduce overall sympathetic nervous system activity and attenuate sympathetic
responses to declines in arterial pressure.[439]
Halothane, enflurane, and isoflurane ( Fig.
7-22
) inhibit preganglionic sympathetic efferent activity at clinically
relevant concentrations in vivo.[431]
[433]
[434]
[435]
[436]
Volatile agents reduce postganglionic sympathetic nerve activity.[431]
[436]
Postsynaptic nicotinic receptors in the stellate
ganglion are also blocked by halothane.[440]
[441]
These findings indicate that attenuation of ganglionic transmission represents a
major mechanism by which volatile agents depress sympathetic nerve traffic.[442]
Depression of sympathetic outflow caused by volatile anesthetics has also been suggested
by examination of endogenous plasma norepinephrine kinetics.[443]
[444]
Halothane, isoflurane, and enflurane decrease
plasma concentrations of norepinephrine to various degrees by causing a more pronounced
reductions in norepinephrine spillover than clearance.[443]
[444]
Halothane-induced reductions in norepinephrine
release from postganglionic sympathetic nerves[445]
may also contribute to depression of reflex vasoconstriction in peripheral blood
vessels observed with this agent.[446]
Volatile
anesthetics also attenuate parasympathetic nervous system function. Halothane depresses
vagal nerve efferent activity by direct measurement of parasympathetic nerve activity.
[435]
These findings are supported by the results
of several other studies demonstrating that volatile anesthetics inhibit reflex bradycardia
in response to increases in arterial pressure.[428]
[431]
[436]
[447]
Parasympathetic and sympathetic nervous system outflows appear to be depressed to
equivalent degrees during halothane[436]
[447]
[448]
or isoflurane anesthesia.[431]
The effects of volatile anesthetics on neural control of the cardiovascular
system have been incompletely examined in healthy humans and have not been described
in patients with autonomic nervous system dysfunction. Halothane[174]
and enflurane[449]
produce greater attenuation of
baroreceptor reflex regulation of heart rate than equi-MACs of isoflurane.[175]
Depression of baroreceptor function by these volatile agents may be more profound
compared with fentanyl, diazepam, and nitrous oxide anesthesia.[450]
Baroreceptor-mediated control of peripheral
Figure 7-22
Baseline renal sympathetic efferent nerve activity (NA)
and arterial blood pressure (BP) recorded in a conscious and isoflurane (I)-anesthetized
dog (at 1.5% and 2.5% inspired concentrations). Nerve activity was depressed with
the 2.5% inspired isoflurane. (Adapted from Seagard JL, Elegbe EO, Hopp
FA, et al: Effects of isoflurane on baroreceptor reflex. Anesthesiology 59:511–520,
1983.)
vascular resistance is also attenuated in young volunteers during halothane anesthesia.
[178]
Steady-state anesthetic concentrations of
sevoflurane have been shown to cause greater depression of sympathetic nerve activity
measured directly with microneurography than desflurane at equivalent levels of hypotension.
[188]
These findings parallel results demonstrating
pronounced sympathetic hyperactivity during rapid increases in inspired desflurane
concentration in humans ( Fig. 7-23
).
[42]
[44]
The actions
of volatile anesthetics on baroreceptor reflex control of the circulation may be
profoundly altered during autonomic dysfunction in elderly patients[451]
or in those with essential hypertension, diabetes mellitus, or heart failure.[452]
Further investigation is required to test these hypotheses.
