Systemic Hemodynamics
Volatile anesthetics cause direct negative chronotropic actions
in vitro by depressing sinoatrial node activity.[173]
However, alterations in heart rate in vivo are determined
Figure 7-15
Histograms depict the ratio of the left atrial (LA) A
loop to the total pressure-volume diagram area (A/A+V, top panel),
the ratio of LA conduit to total reservoir volume (CV/RV, middle
panel), and LA-left ventricular coupling (Ees
/ELV
,
bottom panel) under baseline conditions (Control)
and during the administration of 0.6, 0.9, and 1.2 minimum alveolar concentrations
(MACs) of desflurane (black bars), sevoflurane (red
bars), or isoflurane (gray bars). *,
Significantly (P < .05) different from the control
values; † significantly (P < .05) different
from 0.6 MAC. (Adapted from Gare M, Schwabe DA, Hettrick DA, et al: Desflurane,
sevoflurane, and isoflurane affect left atrial active and passive mechanical properties
and impair left atrial-left ventricular coupling in vivo: Analysis using pressure-volume
relations. Anesthesiology 95:689–698, 2001.)
primarily by the interaction of volatile agents and baroreceptor reflex activity.
[174]
[175]
Halothane
does not appreciably change heart rate in humans[6]
because it attenuates baroreceptor reflex responses.[176]
[177]
[178]
Heart
rate increases to various degrees with enflurane, but these increases may be insufficient
to preserve cardiac output.[11]
[179]
Isoflurane increases heart rate in response to simultaneous decreases
in arterial pressure.[12]
These findings occur
with this volatile agent because baroreceptor reflexes are relatively preserved compared
with equi-MACs of halothane and enflurane.[175]
Desflurane also causes dose-related increases in heart rate in humans.[37]
[38]
[180]
Desflurane-
and isoflurane-induced tachycardia may be more pronounced in pediatric patients or
in the presence of vagolytic agents and, conversely, may be attenuated in neonates
[181]
and geriatric patients or by the concomitant
administration of opioids.[182]
[183]
Rapid increases in the inspired desflurane concentration at greater than 1 MAC may
be associated with further transient increases in heart rate and arterial pressure
resulting from sympathetic nervous system activation.[42]
[44]
Similar increases in heart rate are observed
when the inspired isoflurane concentration is rapidly increased.[44]
The cardiovascular stimulation induced by rapid increases in desflurane or isoflurane
concentration in humans results from activation of tracheopulmonary and systemic
receptors[45]
and is attenuated by pretreatment
with β1
-adrenoceptor antagonists, α2
-adrenoceptor
agonists, or opioids.[43]
In contrast to the findings
with isoflurane and desflurane, sevoflurane neither alters heart rate[184]
[185]
[186]
[187]
nor causes cardiovascular stimulation during rapid increases in anesthetic concentration
in humans.[188]
All modern volatile anesthetics cause concentration-related decreases
in arterial pressure.[6]
[11]
[12]
[37]
[180]
[184]
The mechanism by which these anesthetics
reduce
arterial pressure differs among anesthetics. Decreases in arterial pressure produced
by halothane and enflurane can be primarily attributed to reductions in myocardial
contractility and cardiac output.[1]
In contrast,
decreases in arterial pressure associated with isoflurane, desflurane, and sevoflurane
anesthesia occur as a result of reductions in LV afterload,[143]
[144]
whereas myocardial contractility is relatively
preserved.[1]
Isoflurane, desflurane, and isoflurane
maintain cardiac output because these agents produce less pronounced reductions in
myocardial contractility and greater decreases in systemic vascular resistance than
does halothane or enflurane in humans.[34]
[186]
[189]
Isoflurane and desflurane may also preserve
autonomic nervous system regulation of the circulation to a greater degree than other
volatile anesthetics.[42]
[175]
[188]
The baroreceptor reflex-mediated tachycardia
that occurs during isoflurane and desflurane anesthesia maintains cardiac output
despite simultaneous declines in myocardial contractility and stroke volume. Declines
in arterial pressure produced by volatile anesthetics may be attenuated by surgical
stimulation or concomitant administration of nitrous oxide.[38]
[190]
Volatile anesthetics also cause modest, dose-related
increases in RA pressure in humans.[34]
[189]
These effects probably occur as a result of direct negative inotropic actions.
The vasodilating effects of isoflurane, desflurane, and sevoflurane cause less pronounced
increases in right atrial pressure than those observed during halothane or enflurane
anesthesia.
The cardiovascular effects of volatile anesthetics are altered
by the duration of anesthesia. Increases in myocardial contractility and cardiac
output and decreases in LV preload and afterload occur after several hours of constant-MAC
anesthesia.[6]
[12]
[37]
[179]
[191]
Heart rate may also increase during prolonged halothane[6]
[191]
or enflurane[179]
anesthesia, but arterial pressure remains constant. Recovery from circulatory depression
is greatest during halothane anesthesia[191]
and
less pronounced during prolonged administration of isoflurane[12]
and desflurane.[37]
The time-dependent improvements
in hemodynamics observed with volatile anesthetics are antagonized by propranolol
and may result from enhanced sympathetic nervous system activity.[192]
The systemic hemodynamic effects of volatile agents in the presence
of LV dysfunction are similar but not identical to those observed in the normal heart.
Volatile anesthetics, including isoflurane, modestly increase or do not affect heart
rate in experimental animals with pacing-induced or doxorubicin-induced dilated cardiomyopathy
[65]
[193]
and in
patients with coronary artery disease and LV dysfunction.[62]
[64]
[194]
[195]
These findings may be attributed to altered baroreceptor reflex activity, β1
-adrenoceptor
downregulation, and increases in central sympathetic and withdrawal of parasympathetic
nervous system tone associated with heart failure.[196]
Isoflurane and halothane cause pronounced reductions in LV end-diastolic pressure
and chamber dimension in cardiomyopathic dogs concomitant with decreases in mean
arterial pressure.[65]
These findings support previously
observed declines in pulmonary artery pressures during isoflurane, enflurane, and
halothane anesthesia in patients with coronary artery disease and heart failure[62]
[64]
[194]
[195]
and indicate that venodilation represents a major hemodynamic consequence of these
anesthetics in experimental and clinical heart failure. In contrast to the findings
in normal dogs, isoflurane did not beneficially influence, and halothane detrimentally
affected, the determinants of LV afterload in cardiomyopathic dogs.[147]
As a result of these actions and the simultaneous declines in LV preload and myocardial
contractility, cardiac output may be more profoundly reduced during isoflurane or
halothane anesthesia in the presence of preexisting LV dysfunction.[147]
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