Inhaled Anesthetics:
Cardiovascular Effects
- Dose-dependent & drug-specific
circulatory effects,
e.g.:
- Desflurane (Suprane) and
sevoflurane (Sevorane, Ultane) -- similar
to older inhaled anesthetics;
- Sevoflurane (Sevorane,
Ultane): characteristics of both
isoflurane (Forane) and halothane (Fluothane)
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Manifestations of
drug-mediated circulatory effects-- changes in:
Heart rate
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Stroke volume
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Peripheral vascular resistance
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Blood pressure
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Right atrial pressure
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Cardiac rhythm
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Coronary blood flow
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Cardiac output
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- Inhalational
anesthetic effects on circulation will be
influenced by:
- Controlled ventilation vs.
spontaneous breathing
- Existing heart disease
- Presence of cardioactive
drugs
- Mechanisms by which
inhalational agents influence the circulatory
system:
- Changing myocardial
contractility
- Affecting peripheral vascular
smooth muscle tone
- Altering autonomic nervous
system activity
- Mean Arterial Pressure
(MAP): inhalational agents
- Halothane (Fluothane), and
sevoflurane (Sevorane, Ultane),
isoflurane (Forane), desflurane (Suprane): produce similar, dose-dependent
decrease in MAP in healthy volunteers
- Greater
MAP decrease observed than with
surgical stimulation
- Reduction
in MAP following volatile
anesthetic administration may be
due to the sum of:
- Reduced sympathetic
activation caused by
preoperative anxiety
- Direct pharmacological
effects of volatile
anesthetics
- Nitrous oxide:
- No change
or slight increase in systemic
blood-pressure
- Substitution of nitrous
oxide for some volatile
anesthetic proportion reduces the
BP magnitude decrease produced by
the volatile anesthetic alone
(equal MAC).
- Halothane (Fluothane):
mechanism of blood pressure reduction:
- Reduced myocardial
contractility and reduced cardiac
output
- Isoflurane (Forane),
desflurane (Suprane), sevoflurane
(Sevorane, Ultane): mechanism of blood
pressure reduction:
- Reduced systemic
vascular resistance
- Heart rate: Inhalational
agents
- Increased
rate in healthy individuals:
- Isoflurane (Forane)
- Desflurane (Suprane)
- Sevoflurane (Sevorane, Ultane) (> 1.5 MAC)
- Heart rate in surgical patients: sensitive to a number of
variables: e.g. --
- Isoflurane (Forane)-mediated increase in
heart rate prevented by
preoperative morphine or fentanyl
(Sublimaze) administered just
before induction
- Patients
apprehension/anxiety (excessive sympathetic
activity) increases preoperative
heart rate and may reduce a
further increase due to the
volatile anesthetic
- Excessive
parasympathetic tone may
predispose to a greater
than anticipated increase
in heart rate during
anesthetic administration
- Halothane (Fluothane):
- Heart rate
unchanged; BP decreased
- Mechanisms:
- Halothane (Fluothane)-mediated
baroreceptor-reflex
depression
- Reduced phase 4
depolarization (sinus
node suppression by
halothane (Fluothane))
- Halothane (Fluothane): --
generalized reduction in
cardiac conduction
velocity
- Desflurane (Suprane) (0.5 MAC):
- Reduced systemic
blood-pressure (similar to
isoflurane (Forane))
- No increased heart
rate compared to isoflurane
(Forane) {at 0.5 MAC}
- Isoflurane (Forane):
- Neonates:
- Reduced blood pressure;
no increase in heart rate
- Mechanism: - reduced
carotid sinus reflex
- Elderly
patients: attenuated heart rate
responses
- Younger
patients: increased heart rate
{promoted by vagolytic drugs,
e.g. atropine, pancuronium (Pavulon)}
- Cardiac Output/Stroke
Volume
- Halothane (Fluothane):
dose-dependent decreased in cardiac
output (normal volunteers)
- Isoflurane (Forane),
desflurane (Suprane), sevoflurane (Sevorane, Ultane): no effect on cardiac
output in normal volunteers
- Sevoflurane (Sevorane, Ultane):
- Decreased cardiac
output at 1 & 1.5 MAC
- Minimal effect at 2
MAC
- Generally: volatile
anesthetics decrease left ventricular
stroke volume by about 15% to 30%
(calculated)
- Cardiac output, in
patients, maybe minimally
affected since many volatile
anesthetics increase heart rate (
compensating for a decrease in
stroke volume)
- Nitrous oxide: slightly
increased cardiac output (nitrous oxide
has a slight sympathomimetic effect)
- Isoflurane (Forane):
- Good maintenance of
heart rate
- Minimal cardiac
output depression
- Reduced impact of
isoflurane (Forane) on myocardial
contractility may be secondary to
its higher anesthetic potency
compared halothane (Fluothane)
--i.e., the brain is depressed at
a concentration less than that
required to depress cardiac
contractility
- Systemic Vascular
Resistance:
- Halothane (Fluothane):
minimal effect on systemic vascular
resistance in normal volunteers
- Some organ level
vasodilation, i.e. cerebral
vasodilation and significant
cutaneous vessel vasodilation
- These effects
offset by no change or
vasoconstriction in other
vascular beds
- Isoflurane (Forane),
desflurane (Suprane), sevoflurane
(Sevorane, Ultane): decreased systemic
vascular resistance in normal volunteers
- All four agents reduce
systemic blood-pressure -- only halothane
(Fluothane) does so by primarily decreasing
cardiac output {reduced myocardial
contractility}
- The other agents do
so by reducing vascular
resistance.
- Isoflurane (Forane) --
Mechanism of systemic vascular resistance
decrease:
- Significant increase
in skeletal muscle blood flow
- Increased cutaneous
blood flow
- Increased cutaneous flow
is characteristic of all
volatile anesthetics {in
this condition peripheral
venous blood provides an
alternative to arterial
blood sampling to
evaluate pH and PaCO2}
- Duration of Anesthetic
Administration and Cardiac Effects:
- Administration of a volatile
anesthetic for longer than 5 hr results
in the recovery from depressing effects
-- i.e.:
- At constant MAC:
cardiac output returns to normal
after five hours
- Heart rate
may remain increased,
systemic blood-pressure
is unchanged {increase in
cardiac output is
balanced by decreases in
systemic vascular
resistance}
- Recovery with time
-- most apparent with halothane
(Fluothane); least apparent with
isoflurane (Forane) {note that
isoflurane (Forane) does not
significantly change cardiac
output even at 1 hour}
- Mechanism:
- Probably a
beta-adrenergic response,
since propranolol
(Inderal) pre-treatment
prevents cardiovascular
recovery with increased
anesthetic administration
time.
- Pulmonary Vascular
Resistance
- Inhalational
agents: limited/not predictable effect on
pulmonary vascular bed smooth muscle
- Nitrous oxide:
increased pulmonary vascular resistance
in patient with pulmonary hypertension
(preexisting)
- Neonate: sensitive
to nitrous oxide-mediated pulmonary
vasculature vasoconstriction (independent
of preexisting pulmonary hypertension)
- Congenital heart
disease: nitrous oxide-mediated
increasing pulmonary vascular resistance
may cause increased right-to-left intracardiac
blood shunting (May worsen arterial
oxygenation)
- Cardiac Arrhythmias:
- Volatile anesthetics: range
of myocardial sensitizing effects to
epinephrine-induced arrhythmias
- Greatest sensitizing
effect: halothane (Fluothane)
- Minimal/not
apparent: isoflurane (Forane),
desflurane (Suprane), sevoflurane (Sevorane,
Ultane)
- Lidocaine (Xylocaine) (0.5%)
in submucosal-injected epinephrine
reduces myocardial sensitivity to
epinephrine
- Coronary Blood Flow:
- Volatile anesthetics: cause
coronary vasodilation
- target vessels: 20
microns - 200 microns in diameter
- Isoflurane (Forane):
preferential dilation of small coronary
resistance vessels (relative to larger
conductance vessels)
- Isoflurane (Forane):
greater vasodilatory effects
compared to halothane (Fluothane)
or enflurane (Ethrane) (but less
than adenosine
- Preferential
dilation of small coronary
resistance vessels may cause
blood redistribution from
ischemic to relatively
nonischemic areas, known as
"coronary steal syndrome"
- "Coronary steal
syndrome" more
likely to be seen with
potent coronary vasodilators, e.g. adenosine
- Evidence of intraoperative
myocardial ischemia based upon ST segment
ECG changes:
- Nitrous oxide-isoflurane (Forane)
anesthesia
- Greater
incidence of ischemia in patients
undergoing CABG surgery when
anesthetic included isoflurane
(Forane) {relative to enflurane (Ethrane)}
- Factors
predisposing to "coronary steal
syndrome":
- Total
occlusion of the major artery
with collateral flow distal also
impeded by significant vessel
stenosis (> 90%)
- About 12%
of patients may have requisite
anatomy that predisposes to
"coronary steal
syndrome"
- Ischemia
incidence in patients with
predisposing "coronary steal
syndrome" anatomy is
comparable in patients receiving
isoflurane (Forane), halothane
(Fluothane), enflurane (Ethrane),
or sufentanil (Sufenta).
- Generally, it is more likely
that a patient {with or without coronary
artery disease and without tachycardia or
hypotension} will experience myocardial
ischemia with isoflurane (Forane)
compared to halothane (Fluothane).
- Desflurane
(Suprane) & sevoflurane (Sevorane,
Ultane): no coronary vasodilation = no
possibility of "coronary steal
syndrome"
- Nitrous oxide: no
evidence for induction of myocardial
ischemia in patients with coronary artery
disease when nitrous oxide is an adjuvant
to fentanyl (Sublimaze)
- Significant
factors predisposing to myocardial
ischemia development:
- Presence/absence
of beta-adrenergic block
- Changes in
systemic blood-pressure
- Changes in
heart rate
- Perioperative
incidence of myocardial ischemia is
usually a reflection of underlying
coronary artery disease [as opposed to a
consequence of a particular anesthetic
used}
- Avoiding
perioperative myocardial ischemia:
- Inclusion of opioids
in the anesthetic protocol
- Prior treatment with
beta-adrenergic receptor blockers
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