Drug

EEG

Nitrous Oxide
Dose dependent; as dose of
anesthetic approaches 1 MAC,
the frequency on the EEG
decreases, and the max
voltage occurs

CBF

As vasodilator MORE potent

than isoflurine.

Nitrous>iso>des>sev

Isoflurane
Dose dependent; as
dose of anesthetic
approaches 1 MAC, the
frequency on the EEG
decreases, and the max
voltage occurs
Neuroprotective
effects; does not alter
the responsiveness of
the cerebral circulation
to changes in PaCO2.

Desflurane
Dose dependent; as dose of
anesthetic approaches 1 MAC,
the frequency on the EEG
decreases, and the max
voltage occurs

Sevoflurane
Dose dependent; as dose of
anesthetic approaches 1 MAC,
the frequency on the EEG
decreases, and the max
voltage occurs

Comments:
As the dose approaches
1MAC, the frequency on
the EEG decreases, and
the max voltage occurs.

Dose-dependent increase in

Dose-dependent increase in

Increase

Increase

Anesthetic induced
changes are independent
of BP; do not alter
responsiveness of
cerebral circulation to
changes in PaO2.
Dose-dependent
decreases; not
predictably provided
ALL increase ICP;
Recommendation:
hyperventilate- CO2

CBF; Nitrous>iso>des>sev

CBF; Nitrous>iso>des>sev

>Decrease

CMO2

ICP

Increase

Increase

CSF

No increased production

Conscious memory
BP

Suppressed (0.6 MAC)

No effect to moderate
increase

No increased
production
Suppressed (0.45 MAC)

<30mmHg

HR

CI

SVR

> FALL due to

vasodilation (SVR)

Dose-dep, but even Low

dose

Dose dep fall; vasodilation

(SVR)

Dose dep fall; vasodilation

(SVR)

due to sympathetic outflow

from irritation to tissues
after inhaling coughing,
gagging. Req higher dose.

No f; despite decrease in BP;

suggesting depression of the
carotid sinus reflex response

Volatile anesthetics
produce dose-dep in BP.
Tx: Provide surgical
stimulation and
substitution of N.O. to
decrease the magnitude
of BP decline.
Advanced age and opioids
may blunt HR response.
Enhanced HR responses
with young pts and with
drugs with vagolytic
properties
(anticholinergics)

Maintains CI with a slight

bump due to sympathetic
outflow
All volatiles cause some
degree of vasodilation

CO

Modest increase reflecting

mild sympathomimetic effect

RAP

Slight increase due to

increased pulm vascular
resistance from
sympathomimetic effects
May increase esp in pts with
hypertension.
Caution: pts with pulm HTN

Peripheral
vascular
resistance
Dysrhythmias

Coronary blood
flow

Rate and amount

of MAC f

No significant decrease

No significant decrease

No significant decrease

Possible explanation of
decreased impact of iso,
des, and sev on
myocardial contractility
may be the greater
anesthetic potency (more
readily depress the brain)

Dose-dependent
decrease that parallel
decrease in BP

Dose-dependent decrease that

parallel decrease in BP

Dose-dependent decrease
that parallel decrease in BP

Alkane structure
decreases drug ability
to sensitize heart to
epi resulting in
arrhythmias
More potent
vasodilator and causes
redistribution of
coronary blood flowcoronary steal areas
with >90% stenosis

Alkane structure decreases

drug ability to sensitize heart
to epi resulting in arrhythmias

Alkane structure decreases

drug ability to sensitize heart
to epi resulting in arrhythmias

Volatile anesthetics exert

little or NO predictable
effect on pulmonary
vascular smooth muscle
Halothane sensitizes
heart to epi; making it
susceptible to
dysrhythmias

Does not present coronary

steal properties

Caution with angina and

hx MI. (Iso)

Rapid increases in MAC

increases sympathetic
nervous system activity
(catecholamines release),
HR, & Bp, more than
equivalent increase in iso
Small increases in
concentration to >6% is
more likely to cause
transient increase in HR,
BP, and plasma epi
concentration than similar
1% increases below 5%.

Admin of Fentanyl,
esmolol, or clonidine 5 min
before an abrupt increase
in anesthetic blunts
evidence of CV
stimulation. Note:
fentanyl may be most
useful since it blocks
increases in HR & BR but
has minimal CV effects
and little postanesthetic
sedation..

Spontaneous breathing: Volatile anesthetics: Vented pts maintain normocapnia by increasing systemic BP and HR, while decreasing SVR. (slide 40)

Preexisting disease and drug therapy: Whatever the drug or disease is, the effects are additive
Mechanism: Circulatory Effects: Direct myocardial depression
Inhibition of CNS sympathetic outflow
Peripheral autonomic ganglion blockade
Attenuated carotid sinus reflex activity
Decreased formation of cAMP
Decreased influx of Ca ions through slow channels
Mask Induction agent: most prominent- Sevoflurine (peds); nitrous can be used by not high enough concentration alone.

Solubility
Isoflurine
Nitrous Ox
Desflurine
Sevoflurine

Blood :
Gas
1.46
0.46
0.42
0.69

Brain :
Blood
1.6
1.1
1.3
1.7

Drug
Nitrous Oxide
Isoflurane
Desflurane
Sevoflurane

Muscle : Blood

MAC %
105
1.2
6
2

2.9
1.2
2
3.1

Fat :
Blood
44.9
2.3
27.2
47.5

Vapor Pressure
Liquid
240
681
160

Oil : Gas
98
1.4
18.7
55