reflex

Stimulus

Cardiac output
regulation

When neither the

contractility nor the HR
is compromised, this
mechanism ensures
that the return of blood
flow to the heart will
maintain CO.
Hypertension resulting
in baroreceptor
stimulation; carotid
baroreceptors send
afferent response via
hering and
glossopharyngeal
nerves (CNIX); aortic
baroreceptors send
afferent response via
the vagus nerve (CNX)
Forced expiration
against a closed glottis
mediated via
baroreceptors

Baroreceptor
reflex

Valsalva
maneuver

Oculo cardiac
reflex

Celiac reflex

Traction on the
extraocular muscles
(especially medial
rectus) or pressure on
the globe causes an
afferent response via
the trigeminal nerve
(CNV) and results in an
efferent vagal response
via the vagus nerve
(CNX)
Traction or pressure on
structures within
abdominal and thoracic
cavities causes vagal
nerve stimulation

Response

Anesthesia
considerations
Many of the factors that
affect CO also affect the
MAP. Some of the
reflexes are listed below
and they alter the CO are
described.

Decrease heart rate,

decreased contractility,
peripheral vasodilation
from efferent response
via the vagus nerve
(CNX)

The baroreceptor
response is inhibited by
volatile anesthetic
agents in a dosedependent manner and
results in a decreased
ability of the
baroreceptors to respond
to BP changes when
these agents are used.

Decreased heart rate,

decreased contractility,
peripheral vasodilation
from efferent response
via the vagus nerve
(CNX)

Epidural anesthesia can

be used. General
anesthesia is preferred. If
hypotension occurs
during anesthesia, alphaagonists such as
phenylephrine can help.
Titration of anesthetic
agents and adequate
volume loading is
essential to safely
conduct anesthesia in
this clinical setting.
Response can be
inhibited by an
anticholinergic agent
(atropine or
glycopyrrloate)

Bradycardia,
hypotension, and
arrhythmias

Bradycardia,
hypotension and apnea.

Clinically, the celiac

reflex can be initiated
indirectly as a result of a
pneumoperitoneum.
Celiac reflex is frequently
resolved by stopping the
initiating stimulus.

Bainbridge
reflex

Hypervolemia,
increased venous
return causes
stimulation of atrial
stretch receptors

Increased HR, decreased

BP, decreased systemic
vascular resistance,
diuresis.

Cushing reflex

Increased intracranial
pressure resulting in
cerebral ischemia

Sympathetic nervous
stimulation resulting in
increased BP

Chemoreceptor
reflex

Decreased oxygen
saturation, increased
CO2, increased
hydrogen ion
concentration;
peripheral
chemoreceptors
located in the carotid
body and aortic arch.

Increased respiratory
drive, increased blood
pressure

This reflex relates to the

characteristic but
paradoxical slowing of
the heart seen with
spinal anesthesia.
Blockade of the
sympathetic nervous
system at T1-T4 levels
ablates the efferent limb
of the cardiac
accelerator nerves.
(therefore, unopposed
vagus to cause
bradycardia.) The
primary defect in the
development of spinal
hypotension is a
decrease in venous
receptors to cause
bradicardia. Reflex
tachycardia is the usual
response to hypotension
or acidosis from other
causes. Drug of choice
for bradycardia is
isoproterenol which
causes an increase in the
discharge rate of the
donor SA node by direct
ction.
Use medications to
decrease ICP or
correction of ICP via
other methods for
example mannitol and
decrease cerebral
ischemia to correct
cushing reflex.
This reflex can be
inhibited by the volatile
anesthetic agents in a
dose-dependent manner.
Thus if residual volatile
agent is present during
the emergence from
anesthesia, the threshold
for breathing will be
increased, necessitating
a higher PaCO2 prior to
spontaneous
respirations.