(with wide pulse pressure)
can be caused either by conditions of decreased
aortic compliance, often due to arteriosclerosis
or to increased stroke volume.
As blood volume returning to the
heart increases, preload increases and
there is enhanced filling with
ventricular dilation.
According to Starling's Law,
increased ventricular stretch usually
leads to increased contractility.
Increased preload and
increased contractility lead to increased
stroke volume and ultimately an increase
in arterial pressure, all other factors
remaining equal.
Some antihypertensive drugs
decrease preload.
Heart rate: Since the product of heart
rate and stroke volume equals cardiac output, an
increase in heart rate will increase arterial
blood pressure, all other factors remaining
equal.
Some antihypertensive agents
decrease heart rate (ß-adrenergic
receptor antagonists, e.g.).
Heart Rate
X Stroke Volume = Cardiac Output
Cardiac
Output X Peripheral Resistance = Arterial
Pressure
Peripheral resistance: For a given
cardiac output, blood pressure depends only on
peripheral resistance. Some antihypertensive
drugs act to reduce peripheral resistance.
A
principal mechanism for arterial blood pressure
control is the baroreceptor reflex.
The reflex is initiated by activation
of stretch receptors located in the wall of most
large arteries of the chest and neck.
A high density of baroreceptors is
found in the wall of each internal carotid artery
(just above the carotid bifurcation i.e. carotid
sinus) and in the wall of the aortic arch.
As pressure rises and especially
for rapid increases in pressure:
baroreceptor input to the tractus
solitarius of the
medulla results in inhibition of the
vasoconstrictor center and excitation of
the vagal centers and therefore:
a vasodilatation of the veins and
arterioles in the peripheral vascular
beds and negative chronotropic and
inotropic effects on the heart occurs.
(slower heart rate with reduced force of contraction)
There is probably excessive concern
about interaction potential between anesthetics
and antihypertensive drugs.
Areas of concern for administration
of anesthetic to patients treated with
antihypertensive medications:
Reduced sympathetic nervous
system activity--manifestations:
Orthostatic hypotension
Excessive
systemic blood-pressure responses
(decreases) to:
acute
blood loss
body
position changes
decreased
venous return cause by
positive-pressure
ventilation
Reduced
sensitivity to indirect-acting
sympathomimetic agents (cause by
antihypertensive drugs that
deplete norepinephrine from nerve
terminals
Possible
enhanced response to
catecholamines and direct-acting
sympathomimetics following
sympathetic nervous system
blockade (reduced
alpha-adrenergic receptor tone with loss of
tonic stimulation)
Altered physiological
response to sympathomimetic agents
Sedation
Maintenance of antihypertensive drug
treatment during perioperative time frame:
Fewer systemic
blood-pressure and heart rate
fluctuations during anesthesia
Decreased likelihood of
cardiac dysrhythmias
Conclusion:
Previously
effective antihypertensive drug
therapy should be continued
during the perioperative period.
The
pharmacology of the particular
antihypertensive drug should be
considered in the development of
the anesthesia plan.
Stoelting, R.K., "Antihypertensive Drugs",
in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven
Publishers, 1999, 302-312.
above to
begin the lecture
