blood pressure regulation

1. MECHANISMS TO CONTROL
BLOOD PRESSURE
PRESENTER :- DR RAVE RANJAN KUMAR
MODERATOR :- DR ZIA ARSHAD

2. ARTERIAL BLOOD PRESSURE
MAP is proportionate to the product of SVR ×
CO. This relationship is based on an analogy to
Ohm’s law, as applied to the circulation:
MAP − CVP ≈ SVR × CO
Because CVP is normally very small compared
with MAP the former can usually be ignored.
Hypotension is the result of a decrease in SVR,
CO, or both.
The largest pressure drop, nearly 50%, is across
the arterioles, and the arterioles account for the
majority of SVR.

3. MAP may be estimated by the following formula:
MAP = Diastolic pressure + Pulse pressure/3
Pulse pressure is the difference between systolic
and diastolic blood pressure.
Arterial pulse pressure is directly related to
stroke volume, but is inversely proportional to
the compliance of the arterial tree.
Thus, decreases in pulse pressure may be due to
a decrease in stroke volume, an increase in SVR,
or both.

4. CONTROL OF
THE SYSTEMIC VASCULATURE
AUTONOMIC CONTROL
• is primarily sympathetic.
• passes out of the spinal cord at all thoracic
and first two lumbar segments.
• innervate all parts of the vasculature except for
capillaries.
• regulate vascular tone which serve to regulate
blood pressure and the distribution of blood
flow to the various organs.

5. The vasculature has sympathetic
vasoconstrictor and vasodilator fibers.
• Sympathetic-induced vasoconstriction (via α1
adrenergic receptors) -- in skeletal muscles,
kidneys, gut and skin.
• Vasodilatory fibers -- in skeletal muscles,
mediates increased blood flow (via β-2-
adrenergic receptors) in response to exercise.

6. Vasomotor Centers
• Controls vascular tone and autonomic influences on the
heart.
• located in the reticular formation of the medulla and
lower pons.
• Vasoconstriction is mediated by the antero-lateral areas
of the lower pons and upper medulla, responsible for
adrenal secretion of catecholamines, as well as the
enhancement of cardiac automaticity and contractility.
• Vasodilatory areas, are located in the lower medulla,
are also adrenergic, but function by projecting inhibitory
fibers upward to the vasoconstrictor areas.
• Areas in the postero-lateral medulla receive input from
both the vagal and the glossopharyngeal nerves, important
role in mediating a variety of circulatory reflexes.

7. ENDOTHELIUM-DERIVED
FACTORS
• vasodilators (nitric oxide, prostacyclin[PGI2]),
Nitric oxide synthesized from arginine by
nitric oxide synthetase, binds to guanylate
cyclase , increases c-GMP levels and produces
vasodilation.
• vasoconstrictors ( endothelins,thromboxane A
-2), Endothelins are released in response to
thrombin and epinephrine.

8. Control of Arterial Blood Pressure
Immediate Control
• Minute-to-minute control
• Mediated by autonomic nervous system
reflexes :-
• Baroreceptor Reflexes
• Chemoreceptor Reflexes
• Bezold-Jarisch Reflex
• Atrial Reflexes
• Central Nervous System Ischemic Reflex

9. Baroreceptor Reflex
• Peripheral baroreceptors are located at the
bifurcation of common carotid arteries (carotid
sinus) and the aortic arch.
• Elevations in blood pressure increase
baroreceptor discharge. Carotid baroreceptors
send afferent signals to the depressor portion of
the vasomotor center via Hering’s nerve (a
branch of the glossopharyngeal nerve), whereas
aortic baroreceptor via the vagus nerve.
• leading to decrease in vasoconstrictive impulses
causing vasodilation throughout the peripheral
circulation, decreased heart rate, and decreased
myocardial contractility.

10. • Responsible for minimizing changes in blood pressure
that are caused by acute events, such as a change in
posture,blood loss and shock.
• Carotid baroreceptors sense MAP most effectively
between pressures of 80 and 160 mm Hg.
• Adaptation to acute changes in blood pressure occurs
over the course of 1–2 days, rendering this reflex
ineffective for longer term blood pressure control.
• All volatile anesthetics depress the normal
baroreceptor response.
• Patients with chronic hypertension have a decreased
baroreceptor reflex response.

11. Chemoreceptor Reflex
• located in the carotid bodies and aortic body
• responds to hypotension (SBP < 80 mmHg),
acidosis and hypoxia (Pao2 < 60 mm Hg )
• Impulses from the chemoreceptors are
transmitted to the vasomotor center leading
to increased sympathetic activity which
increases blood pressure towards normal.

12. Atrial Reflexes
• The right atrial wall and cavoatrial junction
contains low-pressure atrial stretch receptors.
• An increase intravascular volume causes an
increase in atrial pressure stimulating these
receptors. They send their impulses through
vagal afferents to inhibit parasympathetic
activity which leads to increase in heart rate
(Bainbridge reflex).
• The increase in heart prevents accumulation
of blood in the atria, veins, or pulmonary
circulation.

13. Bezold-Jarisch Reflex
• A decrease in left ventricular volume activates
chemoreceptors and mechanoreceptors present
in the LV wall which sends impulses through vagal
afferents leading to bradycardia.
• This compensatory decrease in heart rate allows
for increased ventricular filling, but this also
exacerbate hypotension.
• The bradycardia and hypotension that can occur
during spinal or epidural anesthesia and during
reperfusion of ischemic myocardium have been
attributed to this reflex.

14. Central Nervous System Ischemic
Reflex
• The Cushing reflex is a central nervous system
ischemic reflex response that results from
increased intracranial pressure.
• The initial reflex is a direct CNS sympathetic
stimulation leading to increased heart rate,
contractility and blood pressure in an effort to
increase cerebral perfusion.
• This is followed by reflex bradycardia mediated by
baroreceptors reflex as a result of increased
peripheral vascular tone.

15. Intermediate Control
• In the course of a few minutes
• Sustained decreases in arterial pressure,
together with enhanced sympathetic outflow,
activate the renin–angiotensin–aldosterone
system, increases secretion of arginine
vasopressin (AVP), and alter normal capillary
fluid exchange.
• Both angiotensin II and AVP are potent
arteriolar vasoconstrictor. Angiotensin constricts
arterioles via AT 1 receptors. AVP mediates
vasoconstriction via V 1 receptors and exerts its
antidiuretic effect via V 2 receptors.

16. Long-Term Control
• Apparent within hours of sustained changes in
arterial pressure.
• The kidneys alter total body sodium and water
balance to restore blood pressure to normal.
Hypertension increases sodium and water
excretion. The resultant decrease in blood
volume leads to decreases in cardiac output
and systemic blood pressure.
• Contrasts with rapid-acting to moderately rapid-
acting mechanisms, which cannot return systemic
blood pressure entirely back to normal.

17. AUTOREGULATION
• Most tissue beds regulate their own blood
flow (autoregulation). Arterioles generally dilate
in response to reduced perfusion pressure or
increased tissue demands and vice-versa.
• Due to both an intrinsic response of vascular
smooth muscle to stretch and the accumulation of
vasodilatory metabolic by-products like K + , H + ,
CO2, adenosine, and lactate.