BLOOD PRESSURE

Outline
• Definitions
• Blood pressure
• Determinant of blood pressure
• Measurement of blood pressure
• Regulation of blood pressure
– Short term
– Long term
 Definitions:

• Blood pressure is the force exerted by

circulating blood per unit surface area on the
walls of blood vessels.
• The pressure of the circulating blood
decreases as blood moves through arteries,
arterioles, capillaries, and veins; the term
blood pressure generally refers to arterial
blood pressure, i.e., the pressure in the
larger arteries.
• Units = mmHg / cmH2O
 Definitions (cont’d)
• Systolic pressure(SBP) is defined as the peak
pressure generated during systolic contraction.
• Diastolic pressure(DBP) is the lowest pressure
during diastolic relaxation.
• Pulse pressure(PP) is the difference between the
systolic and diastolic pressure.
• Mean arterial presssure (MAP) is average pressure
throughout the cardiac cycle.
MAP= [(SBP)+2(DBP)] / 3
1 mmHg = 1.36 cmH2O.
Of 2 components:
– systolic … (= max press reached) = 110-130 mmHg.
– diastolic … (= min press reached) = 70-90 mmHg
 Factors affecting BP
• Sex :- M > F …due to hormones/ equal at menopause.
• Age:- Elderly > children …due to atherosclerosis.
• Emotions:-  due to secretion of adrenaline & noradrenaline
• Exercise:-  due to  venous return.
• Hormones:-  (e.g. Adrenaline, noradrenaline, thyroid H).
• Gravity:-  Lower limbs > upper limbs.
• Race:- Orientals > Westerns … ? dietry factors, or weather.
• Sleep:-  due to  venous return.
• Pregnancy:-  due to  metabolism.
 Factors determining Arterial Blood Pressure:

Blood Pressure = Cardiac Output X Peripheral Resistance

(BP) (CO) (PR)

Flow Diameter of
arterioles

BP depends on:
1. Cardiac output  CO = SV X HR.
2. Peripheral resistance.
3. Blood volume.
 Measurement of Blood Pressure:

• Usually we measure two types of Blood Pressure

i.e. NIBP (non invasive) and IBP (invasive).
• NIBP: it can be measured by following ;

• Palpation:
– Inflating the cuff to a limit ,deflating it by 2mg per
beat and measuring the cuff pressure at which
arterial pulse begins gives the SBP. It can’t
measure DBP.
• Auscultation:
– Deflating the cuff from a limit ,appearance of
korotkoff indicates SBP and muffling denotes DBP. It
can’t detect the “Auscultatory gap”
• Oscillometry:
– It based on on change in the magnitude of
oscillation.it is very sensitive to movement and also
can’t measure BP during Shock.
• Doppler:
– It measure BP by determining the flow distal to the
artery. Previosly doppler only to measure SBP but
now use of piezoelectric crystal in doppler can
detect both SBP & DBP.
 Auscultation

• BP is measured with a sphygmomanometer usually

at the brachial artery.
Equipment
• A (functioning) sphygmomanometer
• An appropriately sized cuff
• Stethoscope.
 Theory

• A cuff is applied to the upper arm and inflated so as

to cut off the arterial supply.
• The pressure is released slowly and a stethoscope
used to listen for the blood flow.
• When the pressure in the cuff equals the systolic
blood pressure, blood will audibly pulse through the
artery.
• When the cuff pressure falls below the diastolic
blood pressure, the blood will flow continuously and
the sound of intermittent blood flow will disappear.
 Procedure / Technique
• The patient should be sitting, relaxed for 5 minutes
beforehand.
• Apply the cuff to the upper arm with the air bladder
anteriorly (over the brachial artery).
• Using your left arm, support the patient's arm so that it
is held horizontally at the level of the mid-sternum.
• Close the valve (may be a screw or lever), monitor the
patient's radial artery, and inflate the cuff until the
radial pulse is no longer palpable.
• Listen over the brachial artery at the antecubital fossa
using the diaphragm or the bell of the stethoscope
whilst deflating the cuff at a rate of 2-3mmHg/sec.
• Note the point at which the pulsation is audible
(Korotkoff* phase I “the systolic BP”)
• And the point at which the sounds disappear (Korotkoff
phase V”the diastolic BP).
• Record the BP as systolic/diastolic to the nearest
2mmHg.
• In some normal people, the sounds may not disappear
completely. In this case, a distinct muffling of the noise
(Korotkoff phase IV) should be used to indicate the
diastolic BP.
• BP recording may be particularly difficult in a noisy
hospital ward at the time of an emergency (which is
when doctors are most often asked to record the BP) or
when the BP is very low. In this case, a rough
estimation of the systolic BP may be made by feeling
for the return of the radial pulse as the cuff is deflated.
(palpation method)
 Invasive Blood Pressure (IBP):
• It is a method of measuring blood pressure
internally by using a sensitive IV catheter inserted
into an superficial artery . This provides a more
accurate reading of the patent's current blood
pressure.
Indication:
• Procedure where continuous BP monitoring
required.
• Failure of NIBP measurement.
• Repeated blood sampling.
• Planned Pharmacological or mechanical
cardiovascular manipulation.
• IBP is avoided in the absence of collateral
circulation which to be elicited by doing Allen test.
• In the wave form the SBP,DBP,MAP is determined by
the upstroke, down stroke and area under the
pressure curve respectively.
• Complications include distal ischemia, bleeding,
embolisation,infection and fistula formation.
 Classification of High Blood Pressure for Adults
Aged 18 Years and Older

Category Systolic Diastolic

Normal < 120 < 80
Pre Hypertension 120-139 80-89
Hypertension: 140 - 159 90 - 99
Stage-1
Stage-2 >160 >100

Based on the average of 2 or more properly measured, seated, BP

readings on each of 2 or more office visits.
 Regulation of BP
• There are two basic mechanisms for regulating blood
pressure:
(1) short-term mechanisms.
regulate blood vessel diameter, heart rate and
contractility
(2) long-term mechanisms.
regulate blood volume
• Blood Pressure = cardiac output x peripheral resistance
• Any change in cardiac output, blood volume or peripheral
resistance will lead to a change in blood pressure.
• Short term control of Blood pressure is mediated by the :

I. nervous system
II. Chemicals

• That control blood pressure by changing peripheral

resistance. ( in sec or minutes)
• Rapidity of response (beginning within seconds and often
increasing the pressure to 2X normal (5 to 10 seconds).
• Sudden inhibition of nervous cardiovascular stimulation
can decrease the arterial pressure (one half normal)(10-
40 seconds).
 I. Nervous System
• Control BP by changing blood distribution in the body and by
changing blood vessel diameter.
• Sympathetic & Parasympathetic activity will affect veins, arteries
& heart to control HR and force of contraction
The vasomotor center
• Cluster of sympathetic neurons found in the medulla.
• It sends efferent motor fibers that innervate smooth muscle of
blood vessels.
Sympathetic activity Sympathetic activity

VASOCONSTRICTION VASODILATATION
Short-term Regulation of Rising Blood Pressure

Rising blood pressure

Stretching of arterial walls

Stimulation of baroreceptors in carotid

sinus, aortic arch, and other large
arteries of the neck and thorax

Increased impulses to the brain

 Baroreceptors
• The best known of nervous mechanisms for arterial
pressure control (baroreceptor reflex)
• Baroreceptors are stretch receptors found in the
carotid body, aortic body and the wall of all large
arteries of the neck and thorax.
• Respond progressively and effectively at 60-180 mm
Hg.
• Respond more to a rapidly changing pressure than
stationary pressure.
High pressure baroreceptors respond to stretch in
the aortic arch and carotid sinus.

sinus nerve

depressor nerve
Carotid and Aortic Baroreceptors
Baroreceptors
 Effect of Baroreceptors

Baroreceptors entered the medulla (tractus solitarius)

Secondary signals inhibit the vasoconstrictor center of medulla

and excite the vagal parasympathetic center

EFFECT
DECREASED HEART RATE AND
VASODILATATION OF THE
STRENGTH OF HEART
VEINS AND ARTERIOLES
CONTRACTION

Therefore, excitation of baroreceptors by high pressure in the arteries

reflexly causes arterial pressure to decrease (as decrease in PR and CO)

NOTE : Conversely, low pressure has opposite effects,reflexly causing the pressure rise
back to normal.
 Increased Parasympathetic Activity

Effect of increased parasympathetic and decreased

sympathetic activity on heart and blood pressure:
• Increased activity of vagus (parasympathetic) nerve
• Decreased activity of sympathetic cardiac Nerves
• Reduction of heart rate
• Lower cardiac output
• Lower blood pressure
 Decreased Sympathetic Activity

Effect of decreased sympathetic activity on arteries

and blood pressure:
• Decreased activity of vasomotor fibers (sympathetic
nerve fibers)
• Relaxation of vascular smooth muscle
• Increased arterial diameter
• Lower blood pressure
 Short-term Regulation of Falling Blood Pressure
Baroreceptors inhibited

Decreased impulses to the brain

Decreased parasympathetic activity,

increased sympathetic activity

Effects
Heart Vessels Adrenal gland
increased heart rate and increased vasoconstriction release of epinephrine and
increased contractility norepinephrine which enhance heart rate

Contractility and vasoconstriction

Increased blood pressure

• Sympathetic Activity on Heart and Blood Pressure

Effect of Increased Sympathetic Activity on Heart and

Blood Pressure:
• Increased activity of sympathetic cardiac nerves
• Decreased activity of vagus (parasympathetic) nerve
• Increased heart rate and contractility
• Higher cardiac output
• Increased blood pressure
 Vasomotor Fibers

• Effect of Increased Sympathetic Activity on

Arteries and Blood Pressure:
• Increased activity of vasomotor fibers
(sympathetic nerve fibers)
• Constriction of vascular smooth muscle
• Decreased arterial diameter
• Increased blood pressure
Effect of increased sympathetic activity
on adrenal glands and blood pressure:
• Increased sympathetic impulses to adrenal
glands.
• Release of epinephrine and norepinephrine to
bloodstream.
• Hormones increase heart rate, contractility and
vasoconstriction. Effect is slower-acting and
more prolonged than nervous system control.
• Increased blood pressure.
II. Chemoreceptor
 Chemoreceptor
• Chemosensitive cells that respond to changes in pCO2 and
pO2 and pH levels (Hydrogen ion).

pO2 and pH
pCO2 


Stimulation of
vasomotor center

CO  HR vasoconstriction

BP (speeding return of blood

to the heart and lungs)
Chemoreceptor
 CNS Ischemic Response
Severe decrease blood flow to brain

Cerebral hypoxia

Vasomotor center stimulated – causes powerful

vasoconstriction
( INCREASE SYMPATHETIC DISCHARGE – Norepinephrine)

Increase blood pressure & blood flow

 Cushing Reaction
(Special type of CNS Ischemic Response)

Increased pressure of cerebrospinal fluid (cranial vault)

Increase intracranial tension

Compress whole brain & arteries in the brain

Cuts off blood supply to brain

CNS Ischemic Response initiated & arterial pressure rises

Relieve brain ischemia

Blood vessel effect
Innervation of blood vessels
➢ Sympathetic
vasoconstrictor fiber
➢ Distribution: Almost all
segments of the circulation.
➢ The innervation is powerful
in the kidneys, gut, spleen
and skin
➢ is less potent in both skeletal
and cardiac muscle and in the
brain.
Innervation of blood vessels

➢Almost all vessels, such as arteries, arterioles,

venules and veins are innervated.
➢except the capillaries, precapillary sphincters and
most of the metarterioles.

➢Tone: Usually the sympathetic vasoconstrictor

fibers keep tonic.
Parasympathetic nerve fiber to peripheral
vessels
• Parasympathetic nerve fibers innervate
vessels of the blood vessels in
– Meninges
– salivary glands
– liver
– viscera in pelvis
– external genitals

• Importance: Regulate the blood flow of these

organs in some special situations.
 Cardiac Centres (Higher Centres)

1. Cardio Acceleratory Centre sends sympathetic neurones down the spine to

between T1 and T5, where they exit to the periphery.

2. Cardio Inhibitory Centre originates with the Vagus Nucleus in the medulla
and this parasympathetic nerve leaves the cranium as the Vagus (X) Nerve.

3. Vasomotor Centre - is a cluster of sympathetic fibres in the Medulla.

- transmits impulses via sympathetic vasomotor fibres
from T1 to L2 to blood vessels (arterioles)

Vasoconstriction is caused by increased frequency of impulses (Noradrenaline)

Vasodilation is caused by decreased frequency of impulses.
Brainstem contains:

Pons
Medulla

In the Medulla are the:

Cardiac Acceleratory Centre

Cardiac Inhibitory Centre
Vasomotor Centre
 Short-Term Regulation
(minute to minute regulation)

• Rapidly Acting Pressure Control Mechanisms, Acting Within

Seconds or Minutes.

A. Baroreceptor reflexes (60 – 100 mmHg)

Change peripheral resistance, heart rate, and stroke volume in
response to changes in blood pressure
B. Chemoreceptor reflexes (40 – 60 mmHg)
Sensory receptors sensitive to oxygen lack, carbon dioxide
excess, and low pH levels of blood
C. Central Nervous System ischemic response (< 40 mmHg)
Results from severe decrease blood flow to the brain
 Baroreceptor reflexes
Baroreceptors are found in :
• Carotid Sinuses (blood going to brain) by glossopharyngeal nerve
• Aortic Arch (systemic blood going to body) by vagus nerve

As MAP increases this stretches the receptors and they send a fast train of
impulses to the Vasomotor Centre. After the signals enter the tractus solitarius,
secondary signals inhibit vasoconstrictor centres and excite the vagal
parasympathetic center. This results in a decrease in the frequency of impulses
from the Vasomotor Centre and arterioles dilate. Final result is vasodilation and
decreased MAP.

* CIC activity increases (stimulating the Vagus nerve) - decreases HR and SV.

* CAC activity decreases (inhibiting Sympathetic nerves) - decreases CO.

 Hormonal regulation:

■ NA  vasoconstriction.
■ A  vasoconstriction (except in sk. ms.).
■ Angiotensin II  vasoconstriction.
■ Vasopressin  vasoconstriction.
 Substances that cause vascular
smooth muscle relaxation (↓BP)
Chemical Physiologic role Source Type
Nitric oxide Paracrine mediator Endothelium Local

Atrial natriuretic Reduce blood pressure Atrial Hormonal

peptide myocardium,
brain
Vasoactive intestinal Digestive secretion, Neurons Neural,
peptide relax smooth muscle hormonal
Histamine Increase blood flow Mast cells Local,
systemic
Epinephrine (b2) Enhance local blood Adrenal medulla Hormonal
flow to skeletal
muscle, heart, liver
Acetylcholine Erection of clitoris, Parasympathetic neural
(muscarinic) penis neurons
Bradykinin Increase blood flow Multiple tissues Local
via nitric oxide
Adenosine Enhance blood flow to Hypoxic cells local
match metabolism
 Substances causing contraction in
vascular smooth muscle (↑BP)

Chemical Physiologic role Source Type

NE (a ) Baroreceptor reflex Sympathetic Neural
neurons
Endothelin Paracrine Vascular Local
endothelium
Serotonin Platelet aggregation, smooth Neurons, digestive Local, neural
muscle contraction tract, platelets
Substance P Pain, increased capillary Neurons, digestive Local, neural
permeability tract
Vasopressin Increase blood pressure Posterior pituitary Hormonal
during hemorrhage
Angiotensin Increase blood pressure Plasma hormone Hormonal
II
Prostacyclin Minimize blood loss from endothelium local
damaged vessels before
coagulation
Regulation of Blood Volume
 Regulation of Blood Volume:

■ A long-term regulatory mechanism.

■ Mainly renal:
1. Renin-Angiotensin System.
2. Anti-diuretic hormone (ADH), or vasopressin.
3. Low-pressure volume receptors.
 1. Renin-Angiotensin System:

■ Most important mechanism for Na+ retention in

order to maintain the blood volume.

■ Any drop of renal blood flow and/or  Na+, will

stimulate volume receptors found in juxtaglomerular
apparatus of the kidneys to secrete Renin which will
act on the Angiotensin System leading to production
of aldosterone.
• Renin-Angiotensin System:
 renal blood flow &/or  Na+

++ Juxtaglomerular apparatus of kidneys

(considered volume receptors)

Renin

Angiotensinogen Angiotensin I
Converting
(Lungs)
enzymes
Angiotensin III Angiotensin II
(powerful (powerful
vasoconstrictor) vasoconstrictor)
Adrenal
cortex
Aldosterone Corticosterone
2. Anti-diuretic hormone (ADH), or vasopressin:

■ Hypovolemia & dehydration will stimulate the

osmoreceptors in the hypothalamus, which will lead
to release of ADH from posterior pituitary gland.

■ ADH will cause water reabsorption at kidney tubules.

 3. Low-pressure volume receptors:

■ Atrial natriuritic peptide (ANP) hormone, is secreted

from the wall of right atrium to regulate Na+ excretion
in order to maintain blood volume.