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Arterial Blood Pressure

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Arterial Blood Pressure

Arterial blood pressure

“Blood pressure” generally refers to arterial blood pressure

Definition - ‘B.P.’ is the lateral

pressure exerted by the column of blood on the walls of the arteries’ It is not steady Fluctuates during

the Cardiac Cycle

Arterial blood pressure

During ventricular systole B.P is higher than that during diastole

Systolic B.P -the peak pressure during the ventricular systole

Diastolic B.P -the minimum pressure during ventricular diastole

Arterial blood pressure

Pulse pressure - the difference between systolic and diastolic B.P

Mean arterial blood pressure – It is the average pressure throughout the cardiac

cycle

PulsePressure

Arterial blood pressure

Mean B.P –

Normally diastole is longer than systoleThus mean arterial BP is not the arithmetic mean of systolic and diastolic BP

Mean BP = Diastolic B.P + 1 of pulse pressure

Mean BP = SBP + (2xDBP)

Clinically important BP is SBP & DBP and not mean BP

3

3

Arterial blood pressure

Arterial blood pressurePressure – depends onthe amount

of bloodAmount ofBloodEntering – cardiac output

Amount ofBlood leaving – determined by resistanceto flow

Determines mainlysystolic BP

Determines mainlydiastolic BP

Arterial blood pressure

A concept:

B.P. = Cardiac output x Total peripheral resistance

BP = CO x TPRThis equation holds true for actual values of

the above parameters

But, clinically neither the CO nor the TPR is measured routinely.

Total peripheral resistance

total peripheral resistance (TPR) refers to the resistance to blood flow offered by all of the systemic vasculature excluding the pulmonary vasculature.

R = 8Lv

r4

R = resistance

L = length of the blood vesselv = viscosity of bloodr = radius of the blood vessel

Total peripheral resistance

TPR is therefore determined by those factors that

influence vascular resistance in individual vascular beds.

The main site of vascular resistance within the circulation is at the ARTERIOLAR level.

TPR is primarily determined by changes in blood vessel diameters

vasodilataion – increase in vessel diametervasoconstriction – decrease in vessel diameter

Changes in blood viscosity will also affect TPR

Control of arterioles

The blood vessels are controlled by

1. Central mechanisms Neural mechanisms Circulating hormones

2. Local mechanisms Local factors

Tissue factors Endothelial factors

Myogenic factors

Control of arterioles

Arteriolar tone Vascular tone refers to the degree of constriction High

arteriolar tone) / dilatation (low arteriolar tone) of an arteriole

Control of arteriolar tone – central mechanisms

Central mechanisms are –

Neural and endocrine

Regulate a systemic factor Blood pressure Body temperature

Control of arteriolar tone – central mechanisms

1. Neural control

Mostly sympathetics – cause vasoconstriction in most arterioles via alpha 1 receptors.Beta 2 receptors cause vasodilatation e.g. in skeletal muscle

Parasympathetics – in some organs only e.g. external genitalia

Control of arteriolar tone – central mechanisms

2. Hormonal control Adrenalin binds to the beta 2 adrenoceptors to cause

vasodilation in some organs Angiotensin II Antidiuretic hormone Atrial natriuretic peptide

Control of arteriolar tone – Local mechanisms

Local mechanisms are useful for modifying blood flow in a limited area (e.g. one organ or one area of the body)

They are dependent on 1. Metabolic activities of that area2. Pressure within the blood vessels in that area3. Vascular endothelium

Control of arteriolar tone – Local mechanisms

1. Metabolic mechanisms of vasodilation

There is a close coupling between the metabolic activity and blood flow in most organs of the body

an increase in tissue metabolism, as occurs during muscle contraction, will lead to an increase in blood flow (active hyperaemia)

Control of arteriolar tone – Local mechanisms

Local factors causing vasodilation

CO2 excess – hypercapnia H+

Lactic acid Inorganic phosphates

Control of arteriolar tone – Local mechanisms

2. Myogenic MechanismsAutoregulation Autoregulation – the intrinsic ability of an organ to

maintain a constant blood flow despite changes in perfusion pressure.

for example, if the pressure within the arterioles of an organ is decreased blood flow will initially fall this results in dilatation of the arterioles due to the

reduction in stretch blood flow then returns towards normal levels over the

next few minutes this autoregulatory response occurs independently of

any neural or humoral influences and therefore is intrinsic to the organ

Control of arteriolar tone – Local mechanisms

3. Other factors influencing vascular tone – some increase and some decrease arteriolar tone.

Endothelial factors prostacyclin - vasodilatation nitric oxide - vasodilatation endothelin - vasoconstriction

Local hormones/chemical substances thrombaxane, other arachidonic acid metabolites histamine Bradykinin

These factors interact with each other through many mechanisms and help fine-tune the vascular tone

Normal BP

Physiological variations in BPAgeGenetic – racial differencesGenderBody buildSleepPostureRespirationExerciseEmotion and stressPain

Normal BP

Because of the multitude of factors affecting blood pressure it is impossible to determine the normal blood pressure for any individual

In general, blood pressure is said to be normal if at rest –

systolic is 130 mmHg or lessANDdiastolic is 80 mmHg or less

A BP of more than 140/90 mmHg is generally considered to be high

Regulation of BP

The primary goal of the cardiovascular system is the maintainance adequate tissue perfusion

Blood pressure is one major factor that affects tissue perfusion

In order to maintain adequate tissue perfusion the body regulates blood pressure (through the regulation of cardiac output and arteriolar diameter)

Regulation of BP

The blood pressure –

Mostly maintained constant

Increased when necessary (e.g. exercise)

Even allowed to fall a little if appropriate (e.g. sleep)

Maintenance of BP

Short term – minutes to hours, neuro-humoral

Long term – hours to days, renal and endocrine

Maintenance of a constant BP

Short term – neuro-humoral

Mostly neural mechanisms. Hormones (adrenaline) also contribute

This regulation is quick acting (seconds – minutes)

A negative feedback mechanism

Maintenance of a constant BP

Arterial baroreceptors are located in the carotid sinus (at

bifurcation of external and internal carotids)

in the aortic arch

The sinus nerve, a branch of the glossopharyngeal nerve (IX cranial nerve), innervates the carotid sinus. The aortic arch baroreceptors are innervated by the vagus nerve The baroreceptors are tonically active

Arterial baroreceptors

Arterial baroreceptors are sensitive to stretching of the walls of the vessels in which the nerve endings lie.

Stretching occurs when arterial pressure increases

Arterial baroreceptors

The baroreceptors send impulses to the vasomotor centre and cardiac centres (cardioacceleratory & cardioinhibitory) in the medulla oblongata

Impulses along the vagusand glossopharyngeal nerves inhibit the medullary centres

The normal activity of the centres is to activate the sympathetics and inhibit parasympathetics

Increased baroreceptor activityreduce sympathetic activityand enhance parasympathetics

Arterial baroreceptors

A decrease in arterial pressure results in decreased baroreceptor firing

The CVS centers respond by increasing sympathetic outflow and decreasing parasympathetic outflow

TPR

Arterial baroreceptors

Influences on medullary centres

Baroreceptors

Peripheralchemoreceptors

Pain receptors

Temperaturecentre

Proprioceptors

Intracranialpressure

O2 and CO2

partial pressures

Respiratory centre

Temperature receptors

Cerebralcortex

Baroreceptors are only one of many factors influencing the medullary centers

Local short term regulation

Some factors affect the heart directly and influence

•Heart rate

•Force of contraction

Long term – hours to days, renal & endocrine

through maintaining blood volume

Renin angiotensin aldosterone mechanism Other renal mechanisms Vasopressin Atrial natriuretic peptide Thirst

Regulation – Long term

Secretion of renin –From the Juxta-glomerular apparatus (in kidney)

Major stimuli - sympathetic stimulation (as does occur in arterial

hypotension) renal artery hypotension decreased sodium delivery to the distal tubules

Renin angiotensin aldosterone mechanism

Renin angiotensin aldosterone mechanism

Renin

Angiotensinogen

Angiotensin I

Angiotensin II

Increased aldosterone secretion

Vasoconstriction

Thirst

Angiotensin converting enzyme

Kidneys also regulate blood volume by adjusting the excretion of water and sodium into the urine through mechanisms other than renin-angiotensin-aldosterone pathway

Other renal mechanisms

Angiotensin II Hyperosmolality Decreased blood volume

Absorption of waterIn kidney

Vasoconstriction Thirst

Atrial natriuretic peptide

Atrial Natriuretic Peptide

Decreased renin secretion

Increased excretion of Sodium and water

Atrial distension