# Arterial Blood Pressure

## Presentation on theme: "Arterial Blood Pressure"— Presentation transcript:

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 Pulse Pressure

Arterial blood pressure
Mean B.P – Normally diastole is longer than systole Thus 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
Pressure – depends on the amount of blood Amount of Blood leaving – determined by resistance to flow Amount of Blood Entering – cardiac output Determines mainly systolic BP Determines mainly diastolic BP

Arterial blood pressure
A concept: B.P. = Cardiac output x Total peripheral resistance BP = CO x TPR This 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 R = resistance L = length of the blood vessel v = viscosity of blood r = radius of the blood vessel r4

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 diameter vasoconstriction – 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
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 Metabolic activities of that area Pressure within the blood vessels in that area Vascular endothelium

Control of arteriolar tone – Local mechanisms
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 Hypoxia Adenosine K+ CO2 excess – hypercapnia H+ Lactic acid Inorganic phosphates

Control of arteriolar tone – Local mechanisms
2. Myogenic Mechanisms Autoregulation 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 BP Age
Genetic – racial differences Gender Body build Sleep Posture Respiration Exercise Emotion and stress Pain

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 less AND diastolic 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 a constant BP
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

Arterial baroreceptors
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 vagus and glossopharyngeal nerves inhibit the medullary centres The normal activity of the centres is to activate the sympathetics and inhibit parasympathetics Increased baroreceptor activity reduce sympathetic activity and 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

Influences on medullary centres
Baroreceptors are only one of many factors influencing the medullary centers Baroreceptors Temperature centre Peripheral chemoreceptors Cerebral cortex Pain receptors O2 and CO2 partial pressures Proprioceptors Intracranial pressure Respiratory centre Temperature receptors

Local short term regulation
Some factors affect the heart directly and influence Heart rate Force of contraction

Regulation – Long term Long term – hours to days, renal & endocrine
through maintaining blood volume Renin angiotensin aldosterone mechanism Other renal mechanisms Vasopressin Atrial natriuretic peptide Thirst

Renin angiotensin aldosterone mechanism
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
Angiotensinogen Renin Angiotensin I Angiotensin converting enzyme Increased aldosterone secretion Vasoconstriction Angiotensin II Thirst Increased ADH secretion

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