Normal blood pressure




BP is the pressure of the blood on the vessel walls

Normally refers to the BP in the systemic arterial system

Required for the perfusion of all tissues

It is vital to always maintain perfusion of central organs, eg heart, brain, kidney

The pressure required to achieve this perfusion varies, it will be lower in children eg. at 2 years normal systolic might be 95 mmHg

After age 14 adult values may be used


Measured relative to atmospheric pressure, ie. BP is the pressure of the blood greater that that of the atmospheric not relative to a vacuum, normal barometric pressure is 760 mmHg, so 120 mmHg is really 120 +760 =880


Normal BP should be determined after several measurements of different occasions


Systolic - the pressure generated by ventricular contraction


Diastolic - the pressure in the arterial system when the heart is not contracting maintained by the elastic recoil of the large arteries


Systemic blood pressure - the pressure in the systemic arterial system 120/80


Pulmonary blood pressure - pressure in the pulmonary arterial system  25/8


Venous pressure - eg. arm veins 6 - 8 mmHg


Capillary blood pressure - arterial end 32 mmHg, venous end 12 mmHg


Factors determining blood pressure


Blood pressure         =          cardiac output  x  peripheral resistance


Cardiac Output         =          heart Rate  x stroke volume


The arterioles are the key determinant of peripheral resistance


Blood viscosity

High blood viscosity            eg. polycythaemia will raise BP

Low blood viscosity                         eg. after IVI of large volumes of saline, BP will be lowered



Neuronal control


Vasomotor centre

Arterioles naturally relax in the absence of a nerve supply from the sympathetic NS


Sympathetic stimulation causes arterioles to vasoconstrict by innervation of the smooth muscular walls


This tone originates in the Vasomotor centre in the medulla and lower third of the pons


More VMC outflow ---- more vasoconstriction ----- increased BP


VMC also controls heart rate and stroke volume and venous vasotone


*           Heart Rate increase -------

*           Cardiac Output increase -------

*           Arteriole vasoconstriction -------

*           Venoconstriction ---- increased venous return -------


As the effects of the VMC are transmitted via the sympathetic NS the terminal transmitter molecule is noradrenaline (norepinephrine)


Other factors effecting the VMC

Higher influences, eg. stress, anxiety, anger

Higher influences can also lead to a fall in BP even causing a faint

Low O2 will stimulate the VMC, so BP will rise in the early stages of hypoxia

Low CO2 causes reduced VMC activity so lowers BP




Pressure receptors located in the arterial walls in the area of the aortic arch and internal carotid arteries


Baroreceptors in aortic arch communicate with VMC via the vagus


Baroreceptors in carotid sinus at the bifurcation of the internal and external carotid arteries communicate with the VMC via a branch of the glossopharyngeal nerve


The greater the BP the more baroreceptor nerve activity there is. These impulses inhibit the activity of the VMC.


The baroreceptor firing acts as a brake on the VMC and is a form of negative feedback


If BP starts to fall Baroreceptor firing will reduce allowing the VMC outflow to increase which will cause vasoconstriction, increased Cardiac Output, venoconstriction  and so increase BP


If BP rises there will be increased baroreceptor firing inhibiting the VMC outflow allowing the arterioles to vasodilate, Cardiac Output to reduce, veins to dilate and so reduce BP


Endocrine control


Renin - angiotensin

When renal perfusion is reduced the kidney responds by producing the endocrine product renin


The renin splits a plasma protein called angiotensinogen into a small peptide called angiotensin I


A converting enzyme present in the lungs converts angiotensin I into an even smaller peptide called angiotensin II which also gives rise to angiotensin III


Angiotensin II and III are very potent vasoconstrictors and also cause thirst


The renin - angiotensin system occurs after blood loss and takes about 20 minutes


Adrenal gland

Cortex            - aldosterone increases salt reabsorption

Medulla          - Adrenaline and nor adrenaline


Long term regulation

The kidneys achieve this by controlling the volume of body fluids


When arterial pressure rises urine production increases, reduced plasma volumes reduce venous return so reduce blood pressure, this is why diuretics may control some forms of hypertension.


When BP is low urine volumes are reduced to conserve intravascular volume


Antidiuretic hormone


BP recording


Sphygmomanometer;   Sphygmos - pulse,  Manometer - a measuring instrument


Factors effecting blood pressure readings


Correct use of equipment

Centre of cuff should be over the brachial artery

Place rubber tubes superiorly to clear antecubital fossa

Lower edge of cuff should be 2 - 3 cm above brachial palpation point


Correct size of cuff and bladder

Bladder too small - overestimation of BP, therefore over diagnosis and treatment

Bladder too large - underestimation of BP

A cuff of 12 x 26 cm covers most adult arms with an average circumferences of 30 cm

Use 12 x 40 for big arm circumferences

Use 12 x 18 for smaller arms

40% x 80% of upper arm mid point circumference


Variability of blood pressure








Bladder distension

White coat syndrome


Circadian - lowest during sleep

Posture - BP increases from lying to sitting to standing

Arm support - support to prevent isometric exercise which may raise BP by up to 10%

Arm position - should be level with the heart, difference may be up to 10 mmHg

Arm above heart level - Reading reduced

Arm below heart level - BP increased

Which arm - take the highest reading as accurate


Practical points

Top of meniscus - eye should be level with the mercury

Measure in both arms on first visit

Inflate to 30 mmHg above palpated systolic

Record accurate to 2mmHg


Korotkov sounds

Phase I      first beat

Phase II     sound may soften and there may be a gap

Phase III    sounds become louder and crisper

Phase IV   the distinct abrupt muffling of the sounds

Phase V    the point when the sounds disappear


Record the first and the last sound except in pregnancy, anaemia, elderly and children
























A sustained elevation of BP

Moderate      SBP > 140     DBP > 90

Definite          160/100

That level of blood pressure above which investigation and treatment do more good than harm, (Professor Geoffrey Rose)



Essential (primary)   - most cases of hypertension

Secondary                 - 2 - 5% of cases

Benign                       - asymptomatic with long term end organ damage

Malignant                  - often a history of benign, rapid severe rise, most common in black men


Clinical picture


Often there are no symptoms until the patient has end organ damage as in CVA, MI, renal or retinal damage



Cerebral oedema - capillary damage

Nausea and vomiting


Neurological deficit

Visual disturbance - pressure effects on visual nerve pathways




A family history is common in essential hypertension



Renal disorders (80% of secondary cases)


Some drugs, eg oestrogen

Cardiovascular disorders

Adrenal disease





Some differences but probably mostly related to environmental factors


Increasing age

Seems to be related to lifestyle factors, rural non-westernised populations do not show an increase with age



Increased salt is a factor for populations, for individuals some are salt sensitive and some are not

Increasing salt in the diet increases BP, reducing salt in the diet reduces BP



Increased potassium in diet seems to lower BP slightly

Diets rich in fruit and vegetables may also lower BP



Fat people tend to have higher blood pressures than thin people

Greater body mass to perfuse increases cardiac workload



Alcohol intake and BP have a close positive relationship



Acute stress raises BP but there is little evidence that chronic stress is a factor



Acute exercise increases BP, however increased levels of exercise lower BP overall

Reduces sympathetic excitability

Increased insulin receptivity --- reduced insulin levels ---- reduced sympathetic stimulation

Increased oxygen uptake from capillaries

Reduced weight



In essential hypertension the cardiac output is raised in the early stages of the condition but normal in the later stages, in the later stages there is increased peripheral resistance


Sympathetic overactivity ----- increased cardiac output ----- vascular changes ---- baroreceptor reflexs operate at higher pressures -------- increased peripheral resistance -------- increased BP


Atheroma develops in larger arteries


Hypertension ------ hypertrophy of connective tissues and smooth muscle cells in the intima and media causes arteriole thickening


Deposition of collagen in walls causes loss of elasticity


High pressure forces proteins such as fibrinogen into arterial walls


Arteriosclerosis, possible calcification


Reduced perfusion of tissues despite high blood pressures



Risk of morbidity and mortality rises continuously but is steeper at higher pressures


High BP causes death from stroke, myocardial infarction, heart failure, renal failure


Hypertension is a risk factor for development of atherosclerosis


Under the age of 45 diastolic pressure is a more accurate predictor of cardiovascular risk than systolic


Over the age of 45 systolic pressure is a more accurate predictor of cardiovascular risk than systolic, demonstrated in the over 60


Smoking, hypertension and hyperlipidaemia have a synergistic effect on cardiovascular risk


Cerebrovascular disease

Blood vessels become more rigid - fibrous tissue replaces smooth muscle ------ vessel wall weakening ------- aneurysm -------- haemorrhage ------- CVA


Atheroma increases risk of thromboembolic stroke


Heart disease

Coronary arterial disease - hypertension is a major risk factor


Congestive cardiac failure - increased ventricular work load ------ hypertrophy -----  cardiomegaly ------ LVF


Angina may occur from CHD or as a result of the increased oxygen demand from myocardial hypertrophy


Peripheral vascular disease

Hypertension contributes to arterial disease effecting the aorta and peripheral arterial vessels


Renal complications

Hypertension ---- narrowed lumen of intra-renal vessels ---- renal arterial stenosis ------ ischaemia ------ reduced glomerular filtration ----- retention of water and sodium ------- increased BP


Renal ischaemia ------ ultimately death of nephrons ------ progressive renal atrophy and scaring ------- renal failure


Renal hypoperfusion ------ secretion of renin  ------  increased severity of hypertension


Retinal damage

Damage of retinal vessels ----- haemorrhage ----- visual loss


The state of retinal vessels is a good indicator of the condition of other vessels in the heart, kidney, brain etc.


Advantages of treatment

Reduction of all end organ complications -------- overall improved survival figures


Severe hypertension

80% 2 year mortality transformed into 80% 5 year survival


Reduction of stroke

35 - 40%

Nearly all strokes caused by hypertension are preventable


Reduction in MIs

More pronounced in older people - 20 - 25%

Results for pooled data suggest 16%



Chest X ray                           ECG                           Echocardiography               Urine

Serum lipids                          Renal function



In young patients exclude secondary causes

Persuade asymptomatic patients that treatment is necessary

Correct life style factors

Antihypertensive drugs

Take time to promote compliance, (side effects are usually immediate while the benefits are long term)

The object is to decrease BP to below 90 diastolic and to below 160 systolic

Treatment should be commenced at the lowest dose and titrated as necessary


First line treatments


Thiazide diuretics eg bendrofluazide 5 mg/day

Promote a moderate diuresis

Increased sodium and water excretion

Direct dilation of arterioles

Hypokalaemia is not usually a problem but if it is the thiazide should be combined with a potassium sparing diuretic, eg spironolactone

Potassium sparing diuretics are not effective hypotensives on their own


B Blockers

Mechanism of action somewhat unclear

Probably act via the CNS but also reduce renin production, the force of cardiac contraction and reduce anxiety

Eg. Propranolol 80 mg twice daily, Atenolol 50 - 100 mg daily, Oxprenolol 80 mg twice daily


Other treatment options


ACE inhibitors

Angiotensin converting enzyme inhibitors

Prevents the formation of angiotensin II which is a powerful vasoconstrictor and indirect facilitator of the sympathetic nervous system

Suppress aldosterone secretion


Angiotensin II antagonists Direct antagonism of angiotensin II at its vasoconstrictor receptor sites


Ca++ antagonists

Blocks the inward flow of CA++ into muscle cells so reduce the availability of intracellular CA++ for muscle contraction

Reduces the muscular tone in the vasculature



Exclude secondary causes

Persuade the asymptomatic

Life style

Antihypertensive drugs

Promote compliance

Aim - below 90 diastolic      below 160 systolic

Commence at lowest dose and titrated