Hypertension

Discuss blood pressure in arteries and veins

Systolic -

Diastolic -

The diastolic is most important during assessment

Systemic as opposed to pulmonary

> ¹⁴⁰/₉₀ mm of Hg

Factors - cardiac output, blood volume, (venous return), peripheral resistance.

Control of BP

Kidney

Reduced blood flow causes secretion of Renin

Adrenal gland

Medulla - adrenalin and noradrenalin

Cortex - aldosterone causes retention of salt and water

Adrenal cortex is controlled by the Pituitary gland

Pressure receptors

Baroreceptors in arch of aorta and carotid arteries pass information to the VMC which gives out sympathetic information to arterioles

BP varies throughout the day depending on activity

Tends to rise with age

Factors effecting readings

White coat syndrome Emotion Exercise Meals

Tobacco Alcohol Temperature Pain

Aetiology of hypertension

Essential and secondary

Kidney damage

Adrenal medullary tumour, excess aldosterone production usually secondary to pituitary disorder

Expanding SOL

90% idiopathic, termed essential hypertension.

Factors

Race Genetic Obesity Alcohol intake

Salt intake Potassium intake Exercise Stress

Clinical features

Often no clinical features - screening important

Headaches Nose bleeds?

Effects

Fibrous material is deposited in the walls of arterioles, often effecting renal vessels.

Ventricular hypertrophy

Atherosclerosis

Aneurysm formation, eg. berry type

Retinal damage

Mortality

Heart failure and MI 60%

Renal failure 30%

Thrombosis or haemorrhage of cerebral arteries 10%

Prognosis

Factors

Level of hypertension

Presence of renal and cardiac involvement

Gender (men do worse than women)

Age (young do worse than older)

Treatments

Aim - DBP - below 90 in young people, below 100 in older people

SBP - less than 160 mm Hg

Weight reduction

Reduce C₂H₅OH

Reduce NaCl

Increase potassium

Regular exercise

Biofeedback, relaxation

Antihypertensives

Diuretics Beta – blockers ACE inhibitors

Calcium channel blockers Alpha - blockers

Other conditions

Malignant Hypertension - very high BPs

Pre - eclamptic toxaemia of pregnancy

Normal blood pressure

Introduction

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

Baroreceptors

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

Emotion

Exercise

Meals

Tobacco

Alcohol

Temperature

Pain

Bladder distension

White coat syndrome

Age

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

Hypertension

Definition

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)

Forms

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

Benign

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

Malignant

Cerebral oedema - capillary damage

Nausea and vomiting

Headache

Neurological deficit

Visual disturbance - pressure effects on visual nerve pathways

Causes

Essential

A family history is common in essential hypertension

Secondary

Renal disorders (80% of secondary cases)

Pregnancy

Some drugs, eg oestrogen

Cardiovascular disorders

Adrenal disease

Factors

Race

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

Salt

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

Potassium

Increased potassium in diet seems to lower BP slightly

Diets rich in fruit and vegetables may also lower BP

Obesity

Fat people tend to have higher blood pressures than thin people

Greater body mass to perfuse increases cardiac workload

Alcohol

Alcohol intake and BP have a close positive relationship

Stress

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

Exercise

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

Pathophysiology

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

Complications

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%

Investigations

Chest X ray ECG Echocardiography Urine

Serum lipids Renal function

Treatment

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

Diuretics

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

Treatment

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