Hypertension Flashcards
BP determined by:
Rate of blood flow produced by heart (CO)
Resistance of blood vessels to blood flow
BP equation
BP= CO x SVR
Systolic BP
the maximum BP during ventricular contraction
Diastolic BP
the minimum level of BP measured between contractions of the heart
High normal BP (prehypertension)
Systolic 130-139
Diastolic 85-89
Hypotension
Systolic BP <90mmHg
Diastolic BP <60mmHg
Postural hypotension
Present if SBP decrease in standing >20mmH or DBP >10mmHg
Hypertension
Persistent systolic >140mmHg, diastolic >90mmHg
Hypertension epidemiology
16 million ppl in UK
30% W, 32% M
Generally increases with age
Framingham Study
6x increase in stroke
3x increase cardiac death
2x likelihood peripheral arterial disease
CV mortality risk proportional to increase in BP
Adults 40-69
Each 20/10mmHg increase in BP doubles risk of mortality from stroke, ischaemic HR + other vascular causes
Hypertension optimal treatment trial (HOTT)
Largest interventional trial in hypertension
Lowest incidence of major CV events occurred at an achieved Diastolic BP of 83mmHg
Diabetics: Diastolic BP < 80mmHg gives 51% lower risk of CHD compared to >90mmHg
Concentric hypertrophy
Stroke volume decreased
Tachycardia necessary for normal CO
Vascular disease deaths
same as cancer
Eccentric hypertrophy
Lower SP
reduces DV
often leads to HF
Hypertensive retinopathy
Chronic hypertension damaging retinal BVs
Signs of damage to retinal vessels
Silver or Copper wire arterioles Retinopathy lesions (microaneurysms, blot+flame haemorrhages, cotton wool spots, swelling of optic disc)
Silver or Copper wire arterioles
Centre of the arteriole shines due to reflected light
Hearing loss
Combination of hypertension + diabetes is a major risk factor
Primary Hypertension
90-95%
No obvious underlying cause
Strong polygenic familial trend
Secondary Hypertension
5%
Clear underlying cause including- renal/renovascular disease, endocrine disease, coarctation of aorta, iatrogenic, thyroid
Endocrine disease- 2ndary hypertension
Phaeochomocytoma (tumour of chromaffin cells)
Cushings syndrome (adrenal cortical tumour)
Conn’s syndrome (hypersecretion of aldosterone)
Acromegaly + hypothyroidism
Chronic hypertension
Associated mainly with pathology in renin-angiotensin system
BP control factors
Baroreceptors in carotid artery
Renin-angiotensin aldosterone system
Possible Hypertension causes
Impaired NO production (decreased)
Elevated renin release
Reduced atrial natriuretic peptide release
NO function
Gas diffuses into underlying smooth muscle + relaxes it
Balances vasoconstrictor effects of angiotensin + noradrenaline
Atrial natriuretic peptide
Released from heart muscle cells in atrial wall if increased atrial BV
Reduces the ECF vol. by increasing sodium excretion
Dilates glomerular afferent arterioles, constricts efferent arterioles, relaxes mesangial cells
Increases GFR –> increase in water excretion
Hypertension + diabetes
Hypertension present in about 40% of patients with Type II diabetes at age 45–> rises to 60% age 75
Obesity + primary hypertension
high levels of leptin increase vasoconstriction- may increase peripheral resistance
Associated with hyperinsulinaemia + insulin resistance–> increases BP, damages endothelial walls, decreases NO + ANP production
Metabolic syndrome
Central obesity, hypertension + insulin resistance
Increase risk of stroke + serious vascular disease
Treatment Under 55
ACE or ARB
Treatment over 55 or African or Caribeean
Calcium channel blocker
Treatment diuretic
Thiazide-like diuretic
e.g. chlortalidone or indapamide
Conventional thiazide
e.g. Bendroflumethiazide or hydrochlorothiazide
BB as treatment
ACE inhibitor intolerance
Women of child bearing potential
Ppl with increased sympathetic drive
STEP 2 treatment
CCB with ACE inhibitor or AB
Step 3 treatment
3 drug combination of ACE inhibitor/ARB, CCB + thiazide like diuretic
Step 4
ACE inhibitor/ARB, CCB + diuretic classed as resistant hypertention
