Systemic Hypertension

10.11.06

What is it?
• What is normal BP?
• Usually given in mmHg as 100 + age, but only in Western populations.
• What is abnormal level?
• Very variable definition - some debate about whether to treat ostensibly healthy population who are not symptomatic but may be at slight risk of complications.
• Diastolic >90 usually given as threshold level.
• Systolic >140 over period also - hypertension.

Prevalence/types
• Gives prevalence ~25%, increasing with age >50 years.
• More common in females (But less severe in older female group).
• 90-95% is essential type.
• Most of secondary type due to renal disorders (but others possible: endocrine, vascular, Neurogenic).
• Malignant (accelerated) hypertension: can occur in both essential and secondary types - ~5% hypertensive patients develop this.

Mechanisms
• BP = cardiac output x peripheral resistance.
• Concept of autoregulation - especially brain and kidney (but to some extent, all vessels).
• Cardiac output influenced by volume and cardiac activity factors.

Peripheral resistance influenced by:
• Neural (α, β adrenergic).
• Local (autoregulation, ionic, pH etc.)
• Dilators (prostagladins, kinins).
• Constrictors (angiotensin-II, catecholamine, thromboxane, leukotrienes).
• Also by atheroma affecting compliance of aorta.
• Coarctation.

Derangements
• Renin-angiotensin system: normally accurately controlled feedback mechanism.
• Increased renin important in:
-Unilateral renal artery stenosis.
-Malignant hypertension.
-Vasculitis.
-Pyelonephritis.
-JGA tumours, Wilms' tumour/carcinoma.
-Some cases of chronic renal failure of various causes.
• Sodium homeostasis: as well as angiotensin II, glomerular filtration rate and natriuretic factors have bearing on this.
• Sodium retention most important factor in hypertension of chronic renal failure, with which it is strongly associated.

Mechanisms of essential hypertension
1. Genetic (twins, blood relatives).
-Polygenic inheritance.
-?Role of imprinting.
2. Environment: dietary sodium most important?
-Variation of blood pressure with sodium intake locally.

Possible reasons
• Loss/defect of sodium excretion facility.
• Defect of sodium transport in cell membranes.
• Increased sympathetic response to stress/neurogenic factors.

Renal artery stenosis
• Accounts for 2-4% all hypertension, but treatable.
• Type works by JGA stimulation proportional to degree of stenosis.
• 70% cases due to atheromatous plaque at origin of artery.
• Fibromuscular dysplasia can also occur.

Other causes of secondary hypertension
• Renal.
-Acute glomerulonephritis.
-Renal polycystic disease.
-Renal involvement by vasculitis.
• Endocrine.
-Exogenous hormones.
-Steroid-producing tumours.
-Thyroid.
-Phaeochromocytoma.
• Neural.
-Acute stress.
-Sleep apnoea.
-Raised intracranial pressure.
-Psychological.
§Note: blood pressure can be lowered in some people by biofeedback methods.

Effects of hypertension: kidney
• Benign nephrosclerosis.
-Small granular kidneys with narrowed vessels and resultant ischaemic atrophy, glomerulosclerosis and tubular atrophy.
-Fibroelastic hyperplasia in larger arteries.
-Does not usually cause renal failure but will have reduced reserve.

Cerebral effects of benign hypertension
• Intracerebral haemorrhage + subarachnoid.
• Lacunae (minute infarcts in deep portions of brain e.g. basal ganglia and white matter).
• Subcortical leukoencephalopathy: diffuse loss of hemispheric white matter leading to dementia (probably ischaemic).

Hypertensive heart disease
• Left ventricular hypertrophy, usually of concentric type. LV >200g. May occur even at 140/90 i.e. 25% of population.
• Heart undergoes hypertrophy as result of increased workload.
• Eventually, leads to ischaemic fibrosis and decompensation.
• Can be diagnosed only in absence of other causes e.g. aortic stenosis.
• Coronary atherosclerosis interacts with (and is worsened by) hypertension.
• If blood pressure controlled, some evidence hypertrophy may regress. Especially true of ACE inhibitors.

Malignant hypertension - clinical features
• Diastolic >130, papilloedema, encephalopathy, renal failure and cardiac insufficiency.
• Often present with headaches/scotomas.
• May have hypertensive crises.
• Real emergency. Now 50% 5-year survival - much improved from previous rate.

Pathogenesis
• Very high levels of renin, angiotensin II and aldosterone.
• Interacts with endothelial damage to cause intravascular thrombosis, with more ischaemia and vicious circle.
• Sometimes coagulation may come first.
• Renal failure results from profound ischaemia.

Effects: kidney
• Malignant nephrosclerosis.
-Strongly correlated with previous benign hypertension/renal disease of another type.
-2 main changes.

Effects: brain
• Encephalopathy: associated with malignant hypertension, eclampsia and acute nephritis.
• Headache, drowsiness, stupor and coma.