2. What is hypertension?
A.k.a high blood pressure.
Is basically the force which the blood exerts on the walls of blood vessels.
Simply defined as a systolic BP of >140mmHg and/or diastolic BP of >90mmHg.
Is a major cause of premature vascular disease, leading to cerebrovascular events,
ischaemic heart disease & peripheral vascular disease.
Mortality rises with increasing BP.
The prevalence may be 30-45% of the general population.
3. (cont’d)
Present in more than half of cases of myocardial infarction, stroke & chronic renal
disease.
It is included in the “metabolic syndrome”, along with hyperglycemia, insulin
resistance, dyslipidemia, & obesity.
In 95% of patients, HTN occurs without an identifiable cause, a condition referred to
as primary hypertension.
Secondary hypertension is a result of a number of diseases including:
Renal artery stenosis, most forms of chronic renal disease. diabetes mellitus, primary
elevation of aldosterone levels, Cushing syndrome, hyperthyroidism, coarctation of the
aorta & renin-secreting tumors.
Atherosclerosis as well.
4. Classification
Classification SBP (mmHg) DBP (mmHg)
Normal <120 <80
Prehypertension 120-139 80-89
Stage I Hypertension 140-159 90-99
Stage II Hypertension 160-179 100-109
Severe Hypertension ≥180 ≥110
5. Measuring BP
BP should be measured in a quiet room; the patient should be seated.
With an outstretched & supported arm at level of heart (recommended)
If possible, measure in both arms with the highest reading taken for subsequent referral.
If postural hypotension is suspected, then BP should be repeated after 1 minute of standing.
Ensure to prevent occurrence of “white coat syndrome”
That is patients exhibit a BP level above the normal range, in a clinical setting, though they do not exhibit
it in other settings
Believed to be due to anxiety experienced during a clinic visit.
6. BP Formula
BP is the product of cardiac output & systemic vascular resistance to blood flow.
Primary hypertension results from an imbalance in the interactions between these mechanisms.
B.P=C.O×S.V.R
Both of these functions are critically influenced by renal function & sodium homeostasis.
Reduced GFR causes sodium retention & volume expansion, which should be compensated
by a decrease in tubular sodium reabsorption.
Impaired renal tubular sodium handling & reduced GFR are likely to be important in HTN that
afflicts patients with CKD due to diabetes or aging.
7. RAA System
The renin-angiotensin-aldosterone axis is a hormonal & tissue based system that regulates BP, & fluid
and electrolyte balance.
Is important in regulation of normal BP, and dysregulation of RAAS is implicated in over 2/3 of the cases
of HTN.
Renal artery occlusion (decreased perfusion) or dietary salt restriction leads to increased renal secretion
of renin-from juxtaglomerular cells.
Renin (protease) cleaves angiotensinogen from the liver into angiotensin I (mild vasoconstrictor) which is further
broken down in lungs by an enzyme (angiotensin-converting enzyme) into angiotensin II (potent vasoconstrictor).
Angiotensin II causes vasoconstriction (increases SVR) & also affects centers in the brain that control sympathetic
outflow & stimulate adrenal aldosterone release.
Aldosterone increases sodium reabsorption by the renal tubules.
The net effect of all these actions is increased in total body fluid.
8. (RAA system cont’d)
Thus, the RAA system elevates BP by 3 mechanisms:
Increased sympathetic output
Increased mineralocorticoid secretion
Direct vasoconstriction
Angiotensin II also stimulates thirst.
Stimulates cardiac hypertrophy & vascular hypertrophy.
9. ANF (Atrial Natriuretic Factor)
The RAAS axis is antagonized by atrial natriuretic factor
ANF is a polypeptide hormone secreted by specialized cells in the cardiac atria.
ANF binds to specific receptors in the kidney & increases urinary sodium excretion, thereby
opposing angiotensin II-induced vasoconstriction.
ANF depresses steroidogenesis, especially mineralocorticoid synthesis.
It inhibits thyroid synthesis whereas its production is enhanced by thyroid hormones.
It acts on the kidney to increase sodium excretion & GFR
Inhibits renin secretion
10. Investigations
Urinalysis for protein, albumin; creatinine ratio & haematuria
Blood tests for glucose, electrolytes, creatinine, estimated glomerular filtration rate (eGFR), & total
and HDL cholesterol
Fundoscopy to detect hypertensive retinopathy:
Grade I-tortuosity of the retinal arteries with increased reflectiveness (silver wiring)
Grade II-grade I plus the appearance of arteriovenous nipping, produced when thickened retinal arteries
pass over the retinal veins
Grade III-grade II plus flame-shaped haemorrhages & soft (‘cotton wool’) exudates due to small infarcts
Grade IV-grade III plus papilloedema (blurring of optic disc)
A 12-lead ECG to detect left ventricular hypertrophy.
11. Management:
Lifestyle interventions:
Diet: high consumptions of vegetables & fruits and low-fat diet.
Regular physical exercise: 30min of moderate-intensity aerobic exercise 5-7 days/week)
Reduction in alcohol intake (<140g/week men, <80g/week women)
Reduction in dietary sodium intake (5-6g/day) & use of low-sodium salt.
Smoking cessation
Weight reduction (BMI 25kg/m(^2), waist circumference <102cm men, <88cm women)
12. (cont’d)
Pharmacological Therapy:
Treatment should be offered to all people under 80yo with stage 1 hypertension & at least one of
the following risk factors:
Target organ damage
Cardiovascular disease
Renal disease diabetes
10-year cardiovascular risk
Patients <40yo with no risk factors should be referred to a specialist to exclude secondary causes of
hypertension
All patients with stage 2 should be offered treatment
13. (cont’d)
The target for treated patients is <140/90 mmHg in patients below 80yo.
<150/90 mmHg in patients of 80yo and above.
