0 11
Avatar for dr
Written by
1 year ago


·        BP chronically elevated

·        Persistently raised BP measured at past 2 visits and systolic and diastolic pressure or both >140/90mmHg

·        Resistant hypertension – BP >140/90mmHg despite taking full doses of at least 3 antihypertensives including a diuretic

·        Pseudo-hypertension – in old patients, BP recordings are high but without evidence of EOD, d/t non-compressible sclerotic brachial artery where a higher pressure is required to compress the artery

·        Pseudo-resistant hypertension – BP levels persistently above normal values at clinic measurements but who do not have resistant hypertension – eg poor BP measuring techniques, white coat hypertension, poor compliance



1.      Primary/ essential HT (5%)

·        Renal dysfunction, peripheral resistance vessel tone, endothelial dysfunction, autonomic tone, insulin resistance and neurohumoral factors

·        Genetic factors - Black Americans and Japanese

·        Environmental factors - high salt intake, heavy consumption of alcohol, obesity, lack of exercise and impaired intrauterine growth


2.      Secondary hypertension (5%)

·        Alcohol

·        Obesity

·        Pregnancy (pre-eclampsia)

·        Renal disease

o   Renal vascular disease

o   Parenchymal renal disease, particularly glomerulonephritis

o   Polycystic kidney disease

·        Endocrine disease

o   Phaeochromocytoma

o   Cushing's syndrome

o   Primary hyperaldosteronism (Conn's syndrome)

o   Glucocorticoid-suppressible hyperaldosteronism

o   Hyperparathyroidism

o   Acromegaly

o   Primary hypothyroidism

o   Thyrotoxicosis

o   Congenital adrenal hyperplasia due to 11-β-hydroxylase or 17α-hydroxylase deficiency

o   Liddle's syndrome

o   11-β-hydroxysteroid dehydrogenase deficiency

·        Drugs

o   e.g. Oral contraceptives containing oestrogens, anabolic steroids, corticosteroids, NSAIDs, carbenoxolone, sympathomimetic agents

·        Coarctation of the aorta


Blood pressure measurement

·        White coat hypertension – greater r/o cardiovascular disease than normal subjects

·        Average ambulatory daytime (not 24-hour or night-time) BP should be used to guide management decisions



·        Family history

·        Lifestyle (exercise, salt intake, smoking habit) and other risk factors

·        Causes of secondary hypertension such as phaeochromocytoma (paroxysmal headache, palpitation and sweating)

·        Symptoms

o   CVS symptoms

o   CNS

o   Renal

o   Eye

o   Intermittent claudication

·        Adherence to medication, compliance with lifestyle measures

·        Complications such as coronary artery disease (e.g. angina, breathlessness)



·        Radiofemoral delay (CoA)

·        Enlarged kidneys (polycystic kidney disease)

·        Abdominal bruits (renal artery stenosis)

·        Facies, habitus of Cushing’s syndrome

·        Central obesity

·        Hyperlipidemia – tendon xanthomas

·        LVH (apical heave)

·        Accentuation of aortic component of S2

·        S4

·        Hypertensive retinopathy

·        Evidence of PVD

·        Fundoscopy

·        CNS – TRO CVA


Target organ damage

·        Blood vessels

o   Larger arteries (>1mm diameter) - Internal elastic lamina – thickened; Smooth muscle – hypertrophied; Fibrous tissue deposition; Walls – less compliant

§  Aortic aneurysm

§  Aortic dissection

§  RAAS activation – reduced renal blood flow

o   Smaller arteries (<1mm diameter) - Walls – hyaline arteriosclerosis; Lumen – narrows

§  Microaneurysm


·        CNS

o   Stroke

§  Cerebral haemorrhage

§  Cerebral infarction

o   TIA

o   Carotid atheroma

o   Subarachnoid haemorrhage

o   Hypertensive encephalopathy

§  High BP

§  Neurological symptoms - transient disturbances of speech or vision, paraesthesiae, disorientation, fits and loss of consciousness

§  Papilloedema

§  CT scan - haemorrhage in and around the basal ganglia

·        Retina

o   Papilloedema

o   Cotton wool exudates

o   Hard exudates

o   Microaneurysms

o   CRVO

·        Heart

o   APO

o   CAD

o   LVH – forceful apex beat, S4 (high incidence of cardiovascular complications)

o   AF – d/t diastolic dysfunction caused by left ventricular hypertrophy or the effects of coronary artery disease

o   LVF – in absence of CAD when renal function hence sodium excretion is impaired

·        Kidneys

o   Proteinuria

o   Progressive renal failure – damage to renal vasculature

o   ARF


Malignant/ accelerated phase hypertension

·        May complicate hypertension of any aetiology

·        Characterized by

o   Accelerated microvascular damage with necrosis in the walls of small arteries and arterioles ('fibrinoid necrosis')

o   Intravascular thrombosis

·        Diagnosis

o   High BP

o   Rapidly progressive end organ damage

§  Retinopathy (grade 3 or 4)

§  Renal dysfunction (especially proteinuria)

§  Hypertensive encephalopathy

·        Complication - ventricular failure à death



All patients

·        Urine

o   Urinalysis* for blood (dysmorphic red cells – glomerular disease), protein and glucose – renal parenchymal disease, long standing hypertension

o   FBC – anemia (CRF), polycythemia (Cushing)

·        Blood

o   Blood urea, electrolytes and creatinine*

§  Hypokalaemic alkalosis - primary hyperaldosteronism/ (more commonly) diuretic therapy

o   Blood glucose

o   Serum total and HDL cholesterol

·        12-lead ECG* (left ventricular hypertrophy, cardiac axis, coronary artery disease)


Selected patients

·        Chest X-ray*: to detect cardiomegaly, heart failure, coarctation of the aorta (notching of inferior rib margins)

·        Ambulatory BP recording: to assess borderline or 'white coat' hypertension

·        Echocardiogram: to detect or quantify left ventricular hypertrophy

·        Renal ultrasound: to detect possible renal disease (unequal size in renal artery stenosis); suprarenal mass

·        Renal angiography/ duplex USG: to detect or confirm presence of renal artery stenosis

·        Urinary catecholamines: to detect possible phaeochromocytoma

·        Urinary cortisol and dexamethasone suppression test: to detect possible Cushing's syndrome

·        Plasma renin activity and aldosterone (aldosterone to renin ratio): to detect possible primary aldosteronism

·        Thyroid studies


* Urgent investigations – hypertensive crisis




·        Quantify cardiovascular risk – to determine whether the likely benefits of therapy will outweigh its costs and hazards

o   Coronary heart disease = 4/3 X 10 year coronary heart disease risk

·        Threshold for intervention

o   >160/100 mmHg

o   >160 mmHg isolated systolic hypertension

o   ≥ 140/90 mmHg +

§  10 year CVD risk of at least 20% OR

§  Existing CVD OR

§  Existing target organ damage

·        Treatment targets


Treatment of hypertension

·        Non-drug therapy - lifestyle measures

o   Correct obesity

o   Reduce alcohol intake

o   Restricting salt intake

o   Regular exercise

o   Increase consumption of fruits, vegetables

o   Quit smoking

·        Drug therapy

o   Thiazides, other diuretics

§  Bendroflumethiazide 2.5mg

§  Cyclopenthiazide 0.5mg 

§  Furosemide 40mg daily     

§  Bumetanide 1mg daily         Loop diuretics

(Loop diuretics – advantageous over thiazides unless there is substantial renal impairment/ used in conjunction with an ACE inhibitor)

o   ACE inhibitors – inhibits conversion of angiotensin I to angiotensin II; care in renal impairment/ renal artery stenosis d/t reduction in filtration pressure in glomeruli, precipitation of renal failure ; check BUSE; a/e - first-dose hypotension, cough, rash, hyperkalaemia and renal dysfunction

§  Enalapril 20mg daily

§  Ramipril 5-10mg daily

§  Lisinopril 10-40mg daily

o   ARB – no cough, better tolerated

§  Irbesatan 150-300mg daily

§  Valsartan 40-160mg daily

o   CCB – useful in elderly; a/e - flushing, palpitations and fluid retention

§  Amlodipine 5-10mg daily

·        A/e – tachycardia, ankle edema, headache

§  Nifedipine 30-90mg daily

§  Diltiazem 200-300mg daily

§  Verapamil 240mg daily             When angina coexists; a/e – bradycardia

o   Beta-blockers    

§  Metoprolol 100-200mg daily

§  Atenolol 50-100mg daily

§  Bisoprolol 5-10mg daily

o   Combined β- and α-adrenoceptor antagonists

§  Labetalol

§  Carvedilol

o   α1-adrenoceptor antagonists (α-blockers)

§  Prazosin

§  Indoramin

§  Doxazosin

o   Drugs acting directly on smooth muscle (a/e – first dose and postural hypotension, headache, tachycardia, fluid retention)

§  Hydralazine

§  Minoxidil – increased facial hair


Combination therapy – synergistic/ complementary actions


·        Adjuvant drug therapy

o   Aspirin

o   Statins


Emergency treatment of malignant hypertension

·        Too rapid BP lowering can compromise tissue perfusion (d/t altered autoregulation) à cerebral damage including occipital blindness; coronary, renal insufficiency

·        Controlled reduction to a level of about 150/90 mmHg over a period of 24-48 hours is ideal

ü  Bed rest

ü  Oral therapy

ü  Parenteral therapy

o   IV/IM labetalol

o   IV glyceryl trinitrate

o   IM hydralazine

o   IV sodium nitroprusside


Refractory hypertension

ü  Non-adherence – most prevalent

ü  Inadequate therapy

ü  Failure to recognize underlying cause


Novel therapies

-        Carotid baroreceptor stimulation

-        Catheter-based renal sympathetic nerve denervation

Hypertensive crisis – acute increase in BP (>180/110) +/- EOD

1.      Hypertensive emergencies – with EOD

a.      Retinal

b.      Cardiac

c.      Neurological

d.      Renal

BP control within a few hours (DBP 100-110 within 24h)

2.      Hypertensive urgencies – no EOD

BP control (DBP 100-110) within 24h



CAD, HF – iv nitroprusside, nitroglycerin

APO – above, iv furosemide, ACEI

Stroke – B-blocker, CCB, diuretic, ACEI



- Oral

  - B-blocker (atenolol, labetalol)

  - ACEI/ARB – captopril

  - CCB – amlodipine

- Parenteral – sodium nitroprusside, GTN, labetalol (ivà oral after BP normalizes), hydralazine, esmolol, nicardipine


Significance:: Diastolic > systolic BP


First choice anti-hypertensive in reducing BP – CCB (“dipine” group) (ACE-I takes time for onset of action) 

$ 0.00
Avatar for dr
Written by
1 year ago