• To know how to detect and diagnose HT and its secondary causes
• To become familiar with updated recommendations for classifying HT
• To understand the treatment option for HT
• To grasp the importance of counselling patients on lifestyle modification to help BP control

[> 50% over 65yo have HT]

• An elevated arterial BP is probably most important public health problem in developed countries
• Common, asymptomatic, easily detectable, usu easily treatable, often leads to lethal complications if left untreated

• Depends on racial and definition of HT
• White suburban population (Framingham Study) nearly 1/5 of Pt have BP > 160/95 while almost 50% have BP > 140/90
• HK: 7% "healthy elderly > 65 yo" suffering from HT (Lau + Lok, 1999)

• 95% primary
• 5% secondary

1. Renal
2. Endocrine
3. Coarctation of aorta
4. Preg-induced HT
5. Neurologic disorder
6. Acute stress, including surgery

• Black race
• Genetic disposition
• DM
• Lack of exercise
• Alcohol
• Distress (?)
• Obesity
• Hyperlipidaemia

• Hereditary - Environment
• Pre-HT (0-30yo)
• Early HT (20-40yo)
• Established HT (30-50yo)

1. Uncomplicated
2. Complicated

1. Accelerated-Malignant course
2. Cardiac - hypertrophy, failure, infarction
3. Large BV - aneurysm, dissection
4. Cerebral - ischaemia, thrombosis, haemorrhage
5. Renal - nephrosclerosis, failure

Significantly increased risk of

• Death
• Stroke
• MI
• Atrial fibrillation
• Heart failure
• Peripheral vascular disease
• Renal impairment

• Left: relative risk of CAD of 1 at DBP at 90 mmHg
• Right: stroke, relative risk greater than one at DBP of 90 mmHg
• Good linear relationship bet incidence and stroke with HT

10-year probability (%)

• HT 6
• HT + H-chol 13
• HT + H-chol + smoking 19
• HT + H-chol + smoking + DM + LVH 44

• Confirm chronic elevation of BP and determine the level Uncovering correctable secondary forms of HT
• Estab a pre-treatment baseline
• Assessing factors that may influence the type of therapy or be changed adversely by therapy (assess Pt risk profile)
• Determining if target organ damage is present (if yes, more committed to starting Tx early)
• Determining whether other risk factors for the development of arteriosclerotic cardiovascular disease are present

• BP is char by large spontaneous variation
• Dx of HT should be based on multiple BP measurements taken on several separate occasions (at least 2 visits over a period of 1 or more weeks, unless severe HT (> 180/110 mmHg) or target organ damage is present - eg. Retinopathy seen in fundi)

• BP should be measured several occasions using a mercury sphygmomanometer or other non-invasive device.
• Use the following procedures when recording BP:

1. Allow the patient to sit for several minutes before measuring the BP
2. use a cuff with a bladder that is 12-13 cm x 35 cm, with a larger bladder for fat arms
3. Use phase 5 Korotkoff sounds (disappearance) to measure the diastolic pressure
4. Measure the BP in both arms at first visit (discrepancy = AS)
5. Measure the BP in standing position in elderly subjects and diabetic patients (prone to postural hypotension - therefore important in drugs that cause postural hT)
6. Place the sphygmomanometer cuff at heart level, whatever the position of the patient

• Definition: in some patient, office BP is persisted increase whereas BP outside clinic is normal, usu by diagnosis by ambulatory or home BP monitoring
• Prevalence: 15-30% of general population, commonly in elderly and pregnancy woman
• Dx: by home or ambulatory BP measure
• Risk: less than sustained HR, probably small risk > than normal people, ? Precursor to HT
• Implications

1. No specific clinical characteristics
2. Must be considered in people with newly diagnosed Ht and before Tx
3. Must be placed in context of overall profile risk
4. Should reassure Pt
5. Need close follow-up, treatment based on patient risk profile & ± target organ damage

• When clinic blood pressure shows unusual variability
• HT is resistant to drug Tx
• When symptoms suggest the possibility of HT
• To Dx "white coat HT"

• Alcohol, caffeine*, nicotine*
• OCP
• NSAID
• Cyclosporine (eg. Transplantation)
• Steroids
• Nasal decongestant, theophylline
• Amphetamines, cocaine
• MAO inhibitors (anti-psychotic drugs)

* = short duration

• Age: men > 55yo, women > 65yo
• Smoking
• Total chol > 6.5 nmol/L
• DM
• Fam Hx premature CV disease

• Cerebrovascular disease - ischaemia stroke, cerebral haemorrhage, TIA
• Heart disease - MI, CAD, CHF
• Renal disease - DM retinopathy, renal failure
• Vascular disease - dissecting aneurysm, PVD

• None
• Elevated BP - headache, dizziness, palpitation, easy fatigue, impotence
• Hypertensive vascular disease - epistaxis, haematuria, blurring vision, episodes of weakness or dizziness, angina dyspnoea
• Underlying disease - secondary HT - primary aldosteronism (polyuria, polydispia, m weakness due to hypo K+)

• Fam Hx - essential HT
• Age ; secondary HT - 35 or after 55
• Urinary symptoms - repeated UTI - chronic PN, nocturia and polydipsia - renal or endocrine disease
• Changes in wt - wt gain - Cushings syndromes, at loss - phaeochromocytoma
• Vascular disease - angina pectoris, cerebrovascular insufficiency, CHF, PVD
• Other risk factors - cigarette smoking, DM, lipid disorders, fam Hx of early deaths due to CV disease
• Pt's lifestyle - diet, physical activity, family status, work, education level

• General appearance - Cushings: round face + truncal obesity
• BP and pulses in 2 upper extremities (supine and standing)

• Ht and wt
• Fundoscopy
• Palpation and auscultation of all peripheral arteries: vascular disease and renal artery stenosis
• CVS examination - LV tilt/ cardiomegaly, 3 and 4th HS, murmur, pulmonary rales

• Urine - pro, blood, gluc, microscopic analysis
• Haemtocrit
• Serum K, Ca, PO4, Cr, urea, fasting gluc
• Total chol, HDL, LDL, chol, triglycerides
• ECG
• TSH
• CXR
• Limited ECHO (LVH)

• General

1. Age < 30 or > 55
2. Severe HT (180/11)
3. Abrupt onset, rapid increase severity, dev to resistance to previously effective Tx

• Specific

1. Phaeochromocytoma symptoms
2. Unexplained hypo K+ (primary aldosteronism)
3. Signs of Cushings syndrome
4. Palpable kidney, renal bruit, abn urinalysis results
5. Delayed or absent femoral pulses (coarctation)

• Renovascular disease - ACEI radionucleide renal scan, renal duplex Doppler flow studies, MRI angiography
• Phaeochromocytoma - 24hr assay for Cr, metanephrines, catecholamines
• Cushings - overnight dexamethasone suppression test or 24hr urine cortisol and creatinine
• Primary aldosteronism: plasma aldosterone : renin ratio

Adherence difficult, comply in first year, long-term default (reassure and constantly remind Pt)

Drugs proven to reduce CVS mortality (ABCD)

• ACEI, BB, ?CCB, Diuretic
• CCB = calcium-channel blocker
• ACEI - best choice for DM and heart failure
• Depends on individual Pt profile
• Alpha-antagonists: lost favour, increase incidence of heart failure

Assess age

• Young: high angiotensin renin system, more responsible to angiotensin inhibition or beta-blocker
• Old: less responsible system, more responsive to CCB and diuretic
• Beta-blockers and diuretics much cheaper, effective at reducing cardiovascular risk
• Do not start with beta-blocker and ACEI (both work on AAA system)
• If A or B fail, add on C or D

* Hypokalaemia K <3.4 mEq/l

• ACEI

1. Unilateral RAS and normal functioning contralateral kidney
2. chronic renal failure with or without DM
3. Need care monitoring of renal function
4. Contraindicated - bilateral RAS

• CCB

1. BP control
2. No contraindications

• Diuretic

1. Relatively contraindicated as it increases renin level
2. Note: one underfunctioning kidney with underperfusion will cause increase in renin anyway

• After stenting - resume bld transfusion

Indications

MALIGNANT HT

• <1% population, 25-50% 5yr mortality
• Marked BP elevation DBP > 140 mmHg
• Papilloedema and retinal haemorrhages and exudates
• HT encephalopathy - severe headache vomiting, visual disturbances (incl transient blindness), transient paralyses, convulsions, stupor and coma
• Cardiac decompensation
• Acute renal failure and oliguria

• HYPERTENSIVE EMERGENCY (IMMED Rx-WITHIN 1 HR)

1. HT encephalopathy
2. Acute heart failure
3. Unstable angina/ MI
4. Dissecting AA
5. Cerebral haemorrhage
6. Renal failure
7. Severe preclampsia

• HYPERTENSIVE EMERG (early Rx- WITHIN 2hr)

1. HT with grade III or IV retinal changes
2. severe preop or perioop HT

• INDICATION FOR EMERGENCY REDUCTION OF BP WITH IV TX

1. Hypertensive encephalopathy - malignant HT, eclampsia
2. Acute LV failure due to HT
3. Dissecting aneurysm
4. Pt cannot take drug (eg. After surgery)
5. Emergency reduction of BP in our condition (eg. Accelerated BP is contraindicated b/c of loss of cerebral autoregulation and consequent risk of cerebral infarction)