Hypertension

🧬 Risk Factors

Modifiable:

• Smoking
• Dyslipidaemia
• Obesity
• Sedentary lifestyle
• Unsafe alcohol intake
• Diet (high salt, processed foods)
• Recreational drug use
• Psychosocial stressors

Non-Modifiable:

• Age >75 years
• Aboriginal and Torres Strait Islander background (ATSI)
• Family history of heart disease (1st degree relative)
• Familial hypercholesterolaemia
• Non-ischemic heart disease (e.g., atrial fibrillation, cardiomyopathy)

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📚 Causes of Hypertension

A. Essential Hypertension (90–95%)

B. Secondary Hypertension (5–10%)

System	Cause	Key Clues
Renal	– Glomerulonephritis – Reflux nephropathy – Renal artery stenosis – Chronic kidney disease (e.g., diabetic nephropathy, PCKD)	Proteinuria, haematuria, renal bruit, bilateral flank masses
Endocrine	– Hyperthyroidism / Hypothyroidism – Primary hyperaldosteronism (Conn’s) – Cushing’s syndrome – Phaeochromocytoma	Fatigue, nocturia, low K+, facial swelling, moon face, episodes of headache + palpitations + sweating
Vascular	– Coarctation of the aorta	Radiofemoral delay, weak lower limb pulses, rib notching
Sleep-related	– Obstructive sleep apnoea	Obesity, snoring, daytime somnolence
Other	– Anaemia – Pregnancy – Immunologic (e.g., PAN)	Varies; systemic features may coexist

C. Medication-induced Hypertension

• Hormonal: OCPs, corticosteroids
• Psychotropics: Clozapine, SSRIs/SNRIs (e.g., venlafaxine, paroxetine, desvenlafaxine, reboxetine)
• Immunosuppressants: Cyclosporine, tacrolimus
• Stimulants/Other: Pseudoephedrine, amphetamines (e.g., duramine), NSAIDs, MAO inhibitors, energy drinks

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📝History Taking

A. BP-related history

• Onset, diagnosis date, past BP trends
• Symptoms of end-organ damage: headache, dyspnoea, chest pain, haematuria
• Features of secondary HTN – as below (G)

B. Previous treatments

• Medications used and side effect

C. Co-morbidities

• Past or current symptoms of
  • ischaemic heart disease
  • heart failure
  • cerebrovascular disease
  • peripheral arterial disease
• Past or current symptoms that suggest chronic kidney disease
  • nocturia
  • haematuria
• Diabetes, CKD, recent weight gain
• Hyperlipidaemia, asthma, psychiatric illness

D. Lifestyle & Risk Factors

• Obesity, poor diet/salt intake
• Alcohol, smoking, physical inactivity
• Analgesic and caffeine intake

E. Family History

• HTN, CVD, stroke, hyperlipidaemia, diabetes
• Alcohol abuse, premature death

F. Social and Psychosocial Factors

• Education level and health literacy
• Family support and household dynamics
• Employment or financial stressors
• Mental health: Depression, anxiety
• Social isolation and coping mechanisms

G. Symptoms Suggestive of Secondary Causes

Symptom	Likely Secondary Cause
Paroxysmal hypertension with headache, palpitations, sweating, pallor	Phaeochromocytoma
Daytime somnolence, snoring, witnessed apnoea, morning headaches	Obstructive Sleep Apnoea (OSA)
Muscle weakness, nocturia, leg cramps, fatigue, particularly with hypokalaemia	Primary Hyperaldosteronism (Conn’s)
Weight gain, easy bruising, proximal myopathy, facial swelling	Cushing’s Syndrome
Fatigue, cold intolerance, weight change, heat intolerance, palpitations	Thyroid dysfunction (hypo/hyperthyroidism)
Headaches, visual symptoms, flushing, sweating	Consider endocrine cause (e.g., Phaeochromocytoma, Hyperthyroidism)
History of recurrent UTIs, flank pain, urinary abnormalities	Reflux nephropathy or chronic pyelonephritis
Family history of renal disease, haematuria, renal colic, abdominal masses	Polycystic Kidney Disease
Intermittent claudication, cold legs, erectile dysfunction, delayed pulses	Coarctation of the Aorta or Peripheral Vascular Disease
Use of medications/substances (e.g., NSAIDs, OCPs, amphetamines, steroids, venlafaxine)	Drug-induced hypertension

🩺 Physical Examination

A. General

• Elevated BP (often only abnormal sign)
• BMI and waist circumference (risk factor & for metabolic syndrome)

B. Cardiovascular

Blood Pressure:

Category	Systolic (mmHg)	Diastolic (mmHg)
Grade 1	140–159	90–99
Grade 2	160–179	100–109
Grade 3	≥180	≥110
Isolated systolic hypertension	>140	<90
Isolated systolic (wide PP)	>160	<70

Factors Affecting Accurate BP Measurement

• Apprehension: Ensure patient is relaxed; rest ≥5 minutes before measuring.
• Caffeine: Avoid 4–6 hours prior.
• Smoking: Avoid 2 hours before.
• Eating: Avoid food intake 30 minutes before.

Strategies for High Initial Readings

• Repeat reading after 10 minutes of rest if:
  • SBP >140 mmHg or DBP >90 mmHg
• Consider home BP monitor or 24-hour Holter BP if:
  • Suspected white coat hypertension
  • Marked variability or discrepancy between office and home readings

Follow-Up Based on Initial BP Readings (Adults ≥18 Years)

Systolic	Diastolic	Follow-up Recommendation
<120	<80	Recheck in 2 years
120–139	80–89	Recheck in 1 year + lifestyle advice
140–159	90–99	Confirm within 2 months + lifestyle
160–179	100–109	Evaluate or refer within 1 month
≥180	≥110	Evaluate and refer within 1 week (or immediately if urgent)

• If systolic and diastolic differ, follow shorter interval.
• Immediate therapy may be needed if DBP ≥115 mmHg or if target organ damage present.
• Mild HTN: Monitor over 3–6 months before initiating meds.

B. Cardiovascular – other:

Sign	Suggestive Diagnosis
Radiofemoral delay, weak/absent femoral pulses	Coarctation of the aorta
Loud A2, displaced apex, heave	Left Ventricular Hypertrophy (due to longstanding HTN)
Systolic abdominal bruit	Renal artery stenosis
Carotid/renal/femoral bruits	Atherosclerotic vascular disease
Peripheral oedema, basal crackles, elevated JVP	Heart failure due to HTN or secondary cardiac disease

C. Renal

• Palpable enlarged kidneys → Suggests Polycystic Kidney Disease
• Abdominal masses/flank tenderness

D. Endocrine

Finding	Suggestive Diagnosis
Cushingoid appearance (central obesity, striae, moon face)	Cushing’s Syndrome
Thyroid enlargement or signs of thyroid dysfunction	Hyper/hypothyroidism
Muscle weakness, especially proximal	Consider Conn’s or Cushing’s

E. Respiratory

• Obesity, snoring, large neck circumference, daytime sleepiness → Suggests OSA

F. Fundoscopy – Keith-Wagener Classification

Grade	Features	Implication
Grade 1	Tortuous arteries, silver wiring	Mild HTN
Grade 2	AV nipping	Moderate HTN
Grade 3	Flame haemorrhages, cotton wool spots	Severe HTN
Grade 4	Papilloedema	Malignant HTN – URGENT

Investigations:

🔹 Baseline Investigations (Recommended for All Patients)

These establish hypertension diagnosis, identify secondary causes, assess for target organ damage, and determine cardiovascular risk.

• Chest X-ray
  ▸ Assess cardiac size and pulmonary vasculature
  ▸ Baseline for future comparison
• Fasting plasma glucose
  ▸ Assess for diabetes or impaired glucose tolerance
• Serum lipids (total cholesterol, HDL, triglycerides; fasting preferred)
  ▸ Evaluate cardiovascular risk
• Serum electrolytes (sodium, potassium)
  ▸ Detect endocrine causes (e.g. primary aldosteronism, diuretics effect)
• Serum creatinine and eGFR
  ▸ Renal function assessment
• Albumin-to-Creatinine Ratio (ACR)
  ▸ Screen for micro/macroalbuminuria (target organ damage)
• Serum uric acid
  ▸ May indicate renal impairment or metabolic syndrome
• Haemoglobin and haematocrit
  ▸ General health status, polycythaemia
• Urinalysis (dipstick and microscopy)
  ▸ Screen for haematuria, proteinuria
  ▸ If positive for blood/protein: send for microscopy and quantification
• 12-lead ECG
  ▸ Assess for LVH, arrhythmias, past infarcts

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🔹 Proteinuria/Albuminuria Assessment

• Recommended for all patients; mandatory for those with diabetes.
• Can be measured via:
  • Urinary albumin/creatinine ratio (ACR)
  • Urinary protein/creatinine ratio (PCR)
  • Reagent strips
  • In spot urine samples or timed urine collections.
• Relationships between different measurement methods are not exact; approximate equivalence is available in standard reference tables.
• Preferred sample: first-void spot urine for ACR assessment.
  • If not possible, any spot urine is acceptable.
• If ACR result is in the macroalbuminuria range, proceed with 24-hour urine collection to quantify total protein.
• Definition of Proteinuria: >500 mg/day protein excretion.
• Urine PCR is an alternative for quantifying and monitoring proteinuria, particularly if albumin-specific measures are unavailable.

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🔹 Ambulatory Blood Pressure Monitoring (ABPM)

• Special BP Presentations:
  • White coat hypertension:
    • Up to 25% of cases
    • Elevated clinic BP, normal home/ambulatory BP
    • Low short-term risk, but may progress
  • Masked hypertension:
    • Normal clinic BP, elevated ambulatory BP
    • Associated with end organ damage, worse prognosis
  • Isolated systolic hypertension (elderly):
    • SBP ≥140 mmHg, DBP <90 mmHg
    • Not benign – needs cautious pharmacological control to 140–160 mmHg

Indications for Ambulatory Blood Pressure Monitoring (ABPM) :

• Suspected white-coat hypertension (e.g., pregnancy)
• Suspected masked hypertension (normal clinic BP, elevated ABPM)
• Suspected nocturnal hypertension or absent dipping
• Hypertension despite treatment
• Borderline hypertension or high CV risk
• Suspected episodic hypertension
• Suspected/confirmed OSA, early pregnancy HTN, syncope/orthostatic symptoms not evident in clinic

Interpretation:

Context	Normal (mmHg)	Hypertension (mmHg)
24-hour average	<115/75	≥130/80
Daytime (awake)	<120/80	≥135/85
Nighttime (asleep)	<105/65	≥120/75

• Nighttime BP should dip by ≥10% compared to daytime
• BP Load: <20% of readings above hypertensive threshold
• Monitor BP variability, morning surge, maximum SBP

Limitations:

• Not reliable in arrhythmias (e.g., AF)
• Not suitable for assessing postural hypotension
• Requires patient diary to correlate symptoms/events

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🔹 Special Investigations for Suspected Secondary Hypertension

Cardiac and Vascular Imaging

• Echocardiogram
  ▸ Assess for left ventricular hypertrophy or cardiac dysfunction
• Carotid Doppler ultrasound
  ▸ Screen for carotid artery stenosis (CV risk assessment)
• Renal artery duplex Doppler
  ▸ Evaluate for renovascular hypertension
• Ankle-Brachial Index (ABI)
  ▸ Assess for peripheral vascular disease

Endocrine Workup

1. Plasma Aldosterone/Renin Ratio (ARR)

• Consider in treatment-resistant HTN, hypokalaemia, or moderate-severe HTN
• Can occur even with normal K⁺
• Referral recommended due to complexity in interpretation during treatment

2. Cushing’s Syndrome

• Dexamethasone Suppression Test:
  • Day 1: 0900h cortisol baseline (optional)
  • 2300h: 1 mg dexamethasone orally
  • Day 2: 0900h cortisol; <50 nmol/L = normal
• 24-hour urinary free cortisol if further confirmation needed

3. Phaeochromocytoma

• Indications: episodic HTN, headache, sweating, palpitations
• Tests:
  • Plasma metanephrines/normetanephrines
  • 24-hour urine collection: metanephrines, normetanephrines, catecholamines

Obstructive Sleep Apnoea (OSA)

• Screening Tools:
  ▸ Epworth Sleepiness Scale
  ▸ STOP-BANG questionnaire
• Diagnostic: Overnight sleep study
• Consider in: resistant HTN, nocturnal HTN, daytime somnolence

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When to Refer

• Suspected secondary hypertension
• Resistant or complex hypertension
• Hypertension in pregnancy
• Endocrine abnormalities (e.g., suspected Conn’s, Cushing’s, phaeochromocytoma)
• Young-onset or rapidly worsening hypertension
• Evidence of target organ damage

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💊 Treatment

Goals:

• Lower BP to <140/90 mmHg (adjust for age/comorbidities)
• Improve CV outcomes and quality of life
• Promote therapeutic partnership

Patient Education & Engagement

Common Misconceptions to Address:

• “BP is cured when controlled”
• “No symptoms = no problem”
• “I don’t need meds if I’m eating well”
• “I can feel when my BP is up/down”

Education Essentials:

• Reassurance + simple instructions
• Clarify importance of long-term treatment
• Emphasise benefit of lifestyle changes alongside meds
• Provide written material

Tips for Compliance:

• Build a strong therapeutic relationship
• Encourage pill routine (e.g. bedtime dosing)
• Set clear goals + review plan
• Recall system/check-ins
• Ask about missed doses + side effects
• Reassess other CV risk factors regularly

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🏃 Non-Pharmacological Management

Recommended for all patients regardless of CVD risk.

Particularly appropriate if BP <160/100 mmHg.

Review lifestyle changes at 3–6 months.

Intervention	Recommendation	Expected BP Reduction
Weight Reduction	Aim for BMI < 25 kg/m² Waist circumference: • <94 cm (men) • <90 cm (Asian men) • <80 cm (women)	Approx. 1 mmHg ↓ per 1% body weight reduction
Salt Reduction	Reduce to ≤4 g/day (Na⁺ ≈100 mmol; 1600 mg) Avoid processed foods and table salt	↓ 4–5 mmHg
Diet Quality	Follow DASH-style or lacto-vegetarian diet: • High in fruits, vegetables, whole grains • Low in saturated fat and total fat • Avoid excess caffeine, liquorice	↓ 8–14 mmHg
Physical Activity	≥150–300 mins/week of moderate-intensity aerobic activity (e.g. brisk walking)	↓ 4–9 mmHg
Alcohol Reduction	Limit to: • ≤2 standard drinks/day • ≤10 standard drinks/week total Follow NHMRC guidelines	↓ 2–4 mmHg
Stress Management	Use relaxation techniques, mindfulness, meditation, CBT if indicated	Variable BP reduction
Smoking Cessation	Does not reduce BP directly but essential for CV risk reduction	Critical for global CV risk
Sleep Apnoea Management	Assess for OSA if high clinical suspicion CPAP if indicated	↓ 2–3 mmHg

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💊 When to Initiate Pharmacological Therapy

Absolute CVD Risk	BP Threshold	Action
Low (<10%)	≥160/100 mmHg (or persistent ≥150/90)	Initiate drug therapy
	140–159/90–99 mmHg	Lifestyle advice + 6–12 month follow-up; initiate drug therapy if not at target
Moderate (10–15%)	≥140/90 mmHg	Start antihypertensive medication if lifestyle fails after 3–6 months
High (>15%)	Any elevated BP	Initiate drug therapy immediately

🔍 CVD Risk Eligibility

• Assess in adults ≥45 years (or ≥35 years for Aboriginal and Torres Strait Islander peoples) without existing CVD.

Treatment Targets

Target Group	BP Goal	Evidence Source
Most patients	<140/90 mmHg	NHFA Guidelines 2016
High CVD risk patients (if safe/tolerated)	<120 mmHg systolic	SPRINT trial, 2015

🧪 SPRINT Trial Summary (2015) – Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults – 2016

• RCT with 9,361 patients >50 years old at high CVD risk.
• Excluded: diabetes, stroke, proteinuria, CHF, eGFR <20
• Outcome:
  ↓ CV events & mortality with intensive target (<120 mmHg SBP)
  NNT = 61 over 3 years
• Adverse effects ↑: hypotension, syncope, AKI, electrolyte disturbance
• Used automated BP measurement → readings are typically lower than clinic BP

Caution: The absolute risk calculator used in SPRINT differs slightly from the Australian model. Use local CVD risk tools for decision-making (www.cvdcheck.org.au).

Immediate Treatment Indications

• Grade 3 HT: SBP ≥180 mmHg and/or DBP ≥110 mmHg
• Isolated systolic HT with widened pulse pressure (>160 / <70)
• Any target organ damage (e.g., LVH, retinopathy, proteinuria)
• Presence of associated clinical conditions (e.g., CKD, IHD)

Avoid in Pharmacological Management:

• Rapid or excessive BP lowering
• Drugs causing postural hypotension, especially in the elderly
• Polypharmacy with overlapping side effects

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MEDICATIONS

First-line options (monotherapy or in some combinations):

• ACE inhibitors
• ARBs
• Calcium channel blockers (CCBs)
• Thiazide/thiazide-like diuretics

Choose based on: age, comorbidities, organ damage, drug interactions, cost, adherence

Not first-line (unless indicated): Beta-blockers: Inferior in stroke and mortality prevention unless specific indications (e.g. heart failure, post-MI)

🧪 1. ACE Inhibitors (ACEi)

Mechanism:

• Inhibit conversion of angiotensin I to angiotensin II (vasoconstrictor)
• Inhibit bradykinin breakdown (vasodilator effect)

Indications:

• First-line for most patients
• Diabetic nephropathy
• Heart failure with reduced ejection fraction (HFrEF)
• Proteinuria

Adverse Effects:

• First-dose hypotension
• Chronic dry cough (bradykinin accumulation)
• Hyperkalaemia (↑ risk with renal impairment)
• Acute kidney injury (especially in renovascular disease, volume depletion, or NSAID use)
• Angioedema (rare, can occur late)

Contraindications:

• Pregnancy
• History of angioedema
• Bilateral renal artery stenosis
• Hyperkalaemia

Common Agents & Doses:

• Captopril: 12.5–50 mg BD
• Enalapril: 5–40 mg daily (1–2 doses)
• Fosinopril: 10–40 mg daily
• Lisinopril: 5–40 mg daily
• Perindopril (arginine): 5–10 mg daily
• Perindopril (erbumine): 4–8 mg daily
• Quinapril: 5–40 mg daily (1–2 doses)
• Ramipril: 2.5–10 mg daily (1–2 doses)
• Trandolapril: 1–4 mg daily

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🧪 2. Angiotensin II Receptor Blockers (ARBs)

Mechanism:

• Block angiotensin II receptors
• No bradykinin effects → less cough and angioedema

Indications:

• Alternative to ACEi when cough or angioedema occurs

Adverse Effects:

• Hyperkalaemia
• Renal impairment
• Rare: cough, angioedema

Contraindications:

• Pregnancy
• Bilateral renal artery stenosis
• Hyperkalaemia
• History of angioedema with ARB

Common Agents & Doses:

• Candesartan: 8–32 mg daily
• Eprosartan: 400–600 mg daily
• Irbesartan: 150–300 mg daily
• Losartan: 50–100 mg daily
• Olmesartan: 20–40 mg daily
• Telmisartan: 40–80 mg daily
• Valsartan: 80–320 mg daily

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💉 3. Calcium Channel Blockers (CCBs)

Mechanism:

• Dihydropyridines: vasodilation via arteriolar smooth muscle
• Non-dihydropyridines: ↓ heart rate and contractility (esp. verapamil > diltiazem)

A. Dihydropyridine CCBs

Adverse Effects:

• Peripheral oedema
• Flushing, headache, dizziness
• Palpitations, reflex tachycardia
• Gingival hyperplasia

Common Agents & Doses:

• Amlodipine: 2.5–10 mg daily
• Felodipine CR: 5–20 mg daily
• Lercanidipine: 10–20 mg daily
• Nifedipine IR: 10–40 mg BD
• Nifedipine CR: 20–120 mg daily

B. Non-Dihydropyridine CCBs

Adverse Effects:

• Bradycardia, AV block
• Heart failure (caution)
• Constipation (verapamil)

Common Agents & Doses:

• Diltiazem CR: 180–360 mg daily
• Verapamil IR: 80–160 mg TDS
• Verapamil CR: 180–480 mg daily (split doses >240 mg)

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🧪 4. Beta-Blockers (β-Blockers)

Mechanism:

• ↓ heart rate and cardiac output
• Some inhibit renin secretion

Indications:

• Hypertension + angina
• Post-MI
• Heart failure (select agents)

Adverse Effects:

• Bradycardia
• Fatigue
• Cold extremities
• CNS effects (vivid dreams, depression)
• Bronchospasm

Contraindications:

• Asthma
• Bradycardia
• AV block (grade II–III)
• Decompensated heart failure

Common Agents & Doses:

• Atenolol: 25–100 mg daily
• Carvedilol: 12.5–50 mg daily (1–2 doses)
• Labetalol: 100–400 mg BD
• Metoprolol: 50–100 mg BD; CR 23.75–190 mg daily
• Nebivolol: 5 mg daily
• Propranolol: 40–320 mg daily (2–3 doses)

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🧪 5. Diuretics

A. Thiazide/Thiazide-like Diuretics

Adverse Effects:

• Hypokalaemia, hyponatraemia
• Postural hypotension
• Hyperuricaemia (avoid in gout)
• ↑ lipids and glucose

Common Agents & Doses:

• Hydrochlorothiazide: 25 mg daily
• Indapamide: 1.5 mg CR daily (preferred over 2.5 mg due to ↓ hypokalaemia)

B. Loop Diuretics (Frusemide)

• Not first-line unless fluid overload present

C. Potassium-sparing Diuretics

Spironolactone (Aldosterone antagonist)

• Doses: 12.5–50 mg for HTN, 50–200 mg for Conn’s, 25–50 mg for HF
• Adverse Effects: hyperkalaemia, hyponatraemia, gynaecomastia, mastalgia, sexual dysfunction

Amiloride:

• Not used alone
• Contraindicated in hyperkalaemia

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🧪 6. Alpha-Blockers

Mechanism:

• Post-synaptic α₁ blockade → vasodilation

Common Agent:

• Prazosin: start 0.5 mg nocte → maintenance 3–20 mg/day in divided doses

Adverse Effects:

• First-dose hypotension
• Postural hypotension

Note: Start low, consider withholding other antihypertensives initially.

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🧪 7. Vasodilators

Hydralazine

• Dose: 50–100 mg daily in 2 doses
• Used for resistant HTN (with β-blocker + diuretic)

Adverse Effects:

• Reflex tachycardia, palpitations, flushing
• Lupus-like syndrome (↑ risk >100 mg/day >6 months)

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🧪 8. Centrally Acting Agents

A. Moxonidine

• Imidazoline receptor agonist
• Dose: 200–600 mcg/day (max 400 mcg per dose)
• Taper on discontinuation
• Adverse Effects: dry mouth, bradycardia, dizziness

B. Methyldopa

• Central α₂ agonist
• Predominantly used in pregnancy
• Dose: 250–2000 mg/day (2–4 doses)
• Adverse Effects: sedation, hepatitis, haemolysis (Coombs +ve)

C. Clonidine

• Central α₂ + imidazoline agonist
• Dose: 50–300 mcg BD
• Taper >7 days to avoid rebound hypertension
• Adverse Effects: sedation, constipation, dry mouth, bradycardia

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🧾 Initiating Treatment: Monotherapy vs. Combination Therapy

🔹 Combination Therapy

Definition: Use of two or more antihypertensive agents from different classes.

Prevalence: Required in up to 50–70% of patients to achieve BP targets.

Advantages:

• Greater BP reduction than doubling the dose of one agent
• Faster onset of BP control
• May reduce clinical inertia
• Fewer medication changes → improved adherence

Limitations:

• Difficult to assess efficacy or side effects of individual drugs
• Attribution of adverse effects is more complex
• PBS may not subsidise single-pill combination products for initial treatment

When to Use:

• Markedly elevated BP at presentation
• High cardiovascular risk
• Informed consent and individualised decision-making required

Effective combinations:

• ACE inhibitor or ARB + thiazide
• CCB + ACE inhibitor or ARB
• β-blocker + diuretic
• Avoid certain combinations (see below)

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❌ Combinations to Avoid

Combination	Reason
ACEi + ARB	No added benefit, ↑ risk of hypotension, syncope, renal dysfunction
ACEi or ARB + K⁺-sparing diuretic	↑ risk of hyperkalaemia
ACEi/ARB + NSAID + diuretic (triple whammy)	Risk of acute kidney injury
β-blocker + verapamil	Risk of complete heart block

🔹 Stepwise Approach Starting with Monotherapy

Advantages:

• Allows evaluation of individual drug efficacy and tolerability
• Easier identification of adverse effects
• May prevent overtreatment in patients responsive to a single agent

Limitations:

• Slower BP control
• May delay reaching targets in high-risk patients

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🎯 Blood Pressure Targets

Group	Clinic BP Target	Ambulatory BP Equivalent (24h / Day / Night)
Uncomplicated Hypertension	<140/90 mmHg	133/84
With comorbidities (e.g. CAD, CKD, DM, Stroke, TIA, Proteinuria >300 mg/day, ATSI)	<130/80 mmHg	125/76

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effective antihypertensive drugs for clinical conditions

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📌 Strategies to Maximise Adherence

Communication

• Express empathy and build rapport
• Involve patients in decision-making
• Ask about medication adherence regularly
• Discuss consequences of non-adherence (e.g. stroke, MI)

Tailored Education

• Provide written instructions
• Involve family/caregivers if appropriate
• Use home BP monitoring
• Recommend Home Medicines Review where suitable
• Discuss side effects proactively

Motivation

• Explain long-term benefits of treatment
• Reinforce that therapy may be lifelong
• Address new symptoms or quality-of-life concerns
• Screen for and manage depression or other psychosocial barriers
• Reinforce lifestyle changes during follow-up

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Causes of Apparent or True Drug Resistance

A. Lifestyle & Dietary Contributors

• Obesity
• Sedentary lifestyle
• High sodium intake
• Excessive alcohol consumption

B. Medication-Related Causes

• NSAIDs (ibuprofen, naproxen)
• Oral contraceptives
• Nasal decongestants
• Corticosteroids or herbal preparations

C. Secondary Hypertension Causes

• Primary hyperaldosteronism
• Renal artery stenosis
• Chronic kidney disease
• Obstructive sleep apnoea
• Phaeochromocytoma
• Cushing’s syndrome
• Coarctation of the aorta

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as per Murtagh:

Hypertensive Emergencies

A hypertensive emergency is a rare but life-threatening condition where severely elevated blood pressure (BP) causes acute target organ damage.

Common Presentations

• Hypertensive encephalopathy
• Acute ischaemic or haemorrhagic stroke
• Acute left ventricular failure with pulmonary oedema
• Aortic dissection
• Eclampsia

Symptoms may include:

• Severe headache
• Confusion or altered mental state
• Chest pain, dyspnoea, or neurological deficits (depending on the organ involved)

Immediate Management

• Urgent referral to the emergency department for continuous monitoring and tailored treatment.
• BP reduction must be cautious:
  • Target a ≤25% reduction in BP within the first 2 hours
  • Then reduce to approximately 160/100 mmHg within 2–6 hours
• Avoid rapid BP drops due to the risk of cerebral, myocardial, or renal hypoperfusion.

Pharmacological Options

• First-line: IV sodium nitroprusside (ICU setting)
• Alternatives: Oral dihydropyridine calcium channel blockers (e.g. nifedipine) or ACE inhibitors
• In eclampsia or severe pre-eclampsia, add IV magnesium sulphate to reduce maternal morbidity and risk of seizures.

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Hypertension in Children and Adolescents

Challenges in Paediatric BP Monitoring

• Less frequent screening
• Cuff size availability
• Difficulty in measurement (especially in toddlers/infants)

Screening Indications

• Children of hypertensive parents
• Signs suggestive of secondary hypertension:
  • Recurrent headaches, visual changes
  • Seizures
  • Abdominal pain
  • Use of corticosteroids/oral contraceptives
• High-risk comorbidities (e.g. renal disease, diabetes, cardiac/urological abnormalities)

Common Causes

• Essential hypertension is still more common overall
• Secondary causes more proportionally represented than in adults:
  • Renal parenchymal disease
  • Renal artery stenosis

Normal Paediatric BP Thresholds

Age (years)	Normal Upper Limit (mmHg)
≤5	110/75
6–9	120/80
10–13	125/85
14–18	135/90

Measurement Technique

• Use appropriately sized cuff: bladder width should cover ~75% of upper arm length.
• In children, Korotkoff phase 4 (muffling) is often used for diastolic BP due to absence of phase 5.

Management

• Non-pharmacological strategies (e.g. weight reduction in obesity) often sufficient.
• First-line: ACE inhibitors or calcium-channel blockers
• Diuretics are second-line.
• Avoid ACE inhibitors in post-pubertal females due to teratogenicity.
• Consider paediatric specialist referral in most cases.

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Hypertension in the Elderly

Epidemiology

• Prevalence increases linearly with age.
• Isolated systolic hypertension is common and warrants treatment.

Treatment Principles

• Start low, go slow: initiate at half adult dose to minimise adverse effects.
• Gradual BP reduction is preferred to avoid hypotension or falls.
• Monitor closely for drug interactions (e.g. NSAIDs, psychotropics, antiparkinsonian agents).

Non-Pharmacological Measures

• Sodium restriction is particularly effective in the elderly.

Pharmacological Management

• First-line:
  • Indapamide (preferred) or low-dose thiazide diuretics
  • Monitor electrolytes 2–4 weeks post-initiation
  • Add a potassium-sparing diuretic if hypokalaemia occurs
• Second-line:
  • ACE inhibitors or ARBs, especially if heart failure is present
• Other agents:
  • Calcium channel blockers (e.g. amlodipine)
  • Beta-blockers (if angina or intolerant to other classes)
  • Note: verapamil may cause constipation

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Deprescribing and Step-Down Therapy in Mild Hypertension

Rationale

• Long-term pharmacotherapy may not be necessary for all patients.
• Step-down should be considered if BP has been well controlled for several months to years.

Deprescribing Strategy

• Gradual dose reduction or withdrawal of one agent at a time.
• Monitor BP regularly during and after tapering.
• Avoid abrupt cessation (“drug holiday”)—risk of rebound hypertension.

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When to Refer

Referral to a specialist or hospital setting is appropriate in the following scenarios:

• Refractory hypertension: inadequate control despite multiple agents
• Suspected white coat hypertension: consider ambulatory BP monitoring
• Severe hypertension: diastolic BP >115 mmHg
• Hypertensive emergencies: with signs of target organ damage
• Evidence of end-organ damage not responding to standard management
• Significant renal impairment (eGFR <30 mL/min/1.73 m²)
• Identified secondary cause of hypertension that is potentially reversible