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)

📚 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

📝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

🔹 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.

🔹 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

🔹 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

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

💊 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

🏃 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

💊 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

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

🧪 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

💉 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)

🧪 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)

🧪 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

🧪 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.

🧪 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)

🧪 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

🧾 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)

❌ 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

🎯 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

effective antihypertensive drugs for clinical conditions

📌 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

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

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.

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.

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

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.

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