based on National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults – 2016. Melbourne: National Heart Foundation of Australia, 2016.

Risk factors

Modifiable risk factors

Smoking
Dyslipidaemia
Overweight or obesity
Physical inactivity
High salt intake
Highly processed diet
Excess alcohol intake
Recreational drug use, especially stimulants
Psychosocial stress and poor sleep
Obstructive sleep apnoea
NSAID use and other medication contributors

Non-modifiable risk factors

Increasing age
Family history of hypertension, premature cardiovascular disease or stroke
Aboriginal and Torres Strait Islander background
Familial hypercholesterolaemia
Established cardiovascular disease
Chronic kidney disease
Diabetes

Causes of hypertension

Primary / essential hypertension

Accounts for most adult hypertension.
Usually multifactorial.
Associated with:
- Age
- Genetics
- Obesity
- Salt intake
- Alcohol
- Physical inactivity
- Metabolic syndrome
- Sleep apnoea

Secondary hypertension

Consider secondary causes when hypertension is:

Young onset, especially age <30 years
Severe at presentation
Abrupt onset or rapidly worsening
Resistant to treatment
Associated with hypokalaemia
Associated with renal impairment or proteinuria
Episodic or paroxysmal
Associated with suggestive clinical features

System	Causes	Clinical clues
Renal	CKD glomerulonephritis reflux nephropathy polycystic kidney disease renal artery stenosis	Proteinuria haematuria renal impairment renal bruit recurrent UTIs flank pain enlarged kidneys
Endocrine	Primary aldosteronism thyroid disease Cushing syndrome phaeochromocytoma	Hypokalaemia nocturia cramps weight change proximal weakness sweating palpitations episodic headaches
Vascular	Coarctation of the aorta	Radiofemoral delay weak femoral pulses upper-limb hypertension
Sleep-related	Obstructive sleep apnoea	Snoring witnessed apnoea morning headache daytime somnolence obesity large neck circumference
Pregnancy-related	Pre-eclampsia gestational hypertension	Pregnancy proteinuria headache visual symptoms RUQ pain
Drug/substance-induced	NSAIDs corticosteroids OCP venlafaxine/SNRIs stimulants pseudoephedrine cyclosporine tacrolimus cocaine/amphetamines excess caffeine/energy drinks	Medication or substance exposure

History taking

BP-related history

Ask about:

Date of diagnosis
Previous BP readings and trends
Home BP readings, if available
White coat effect or anxiety with measurements
Medication adherence
Symptoms suggestive of severe hypertension or end-organ damage:
- Headache
- Visual symptoms
- Chest pain
- Dyspnoea
- Neurological symptoms
- Haematuria
- Reduced urine output

Cardiovascular history

Ask about symptoms or history of:

Ischaemic heart disease
Myocardial infarction
Angina
Heart failure
Stroke or TIA
Peripheral arterial disease
Atrial fibrillation or other arrhythmia

Renal history

Ask about:

CKD
Diabetes
Haematuria
Proteinuria
Nocturia
Recurrent UTIs
Flank pain
Renal stones
Family history of renal disease or polycystic kidney disease

Secondary hypertension screen

Symptom pattern	Possible cause
Episodic headache palpitations sweating pallor	Phaeochromocytoma
Snoring witnessed apnoea daytime sleepiness morning headache	OSA
Muscle weakness cramps nocturia hypokalaemia	Primary aldosteronism
Weight gain proximal weakness easy bruising purple striae facial rounding	Cushing syndrome
Heat intolerance palpitations tremor weight loss	Hyperthyroidism
Cold intolerance fatigue weight gain	Hypothyroidism
Recurrent UTIs flank pain urinary abnormalities	Reflux nephropathy/chronic pyelonephritis
Haematuria renal colic abdominal masses family history	Polycystic kidney disease
Claudication cold legs erectile dysfunction delayed pulses	Peripheral arterial disease or coarctation
NSAIDs OCP steroids stimulants venlafaxine decongestants	Drug-induced hypertension

Lifestyle and psychosocial history

Ask about:

Smoking
Alcohol intake
Recreational drugs
Diet, especially salt and processed food intake
Exercise
Weight gain
Sleep quality
OSA symptoms
Work stress
Financial stress
Mental health
Health literacy
Family support
Social isolation

Family history

Ask about:

Hypertension
Stroke
Ischaemic heart disease
Diabetes
Dyslipidaemia
Familial hypercholesterolaemia
CKD
Premature cardiovascular death

Physical examination

General examination

BMI and waist circumference.
Look for features of metabolic syndrome.
Look for signs of endocrine disease:
- Cushingoid appearance
- Thyroid enlargement
- Tremor
- Proximal myopathy

BP exam

Confirm BP using correct technique.
Measure both arms initially.
Assess for postural hypotension if older, symptomatic, diabetic, frail or on treatment.

BP classification in adults

Category	Systolic BP	Diastolic BP
Optimal	<120	and <80
Normal	120–129	and/or 80–84
High-normal	130–139	and/or 85–89
Grade 1 hypertension	140–159	and/or 90–99
Grade 2 hypertension	160–179	and/or 100–109
Grade 3 hypertension	≥180	and/or ≥110
Isolated systolic hypertension	>140	and <90

Use the higher category if systolic and diastolic readings fall into different categories.

Practical accurate BP measurement checklist

Clinic BP should be used for Australian absolute CVD risk calculators.

Using home or ambulatory BP in risk calculators may underestimate absolute CVD risk.

BP diagnosis should be based on:

Multiple readings
Several separate occasions
Correct technique
Use the correct cuff
Validated device
Wrist and finger BP devices are not recommended.

Ensure the patient is:

Seated comfortably
Rested for at least 5 minutes
Back supported
Feet flat on the floor
Legs uncrossed
Arm supported at heart level
Avoid talking during measurement.
Ideally avoid:
- Caffeine before measurement
- Nicotine before measurement
- Exercise immediately before measurement
Measure BP in both arms initially.
Use the arm with the higher reading for future measurements.
Take at least 2 readings, separated by 1–2 minutes.
If readings differ significantly, take additional readings and average the later readings.

Strategy if the initial clinic BP is high

Confirm technique:
- Correct cuff.
- Patient rested.
- Arm at heart level.
- No talking.
- Repeat after rest.
Repeat BP:
- Take at least a second reading.
- If still elevated, consider further readings.
Assess severity:
- Mild/moderate elevation: arrange follow-up and out-of-clinic confirmation.
- Severe elevation: assess for target-organ damage.
Offer confirmation with:
- ABPM and/or
- HBPM
  if clinic BP is ≥140/90 mmHg or hypertension is suspected.
If symptoms or signs of acute organ damage:
- Treat as possible hypertensive emergency.
- Urgent ED/hospital assessment.

Clinic BP vs HBPM vs ABPM

Clinic BP

Easy and available.
Used in most historical treatment trials.
Used in absolute CVD risk calculators.
Can be affected by white-coat effect.

HBPM

Convenient.
Useful for long-term monitoring.
Improves patient involvement.
Requires correct device and technique.

ABPM

Best for full 24-hour profile.
Captures nocturnal hypertension.
Helps distinguish white-coat and masked hypertension.
Strong prognostic value.
Less available and less convenient.

Guideline position

If clinic BP ≥140/90 or hypertension suspected, offer HBPM and/or ABPM to confirm BP level.

White-coat hypertension

Definition

Elevated clinic BP.
Normal out-of-clinic BP.
Applies to untreated patients.

Diagnosis

Requires HBPM or ABPM.

Clinical importance

Avoids unnecessary medication.
But not entirely benign:
- Can progress to sustained hypertension.
- May have increased CVD risk compared with true normotension.

Management

Lifestyle advice.
Assess absolute CVD risk.
Regular follow-up.
Repeat HBPM/ABPM if BP pattern changes.
Drug therapy may be considered if:
- High absolute CVD risk.
- Target-organ damage.
- Progression to sustained hypertension.

Masked hypertension

Definition

Normal clinic BP.
Elevated home/ambulatory BP.
Applies to untreated patients.

Why important

Easy to miss.
Associated with increased cardiovascular events and mortality compared with true normotension.

Suspect in

Normal clinic BP but:
- LVH.
- Albuminuria.
- CKD.
- Diabetes.
- High CVD risk.
- OSA.
- Heavy alcohol use.
- Smoking.
- Strong family history.
- Workplace or stress-related BP elevation.

Management

Confirm with HBPM/ABPM.
Treat according to confirmed BP and total risk.
Address lifestyle and risk factors.

Cardiovascular examination

Finding	Possible implication
Displaced apex beat	LVH or cardiomegaly
Heave	Longstanding pressure overload
Loud A2	Longstanding hypertension
Carotid bruit	Atherosclerotic disease
Abdominal bruit	Renal artery stenosis
Femoral bruit	Peripheral arterial disease
Weak femoral pulses / radiofemoral delay	Coarctation
Peripheral oedema, raised JVP, basal crackles	Heart failure

Renal examination

Look for:

Renal bruit
Palpable enlarged kidneys
Abdominal masses
Flank tenderness
Peripheral oedema

Respiratory / OSA assessment

Look for:

Obesity
Large neck circumference
Crowded oropharynx
Signs of hypoventilation or cardiorespiratory disease

Fundoscopy

Grade	Findings	Meaning
Grade1	Arteriolar narrowing / tortuosity	Mild hypertensive retinopathy
Grade2	AV nipping	Moderate hypertensive retinopathy
Grade3	Flame haemorrhages, cotton wool spots	Severe hypertension
Grade4	Papilloedema	Malignant hypertension / emergency

Investigations

Baseline investigations for most patients

These assess cardiovascular risk, target-organ damage and secondary causes.

UEC, creatinine and eGFR
Sodium and potassium
Urine ACR
Urinalysis for blood and protein
Fasting lipids
HbA1c or fasting glucose
ECG
Consider FBC
Consider LFTs
Consider TSH if clinically indicated

Proteinuria/Albuminuria Assessment

Assess kidney damage in patients with hypertension using:
- Serum creatinine / eGFR
- Urine albumin:creatinine ratio — ACR
- Blood pressure
Urine ACR is the preferred screening test for albuminuria.
Use a first-morning spot urine sample where possible.
A random spot urine sample is acceptable if first-morning urine is not practical.
Do not rely on urine dipstick/reagent strip for detecting low-grade albuminuria.
If ACR is abnormal:
- Repeat ACR twice over the next 3 months.
- Confirm albuminuria if at least 2 out of 3 results are abnormal.
- Exclude transient causes such as UTI, fever, recent heavy exercise, menstruation, heart failure or acute illness.
Use PCR or 24-hour urine if:
- heavy proteinuria suspected
- nephrotic syndrome suspected
- ACR and clinical picture do not match
- non-albumin proteinuria suspected
- nephrologist requests quantification.

Albuminuria category	Male ACR	Female ACR	Meaning
Normal	<2.5 mg/mmol	<3.5 mg/mmol	No albuminuria
Moderately increased albuminuria	2.5–25 mg/mmol	3.5–35 mg/mmol	Previously called microalbuminuria
Severely increased albuminuria	>25 mg/mmol	>35 mg/mmol	Previously called macroalbuminuria

Category	ACR	Approx albumin excretion	PCR	Approx total protein excretion
Moderately increased albuminuria / old “microalbuminuria”	Male 2.5–25 mg/mmol; Female 3.5–35 mg/mmol	30–300 mg/day albumin	Male 4–40 mg/mmol; Female 6–60 mg/mmol	50–500 mg/day protein
Severely increased albuminuria / old “macroalbuminuria”	Male >25 mg/mmol; Female >35 mg/mmol	>300 mg/day albumin	Male >40 mg/mmol; Female >60 mg/mmol	>500 mg/day protein

Note:

ACR is not simply the same as PCR.
ACR measures albumin only.
PCR measures all protein.
Therefore:
- PCR is usually higher than ACR, because total protein includes albumin plus non-albumin proteins.
- But the exact relationship depends on the underlying pathology.

Test	What it estimates	Main use
ACR	Albumin excretion	Preferred CKD/CVD risk screening test
PCR	Total protein excretion	Quantifying total proteinuria
24-hour urine protein	Actual total protein lost per day	Specialist quantification, nephrotic-range proteinuria, unusual cases

1. ACR = albumin-specific test

Urine ACR = albumin : creatinine ratio

It measures:

urinary albumin concentration ÷ urinary creatinine concentration

It is best for detecting albuminuria, especially early glomerular kidney disease.

In hypertension, diabetes and CKD screening, ACR is preferred because it is more sensitive than PCR for clinically important low-level albuminuria. Kidney Health Australia states that urine ACR is more sensitive than PCR for detecting lower amounts of clinically important albuminuria, and dipstick protein is no longer recommended for CKD detection because sensitivity and specificity are suboptimal.

2. PCR = total protein test

Urine PCR = total protein : creatinine ratio

It measures:

total urinary protein concentration ÷ urinary creatinine concentration

This includes:

albumin
globulins
tubular proteins
light chains, e.g. myeloma protein
other non-albumin proteins

So PCR is useful when you want to quantify total proteinuria, particularly if non-albumin proteinuria is suspected.

3. 24-hour urine protein = measured daily protein excretion

A 24-hour urine collection measures total protein excretion over a full day.

It reports: mg/day or g/day of protein loss

Best for:

nephrotic-range proteinuria assessment
specialist workup
unusual or discordant results
when spot urine tests may be unreliable

Historically, this was the reference method for quantifying proteinuria. In routine GP practice, it is used less often because spot ACR/PCR is easier and usually adequate.

Example

If a patient has diabetic nephropathy or hypertensive nephrosclerosis:

Most urinary protein is albumin.
ACR and PCR may broadly correlate.

If a patient has tubular disease or myeloma/light-chain proteinuria:

There may be significant non-albumin protein.
PCR may be high while ACR is relatively less elevated.

When to Consider Nephrology Referral

Consider renal referral if any of the following:

eGFR <30 mL/min/1.73 m²
Rapidly declining eGFR
Persistent macroalbuminuria / severely increased albuminuria
Haematuria plus albuminuria
Suspected glomerulonephritis
Resistant hypertension
Unclear cause of CKD
Nephrotic syndrome features: heavy proteinuria, hypoalbuminaemia, oedema
Electrolyte complications, e.g. recurrent hyperkalaemia

Home BP monitoring

When useful

Confirm diagnosis.
Assess white-coat hypertension.
Assess masked hypertension.
Monitor treatment response.
Improve patient engagement.
Assess possible overtreatment/hypotension.
Assess suspected resistant hypertension.

How to perform HBPM

Use validated upper-arm device.
Patient should be trained.
Measure:
- Morning before breakfast and before medications.
- Evening before bed.
Sit quietly for 5 minutes.
Take 2 readings, 1 minute apart.
Record all values.
Ideally measure over several days.
Avoid selectively recording only “good” readings.

Interpretation

Home BP hypertension threshold:
- ≥135/85 mmHg

Practical GP interpretation

HBPM is very useful in routine Australian general practice.
It helps avoid overtreatment of white-coat hypertension.
It can identify undertreatment where clinic BP appears controlled but home BP remains elevated.

Ambulatory BP monitoring

What ABPM provides

24-hour BP profile.
Daytime BP.
Night-time BP.
24-hour average.
Dipping status.
BP variability.
Morning surge.

When ABPM is especially useful

Suspected white-coat hypertension.
Suspected masked hypertension.
Resistant hypertension.
Episodic hypertension.
Postural or post-prandial hypotension.
Suspected nocturnal hypertension.
CKD.
Diabetes.
OSA.
High CVD risk with uncertain clinic readings.

Interpretation:

Diagnostic thresholds by measurement method

Method	Hypertension threshold
Clinic BP	≥140 and/or ≥90
ABPM daytime / awake	≥135 and/or ≥85
ABPM night-time / asleep	≥120 and/or ≥70
ABPM 24-hour average	≥130 and/or ≥80
Home BP monitoring	≥135 and/or ≥85

Dipping

Normal:
- Night-time systolic BP falls by at least ~10%.
Non-dipping:
- Associated with increased cardiovascular risk.
- Seen more often in OSA, CKD, diabetes and autonomic dysfunction.

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

International and local guidelines differ in their recommendations and prescriptiveness in relation to screening for secondary causes of hypertension. In general, patients with hypertension and any of the following characteristics should be screened:^1,3

age of onset less than 40 years
abrupt onset of hypertension
abrupt worsening of hypertension despite previously good control
hypertensive urgency or emergency
resistant hypertension (blood pressure ≥140/90 mmHg despite the consistent use of three antihypertensive drugs including a diuretic, or a need for four or more drugs to control the blood pressure)
target organ damage disproportionate to the degree of hypertension
family history of early-onset hypertension, stroke before the age of 40 years, or primary aldosteronism
clinical clues
- hypokalaemia (may occur in primary aldosteronism)
- higher elevation than expected (>20%) of serum creatinine after starting an ACE inhibitor or angiotensin receptor antagonist (may suggest renovascular hypertension)
- paroxysmal hypertension or episodes suggestive of catecholamine excess (suggestive of phaeochromocytoma).

Cardiac and Vascular Imaging

Echocardiogram
- Consider if:
  - Suspected LVH.
  - Heart failure symptoms.
  - Murmur.
  - Abnormal ECG.
  - Dyspnoea.
  - Longstanding hypertension.
  - Suspected structural heart disease.
  - suspected Aortic coarctation
Carotid Doppler ultrasound
▸ Screen for carotid artery stenosis (CV risk assessment)
Renal ultrasound
- Consider if:
  - CKD.
  - Abnormal urinalysis.
  - Suspected renovascular disease.
  - Recurrent UTI/stones.
  - Renal asymmetry concern.
Renal artery imaging
- Consider if:
  - Resistant hypertension.
  - Sudden onset/worsening hypertension.
  - Flash pulmonary oedema.
  - Abdominal bruit.
  - Worsening renal function after ACEi/ARB.
  - Young woman with possible fibromuscular dysplasia.
  - Older patient with atherosclerotic disease.
Ankle-Brachial Index (ABI)
- Assess for peripheral vascular disease
- Consider if:
  - Claudication.
  - Diabetes.
  - Smoking history.
  - Older age.
  - Peripheral pulse abnormality.
  - Vascular bruit.
  - Non-healing lower limb wound.

Endocrine Workup

1. Plasma Aldosterone/Renin Ratio (ARR)

Aldosterone–renin ratio, used to screen for primary aldosteronism
- Renin suppressed/low
- Aldosterone inappropriately normal or high
- Therefore ARR elevated
Consider in
- treatment-resistant HTN
- hypokalaemia
- Adrenal incidentaloma
- Young onset hypertension
- Family history of early hypertension/stroke.
Can occur even with normal K⁺
Is best done before starting antihypertensives, but if already treated, medication switching is often needed to reduce false positives and false negatives.
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
Measuring a morning or random serum cortisol is not recommended owing to a low sensitivity and specificity for Cushing’s syndrome

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
Physical activity	150–300 min/week moderate activity or 75–150 min/week vigorous activity Practical examples – Brisk walking. – Cycling. – Swimming. – Gym program. – Resistance bands. – Supervised exercise physiology if complex comorbidity. Cautions If symptomatic CVD, unstable angina, severe aortic stenosis, decompensated heart failure or severe uncontrolled hypertension: Assess before vigorous exercise. Start low and build gradually in older/frail patients.
Resistance exercise	Muscle strengthening at least 2 days/week
Weight Reduction	Aim for BMI < 25 kg/m² Waist circumference: • <94 cm (men) • <90 cm (Asian men) • <80 cm (women) Practical approach – Measure BMI and waist. – Avoid weight stigma. – Set realistic goals: 5–10% weight loss can be clinically meaningful. Consider: – Dietitian. – Exercise physiologist. – Behavioural strategies. – Sleep and stress management. – Screening for binge eating or depression where relevant.
Salt Reduction	Reduce to ≤4 g/day (Na⁺ ≈100 mmol; 1600 mg) Advise: – Avoid adding salt. – Read labels. – Choose low-salt options. – Reduce processed meats, packaged soups, sauces, takeaway foods.
Diet Quality	5 serves vegetables + 2 serves fruit/day DASH-style principles More: – Vegetables. – Fruit. – Wholegrains. – Low-fat dairy. – Nuts/legumes. – Fish. Less: – Processed food. – Added salt. – Saturated fat. – Sugary drinks. – Excess alcohol.
Alcohol Reduction	Limit to: • ≤2 standard drinks/day • ≤10 standard drinks/week total Follow NHMRC guidelines
Stress Management	Use relaxation techniques, mindfulness, meditation, CBT if indicated
Smoking Cessation	Does not reduce BP directly but essential for CV risk reduction
Sleep Apnoea Management	Assess for OSA if high clinical suspicion CPAP if indicated

When to Initiate Pharmacological Therapy

Using the 2023 Australian CVD risk framework, with 2016 NHFA hypertension BP treatment principles

CVD risk category	BP / clinical context	Action
Low risk	5-year CVD risk <5% and BP below severe range	Lifestyle advice, confirm BP with HBPM/ABPM where appropriate, monitor
Low risk + severe/persistent hypertension	Persistent BP ≥160/100 mmHg	Start antihypertensive drug therapy
Intermediate risk	5-year CVD risk 5% to <10% with persistent hypertension, especially ≥140/90 mmHg	Lifestyle advice + shared decision-making consider antihypertensive therapy depending on – BP level – patient preference – comorbidities – target-organ damage
High risk	5-year CVD risk ≥10% with elevated BP	Start BP-lowering pharmacotherapy unless contraindicated or clinically inappropriate
Clinically high-risk patients	Established CVD clinically significant CKD familial hypercholesterolaemia target-organ damage IHD heart failure PAD	Treat as high risk; do not rely only on calculator
Severe hypertension	Persistent ≥180 systolic and/or ≥110 diastolic, or symptoms/signs of acute target-organ damage	Same-day urgent assessment if acute organ damage suspected; otherwise prompt treatment and close follow-up

The older NHFA 2016 guideline used low risk <10%, moderate risk 10–15%, high risk >15%;
its key recommendations were:
- lifestyle advice for all
- start treatment in low-risk patients if persistent BP ≥160/100, and
- start treatment in moderate-risk patients if persistent BP ≥140/90.
It also recommended confirming clinic BP ≥140/90 with ambulatory or home BP monitoring where possible.
The newer Australian CVD risk framework now defines
- low risk as <5%
- intermediate as 5% to <10%
- high risk as ≥10% over 5 years.

CVD risk assessment eligibility

Assess CVD risk in people without known CVD:	When to assess CVD risk
General population	45–79 years
People with diabetes	35–79 years
First Nations people	30–79 years
First Nations people aged 18–29 years	Assess individual CVD risk factors rather than using the calculator
Known CVD	Do not calculate primary prevention risk; manage as secondary prevention

Treatment targets

Target group	BP goal	Notes
Most uncomplicated hypertension	<140/90 mmHg	Standard NHFA 2016 target
Diabetes + hypertension	<140/90 mmHg	Lower systolic target only in selected cases, especially where stroke prevention is prioritised
CKD + hypertension	NHFA 2016: <140/90 mmHg	CKD-specific guidance may use tighter targets, especially with albuminuria; ACEi/ARB preferred if albuminuria
Prior stroke/TIA	<140/90 mmHg	Secondary prevention
Previous MI	Usually at least <140/90 mmHg, lower if tolerated	ACEi and beta-blocker recommended for hypertension and secondary prevention
Selected high CVD-risk patients	Consider SBP <120 mmHg only if safe/tolerated	Requires close monitoring for hypotension, syncope, electrolyte disturbance and AKI
Older/frail/falls risk/postural hypotension	Individualise	Start low, titrate slowly, avoid overtreatment

The NHFA 2016 guideline recommends a target of <140/90 mmHg or lower if tolerated once treatment is started. It allows consideration of SBP <120 mmHg only in selected high-risk populations and specifically recommends close follow-up for hypotension, syncope, electrolyte abnormalities and acute kidney injury.

For diabetes and CKD, the NHFA 2016 guideline also lists <140/90 mmHg as the formal target, with ACEi/ARB preferred in CKD when albuminuria is present.

SPRINT Trial (Systolic Blood Pressure Intervention Trial)

RCT of 9,361 adults ≥50 years with increased CVD risk.
SPRINT participants were high-risk:
- Age >50.
- SBP >130.
- Estimated 10-year CVD risk at least 20%.
- Many had prior vascular disease or mild–moderate CKD.
SPRINT did not include patients with diabetes.
Compared intensive SBP target <120 mmHg vs standard target <140 mmHg.
Intensive treatment reduced major CVD events and mortality.
Approximate NNT: 61 over 3.3 years for the primary composite CVD outcome.
Increased adverse effects:
- Hypotension.
- Syncope.
- AKI.
- Electrolyte abnormalities.
SPRINT is not applied universally because it studied a
- selected high-CVD-risk population
- excluded
  - Diabetes
  - Previous stroke
  - Congestive heart failure
  - Significant proteinuria
  - eGFR <20 mL/min/1.73 m²
  - Polycystic kidney disease
  - Patients with adherence concerns
  - Some frail or institutionalised patients.
- Used automated office BP readings that are generally lower than routine clinic BP.
Intensive SBP targeting <120 mmHg reduced CVD events and mortality but increased hypotension, syncope, AKI and electrolyte abnormalities.
Therefore, Australian guidance keeps <140/90 mmHg as the usual target and reserves SBP <120 mmHg for selected high-risk patients where safe, tolerated and closely monitored

Immediate treatment or urgent assessment indications

Situation	Action
Hypertensive emergency: severe BP with acute target-organ damage	Urgent ED/hospital assessment
Severe hypertension: SBP ≥180 and/or DBP ≥110	Recheck correctly; assess for emergency symptoms/signs; prompt therapy and close follow-up if no acute organ damage
Persistent BP ≥160/100	Start drug therapy, even if calculated CVD risk is low
Target-organ damage	Treat as high risk; start pharmacological therapy
Associated clinical conditions: CKD, IHD, prior stroke/TIA, diabetes with hypertension, heart failure, PAD	Usually requires pharmacological treatment as part of global CVD risk management
Resistant hypertension	Check adherence, white-coat effect, secondary causes, NSAIDs/alcohol/salt/OSA; consider specialist advice

Avoid in pharmacological management

Avoid rapid or excessive BP lowering unless hypertensive emergency is being managed in an appropriate acute-care setting.
Avoid overtreatment in older/frail patients.
Check standing BP when risk of postural hypotension is present.
Avoid drug combinations with overlapping adverse effects where possible.
Avoid ACE inhibitor + ARB combination.
Avoid beta-blockers as first-line therapy for uncomplicated hypertension.
Use caution with:
- Diuretics in hyponatraemia, gout, dehydration or frailty.
- ACEi/ARB in AKI, hyperkalaemia, bilateral renal artery stenosis or pregnancy.
- Non-dihydropyridine CCBs with beta-blockers due to bradycardia/heart block risk.
- Aldosterone antagonists in CKD/hyperkalaemia risk.

MEDICATIONS

First-line antihypertensive drug classes

ACE inhibitor.
ARB.
Calcium channel blocker.
Thiazide/thiazide-like diuretic.

Not preferred first-line for uncomplicated hypertension

Beta-blockers.

Reason:

Less favourable balance of efficacy and safety compared with other first-line options for uncomplicated hypertension.

Avoid

ACE inhibitor + ARB combination.
Dual renin–angiotensin system blockade due to increased adverse effects.

🧪 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

ACE inhibitors and renal function

A small rise in creatinine or small fall in eGFR is common after starting an ACE inhibitor. This is usually a haemodynamic effect, not direct structural kidney damage.

Why eGFR can fall after starting an ACE inhibitor

ACE inhibitors reduce angiotensin II.

Angiotensin II normally constricts the efferent arteriole, which is the “outflow pipe” from the glomerulus.

This helps maintain pressure inside the glomerulus and supports filtration.

Think of the glomerulus like a coffee filter:

Situation	What happens
Before ACE inhibitor	Angiotensin II keeps the efferent arteriole relatively tight, maintaining pressure inside the glomerulus
After ACE inhibitor	Efferent arteriole dilates
Result	Glomerular pressure falls, so filtration pressure drops
Blood test effect	eGFR may fall and creatinine may rise slightly

So the kidney is not necessarily “injured”. It may simply be filtering at a lower pressure.

What does “haemodynamic fall in eGFR” mean?

A haemodynamic fall means the eGFR falls because of a change in kidney blood flow and pressure, not because the kidney tissue has been damaged.

ACE inhibitors reduce intraglomerular pressure. This can cause a predictable early fall in eGFR.

This effect is often acceptable because lowering glomerular pressure can be kidney-protective long-term, especially in:

Situation	Why ACE inhibitors are useful
Diabetes with albuminuria	Reduce albuminuria and slow CKD progression
Proteinuric CKD	Reduce intraglomerular pressure and protein loss
Heart failure with reduced ejection fraction	Improve mortality and symptoms
Hypertension	Lower BP and reduce cardiovascular risk

Does the eGFR return to normal?

Not always.

When we say the eGFR “stabilises”, we usually mean:

The eGFR drops a little after starting the ACE inhibitor, then stops falling and remains steady.

It does not necessarily return to the original baseline.

Example:

Time	eGFR
Before ACE inhibitor	70
1–2 weeks after starting	58–62
4 weeks later	60
3 months later	59–62

This is considered stable, even though the eGFR did not return to 70.

When might eGFR return closer to baseline?

The eGFR may improve closer to baseline if the initial fall was partly due to a reversible factor, such as:

Reversible factor	Example
Dehydration	Vomiting, diarrhoea, poor oral intake
Over-diuresis	Frusemide, thiazide, spironolactone
NSAID use	Ibuprofen, naproxen, celecoxib
Low BP	Postural hypotension, overtreatment
Intercurrent illness	Sepsis, acute infection

Example:

Time	eGFR
Baseline	70
ACE inhibitor started while dehydrated and taking NSAIDs	42
ACE inhibitor held, fluids given, NSAID stopped	65

This pattern suggests AKI physiology, not just the expected mild haemodynamic change.

Does BP drop too?

Yes. ACE inhibitors usually lower blood pressure, which is the intended effect.

Mechanism	Effect
Less angiotensin II	Less vasoconstriction
Less aldosterone	Less sodium and water retention
More bradykinin	More vasodilation

BP can fall more noticeably:

after the first dose
after dose increases
in older adults
if volume depleted
if taking diuretics
if already on multiple antihypertensives

BP drop: expected versus concerning

Finding	Interpretation
Mild BP reduction, asymptomatic	Expected
Dizziness or postural symptoms	Dose may be too high, or patient may be volume depleted
Symptomatic systolic BP <90–100 mmHg	Concerning
Large eGFR fall plus low BP	Consider renal hypoperfusion or AKI

Interpreting renal function after starting an ACE inhibitor

NICE CKD guideline NG203

Threshold	NICE recommendation
eGFR fall <25% or creatinine rise <30%	Do not modify the ACEi/ARB dose; repeat test in 1–2 weeks
eGFR fall ≥25% or creatinine rise ≥30%	Investigate other causes: – Bilateral renal artery stenosis – Renal artery stenosis in a single functioning kidney – Volume depletion – NSAID use – Over-diuresis – Severe heart failure / low renal perfusion if no other cause is found, stop or reduce ACEi/ARB
K⁺ ≥6.0 mmol/L	Stop renin–angiotensin system antagonist after stopping other hyperkalaemia-promoting medicines

NICE also recommends checking serum potassium and eGFR before starting, then repeating 1–2 weeks after starting and after each dose increase

Renal Artery Stenosis

In bilateral renal artery stenosis, both kidneys have reduced blood flow coming in through narrowed renal arteries. Because the kidneys are under-perfused, they rely heavily on angiotensin II to keep filtration pressure up. When renal artery stenosis reduces blood entering the kidney, the kidney compensates by producing renin → angiotensin II..Angiotensin II preferentially constricts the efferent arteriole. This is like partially closing the outflow pipe to maintain pressure inside the filter.

ACE inhibitor blocks angiotensin II production.

So:

Renal artery stenosis already reduces blood coming into the kidney.
The kidney is depending on angiotensin II to constrict the efferent arteriole.
ACE inhibitor removes that efferent constriction.
Efferent arteriole dilates.
Glomerular pressure drops sharply.
GFR falls significantly.
Creatinine rises, sometimes causing AKI.

Simple analogy

Think of the glomerulus as a water filter.

Scenario	What happens
Normal kidney	Good water flow into filter; ACEi lowers pressure slightly
Bilateral renal artery stenosis	Poor water flow into filter; kidney tightens exit pipe to maintain pressure
Add ACEi	Exit pipe opens → pressure collapses → filtration falls

Why bilateral is worse than unilateral

Situation	Effect of ACEi
One renal artery stenosed, other kidney normal	Normal kidney can usually maintain overall renal function
Both renal arteries stenosed	Both kidneys lose filtration pressure → large creatinine rise
Single functioning kidney with renal artery stenosis	Same risk as bilateral disease

Clinical clue

A major clue is:

Creatinine rises >30% after starting an ACE inhibitor or ARB.

Practical monitoring

Check UEC/eGFR and potassium:

before starting
around 1–2 weeks after initiation
around 1–2 weeks after dose increases
sooner if the patient is frail, has CKD, is on diuretics, or becomes acutely unwell

Key point

A mild early fall in eGFR after starting an ACE inhibitor is often expected and acceptable.

The main concern is not the fall itself, but whether it is:

too large
progressive
associated with hyperkalaemia
associated with symptomatic hypotension
occurring in the context of dehydration, NSAIDs, diuretics, sepsis, or possible renal artery stenosis

🧪 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

Common effective combinations

Combination	Comment
ACEi or ARB + CCB	Common, effective
ACEi or ARB + thiazide/thiazide-like diuretic	Common, effective
CCB + thiazide/thiazide-like diuretic	Useful alternative
ACEi + ARB	Avoid

❌ 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

Practical sequence

Confirm hypertension.
Start lifestyle advice.
Start first-line medication if threshold met.
Review BP response and side effects.
If not at target:
- Check adherence and technique.
- Increase dose or add second first-line drug.
If still not controlled:
- Use two-drug combination at adequate doses.
If still not controlled:
- Add third drug, usually including a diuretic.
If still uncontrolled:
- Consider resistant hypertension.
- Check secondary causes.
- Seek specialist advice.

Before escalating

Always check:

Is BP being measured correctly?
Is patient taking medication?
Is there white-coat hypertension?
Are home readings actually controlled?
Is there high salt intake?
NSAID use?
Alcohol?
OSA?
CKD?
Primary aldosteronism?
Drug interactions?

effective antihypertensive drugs for clinical conditions

Hypertension with prior stroke or TIA

Guideline recommendations

Antihypertensive therapy is recommended after TIA/stroke to reduce overall CVD risk.
Any first-line antihypertensive drug that effectively lowers BP can be used.
Target:
- <140/90 mmHg.

Practical notes

Secondary prevention should also include:
- Antiplatelet/anticoagulation where indicated.
- Statin therapy where indicated.
- Diabetes management.
- Smoking cessation.
- Lifestyle advice.
- AF detection.
- Carotid disease assessment where relevant.

Acute stroke

Acute stroke BP management differs.
Do not automatically lower BP rapidly in acute stroke without stroke-specific guidance.

Hypertension with CKD

Key recommendations

Any first-line drug can be used if it effectively lowers BP.
If CKD plus albuminuria:
- ACE inhibitor or ARB should be considered first-line.
Start treatment if BP consistently >140/90.
Target:
- <140/90 mmHg.
More intensive SBP <120 may benefit selected patients if well tolerated.
Avoid dual renin–angiotensin system blockade.
Aldosterone antagonists require caution.

Practical CKD monitoring

Before and after ACEi/ARB/diuretic:

UEC.
Creatinine/eGFR.
Potassium.
Sodium.

Watch for

Hyperkalaemia.
AKI.
Volume depletion.
NSAID use.
Dehydration.
Renal artery stenosis.

Sick-day advice

Consider advising temporary withholding during acute dehydration/illness for:

ACE inhibitors.
ARBs.
Diuretics.
NSAIDs avoidance.

Hypertension with diabetes

Guideline recommendations

Antihypertensive therapy strongly recommended if:
- SBP ≥140 mmHg.
Any first-line drug that effectively lowers BP can be used.
Target:
- <140/90 mmHg.
SBP <120 may be considered where stroke prevention is prioritised, but needs close monitoring.

Practical notes

Check:
- ACR.
- eGFR.
- Retinopathy status.
- CVD risk.
- Foot risk.
ACEi/ARB often preferred if albuminuria.
Avoid overtreatment in:
- Frailty.
- Postural hypotension.
- Falls.
- Autonomic neuropathy.

Hypertension with prior myocardial infarction

Guideline recommendations

ACE inhibitors and beta-blockers are recommended for:
- Hypertension management.
- Secondary prevention after MI.
Beta-blockers or calcium channel blockers are recommended for symptomatic angina.

Practical notes

Consider:
- LV function.
- Heart rate.
- Angina frequency.
- Bradycardia.
- Conduction disease.
- COPD/asthma severity.
- Other secondary prevention therapy:
  - Statin.
  - Antiplatelet.
  - Smoking cessation.
  - Cardiac rehabilitation.

Hypertension with chronic heart failure

Guideline recommendations

ACE inhibitors and selected beta-blockers are recommended.
ARBs are recommended if ACE inhibitor not tolerated.
Evidence-based beta-blockers listed:
- Carvedilol.
- Bisoprolol.
- Metoprolol extended release.
- Nebivolol.

Practical notes

In HFrEF, BP management overlaps with prognostic therapy:
- ACEi/ARB/ARNI.
- Beta-blocker.
- MRA.
- SGLT2 inhibitor, according to newer standards.
- Diuretics for congestion.
Monitor:
- BP.
- HR.
- Weight.
- Renal function.
- Potassium.
- Symptoms.

Hypertension with peripheral arterial disease

Guideline recommendations

Treat hypertension to reduce CVD risk.
Any first-line antihypertensive drug that effectively lowers BP can be used.
Target:
- Consider <140/90 mmHg.
Treatment should be guided by symptoms and contraindications.

Practical notes

PAD management must also include:
- Smoking cessation.
- Statin.
- Antiplatelet if indicated.
- Supervised walking/exercise.
- Diabetes control.
- Foot care.
- Vascular referral if critical limb ischaemia or lifestyle-limiting claudication.

Hypertension in older persons

Guideline recommendations

Any first-line antihypertensive can be used.
Start at the lowest dose.
Titrate slowly because adverse effects increase with age.
For patients >75 years:
- SBP <120 may show benefit if well tolerated, unless concomitant diabetes.
Use clinical judgement in lower-grade hypertension.

Practical older-person assessment

Consider:

Frailty.
Falls history.
Postural BP.
Cognition.
Polypharmacy.
Renal function.
Electrolyte risk.
Life expectancy.
Goals of care.
Medication administration capacity.
Carer support.

Avoid overtreatment

Especially if:
- Dizziness.
- Syncope.
- Recurrent falls.
- Standing hypotension.
- Advanced frailty.
- Limited life expectancy.

Pregnancy

The guideline does not cover pregnancy hypertension in detail.
Use pregnancy-specific guidance, such as SOMANZ.
Important:
- ACE inhibitors and ARBs are contraindicated in pregnancy.
- Pregnancy hypertension requires separate diagnostic and treatment thresholds.

Blood pressure variability

Guideline explanation

Visit-to-visit BP variability is associated with increased CVD outcomes in high-risk patients.
However, there is insufficient direct evidence that choosing drugs specifically to reduce variability improves outcomes independently.
Therefore, drug selection should follow usual evidence-based recommendations rather than variability alone.

Management

Focus on:
- Accurate measurement.
- Medication adherence.
- Lifestyle consistency.
- Alcohol reduction.
- Salt reduction.
- Avoid NSAIDs/stimulants.
- Treat OSA if present.
- Ensure long-acting medication coverage.

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