Hypertension

Hypertension is chronic elevation of arterial blood pressure. Regulation of blood pressure is complex — the autonomic nervous system, the renin-angiotensin-aldosterone system, cardiac output, vascular tone, and renal salt/water handling all contribute, and obesity and vascular stiffness are two of the most important drivers of rising blood pressure with age. Sustained elevation damages the heart, brain, kidneys, and blood vessels over time, and hypertension is the leading modifiable contributor to stroke, myocardial infarction, heart failure, atrial fibrillation, chronic kidney disease, and dementia.^[1]

The 2025 Hypertension Canada primary care guideline makes two changes that reshape day-to-day management: it redefines hypertension as blood pressure consistently ≥130/80 mmHg on correctly performed measurement (down from the older 140/90 mmHg threshold), and it replaces sequential monotherapy with a low-dose single-pill combination — typically an ACE inhibitor or ARB plus a thiazide/thiazide-like diuretic — as the default first step for most adults starting drug therapy.^[1] The degree of blood pressure reduction achieved matters more to cardiovascular risk reduction than which specific drug class is used to get there, which is part of why combining two lower-dose agents from complementary classes is now preferred over pushing a single agent to its maximum dose.^[1]

Usually silent

Hypertension is typically asymptomatic. Most patients feel entirely well, and blood pressure is found incidentally on screening rather than because of symptoms — do not wait for symptoms to prompt measurement. When symptoms are present they are nonspecific (headache, dizziness) and do not reliably track with the degree of elevation, except in a true hypertensive emergency (see Red Flags & Refer). Opportunistic screening at every applicable visit, and at minimum annually, is how most hypertension is actually found.^[1]

• Age.
• Family history of hypertension.
• Overweight or obesity, particularly abdominal obesity.
• Sedentary lifestyle.
• High dietary sodium intake; low dietary potassium intake.
• Excess alcohol intake.
• Smoking.
• Diabetes mellitus.
• Dyslipidemia.
• Chronic kidney disease.
• Obstructive sleep apnea.
• Hypertension during a prior pregnancy.
• Chronic psychological stress.

Drugs and other exogenous factors that can induce or aggravate hypertension

Review every patient's medication and substance-use history for these contributors before assuming a hypertension diagnosis is purely primary — this is a genuinely reversible or modifiable factor in some patients.

• Alcohol (excessive use).
• Bruton tyrosine kinase inhibitors (e.g., ibrutinib, zanubrutinib).
• Calcineurin inhibitors (e.g., cyclosporine, tacrolimus).
• Corticosteroids and anabolic steroids.
• Erythropoietin and analogues.
• Licorice root.
• Midodrine.
• Monoamine oxidase inhibitors (MAOIs).
• NSAIDs, including COX-2 inhibitors.
• Oral contraceptives and other sex hormones.
• High dietary sodium (salt) intake.
• Selective serotonin reuptake inhibitors (SSRIs).
• Serotonin-norepinephrine reuptake inhibitors (SNRIs).
• Stimulants, including cocaine.
• Vasoconstricting, sympathomimetic decongestants.

History

• Duration of hypertension, usual BP level, any sudden change in severity, and any prior hospitalization or emergency visit for hypertensive urgency/emergency.
• Home BP monitoring use, technique, and device (confirm a validated device and correct cuff size), home readings, and any discrepancy from office values.
• Prior antihypertensive drug use — reason for changing or stopping, effectiveness, side effects, and intolerance.
• Drugs or substances that may be causing or aggravating hypertension (see Risk Factors), and drugs that may interact with antihypertensive therapy.
• Adherence to lifestyle recommendations and drug therapy.
• Family history of hypertension, cardiovascular risk factors, and premature cardiovascular disease.
• Smoking and alcohol use, usual physical activity, usual diet and sodium intake, current weight/recent weight change, waist circumference, diabetes, dyslipidemia, and hypertension during a prior pregnancy.
• Cerebrovascular, cardiac, and peripheral vascular symptoms suggesting target-organ damage.
• Symptoms of secondary hypertension — e.g., catecholamine-excess symptoms (pheochromocytoma), hyper-/hypothyroid symptoms, Cushingoid features, or renal/urinary symptoms or a past history of renal disease.

Diagnostic technique

Use a validated automated oscillometric device and a standardized technique — automated office BP (AOBP) is the preferred office/pharmacy method, taking the mean of several automated readings (usually 3-6) with the patient unattended, which minimizes white-coat effect. All in-office measurement remains susceptible to white-coat effect, so out-of-office measurement is required to confirm the diagnosis — either a home BP series (2 readings each morning and evening for 7 days, discard the first day, and average the remaining 24 readings) or 24-hour ambulatory BP monitoring, which is considered the gold standard and is preferred when available. Hypertension is diagnosed when the mean BP is consistently ≥130/80 mmHg.^[1]

Physical exam

• Fundoscopy for hypertensive retinopathy.
• Bruits and peripheral pulses for vascular disease or renovascular hypertension.
• Edema and lung fields for signs of heart failure.
• Heart sounds (a fourth heart sound suggests reduced left ventricular compliance).
• Sustained, displaced apex beat suggesting left ventricular hypertrophy.
• Abdominal mass suggesting polycystic kidneys or aortic aneurysm.
• Neurologic exam for cerebrovascular disease.
• Femoral-radial pulse delay and any murmur suggesting aortic coarctation.

Initial investigations

• Serum potassium, sodium, and creatinine.
• Urinalysis; urine albumin and/or albumin-creatinine ratio in patients with diabetes.
• Fasting glucose and/or HbA1c.
• Lipid panel (total cholesterol, HDL-C, LDL-C, triglycerides — fasting or non-fasting).
• Standard 12-lead ECG.
• Consider renin and aldosterone levels in medication-naive patients.
• Perform a global cardiovascular risk assessment (e.g., Framingham) in every hypertensive patient — this independently determines both the treatment-initiation threshold and target (see Treatment Targets).

• Reduce the risk of stroke, myocardial infarction, heart failure, and other cardiovascular and renal complications.
• Achieve a target systolic BP under 130 mmHg, provided this is well tolerated — the current guideline uses one simplified systolic target for most adults rather than separate population-specific numeric targets.^[1]
• Start drug therapy for BP ≥140/90 mmHg in average-risk adults.
• Start drug therapy earlier, at SBP 130-139 mmHg, in adults at high cardiovascular risk: established cardiovascular disease (coronary artery disease, heart failure, cerebrovascular disease, peripheral artery disease); type 1 or type 2 diabetes mellitus; chronic kidney disease (eGFR under 60 mL/min/1.73m² or albuminuria ≥3 mg/mmol); a 10-year Framingham Risk Score ≥20%; or age ≥75 years.
• If SBP is 130-139 mmHg and the patient is not high risk, start with healthy lifestyle changes alone, continue monitoring BP and other risk factors, and reassess the need for drug therapy every 6-12 months rather than starting a drug immediately.
• Individualize the target in very old age, significant frailty, symptomatic orthostatic hypotension, or limited life expectancy — do not automatically withhold treatment, but do not pursue the under-130 target rigidly either (see Special Populations).
• Minimize the adverse effects of antihypertensive therapy.

Advise every patient — treated or not yet on drug therapy — on a healthy lifestyle to prevent or control hypertension and cardiovascular risk overall:

• Weight loss if overweight, targeting a BMI of 18.5-24.9 kg/m² and a waist circumference under 102 cm (men) or 88 cm (women).
• A healthy diet high in fresh fruits, vegetables, soluble fibre, and low-fat dairy, and low in saturated fat and sodium — e.g., a DASH-style eating plan.
• Sodium intake under 2000 mg (88 mmol) per day.
• Increase dietary potassium (e.g., the fruit/vegetable component of a DASH-style diet) unless the patient is at risk of hyperkalemia — renin-angiotensin-system inhibitor use, other potassium-raising drugs, chronic kidney disease, or a serum potassium above 4.5 mmol/L.
• Regular, moderate-intensity cardiorespiratory physical activity for 30-60 minutes on most days of the week.
• Low-risk alcohol consumption — no more than 0-2 standard drinks per week.
• A smoke-free environment.

Home blood pressure monitoring technique

Recommend a validated, Hypertension Canada-endorsed home BP monitor and train the patient in correct technique (proper cuff size, seated position, arm supported at heart level, no talking during measurement). Use a home BP series to confirm a diagnosis or assess control: 2 readings each morning and evening for 7 days, discard the first day's readings, and average the remaining 24 readings. Reassure patients that some variation in BP throughout the day is normal — the goal is the trend, not any single reading.

Supporting adherence

Poor adherence is a major, correctable cause of uncontrolled blood pressure. Build these strategies into routine care:

• Ensure the patient understands hypertension and its treatment, ideally with both verbal counselling and written patient information.
• Involve family or social support in lifestyle changes.
• Use a simplified regimen — long-acting, once-daily drugs, and a single-pill combination product where appropriate — rather than multiple separate pills.
• Confirm the patient can access and afford the prescribed drugs.
• Anchor pill-taking to an existing daily routine (e.g., alongside brushing teeth).
• For patients with confirmed poor adherence: identify and address the specific reason, consider a dosette box or other adherence-enhancing dispenser, encourage home BP self-monitoring, use pill counts or a marked calendar for refill timing, and involve regular follow-up contact or social work support where needed.

Breastfeeding

Labetalol, nifedipine extended-release, and methyldopa are all considered safe to continue while breastfeeding. If an ACE inhibitor is strongly favoured, captopril, enalapril, benazepril, and quinapril are the preferred agents given lower transfer into breast milk.

Older adults

Use a lower starting dose in older patients, who are often more sensitive to blood-pressure-lowering effects. Beta-blockers are not recommended as initial therapy over age 60 without a compelling indication. A single-pill combination remains reasonable in a fit older adult, but in very old or significantly frail patients — particularly age ≥85, symptomatic orthostatic hypotension, or a limited predicted lifespan — individualize the target rather than rigidly pursuing systolic BP under 130 mmHg, and avoid starting with combination therapy unless BP is very high; a long-acting dihydropyridine CCB is a reasonable single starting agent, followed by a low-dose thiazide/thiazide-like diuretic if further lowering is needed. Do not automatically deprescribe antihypertensive therapy in a frail patient who is tolerating it well, but review the regimen regularly, since progressive frailty can itself lower BP and eventually require deprescribing. Avoid vasodilating beta-blockers, direct vasodilators, and alpha1-blockers where possible in very frail patients given a higher orthostasis risk.^[5]

Renal impairment

Thiazide diuretics become ineffective once creatinine clearance falls below 30-40 mL/min — switch to a loop diuretic instead. An ACE inhibitor or ARB is preferred in proteinuric chronic kidney disease, with close monitoring of potassium and creatinine after starting or increasing the dose. Never combine an ACE inhibitor with an ARB. Avoid ACE inhibitors/ARBs in bilateral renal artery stenosis or unilateral stenosis with a solitary kidney.

Diabetes

An ACE inhibitor or ARB is preferred first-line, especially with albuminuria, renal disease, cardiovascular disease, or additional cardiovascular risk factors — add a dihydropyridine CCB in preference to a thiazide diuretic if further BP lowering is needed in this group.

Hepatic impairment

Use lower starting and maximum doses of ACE inhibitors and other hepatically metabolized agents in significant hepatic impairment, and monitor clinical response and adverse effects more closely.

Titrate therapy approximately every 4 weeks in most patients; use closer follow-up and more frequent titration for severe hypertension, target-organ damage, or high cardiovascular risk. Recheck BP 2-4 weeks after any dose change or new drug. Uncontrolled BP is most often a failure to titrate therapy in response to elevated readings, not true treatment resistance — supplement office readings with home or ambulatory measurement to build confidence in the true BP before intensifying therapy. Assess medication adherence at every visit. Check serum potassium and creatinine within days of starting or increasing an ACE inhibitor, ARB, or potassium-sparing diuretic/spironolactone, then periodically thereafter. Reassess global cardiovascular risk and screen for target-organ damage on an ongoing basis. For a patient managed with lifestyle measures alone (SBP 130-139 mmHg, not high risk), reassess the need for drug therapy every 6-12 months. There is no advantage to routinely moving antihypertensive dosing to bedtime — evening dosing does not improve cardiovascular outcomes compared with morning dosing.^[6]

1. Confirm the measurement technique is correct and obtain out-of-office readings (home BP series or ABPM) before assuming true treatment failure — an elevated office reading with normal out-of-office BP is white-coat effect, not resistant hypertension.
2. Assess and address adherence in a nonconfrontational way — ask directly, consider a dosette box, simplify to once-daily or single-pill combination dosing, and confirm the patient can afford the regimen.
3. Screen specifically for hypertension-aggravating drugs and substances (NSAIDs, decongestants, licorice, oral contraceptives, excess alcohol/sodium — see Risk Factors) as a reversible contributor.
4. Optimize the current regimen to its full effective dose before adding another agent, then add — never substitute — a complementary-class agent rather than cycling between single drugs.
5. If BP remains above target despite 3 optimally dosed drugs including a diuretic (resistant hypertension): obtain 24-hour ambulatory BP monitoring to confirm true resistance and re-confirm adherence. If no nocturnal BP dipping is seen on ABPM, screen for obstructive sleep apnea and consider moving one or more doses to the evening. Add spironolactone (amiloride, bisoprolol, doxazosin, or clonidine are reasonable alternatives) once secondary causes have been considered.^[2]
6. Refer to a hypertension specialist, nephrologist, or internist if BP targets are still not achieved with a regimen the prescriber is comfortable managing, or if secondary hypertension is suspected (see Red Flags & Refer).

• Diagnosing or intensifying treatment based on unstandardized or nonvalidated office BP readings without out-of-office confirmation.
• Substituting a new drug for an existing one instead of adding a complementary-class agent when the first drug alone is not enough.
• Using a beta-blocker as routine initial therapy, especially in patients over 60, without a compelling indication.
• Combining an ACE inhibitor with an ARB — no added benefit, more harm, across every indication.
• Assuming routine bedtime dosing improves cardiovascular outcomes — the TIME trial found no benefit of evening over morning dosing, so dose timing should be chosen for adherence, not a presumed outcome advantage.^[6]
• Missing a hypertension-aggravating drug or substance (NSAIDs, decongestants, licorice, oral contraceptives) as a reversible contributor to poor control.
• Using short-acting (immediate-release) nifedipine for chronic essential hypertension — reserved only for acute severe hypertension in pregnancy.
• Labelling a patient "resistant" without first excluding white-coat effect and nonadherence via out-of-office measurement.
• Missing secondary-hypertension clues (see Red Flags & Refer) and simply cycling through more antihypertensive classes instead of investigating or referring.
• In pregnancy: continuing an ACE inhibitor or ARB after conception, using atenolol, or forgetting ASA for preeclampsia prevention in a patient with chronic hypertension.
• Stopping a beta-blocker or clonidine abruptly — both require tapering to avoid rebound hypertension or ischemia.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Alpha1-Adrenergic Antagonists

Not used as initial hypertension therapy; reserved for special situations such as resistant hypertension or symptomatic benign prostatic hyperplasia.

ACE Inhibitors

First-line only as part of a single-pill combination with a thiazide/thiazide-like diuretic, or for a specific compelling indication. Never combine with an ARB. Contraindicated in pregnancy.

Angiotensin II Receptor Blockers (ARBs)

First-line only as part of a single-pill combination with a thiazide/thiazide-like diuretic, or for a specific compelling indication; generally better tolerated than ACE inhibitors given a lower cough rate. Never combine with an ACE inhibitor. Contraindicated in pregnancy.

Beta-Blockers — Non-Selective

Not first-line for uncomplicated hypertension; reserve for a compelling indication. Taper rather than stop abruptly — abrupt withdrawal can precipitate rebound hypertension and ischemia. Avoid in asthma; contraindicated in 2nd-/3rd-degree heart block without a pacemaker; avoid in severe peripheral arterial disease.

Beta-Blockers — Cardioselective (beta1-selective)

Preferred over non-selective agents when a beta-blocker is indicated, given fewer non-cardiac effects. Same tapering and heart-block cautions as non-selective agents.

Beta-Blockers — With Intrinsic Sympathomimetic Activity (ISA)

ISA agents cause less resting bradycardia than agents without ISA; a minor, infrequently used subgroup.

Combined Alpha1/Beta-Blocker

A reasonable compelling-indication choice when both alpha- and beta-blockade are wanted, and one of the preferred agents in pregnancy.

Calcium Channel Blockers — Dihydropyridine

Older patients with isolated systolic hypertension respond particularly well to this class. Never use a short-acting dihydropyridine (immediate-release nifedipine) for chronic hypertension.

Calcium Channel Blockers — Non-Dihydropyridine

Avoid combining with a beta-blocker without close monitoring given additive bradycardia/AV-block risk; avoid in significant heart failure.

Centrally Acting Agents

Not for initial therapy; reserved for resistant hypertension or specific situations.

Potassium-Sparing Diuretics

Not for initial monotherapy; used as add-on therapy, particularly for resistant hypertension or to offset thiazide-induced hypokalemia.

Thiazide / Thiazide-Like Diuretics

First-line only as part of a single-pill combination with an ACE inhibitor or ARB, or as one of 2 separate pills. Ineffective once creatinine clearance falls below 30-40 mL/min, where a loop diuretic is preferred instead.

Single-Pill Combinations — ACE Inhibitor / Calcium Channel Blocker

Contraindicated in pregnancy.

Single-Pill Combinations — ACE Inhibitor / Diuretic

First-line option when a single-pill combination is preferred over 2 separate pills. Contraindicated in pregnancy. Ineffective at creatinine clearance under 30-40 mL/min.

Single-Pill Combinations — ARB / Diuretic

The preferred first-line single-pill combination class for most adults starting therapy without a compelling comorbid indication. Contraindicated in pregnancy.

Single-Pill Combinations — Beta-Blocker / Diuretic

Only used when a beta-blocker is separately indicated for a compelling reason.

Single-Pill Combination — Calcium Channel Blocker / ARB

Contraindicated in pregnancy.

Calcium Channel Blocker / HMG-CoA Reductase Inhibitor Combination

For a patient with both hypertension and an indication for a statin — a convenience combination rather than a hypertension-specific interaction advantage.

Diuretic / Diuretic Combinations

Combine a thiazide with a potassium-sparing diuretic specifically to reduce thiazide-induced hypokalemia.