Topic breakdown

1. Definition and classification (ACC/AHA vs ESC/ESH thresholds)
2. Epidemiology and risk factors
3. Pathophysiology (RAAS, sympathetic tone, sodium handling, vascular remodeling)
4. Primary vs secondary hypertension (renal, endocrine, drug-induced causes)
5. Clinical features, diagnosis and BP measurement (office, home, ABPM)
6. Target organ damage and complications
7. Lifestyle and non-drug management
8. Drug therapy (ACE inhibitors, ARBs, calcium channel blockers, thiazide-like diuretics, beta blockers, others) and BP targets
9. Resistant hypertension
10. Special situations: pregnancy, elderly, CKD, diabetes, hypertensive emergency and urgency

Brief overview

Topic breakdown

1. Definition and classification (ACC/AHA vs ESC/ESH thresholds)
2. Epidemiology and risk factors
3. Pathophysiology (RAAS, sympathetic tone, sodium handling, vascular remodeling)
4. Primary vs secondary hypertension (renal, endocrine, drug-induced causes)
5. Clinical features, diagnosis and BP measurement (office, home, ABPM)
6. Target organ damage and complications
7. Lifestyle and non-drug management
8. Drug therapy (ACE inhibitors, ARBs, calcium channel blockers, thiazide-like diuretics, beta blockers, others) and BP targets
9. Resistant hypertension
10. Special situations: pregnancy, elderly, CKD, diabetes, hypertensive emergency and urgency

Brief overview

Hypertension: overview and treatment

1. Definition and classification

• ESC/ESH defines hypertension as office BP ≥140/90 mmHg.
• The 2025 AHA/ACC guideline kept the 2017 categories and the <130/80 mmHg goal.
• Hypertensive crisis is BP >180/120 mmHg. It is called an emergency if there is acute target organ damage, and urgency if there is not.

2. Causes and risk factors

• Primary (essential) hypertension is about 90% of cases. Risk factors are age, family history, obesity, high sodium intake, low potassium intake, inactivity, alcohol, stress and sleep apnea.
• Secondary hypertension is about 5 to 10% of cases. Think of it with early onset, severe or resistant BP, or hypokalemia.
  • Renal: parenchymal disease, renal artery stenosis.
  • Endocrine: primary aldosteronism (the most common endocrine cause), Cushing syndrome, pheochromocytoma, thyroid disease.
  • Other: obstructive sleep apnea, coarctation of the aorta.
  • Drugs: NSAIDs, oral contraceptives, decongestants, steroids, licorice, cocaine, calcineurin inhibitors.

3. Pathophysiology

• RAAS overactivity, which causes vasoconstriction and sodium retention.
• Increased sympathetic tone.
• Impaired renal sodium excretion, so the pressure-natriuresis curve shifts.
• Endothelial dysfunction, with reduced nitric oxide.
• Arterial stiffness and vascular remodeling, with insulin resistance and inflammation.

4. Diagnosis

• Measure BP properly: seated and rested, correct cuff size, arm at heart level, average of at least 2 readings on at least 2 occasions.
• Confirm with out-of-office measurement, either home BP monitoring or 24-hour ambulatory BP monitoring (ABPM). This excludes white-coat and masked hypertension.
• Baseline tests:
  • Urea, creatinine/eGFR, electrolytes, glucose and lipids.
  • Urinalysis and urine albumin-creatinine ratio.
  • ECG, with echocardiography if LVH is suspected.
  • Fundoscopy.
  • TSH if indicated.
• Targeted screening:
  • Primary aldosteronism: renin and aldosterone. The 2025 guideline broadened this to all patients with stage 2 or resistant hypertension.
  • Pheochromocytoma: plasma metanephrines.
  • Renal artery stenosis: imaging.
  • Sleep apnea: sleep study.

5. Complications

• Heart: LVH, heart failure, coronary disease, atrial fibrillation.
• Brain: stroke, intracerebral hemorrhage, cognitive decline.
• Kidney: hypertensive nephrosclerosis, CKD.
• Eye: retinopathy.
• Vessels: aortic dissection, aneurysm, peripheral artery disease.

6. Treatment

A. Lifestyle (for all patients)

• Weight loss: about 1 mmHg per kg lost.
• DASH diet.
• Sodium below about 2 g a day.
• Potassium-rich foods, unless CKD or hyperkalemia.
• Aerobic exercise: 150 minutes a week.
• Alcohol limited to 1 to 2 drinks a day or less.
• Stop smoking.

B. When to start drugs (2025 ACC/AHA)

• Start in stage 2 hypertension, usually with two drugs.
• Start in stage 1 if the patient has established CVD, diabetes or CKD, or a 10-year CVD risk ≥7.5% on the new PREVENT calculator.
• In lower-risk stage 1, give lifestyle measures for 3 to 6 months. If BP stays ≥130/80 mmHg, add medication. This is a change from 2017.
• The goal for most adults is <130/80 mmHg. For higher-risk patients, aim for systolic <130 and try to reach <120 where it is tolerated and measured in a standardized way.
• Use single-pill combinations to improve adherence.

C. First-line drug classes

• Mineralocorticoid receptor antagonists (spironolactone, eplerenone) are the best fourth-line drug for resistant hypertension.
• Others are alpha blockers (doxazosin), central agents (clonidine, methyldopa), hydralazine and minoxidil.

D. Practical approach

1. Start two-drug single-pill therapy for stage 2, using an ACE inhibitor or ARB plus a CCB or thiazide-like diuretic.
2. If BP is uncontrolled, move to triple therapy: ACE inhibitor/ARB plus CCB plus thiazide-like diuretic.
3. If still uncontrolled, add spironolactone and check for adherence problems, secondary causes, interfering drugs and white-coat effect. This is resistant hypertension.
4. Review within 2 to 4 weeks after changes, then monthly until at goal. Check potassium and creatinine after starting ACE inhibitors, ARBs or diuretics.
5. For resistant cases, the 2025 guideline adds renal denervation as an adjunct in selected patients.

E. Special situations

• Diabetes or CKD: Target <130/80 mmHg. Use an ACE inhibitor or ARB if albuminuria is present. In CKD, salt restriction comes first, and a small eGFR fall (<30%) after starting an ACE inhibitor or ARB can be acceptable. RAS inhibitors can usually be continued even at low eGFR with monitoring. Avoid amiloride and triamterene in most patients, and monitor potassium with MRAs (Harrison's Principles of Internal Medicine 22E, "Management of Hypertension"). Very low targets may not suit CKD patients.
• Pregnancy: Use labetalol, nifedipine or methyldopa. Avoid ACE inhibitors, ARBs and direct renin inhibitors. Treat severe BP (≥160/110) urgently. Low-dose aspirin is used to prevent pre-eclampsia in high-risk women.
• Elderly: Treat if tolerated, with a gradual start, and watch for orthostatic hypotension. A 2025 Cochrane review (PMID 41065416) covers drug therapy at age 60 and over.
• Black patients: A CCB or thiazide-like diuretic is usually preferred as the first-line choice.
• Acute intracerebral hemorrhage: The 2025 guideline lowers systolic BP to 130 to <140 mmHg for at least 7 days in patients presenting at 150 to 220 mmHg.
• Hypertensive emergency: BP >180/120 mmHg with organ damage (encephalopathy, aortic dissection, acute pulmonary edema, ACS, eclampsia, acute kidney injury). Admit to ICU and use IV agents such as labetalol, nicardipine, clevidipine, nitroprusside or nitroglycerin. Lower mean BP by no more than about 25% in the first hour, then gradually over 24 to 48 hours. Aortic dissection is the exception, where systolic is lowered to <120 mmHg rapidly. Hypertensive urgency without organ damage is managed with oral drugs and outpatient follow-up, not rapid lowering.

7. Follow-up and prevention

• Home BP monitoring and regular visits.
• Statin and aspirin only when otherwise indicated.
• Treat sleep apnea.
• Avoid therapeutic inertia.

1. Grading of blood pressure

ESC/ESH 2018 (also WHO/ISH style grades)

• Office BP: ≥140/90 mmHg.
• Home or daytime ambulatory: ≥135/85 mmHg.
• Night-time ambulatory: ≥120/70 mmHg.
• 24-hour ambulatory: ≥130/80 mmHg.

ACC/AHA (2017, retained in 2025)

JNC 7 (older, still used in some exams)

• Normal: <120/80.
• Prehypertension: 120-139 / 80-89.
• Stage 1: 140-159 / 90-99.
• Stage 2: ≥160 / ≥100.

2. Grading of hypertensive retinopathy

• The Rosen's Emergency Medicine funduscopic scale runs 0 to 4. It is the same except that grade 0 is normal and grade 1 is minimal arterial narrowing.
• Scheie's classification grades arteriolar sclerosis separately: grade 1 is a broadened arteriolar reflex, grade 2 an increased light reflex with AV crossing changes, grade 3 "copper wire" arterioles, and grade 4 "silver wire" arterioles (Textbook of Family Medicine 9e, "Hypertensive Retinopathy Grading").
• Grade 3 and 4 changes indicate accelerated or malignant hypertension. They also raise the possibility of secondary causes such as renovascular disease (Campbell-Walsh Urology, "Diagnosis").
• A simpler modern grouping is mild (grades 1 and 2), moderate (grade 3) and malignant (grade 4).

3. Hypertensive crisis

4. Total CV risk stratification

Clinical features of grade 1 hypertension

1. Symptoms: usually none

• Most people with grade 1 hypertension have no symptoms, and it is found at a routine check-up or screening. This is why it is called the "silent killer".
• Compensated hypertensive heart disease is "typically asymptomatic and is suspected only from discovery of elevated blood pressure on routine physical examination, or from ECG or echocardiographic findings of left ventricular hypertrophy" (Robbins & Kumar Basic Pathology, "Morphology").
• Fuster and Hurst's The Heart notes that even severely raised BP (>180/120 mmHg) is often asymptomatic.
• Adams and Victor's Principles of Neurology notes that headache, dizziness and epistaxis do not occur with any consistency before hypertensive complications.
• Headache, dizziness, palpitations, tinnitus and nosebleeds are often blamed on hypertension. At this grade they are mostly coincidental and not caused by the BP. The AHA also says symptoms are not a reliable guide.

2. History to look for

• Risk factors: family history, salt intake, alcohol, smoking, inactivity, weight gain, stress.
• Contributing drugs: NSAIDs, oral contraceptives, decongestants, steroids, licorice, stimulants.
• Secondary-cause clues: snoring or daytime sleepiness (sleep apnea), episodic sweating, palpitations and headache (pheochromocytoma), muscle weakness or cramps (hypokalemia, aldosteronism), renal disease history.
• Complication clues: chest pain, breathlessness, claudication, transient neurological or visual symptoms.
• Comorbidities: diabetes, dyslipidemia, CKD, gout.

3. Signs on examination

• BP:
  • Properly measured, repeated, and taken in both arms. Check postural change in older patients.
  • Home or ambulatory readings rule out white-coat and masked hypertension.
• General: BMI, waist circumference, and features of Cushing syndrome.
• Cardiac:
  • Normal or a slightly forceful apex beat.
  • A fourth heart sound (S4) from a stiff left ventricle.
  • Loud A2.
• Pulses and bruits: check for radio-femoral delay (coarctation), and listen for renal artery or carotid bruits.
• Abdomen: palpable kidneys (polycystic disease), abdominal aortic aneurysm.
• Fundoscopy: normal or Keith-Wagener-Barker grade 1 to 2 changes (mild arteriolar narrowing, AV nipping). Grade 3 or 4 changes (hemorrhages, exudates, papilledema) are not expected and suggest accelerated hypertension or a secondary cause.
• Edema: none unless there is heart or kidney disease.

4. Investigation findings

• Normal in many patients.
• Possible findings:
  • ECG: early LVH or left atrial enlargement.
  • Urine: mild albuminuria.
  • Blood: raised creatinine, glucose or lipids.
• Hypokalemia with high-normal sodium should prompt aldosterone/renin testing.

5. Key points for exams

1. Grade 1 hypertension is mostly asymptomatic and found incidentally.
2. Physical signs are usually absent or subtle.
3. Check for target organ damage, risk factors and secondary causes.
4. Treatment depends on total CV risk, not on grade alone.
5. In ESC/ESH, drug therapy is considered for grade 1 only in patients with high CV risk, established CVD, or persistent elevation after lifestyle measures. In the 2025 ACC/AHA guideline, stage 1 is treated with drugs in patients with diabetes, CKD or 10-year risk ≥7.5%, or when BP stays ≥130/80 mmHg after 3 to 6 months of lifestyle change.

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