Hypertension

Also known as: High blood pressure

Chronic elevation of systemic arterial blood pressure, a major modifiable risk factor for cardiovascular disease, stroke, and chronic kidney disease. Defined per major guidelines (thresholds vary slightly by society — ACC/AHA vs. ESC/NICE):

ACC/AHA: ≥130/80mmHg (Stage 1: 130-139/80-89; Stage 2: ≥140/90)
ESC/NICE/WHO: ≥140/90mmHg (clinic), ≥135/85mmHg (home/ambulatory average)

Classified by:

Primary (essential) hypertension: ~90-95% of cases, multifactorial (genetic, lifestyle, age-related vascular changes), no single identifiable cause
Secondary hypertension: identifiable underlying cause — renal (renal artery stenosis, CKD, polycystic kidney disease), endocrine (primary aldosteronism, pheochromocytoma, Cushing's syndrome, hyperthyroidism/hypothyroidism, hyperparathyroidism), obstructive sleep apnea, coarctation of aorta, drug-induced (NSAIDs, oral contraceptives, corticosteroids, decongestants, cocaine)
Hypertensive urgency: severely elevated BP (≥180/120) without acute end-organ damage
Hypertensive emergency: severely elevated BP WITH acute end-organ damage (encephalopathy, ACS, aortic dissection, acute pulmonary edema, acute kidney injury, eclampsia)

Usually asymptomatic ("silent killer") — detected on routine screening
Severe hypertension may cause: headache, visual disturbance, epistaxis (poorly correlated with BP level, often coincidental)
Hypertensive emergency symptoms depend on organ affected: chest pain (ACS, dissection — tearing pain radiating to back), dyspnea (pulmonary edema), focal neurological deficit/severe headache/altered consciousness (hypertensive encephalopathy, stroke), visual disturbance (papilledema, retinal hemorrhages)
Examination: fundoscopy (hypertensive retinopathy grading — arteriolar narrowing, AV nicking, hemorrhages/exudates, papilledema in malignant hypertension), signs of secondary causes (radiofemoral delay — coarctation; abdominal bruit — renal artery stenosis; central obesity/striae — Cushing's; paroxysmal symptoms with palpitations/sweating/headache — pheochromocytoma)
Target organ damage assessment: LVH (examination/ECG/echo), retinopathy, proteinuria/renal impairment, peripheral arterial disease

Confirm with out-of-office measurement before diagnosing (avoid white-coat effect): ambulatory BP monitoring (ABPM, gold standard) or home BP monitoring (HBPM) — average of readings over several days
Proper technique essential: seated, back supported, arm at heart level, appropriate cuff size, no caffeine/exercise/smoking 30 min prior, average of ≥2 readings

Investigations (baseline, all patients):

U&E/creatinine/eGFR (renal function, baseline before ACEi/ARB)
Urinalysis (proteinuria, hematuria — renal disease)
Fasting glucose/HbA1c, lipid profile (cardiovascular risk assessment)
ECG (LVH, ischemia, arrhythmia)
Consider echocardiogram if LVH suspected or heart failure symptoms

Screen for secondary causes if: age <30 with no risk factors/family history, resistant hypertension (uncontrolled on 3 drugs including diuretic), sudden onset/worsening, hypokalemia (aldosteronism), paroxysmal symptoms (pheochromocytoma) — aldosterone:renin ratio, plasma/urine metanephrines, renal artery imaging, overnight dexamethasone suppression test as indicated.

Cardiovascular risk assessment: calculate 10-year CVD risk (e.g., ASCVD risk calculator, QRISK) to guide treatment intensity and statin decision.

Lifestyle modification (all patients, foundation of treatment):

Sodium restriction (<2g/day, ~5g salt), DASH diet (fruits, vegetables, low-fat dairy, reduced saturated fat)
Weight loss if overweight/obese (each kg loss ~1mmHg SBP reduction)
Regular aerobic exercise (≥150 min/week moderate intensity)
Alcohol moderation, smoking cessation
Stress reduction

Pharmacological treatment — initiate based on BP level, CV risk, and target organ damage; per ACC/AHA/NICE algorithms:

First-line agents (choice influenced by age, ethnicity, comorbidities):
ACE inhibitors (lisinopril 10mg od, ramipril 2.5-10mg od) or ARBs (losartan 50mg od, candesartan 8-32mg od) — preferred in younger patients (<55, non-Black), diabetes, CKD with proteinuria, heart failure; avoid combining ACEi+ARB; monitor U&E/creatinine and K+ after initiation
Calcium channel blockers (amlodipine 5-10mg od) — preferred first-line in older patients (≥55) and Black patients of any age (per NICE); effective, well-tolerated
Thiazide/thiazide-like diuretics (indapamide 1.5-2.5mg od, chlorthalidone 12.5-25mg od) — alternative first-line, particularly useful add-on
Step 2: combination therapy (ACEi/ARB + CCB, or ACEi/ARB + thiazide) — combination therapy from the outset increasingly recommended for Stage 2/higher BP given superior efficacy and adherence with fixed-dose combinations
Step 3: triple therapy (ACEi/ARB + CCB + thiazide-like diuretic)
Step 4 (resistant hypertension): add spironolactone 25-50mg od (if K+ <4.5 and eGFR adequate — effective given frequent occult primary aldosteronism contribution) or alpha-blocker (doxazosin) or beta-blocker if not tried; consider secondary causes workup and specialist referral
Beta-blockers: not first-line for uncomplicated hypertension but indicated with compelling comorbid indications (post-MI, heart failure, atrial fibrillation rate control) — e.g., bisoprolol 2.5-10mg od

Hypertensive urgency: gradual BP reduction over 24-48 hours with oral agents, no need for IV therapy or hospital admission in absence of end-organ damage — rapid reduction risks cerebral/coronary hypoperfusion.

Hypertensive emergency: hospital/ICU admission, IV antihypertensives (labetalol infusion, nicardipine, sodium nitroprusside, GTN for pulmonary edema/ACS) — target: reduce MAP by no more than 25% in first hour (except aortic dissection — target SBP <120 within 20 min, and ischemic stroke where permissive hypertension often preferred acutely unless thrombolysis planned or extreme elevation).

Targets: generally <130/80mmHg for most adults (ACC/AHA) or <140/90 (ESC/NICE, more lenient in elderly/frail — individualize, avoid orthostatic symptoms/falls in frail elderly); tighter targets in diabetes with proteinuria/CKD per some guidelines.

Monitoring: BP reassessment 2-4 weeks after medication changes, then periodically once controlled (every 3-6 months); annual review of renal function, electrolytes on ACEi/ARB/diuretics, cardiovascular risk reassessment.

References

ACC/AHA hypertension guideline
NICE / ESC hypertension guideline

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Rheumatic Fever

Also known as: Acute rheumatic fever

Rheumatic fever is a delayed, autoimmune complication of group A Streptococcus (Streptococcus pyogenes) pharyngitis, occurring roughly two to four weeks after the initial throat infection.

It results from molecular mimicry, in which antibodies raised against streptococcal antigens cross react with host tissue in the heart, joints, skin, and central nervous system.

It remains a major cause of acquired heart disease in children and young adults in low and middle income settings, where access to prompt treatment of streptococcal pharyngitis is limited.

Recurrent episodes cause cumulative valvular damage, and it is this valvular scarring, known as rheumatic heart disease, that carries the long term morbidity and mortality burden.

Diagnosis is guided by the Jones criteria, which separate major and minor manifestations.

The major criteria are carditis (endocarditis, myocarditis, or pericarditis, often presenting as a new murmur, particularly mitral regurgitation), polyarthritis (classically migratory, affecting large joints), Sydenham chorea (involuntary, irregular movements, often delayed in onset by weeks to months after the preceding infection), erythema marginatum (a evanescent, pink, serpiginous rash with central clearing, typically on the trunk and proximal limbs), and subcutaneous nodules (firm, painless, over extensor surfaces and bony prominences).
The minor criteria include fever, arthralgia (which cannot be counted alongside polyarthritis as a major criterion in the same patient), elevated inflammatory markers (ESR or CRP), and a prolonged PR interval on ECG.

Diagnosis requires evidence of a preceding group A streptococcal infection, together with either two major criteria, or one major plus two minor criteria. A separate, lower threshold applies for recurrent episodes in a patient with known prior rheumatic fever.

Evidence of preceding streptococcal infection is sought through a positive throat culture or rapid antigen test (though these are frequently negative by the time rheumatic fever manifests, given the delay after the original infection), or, more usefully at this stage, elevated or rising anti-streptolysin O (ASOT) or anti-DNase B titres.

Inflammatory markers (ESR and CRP) support the diagnosis as minor criteria and help track disease activity.

ECG is essential, looking for a prolonged PR interval and any arrhythmia.

Echocardiography is required in all suspected cases, both to confirm carditis (which may be subclinical, detected only on echocardiography without an audible murmur) and to assess the severity of any valvular involvement, most commonly mitral regurgitation, less commonly aortic regurgitation.

Differentials include septic arthritis, reactive arthritis, juvenile idiopathic arthritis, systemic lupus erythematosus, viral myocarditis, and infective endocarditis, particularly when carditis is the presenting feature.

Eradication of the streptococcal infection is essential even if throat culture is now negative, using a single dose of intramuscular benzathine penicillin, or oral phenoxymethylpenicillin for ten days if intramuscular treatment is not feasible.

Anti-inflammatory treatment follows separately. Arthritis and fever generally respond well to high dose aspirin or another NSAID (naproxen is a commonly used alternative), continued until symptoms and inflammatory markers settle.

Moderate to severe carditis, particularly with heart failure, is treated with corticosteroids, though evidence for a mortality or long term valvular benefit is limited and steroids are used mainly for symptomatic and hemodynamic control in this context.

Heart failure arising from severe carditis is managed with standard heart failure therapy alongside the anti-inflammatory treatment above (see Heart Failure entry).

Sydenham chorea, when mild, may only require reassurance and supportive care; more significant chorea is treated with carbamazepine or sodium valproate, with antipsychotics reserved for severe, refractory cases.

Secondary prophylaxis is the cornerstone of long term management, given the markedly increased risk of recurrent rheumatic fever and progressive valvular damage with each subsequent episode.

Regular intramuscular benzathine penicillin, typically every three to four weeks, is continued for a minimum duration determined by the presence and severity of carditis: at least five years or until age twenty one for rheumatic fever without carditis, at least ten years or until age twenty five for rheumatic fever with carditis but no residual valvular disease, and lifelong for those with established valvular disease.

Referral: cardiology for all confirmed or suspected carditis, given the need for echocardiographic assessment and monitoring of valvular disease; neurology for significant chorea.

Hypertension

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management