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HYPERTENSION

General Medicine - BDS 3rd Year

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DEFINITION

• Systolic BP (SBP) ≥ 130 mmHg, and/or
• Diastolic BP (DBP) ≥ 80 mmHg

The WHO/JNC 7 definition (still widely used in clinical practice internationally) defines hypertension as BP ≥ 140/90 mmHg. Correct classification requires accurate BP measurement; when SBP and DBP fall in different categories, the higher category is chosen.

• Harrison's Principles of Internal Medicine, 22e, p. 2177
• Lippincott Illustrated Reviews: Pharmacology, p. 288

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CLASSIFICATION

ACC/AHA 2017 Classification (most current)

JNC 7 / WHO Classification (older, still widely used)

Etiological Classification

• No identifiable underlying cause
• Multifactorial: genetic predisposition + environmental factors
• Risk factors: high dietary sodium, obesity, physical inactivity, excessive alcohol, stress, positive family history, advancing age

• Renal: Chronic kidney disease, renovascular disease (renal artery stenosis), polycystic kidney disease
• Endocrine: Primary hyperaldosteronism, Cushing's syndrome, phaeochromocytoma, hyperthyroidism
• Vascular: Coarctation of the aorta
• Drugs: OCP, NSAIDs, corticosteroids, decongestants, cocaine

• Harrison's Principles of Internal Medicine, 22e, p. 2178-2180

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PATHOPHYSIOLOGY

1. Sympathetic nervous system overactivity - increases heart rate, contractility, and vasoconstriction via baroreceptor dysregulation.
2. Renin-Angiotensin-Aldosterone System (RAAS) overactivation - angiotensin II causes vasoconstriction and aldosterone-mediated sodium/water retention, increasing blood volume.

• Lippincott Illustrated Reviews: Pharmacology, p. 290-292

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CLINICAL FEATURES

Symptoms

• Headache - typically occipital, worse in the morning (most common symptom)
• Dizziness / vertigo
• Tinnitus (ringing in ears)
• Palpitations (awareness of heartbeat)
• Epistaxis (nosebleeds)
• Visual disturbances - blurring of vision (due to hypertensive retinopathy)
• Fatigue and breathlessness (if cardiac involvement)
• Chest pain (if associated angina or CAD)
• Facial flushing

Signs on Examination

• Elevated BP on repeated readings
• Cardiovascular: Forceful apex beat, left ventricular heave (LV hypertrophy), accentuated aortic component of S2 (A2), S4 gallop
• Eyes (Fundoscopy): Keith-Wagener-Barker grading of hypertensive retinopathy:
  • Grade I: Arteriolar narrowing, increased light reflex ("silver wiring")
  • Grade II: AV nipping/nicking (crossing changes)
  • Grade III: Flame-shaped haemorrhages and cotton-wool spots (soft exudates)
  • Grade IV: Papilledema (optic disc swelling) - indicates malignant hypertension
• Kidneys: Nocturia, proteinuria (early indicator of renal damage)
• Neurological: Hypertensive encephalopathy - headache, confusion, seizures

• Harrison's Principles of Internal Medicine, 22e

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COMPLICATIONS

1. Cardiac Complications

• Left Ventricular Hypertrophy (LVH) - compensatory response to increased afterload
• Coronary Artery Disease (CAD) - accelerated atherosclerosis
• Myocardial Infarction (MI)
• Heart Failure - initially diastolic dysfunction, later systolic failure
• Cardiac arrhythmias including AF

2. Cerebrovascular Complications

• Haemorrhagic stroke - rupture of Charcot-Bouchard microaneurysms in small perforating arteries
• Ischaemic stroke / TIA - thromboembolism from hypertensive vascular disease
• Hypertensive encephalopathy - acute severe HTN causing cerebral edema
• Vascular dementia - chronic ischaemic white matter damage

3. Renal Complications

• Hypertensive nephrosclerosis - glomerular ischaemia and nephron loss
• Proteinuria and haematuria (early signs)
• Chronic Kidney Disease (CKD)
• End-stage renal disease (ESRD)

4. Ophthalmic Complications

• Hypertensive retinopathy (grades I-IV as above)
• Central retinal artery/vein occlusion
• Visual loss

5. Vascular Complications

• Aortic aneurysm (especially abdominal aortic aneurysm)
• Aortic dissection
• Peripheral arterial disease (PAD)
• Accelerated atherosclerosis throughout the vasculature

6. Hypertensive Crisis

• Hypertensive Urgency: BP > 180/120 mmHg WITHOUT acute target organ damage
• Hypertensive Emergency: BP > 180/120 mmHg WITH acute target organ damage (stroke, MI, aortic dissection, renal failure, pulmonary oedema, hypertensive encephalopathy)

• Harrison's Principles of Internal Medicine, 22e; Park's Preventive & Social Medicine

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MANAGEMENT

Non-Pharmacological (Lifestyle Modifications)

Pharmacological Management

1. Thiazide Diuretics

• Examples: Hydrochlorothiazide, Chlorthalidone, Indapamide
• Mechanism: Initially reduce blood volume via natriuresis; long-term reduce peripheral vascular resistance
• Side effects: Hypokalaemia, hyperuricaemia, hyperglycaemia, hyponatraemia
• Use: First-line; useful in combination therapy

2. ACE Inhibitors (ACEI)

• Examples: Enalapril, Lisinopril, Captopril, Ramipril
• Mechanism: Block ACE → reduce angiotensin II → reduce vasoconstriction + reduce aldosterone → vasodilation + reduced sodium retention; also increase bradykinin (vasodilator)
• Compelling indications: Diabetes, CKD, heart failure, post-MI, LVH
• Side effects: Dry cough (bradykinin-mediated - most common), hyperkalaemia, angioedema, teratogenic (avoid in pregnancy)

3. Angiotensin Receptor Blockers (ARBs)

• Examples: Losartan, Valsartan, Telmisartan, Candesartan
• Mechanism: Block AT1 receptors → same haemodynamic effects as ACEI but no bradykinin accumulation
• Advantage over ACEI: No dry cough, lower risk of angioedema
• Use: Alternative to ACEI; same compelling indications; preferred if ACEI-intolerant

4. Calcium Channel Blockers (CCBs)

• Dihydropyridines: Amlodipine, Nifedipine, Felodipine
  • Primarily vascular smooth muscle → vasodilation → reduce peripheral resistance
  • Side effects: Peripheral oedema, flushing, reflex tachycardia
  • Nifedipine causes gingival hyperplasia (important dental consideration)
• Non-dihydropyridines: Verapamil, Diltiazem
  • Cardiac + vascular effects → reduce heart rate and contractility
  • Avoid in heart failure with reduced EF; cause bradycardia

5. Beta-Blockers (β-Blockers)

• Examples: Atenolol, Metoprolol, Bisoprolol (cardioselective); Propranolol (non-selective)
• Mechanism: Block β1 receptors → reduce heart rate and cardiac output; also reduce renin release
• Compelling indications: Post-MI, angina, heart failure, rate control in AF, thyrotoxicosis
• Side effects: Bradycardia, bronchospasm (avoid in asthma), fatigue, cold extremities, sexual dysfunction, mask hypoglycaemia in diabetics
• No longer first-line unless compelling indication exists

Step-up Approach to Pharmacotherapy

Step 1: Lifestyle modification alone (Stage 1 without high CVD risk)
           ↓ (if target not achieved in 3-6 months)
Step 2: Monotherapy - Thiazide OR ACEI/ARB OR CCB
           ↓ (if target not achieved)
Step 3: Combination of 2 drugs (e.g., ACEI + CCB or ACEI + Thiazide)
           ↓ (if target not achieved)
Step 4: Triple therapy (ACEI + CCB + Thiazide)
           ↓ (Resistant HTN)
Step 5: Add aldosterone antagonist (Spironolactone) or α-blocker or β-blocker

Management of Hypertensive Emergency

• Immediate IV therapy: IV Labetalol, IV Sodium Nitroprusside, IV Nitroglycerin, IV Nicardipine
• Goal: Reduce MAP by no more than 25% in first hour; then gradually to 160/100 over next 2-6 hours
• Avoid over-rapid reduction (risk of cerebral/cardiac ischaemia)

• Lippincott Illustrated Reviews: Pharmacology, 22e, p. 288-306
• Harrison's Principles of Internal Medicine, 22e, p. 2183-2192

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DENTAL CONSIDERATIONS

1. Pre-operative Assessment

• Measure BP at every dental appointment - the dental chair is an ideal screening point; many patients are undiagnosed.
• Defer elective treatment if BP is ≥ 180/110 mmHg (hypertensive urgency level); refer for medical management first.
• Elective surgery can generally proceed if BP is < 160/100 mmHg with close monitoring.
• Review the patient's medical history, current antihypertensive medications, and compliance.

2. Stress and Anxiety Management

• Dental anxiety raises BP significantly via sympathetic activation; this is especially dangerous in hypertensive patients.
• Use adequate pre-operative sedation / anxiolysis (e.g., oral benzodiazepines the night before and morning of procedure).
• Short appointments, morning scheduling (BP is lower), calm and reassuring environment.
• Minimize waiting time in the clinic.

3. Local Anaesthesia and Vasoconstrictors

• Epinephrine (adrenaline) in local anaesthetics is a sympathomimetic that can raise BP and heart rate.
• However, adequate pain control is more important - inadequately controlled pain from an insufficient block releases endogenous catecholamines (in greater amounts than epinephrine in the LA cartridge).
• Safe limits: Use 2 cartridges (3.6 mL) of 1:100,000 epinephrine (= 0.036 mg total) - this is generally safe in controlled hypertensives.
• Avoid high concentrations of epinephrine (1:50,000) in hypertensive patients.
• Avoid gingival retraction cords soaked in epinephrine.
• Non-epinephrine-containing vasoconstrictors (e.g., felypressin) are alternatives but also cause vasoconstriction and can increase BP.
• Patients on non-selective beta-blockers (propranolol): epinephrine can cause unopposed alpha-stimulation → sudden marked rise in BP → reflex bradycardia. Use minimal epinephrine and aspirate carefully.

4. Drug Interactions with Antihypertensives

5. Oral Manifestations of Antihypertensive Drugs

• Nifedipine (CCB) → Gingival Enlargement/Hyperplasia
  • Affects ~20% of patients on nifedipine
  • Mechanism: Inhibition of Ca²⁺-dependent collagen degradation → fibroblast proliferation → gingival overgrowth
  • Starts in the interdental papillae; may involve attached gingiva
  • Exacerbated by poor oral hygiene and plaque
  • Management: Drug substitution (switch to amlodipine, which has lower incidence); improved oral hygiene; surgical gingivectomy if severe
  • Also seen with: Cyclosporine, phenytoin
• ACE Inhibitors (Captopril, Enalapril) → Lichenoid Reactions and altered taste (dysgeusia)
  • Dry mouth (xerostomia) is a less common side effect
• Beta-blockers → Xerostomia (dry mouth)
  • Reduce salivary flow via anticholinergic-like effects
  • Dry mouth → increased caries risk, oral candidiasis, difficulty swallowing/speaking
• Thiazide diuretics → Xerostomia
  • Reduce salivary gland secretion; patients may present with increased caries
• Calcium channel blockers → Peripheral oedema that may include the face/lips

6. Postural (Orthostatic) Hypotension

• Patients on antihypertensives (especially alpha-blockers, thiazides, calcium channel blockers) may experience sudden dizziness/faintness when raised quickly from a supine or reclined position.
• Precaution: Raise the dental chair slowly; let the patient sit upright for 1-2 minutes before standing; support them while standing.

7. Haemostasis and Bleeding

• Hypertensive patients may have fragile, atheromatous vessels that bleed more readily.
• Some antihypertensive medications (e.g., aspirin used as antiplatelet therapy alongside antihypertensives) impair platelet function.
• Check INR if patient is on anticoagulants (warfarin) for associated conditions (AF, DVT).

8. Hypertensive Emergency in the Dental Chair

• Stop dental procedure immediately
• Place patient in semi-recumbent position
• Loosen tight clothing
• Monitor vital signs every 5 minutes
• Administer sublingual nifedipine 5-10 mg (bite the capsule and swallow) or sublingual captopril 25 mg for urgent BP reduction (Note: sublingual nifedipine is controversial in many guidelines - refer to emergency protocol)
• Call emergency services if symptoms of stroke/MI/encephalopathy develop
• Arrange urgent medical referral

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SUMMARY TABLE

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• Harrison's Principles of Internal Medicine, 22e (McGraw-Hill, 2025) - Chapter on Hypertension
• Lippincott Illustrated Reviews: Pharmacology - Chapter 8: Antihypertensive Drugs
• Park's Textbook of Preventive and Social Medicine - Cardiovascular Disease Section
• Comprehensive Clinical Nephrology, 7th Edition - Chapter on Hypertension Classification