Hypertension notes for exam
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Hypertension - Exam Notes
1. Definition & Classification
Blood pressure (BP) risk is continuous - there is no true threshold below which CVD risk disappears. Classification systems exist to guide clinical decision-making.
ACC/AHA 2017 Classification (Adults ≥18 years)
| Category | SBP (mmHg) | DBP (mmHg) | |
|---|---|---|---|
| Normal | <120 | AND | <80 |
| Elevated | 120-129 | AND | <80 |
| Stage 1 Hypertension | 130-139 | OR | 80-89 |
| Stage 2 Hypertension | ≥140 | OR | ≥90 |
- JNC 7 (older, still widely used): Stage 1 = 140-159/90-99; Stage 2 = ≥160/≥100; Prehypertension = 120-139/80-89.
- Any patient on antihypertensive medication is classified as having hypertension, regardless of measured BP.
- Children (<13 yrs): percentile-based classification.
(Fuster and Hurst's The Heart, 15th Edition)
2. Epidemiology
- Affects ~45% of US adults (2017 ACC/AHA definition) or ~32% (≥140/90 cut-off).
- Affects one-third of the global adult population; leading modifiable CVD risk factor.
- Control rates are poor: only ~48% of US adults are controlled to <140/90 mmHg; worldwide control to <140/90 is <14%.
- Non-Hispanic Black Americans have higher prevalence, earlier onset, and worse outcomes; diuretics and CCBs are particularly effective in this group.
- After age 50, SBP (not DBP) is the dominant predictor of CVD risk.
(Harrison's Principles of Internal Medicine 22E; Fuster and Hurst's The Heart)
3. Pathophysiology
Primary (Essential) Hypertension (~90-95% of cases)
No single identifiable cause. Multi-factorial:
Modifiable environmental risk factors:
- Excessive dietary sodium; insufficient dietary potassium
- Overweight/obesity (visceral adiposity, inflammation)
- Physical inactivity
- Alcohol consumption
- Poor diet quality
Mechanisms:
- Overactivation of the Renin-Angiotensin-Aldosterone System (RAAS): angiotensinogen → (renin) → Angiotensin I → (ACE) → Angiotensin II → vasoconstriction + aldosterone release → sodium retention → ↑BP
- Sympathetic nervous system overactivity: increases heart rate, cardiac output, and peripheral resistance
- Impaired renal sodium excretion
- Endothelial dysfunction
- Genetic susceptibility (multiple genes, small effect sizes)
Nondipping BP: Normal BP should fall 10-20% at night (dipping). Nondippers and reverse-dippers have significantly higher stroke, cardiovascular mortality, and all-cause mortality risk. Associated with autonomic imbalance, OSA, salt sensitivity, and renal dysfunction.
(Harrison's Principles of Internal Medicine 22E; Fuster and Hurst's The Heart)
4. Secondary Hypertension (~5-10% of cases)
Suspect when: treatment-resistant HTN; abrupt worsening; disproportionate target-organ damage; lab clues (unexplained hypokalemia, proteinuria, LVH).
| Category | Cause |
|---|---|
| Endocrine | Primary hyperaldosteronism (most common endocrine cause), Pheochromocytoma, Cushing syndrome, Thyroid disease, Hyperparathyroidism |
| Renal | Chronic kidney disease (CKD), Acute kidney injury |
| Vascular | Renovascular disease (renal artery stenosis), Coarctation of the aorta |
| Pulmonary | Obstructive sleep apnea (most common secondary cause overall; >50% of OSA pts have HTN) |
| Gastrointestinal | Obesity |
| Genitourinary | Ureteral/bladder outlet obstruction |
| Drug-induced | NSAIDs, COX-2 inhibitors, corticosteroids, oral contraceptives, cocaine, sympathomimetics (decongestants), cyclosporine/tacrolimus, erythropoietin, amphetamines, alcohol |
Key clue for OSA: sympathetic activation from intermittent hypoxia; direct correlation between OSA severity and BP level/treatment resistance.
(Symptom to Diagnosis - Evidence Based Guide, 4th Ed.; Harrison's Principles of Internal Medicine 22E)
5. Target Organ Damage
- Cardiac: LVH, coronary artery disease, heart failure
- Cerebrovascular: Stroke (ischemic and hemorrhagic), TIA
- Renal: CKD, proteinuria, microalbuminuria
- Vascular: Peripheral artery disease, aortic aneurysm
- Ocular: Hypertensive retinopathy (AV nicking, flame hemorrhages, papilledema in emergency)
6. Evaluation & Workup
Proper BP Measurement
- 5 minutes of rest, seated, arm at heart level, validated cuff
- Two readings per visit, average
- Confirm in both arms (>15 mmHg difference suggests subclavian stenosis)
Measurement Types
| Type | Goal |
|---|---|
| Office BP | Standard screening |
| Home BP monitoring (HBPM) | Goal <135/85 mmHg (average) |
| Ambulatory BP monitoring (ABPM) | 24-hour goal <130/80 mmHg; rules out white coat HTN |
Initial Workup
- Urinalysis, urine albumin/creatinine
- BMP (electrolytes, creatinine, glucose)
- Fasting lipids
- ECG (LVH?)
- Thyroid function if indicated
- Additional if secondary cause suspected: aldosterone/renin ratio, plasma metanephrines, renal Doppler ultrasound, sleep study
7. Lifestyle Modifications (Non-Pharmacological)
Expected SBP reductions:
- DASH diet: -8 to -14 mmHg
- Sodium restriction (<2.3g/day, ideally <1.5g): -2 to -8 mmHg
- Weight loss (per 10 kg): -5 to -20 mmHg
- Aerobic exercise (≥150 min/week): -4 to -9 mmHg
- Limit alcohol (men ≤2 drinks/day; women ≤1): -2 to -4 mmHg
- Increase dietary potassium
(Harrison's Principles of Internal Medicine 22E)
8. Pharmacological Treatment
When to Start Medications
- ACC/AHA 2017: Start at Stage 1 (≥130/80) if 10-year ASCVD risk ≥10%, or known CVD/diabetes/CKD; ALL patients at Stage 2 (≥140/90).
- JNC 8: Threshold ≥140/90 for most; ≥150/90 for patients >60 years (controversial).
- If BP >20/10 mmHg above target: start TWO agents simultaneously.
BP Targets
| Population | Target |
|---|---|
| General adults (ACC/AHA 2017) | <130/80 mmHg |
| JNC 8 <60 years | <140/90 mmHg |
| JNC 8 >60 years | <150/90 mmHg |
| Diabetes/CKD | <130/80 mmHg |
| Home BP | <135/85 mmHg |
Drug Classes & Compelling Indications
| Drug Class | Mechanism | Key Side Effects | Compelling Indications |
|---|---|---|---|
| Thiazide diuretics (HCTZ, chlorthalidone) | Inhibit Na/Cl cotransporter in distal convoluted tubule | Hypokalemia, hyponatremia, hyperuricemia, hyperglycemia, dyslipidemia | Heart failure, high CAD risk, diabetes, stroke, elderly |
| ACE inhibitors (lisinopril, ramipril) | Block ACE, prevent Ang I → Ang II | Dry cough (10-15%), hyperkalemia, angioedema, elevated creatinine, teratogenic | Heart failure, post-MI, diabetes (nephroprotection), CKD, stroke |
| ARBs (losartan, valsartan) | Block AT1 receptor for Ang II | Similar to ACEi but no cough; avoid in pregnancy | Same as ACE inhibitors; use when ACEi cough intolerable |
| Calcium Channel Blockers (CCBs) - Dihydropyridines (amlodipine) | Block L-type voltage-gated Ca²⁺ channel → vasodilation | Peripheral edema, flushing, reflex tachycardia | High CAD risk, diabetes, elderly, Black patients, isolated systolic HTN |
| CCBs - Non-dihydropyridines (diltiazem, verapamil) | Ca²⁺ block + negative chronotropy/inotropy | Bradycardia, heart block, constipation (verapamil) | Angina, atrial fibrillation rate control; avoid with heart failure with reduced EF |
| Beta-blockers (metoprolol, carvedilol) | Block β1 (and β2) adrenergic receptors | Bradycardia, fatigue, bronchospasm, masking hypoglycemia, sexual dysfunction | Post-MI, heart failure with reduced EF, angina, tachyarrhythmias |
| Aldosterone antagonists (spironolactone) | Block mineralocorticoid receptor → Na excretion | Hyperkalemia, gynecomastia | Resistant HTN, heart failure, primary hyperaldosteronism |
| Direct renin inhibitor (aliskiren) | Block renin → ↓ Ang I production | Similar to ARB, diarrhea at high doses | Avoid combining with ACEi or ARB |
Never combine ACEi + ARB + renin inhibitor (dual RAAS blockade increases AKI and hyperkalemia risk without added benefit).
Preferred combination (ACCOMPLISH trial): ACEi + CCB (amlodipine) is superior to ACEi + thiazide for CV outcomes.
(National Kidney Foundation Primer on Kidney Diseases 8e; Textbook of Family Medicine 9e; Harrison's Principles of Internal Medicine 22E)
9. Special Populations
| Population | Preferred Agents |
|---|---|
| Diabetes | ACEi or ARB (renoprotection) |
| CKD with proteinuria | ACEi or ARB first-line |
| Heart failure (reduced EF) | ACEi/ARB + beta-blocker + aldosterone antagonist |
| Post-MI | Beta-blocker + ACEi/ARB |
| Stroke prevention | Thiazide + ACEi (PROGRESS trial) |
| Pregnancy | Methyldopa, labetalol, nifedipine; ACEi/ARBs are CONTRAINDICATED |
| Black patients | Thiazides and CCBs more effective monotherapy; higher doses often needed |
| Elderly | Start low, go slow; prefer thiazide or CCB; risk of orthostatic hypotension and falls |
| Isolated systolic HTN | Thiazide or CCB |
10. Resistant Hypertension
- Definition: BP remains >140/90 despite 3 antihypertensive drugs at maximal doses, including a diuretic.
- Affects ~10% of hypertensive patients.
- Common causes: Non-adherence, white coat effect, secondary HTN (especially OSA, primary aldosteronism, renal artery stenosis), drug interference (NSAIDs, stimulants, OCPs), pseudoresistance (improper technique).
- Management: Rule out secondary causes, optimize existing regimen, add spironolactone 25-50 mg/day (strong evidence).
11. Hypertensive Crisis
| Hypertensive Urgency | Hypertensive Emergency | |
|---|---|---|
| BP | Often >180/120 mmHg | Often >180/120 mmHg |
| Target organ damage | ABSENT | PRESENT |
| Clinical features | Headache, anxiety | Encephalopathy, papilledema, retinal hemorrhages, acute MI, stroke, AKI, pulmonary edema, aortic dissection |
| Setting | Outpatient / ED | ICU admission |
| Treatment | Oral agents (captopril, clonidine, labetalol); gradual reduction over 24-48h | IV vasodilators; reduce MAP by ≤25% in first hour, then gradually to 160/100 over 2-6h |
IV drugs for hypertensive emergency: nitroprusside, labetalol, nicardipine, hydralazine, fenoldopam, esmolol.
Exception - aortic dissection: target SBP <120 mmHg rapidly with labetalol or esmolol + vasodilator.
Warning: Do NOT lower BP too rapidly (risk of organ hypoperfusion, watershed infarcts, blindness).
(Brenner and Rector's The Kidney, 2-Volume Set; Harrison's Principles of Internal Medicine 22E)
12. Quick Exam High-Yield Points
- Hypertension affects 45% of US adults (ACC/AHA 2017 definition).
- Most common secondary cause: OSA.
- Most common endocrine cause: Primary hyperaldosteronism (suspect: hypokalemia + resistant HTN).
- ACEi side effect: Dry cough (bradykinin-mediated); switch to ARB.
- ACEi/ARBs are teratogenic - avoid in pregnancy.
- Chlorthalidone > HCTZ in antihypertensive potency and CV outcomes (longer half-life: 48-72h vs 16-24h).
- ACCOMPLISH trial: ACEi + amlodipine superior to ACEi + HCTZ for CV outcomes.
- ALLHAT trial: Thiazides equally effective as CCBs and ACEi for coronary events.
- SBP matters more than DBP after age 50.
- Nondipping BP (failure to drop ≥10% at night) = independent CV and stroke risk factor.
- Dual RAAS blockade (ACEi + ARB) is contraindicated.
- After BP is controlled, 75% of patients require ≥2 drugs.
- Resistant HTN first add-on: spironolactone.
Sources: Fuster and Hurst's The Heart 15e | Harrison's Principles of Internal Medicine 22E | National Kidney Foundation Primer on Kidney Diseases 8e | Textbook of Family Medicine 9e | Brenner and Rector's The Kidney 2-Volume Set | Symptom to Diagnosis - Evidence Based Guide 4e
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