I-1. Definition & forms of hypertension; secondary hypertension; complications

1. Definition & Diagnosis

• Systemic arterial hypertension = constantly elevated blood pressure in the systemic arteries.
• Result of increased cardiac output and/or increased peripheral resistance.
• Often asymptomatic — the “silent killer”; possible symptoms: headache, dizziness, tinnitus, chest pain, palpitations, nosebleeds, effort dyspnea.
• Most frequent and controllable risk factor for cardiovascular morbidity/mortality; also a leading cause of chronic kidney failure, cognitive disorders, and disability.
• Optimal BP = 115/75 mmHg; cut-off values (when we diagnose and treat) differ by country.

🩺 Diagnosis: Hypertension is confirmed when the average office BP — measured with the patient at rest, on ≥3 occasions (≥1 week apart) and ≥3 times per occasion — reaches or exceeds 140/90 mmHg.

BP categories (office measurement)

Category	Systolic (mmHg)	Diastolic (mmHg)
Optimal	< 120 and	< 80
Normal	120–129 and/or	80–84
High normal	130–139 and/or	85–89
Grade 1 HTN	140–159 and/or	90–99
Grade 2 HTN	160–179 and/or	100–109
Grade 3 HTN	≥ 180 and/or	≥ 110
Isolated diastolic (IDH)	< 140 and	≥ 90
Isolated systolic (ISH)	≥ 140 and	< 90

2. Measurement Methods

• Direct (invasive): intra-arterial catheter, used only in intensive care.
• Indirect (non-invasive): oscillometric automatic monitors, Korotkoff sound auscultation; mercury sphygmomanometers now used only for calibration.
• Auscultation: cuff compresses the brachial artery; 1st Korotkoff sound (sharp knock) = systolic pressure; sound becoming muffled/disappearing (2nd Korotkoff sound, total loss of sound) = diastolic pressure. Sounds are caused by turbulent flow.
• Home measurements give lower values, so cut-offs differ (home ≥135/85).

ABPM (Ambulatory BP Monitoring)

Automatic BP measurement several times a day, usually over 24 h. Helps detect:

• White coat hypertension — high in office, normal at home.
• Masked hypertension — normal in office, abnormally high at certain times of day.
• Disturbed diurnal rhythm — BP normally drops at night; failure to dip suggests severe, progressive disease.

3. Forms / Etiology

• Primary / essential (unknown, multifactorial): 90–95% of cases.
• Secondary (~5%): caused by an underlying condition.
• Monogenic / inherited (rare): single-gene mutation — suspect when HTN appears in children/adolescents.

Monogenic forms

• Affecting kidney function:
  • Liddle’s syndrome — ENaC hyperfunction/overexpression in collecting ducts.
  • Gordon’s syndrome — increased Na⁺ reabsorption (WNK1/WNK4 malfunction → ↑Na-Cl co-transporter).
• Affecting steroid metabolism (adrenal cortex) — excess mineralocorticoid effect:
  • CYP11B2 hyperfunction → ↑aldosterone → Na⁺ retention (AD).
  • Mineralocorticoid receptor hyperfunction (AD).
  • CYP11B1 + CYP17A1 deficiency (congenital adrenal hyperplasia types 4 & 5).

4. Secondary Hypertension (known causes)

• Renal:
  • Renovascular — ↓renal blood flow → RAAS activation → fluid retention (renal artery stenosis: atherosclerosis, fibromuscular dysplasia, etc.).
  • Renal parenchymal — glomerulonephritis, pyelonephritis, obstructive renopathy → ↓GFR / ↑renin → Na⁺ + H₂O retention.
• Mechanical: coarctation of the aorta → high BP in arms/head, low BP in legs.
• Endocrine:
  • Conn’s syndrome (hyperaldosteronism) → salt/water retention.
  • Cushing’s syndrome — high cortisol acting on mineralocorticoid receptors.
  • Hyperthyroidism → isolated ↑systolic; Hypothyroidism → isolated ↑diastolic.
  • Acromegaly (↑GH → salt reabsorption, ↑CO), Phaeochromocytoma (↑catecholamines), Hyperparathyroidism (↑PTH).
• Sleep apnea — hypoxia activates the sympathetic nervous system.
• Iatrogenic/drugs: corticosteroids, oral contraceptives, sympathomimetics, NSAIDs, cocaine, amphetamine.

5. Complications

Heart

• Pressure overload → myocardial hypertrophy & remodeling → ↓compliance (diastolic dysfunction) + systolic dysfunction → heart failure.
• Accelerated coronary atherosclerosis + ↑O₂ demand → ischemic heart disease.

Blood vessels

• Accelerated, vulnerable atherosclerosis → IHD, stroke, aortic aneurysm.
• Vascular remodeling → arterial stiffness, wall thickening, lumen narrowing.
• Arteriosclerosis of small arteries → target-organ damage.

Eyes — Retinopathy

• Early: arterial narrowing/constriction.
• Advanced: permanent narrowing, retinal hemorrhages, cotton-wool spots, drusen, papilledema. Useful marker of long-term severity.

Kidney — Hypertensive nephrosclerosis

• Renal arteriosclerosis with hyaline deposits/wall thickening → interstitial & tubular damage, ischemic nodules; glomerular damage → microalbuminuria, ↓GFR. A frequent cause of renal failure, and it maintains hypertension.

Brain — Vascular dementia & stroke

• Cerebral artery remodeling, stiffness, atherosclerosis, arteriosclerosis of white-matter/basal-ganglia vessels, impaired neurovascular coupling, endothelial dysfunction, right-shifted autoregulation.
• Consequences: ischemic & hemorrhagic stroke, lacunar infarcts (<20 mm), microinfarcts (<1 mm), diffuse white-matter damage → vascular dementia.

Hypertensive crisis

• Sudden BP rise, usually in chronic hypertensives.
• Papilledema — headache, vomiting, visual disturbances, confusion, lethargy, speech disorder, spasms, coma; may involve myocardial ischemia, renal failure, stroke.
• Hypertensive encephalopathy — perfusion pressure exceeds autoregulation → passive arterial dilation, endothelial damage (ROS, ↑BBB permeability, pro-coagulant state) → cerebral edema (mainly parieto-occipital).