Hypertension and Cardiovascular Disease

Hypertension and cardiovascular disease (CVD) are the leading causes of death and disability in the UAE, making this a high-priority area for the DOH (UAE) examination. An estimated 30–40% of adults in the UAE have hypertension, and this is a major driver of the high rates of stroke, coronary artery disease, heart failure, and chronic kidney disease seen in Emirati patients. Nurses must understand the pathophysiology, classification, and management of hypertension, as well as recognise and respond to cardiovascular emergencies.

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🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Hypertension Classification (WHO/ISH):

Category	Systolic (mmHg)	Diastolic (mmHg)
Optimal	< 120	< 80
Normal	120–129	80–84
High Normal	130–139	85–89
Grade 1 Hypertension	140–159	90–99
Grade 2 Hypertension	160–179	100–109
Grade 3 Hypertension	≥ 180	≥ 110
Isolated Systolic	≥ 140	< 90

Hypertensive Crisis — Know the Difference:

Feature	Hypertensive Urgency	Hypertensive Emergency
BP	Severely elevated	Severely elevated
End-organ damage	No	Yes (encephalopathy, MI, stroke, renal failure, eclampsia)
Treatment	Gradual reduction over 24–48h	Immediate reduction in ICU with IV antihypertensives
Hospital admission	Optional	Mandatory

Target Organs Damaged by Hypertension:

• Heart: LVH → heart failure, CAD → angina/MI, atrial fibrillation
• Brain: Stroke (ischaemic and haemorrhagic), TIA, cognitive decline
• Kidneys: Hypertensive nephrosclerosis → CKD
• Eyes: Hypertensive retinopathy (grades I–IV), visual loss

⚡ Exam Tip: In a hypertensive emergency with aortic dissection (tearing chest pain radiating to back), the target BP is the lowest tolerated MAP — reduce by 20–25% immediately but not below 110 mmHg MAP initially.

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🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

1. Antihypertensive Drug Classes

A. ACE Inhibitors (ACEi) — “-pril” drugs:

• Enalapril, lisinopril, ramipril
• Mechanism: Block conversion of angiotensin I → angiotensin II → vasodilation, ↓ aldosterone
• Benefits: Reduce LVH, protect kidneys (reduce proteinuria), improve survival in heart failure
• Side effects: Dry cough (10–15% — due to bradykinin accumulation); angioedema (rare but life-threatening — must stop drug permanently); hyperkalaemia
• CI: Pregnancy, bilateral renal artery stenosis, history of angioedema
• Monitor: Serum creatinine and K⁺ after initiation (↑Cr up to 30% acceptable; more requires stopping)

B. Angiotensin Receptor Blockers (ARBs) — “-sartan” drugs:

• Valsartan, losartan, irbesartan
• Mechanism: Block AT1 receptor (angiotensin II receptor)
• Advantages: No cough (don’t affect bradykinin); can use in patients who developed cough on ACEi
• Similar benefits and precautions to ACEi

C. Calcium Channel Blockers (CCBs):

• Dihydropyridines (amlodipine, nifedipine): Primarily vasodilation; used for hypertension
• Non-dihydropyridines (verapamil, diltiazem): Also ↓ heart rate and contractility
• Side effects: Ankle oedema (dihydropyridines), constipation (verapamil), bradycardia (non-dihydropyridines)
• Can be used in pregnancy ( safer than ACEi/ARBs)

D. Thiazide Diuretics:

• Hydrochlorothiazide, indapamide, chlorthalidone
• Mechanism: ↓ Na⁺ and water at distal convoluted tubule → ↓ blood volume → ↓ BP
• Side effects: Hypokalaemia, hyperuricaemia (precipitates gout), hyperglycaemia, hyponatraemia
• Best combined with ACEi/ARB or potassium-sparing diuretic

E. Beta-blockers:

• Metoprolol, atenolol, bisoprolol, carvedilol
• Mechanism: ↓ Heart rate, ↓ contractility, ↓ renin release
• Benefits: Particularly useful in patients with CAD (secondary prevention post-MI), heart failure, atrial fibrillation
• Side effects: Bradycardia, bronchospasm (avoid in asthma), fatigue, depression, masking of hypoglycaemia symptoms (use with caution in diabetics)
• Do not abruptly discontinue (rebound hypertension)

2. Coronary Artery Disease and Acute Coronary Syndrome

Stable Angina vs ACS:

Feature	Stable Angina	ACS (Unstable Angina + NSTEMI + STEMI)
Trigger	Predictable (exertion, emotion)	Unpredictable; at rest
Duration	< 10 minutes	> 10 minutes; new onset; crescendo
Relief	Rest or nitrates	May NOT relieve with rest/nitrates
Pathology	Fixed atherosclerotic stenosis	Plaque rupture → thrombosis

STEMI (ST-Elevation MI) — The Medical Emergency:

• ECG: ST elevation in contiguous leads; new LBBB
• Presentation: Crushing/pressure chest pain; radiation to left arm/jaw/neck; sweating; nausea; dyspnoea; fear of death
• DOH protocol: MONA is outdated; current best practice is:
  • O₂ if SpO₂ < 94%
  • Aspirin 300 mg (chewed)
  • P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel)
  • Anticoagulation (heparin)
  • Reperfusion: Primary PCI (preferred if available within 90 min) or thrombolysis (if PCI unavailable within 120 min)

NSTEMI vs Unstable Angina:

• Both have elevated troponin (NSTEMI) or normal troponin (UA)
• Both require antiplatelet therapy, anticoagulation, risk stratification
• Early angiography within 24–72 hours for intermediate-high risk NSTEMI/UA

3. Heart Failure

Types:

• Systolic (HFrEF): ↓ Contractility (EF < 40%); ventricles dilated; e.g., ischaemic cardiomyopathy, dilated cardiomyopathy
• Diastolic (HFpEF): Preserved EF; ventricles stiff (impaired relaxation); e.g., hypertensive heart disease, hypertrophic cardiomyopathy

Framingham Criteria for Heart Failure Diagnosis (2 major or 1 major + 2 minor):

• Major: Paroxysmal nocturnal dyspnoea, orthopnoea, elevated JVP, pulmonary crackles, cardiomegaly on X-ray, acute pulmonary oedema, S3 gallop
• Minor: Bilateral ankle oedema, nocturnal cough, dyspnoea on ordinary exertion, hepatomegaly

NYHA Functional Classification:

• Class I: No limitation
• Class II: Slight limitation (comfortable at rest; symptoms with ordinary activity)
• Class III: Marked limitation (comfortable at rest; symptoms with less-than-ordinary activity)
• Class IV: Symptoms at rest

Acute Decompensated Heart Failure — Management:

• Position: Upright (reduce preload — orthopnoea, bilateral crackles)
• Oxygen: Target SpO₂ ≥ 94%
• Loop diuretics: IV furosemide (higher doses if on chronic diuretics)
• Vasodilators: IV nitrates if BP allows (reduce preload)
• Morphine (less used now — controversial)
• Non-invasive ventilation (CPAP/BiPAP) if respiratory failure

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🔴 Extended — Deep Study (3m+)

Comprehensive coverage for students on a longer study timeline.

4. Cardiac Arrhythmias

Atrial Fibrillation (AF) — Most Common Sustained Arrhythmia:

• Irregularly irregular pulse; absent P waves on ECG; fibrillatory baseline
• CHA₂DS₂-VASc score for stroke risk: Congestive heart failure (1), Hypertension (1), Age ≥75 (2), Diabetes (1), Stroke/TIA/TE (2), Vascular disease (1), Age 65–74 (1), Sex category female (1)
• Anticoagulation if score ≥ 2 (warfarin or DOAC)
• Rate control: Beta-blockers, CCBs, digoxin
• Rhythm control: Cardioversion (electrical or pharmacological), antiarrhythmics, catheter ablation

Ventricular Fibrillation (VF) and Pulseless VT — Cardiac Arrest Rhythms:

• VF: Chaotic, irregular waveforms — no effective cardiac output
• Pulseless VT: Wide, bizarre complexes at >100/min — no effective cardiac output
• Treatment: Immediate defibrillation (non-synchronous shock) + CPR
• These are shockable rhythms (unlike asystole and PEA)

Complete Heart Block (Third-Degree AV Block):

• P waves and QRS complexes completely independent (no relationship)
• Ventricular escape rhythm (usually 40–60 bpm) maintains consciousness initially
• Can progress to asystole suddenly — medical emergency
• Treatment: Temporary pacemaker + permanent pacemaker if persistent

5. Stroke — Recognition and Initial Management

FAST Criteria (Recognise Stroke):

• Face: Facial droop, asymmetry
• Arms: Arm drift, weakness
• Speech: Slurred, aphasic, mute
• Time: Call immediately — TIME IS BRAIN

Ischaemic Stroke (87% of strokes):

• Thrombus (large vessel atherosclerosis) or embolus (usually cardiac — AF, valvular disease, paradoxical embolus)
• Treatment window: Thrombolysis (IV alteplase) within 4.5 hours of onset; mechanical thrombectomy up to 24 hours in selected patients
• Door-to-needle time target: < 60 minutes

Haemorrhagic Stroke (13% of strokes):

• Hypertension is the leading cause; anticoagulation (warfarin, DOACs) can precipitate
• CT without contrast: Rule out haemorrhage FIRST (haemorrhage appears hyperdense/white immediately)
• Hypertension management is critical but cautious (CPP = MAP − ICP — over-aggressive BP reduction can reduce cerebral perfusion)

BP Management in Acute Stroke (UAE Protocol):

• Ischaemic stroke: Allow BP up to 220/120 unless thrombolysis planned (then < 185/110)
• Haemorrhagic stroke: Cautious reduction; avoid MAP < 80 or SBP < 140 in first 24 hours without clear indication

Exam Watch: In the UAE, stroke patients are managed in dedicated stroke units or stroke code activation pathways. A common DOH question involves a patient presenting with sudden onset right-sided weakness and slurred speech — the nurse’s priority action is to activate the stroke code and arrange for immediate CT head (to rule out haemorrhage before thrombolysis). Never wait to see if symptoms improve before acting.

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