Pulmonary Hypertension (PH)

Causes (WHO classification)

1.    Pulmonary arterial hypertension (PAH)

o    Idiopathic, connective tissue diseases (e.g., systemic sclerosis), HIV, portal hypertension

2.    Left heart disease

o    LV dysfunction, mitral/aortic valve disease

3.    Lung diseases and hypoxia

o    COPD, ILD, OSA

4.    Chronic thromboembolic pulmonary hypertension (CTEPH)

5.    Miscellaneous (e.g., sarcoidosis)

Clinical features

•    Dyspnoea, fatigue, syncope

•    Loud P2, right ventricular heave

•    Tricuspid regurgitation murmur, raised JVP

Investigations

•    Echo: RV dilatation, elevated pulmonary pressures

•    Right heart catheterisation: gold standard for diagnosis

Treatment

•    Underlying cause

•    PAH-specific: endothelin receptor antagonists (bosentan), PDE-5 inhibitors (sildenafil), prostacyclin analogues

Pulmonary Embolism (PE)

Clinical presentation

•    Sudden-onset dyspnoea, pleuritic chest pain, haemoptysis

•    Tachycardia, hypoxia, possible hypotension if massive

Diagnosis

•    Wells score (clinical probability)

•    D-dimer (if low-intermediate probability)

•    CT pulmonary angiogram (CTPA): gold standard

Treatment

•    LMWH (first-line)

•    DOACs (e.g., apixaban, rivaroxaban) or warfarin after initial anticoagulation

•    Thrombolysis if massive PE with haemodynamic instability

Deep Vein Thrombosis (DVT)

Risk factors

•    Virchow's triad: stasis (immobility), hypercoagulability (malignancy, OCP, thrombophilia), endothelial injury (surgery)

Clinical features

•    Unilateral leg swelling, pain, warmth

Diagnosis

•    Wells score

•    Proximal leg vein ultrasound (first-line)

Treatment

•    Anticoagulation (as for PE)

•    Compression stockings after resolution to prevent post-thrombotic syndrome

Systemic Hypertension

Classification

•    Essential (90–95%)

•    Secondary

o    Renal artery stenosis (young, flash pulmonary oedema)

o    Primary hyperaldosteronism (Conn’s): hypertension + hypokalaemia

o    Phaeochromocytoma: paroxysmal HTN, headache, palpitations, sweating

o    Cushing’s syndrome, thyroid disorders

Targets

•    <140/90 mmHg (clinic)

•    <130/80 mmHg if CKD, diabetes, or target organ damage

First-line treatment

•    <55 years or diabetic: ACE inhibitor

•    55 or Afro-Caribbean: CCB

Aortic Dissection

Presentation

•    Sudden, severe tearing chest/back pain

•    Pulse deficits, asymmetrical BP

•    New aortic regurgitation murmur

Classification

•    Stanford A: ascending ± descending → surgical emergency

•    Stanford B: descending only → medical therapy unless complications

Diagnosis

•    CT angiogram (gold standard)

•    CXR: widened mediastinum

Treatment

•    Control BP (IV labetalol), pain control

•    Surgery for type A

Peripheral Arterial Disease (PAD)

Features

•    Intermittent claudication (pain on exertion, relieved by rest)

•    Critical limb ischaemia: rest pain, ulcers, gangrene

•    Reduced/absent pulses

Diagnosis

•    Ankle–brachial index (ABI):

o    <0.9 diagnostic of PAD

o    <0.5 indicates severe ischaemia

Management

•    Smoking cessation

•    Antiplatelet therapy, statin

•    Supervised exercise program

•    Revascularisation (angioplasty/bypass) if severe

Carotid Artery Disease

Risk

•    TIA or stroke from emboli

Intervention

•    Carotid endarterectomy:

o    Symptomatic stenosis ≥70% (NASCET criteria)

o    Consider 50–69% if high risk

Extra Revision Pearls

•    Loud P2 clue → PH (esp. in young with CTD)

•    RV heave clue → chronic cor pulmonale, PH

•    Stanford A clue → surgery always; can cause tamponade, AR

•    ABI <0.5 clue → limb-threatening ischaemia

•    Conn’s clue → HTN + low K⁺; high aldosterone, low renin

•    Phaeochromocytoma clue → episodic triad + 24h urinary metanephrines

•    Hypertensive urgency vs emergency → end-organ damage defines emergency