Pulmonary hypertension

Overview

Elevated pulmonary arterial pressure - mean PAP (mPAP) ≥20 mmHg on right heart catheterisation
Not a single disease - a haemodynamic state with many causes; WHO group determines management

Presentation

Exertional dyspnoea - cardinal and earliest symptom; fixed elevated PVR prevents increased cardiac output on demand
Exertional syncope/pre-syncope - sinister; RV cannot increase output → drop in systemic cardiac output and cerebral hypoperfusion
Fatigue, chest pain (RV ischaemia), haemoptysis (uncommon)
Signs of RV failure (cor pulmonale): raised JVP, parasternal heave, loud P2, tricuspid regurgitation murmur, hepatomegaly, peripheral oedema
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Exertional syncope in a young woman with progressive breathlessness is a red flag for severe PAH - warrants urgent specialist referral.

Investigations

First-line screening: transthoracic echocardiogram (TTE) - estimates RVSP from TR jet velocity; peak TR velocity >3.4 m/s = high probability PH
ECG: right axis deviation, RBBB, P pulmonale, RV strain (T-wave inversion V1-V4)
CXR: enlarged hilar pulmonary arteries, peripheral pruning, RV enlargement
V/Q scan: essential to exclude Group 4 CTEPH - more sensitive than CTPA for chronic thromboembolic disease; normal V/Q effectively excludes CTEPH
Bloods: BNP/NT-proBNP (RV strain/prognosis), autoimmune screen (ANA, anti-Scl-70, anti-centromere for SSc), HIV, TFTs, FBC
PFTs + DLCO: exclude Group 3; DLCO typically reduced in PAH
Gold standard - right heart catheterisation (RHC): directly measures mPAP, PCWP, PVR, cardiac output; also allows vasoreactivity testing
Pre-capillary vs post-capillary PH on RHC
ParameterPre-capillary (Groups 1,3,4,5)Post-capillary (Group 2)
mPAP≥20 mmHg≥20 mmHg
PCWP≤15 mmHg>15 mmHg
PVR≥2 Wood unitsNormal/low
Targeted PAH therapyAppropriateHarmful - avoid

Management

General (all groups): treat underlying cause, supplemental oxygen if hypoxic, diuretics for RV failure, anticoagulation in CTEPH
Group 1 PAH - targeted vasodilator therapies (3 pathways):
Endothelin receptor antagonists (ERAs): ambrisentan, bosentan, macitentan
PDE-5 inhibitors: sildenafil, tadalafil
Prostacyclin pathway: epoprostenol (IV), iloprost (inhaled), selexipag (oral)
Combination therapy (e.g. ERA + PDE-5i) is standard of care in Group 1
Vasoreactivity testing (RHC): positive responders (minority) can be treated with nifedipine or other CCBs
Group 4 CTEPH: riociguat (soluble guanylate cyclase stimulator); surgical pulmonary endarterectomy if operable - potentially curative
Advanced/refractory disease: lung transplantation (or heart-lung transplant)

Complications

Right ventricular failure (cor pulmonale) - principal cause of death
Atrial arrhythmias - AF/flutter due to RA dilatation; poorly tolerated
Eisenmenger syndrome - longstanding unrepaired left-to-right shunt reverses with cyanosis; precludes surgical repair
Pregnancy - very high maternal mortality (up to 30-50%) in severe PAH; strongly contraindicated

Prognosis

Untreated idiopathic PAH: median survival ~2.8 years from diagnosis
Modern combination therapy: 5-year survival ~60-70% in Group 1
Group 4 CTEPH: best prognosis if surgically resectable endarterectomy successful
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Always exclude CTEPH with a V/Q scan before diagnosing idiopathic PAH - Group 4 is the only potentially curable form of pulmonary hypertension.

Classification (WHO Groups)

Group 1 - Pulmonary arterial hypertension (PAH): idiopathic, heritable (BMPR2 mutation), CTD-associated (esp. systemic sclerosis), congenital heart disease, drugs/toxins
Group 2 - Left heart disease: most common cause of PH overall (HFpEF, HFrEF, valve disease)
Group 3 - Lung disease/hypoxia: COPD, ILD, OSA
Group 4 - CTEPH: chronic thromboembolic pulmonary hypertension - only potentially curable form (surgical endarterectomy)
Group 5 - Unclear/multifactorial: sarcoidosis, haematological disorders
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Targeted vasodilator therapies are only appropriate in Group 1. Giving them to Group 2 (left heart disease) can cause pulmonary oedema and worsen outcomes.