Pulmonary hypertension in the ICU
"The critical early branch point is whether you are facing decompensated pre-existing pulmonary arterial hypertension, or pulmonary hypertension caused by the acute illness — because the treatments diverge sharply. Then the whole management of a failing right ventricle reduces to five levers: fix the trigger, optimise preload, cut afterload, protect coronary perfusion pressure, and support contractility."
Summarised from Irwin & Rippe's Intensive Care Medicine; with Marino's The ICU Book and Oh's Intensive Care Manual.PH = mean pulmonary artery pressure >20 mmHg. The RV is a thin-walled, afterload-intolerant pump — a sudden rise in afterload (PE, hypoxaemia, acidosis) or loss of contractility (RV infarct, sepsis) tips it into failure.
Five groups — because treatment differs
| Group | Mechanism | Examples |
|---|---|---|
| 1 — PAH | Pre-capillary arterial disease | Idiopathic, connective-tissue disease, congenital, drugs |
| 2 — Left heart disease | Post-capillary (raised filling pressures) | HFrEF/HFpEF, valve disease — commonest |
| 3 — Lung disease / hypoxia | Alveolar/vascular | COPD, ILD, OSA, high altitude |
| 4 — Chronic thromboembolic (CTEPH) | Vessel occlusion | Organised chronic PE |
| 5 — Multifactorial/unclear | Mixed | Sarcoid, haematological, metabolic |
They benefit Group 1 (PAH), but can precipitate flash pulmonary oedema in Group 2 and worsen V/Q mismatch/hypoxaemia in Group 3. Identify the group first.
How the right ventricle fails
Afterload rises
Acute PE, hypoxaemia, hypercarbia or acidosis abruptly increase RV afterload.
RV dilates & the septum bows
The failing RV distends and pushes the interventricular septum into the LV (ventricular interdependence).
LV underfills → hypotension
Reduced LV filling drops cardiac output and systemic blood pressure.
RV ischaemia → more failure
Low aortic pressure + high RV wall tension cut RV coronary perfusion → worsening RV function → the spiral tightens.
The therapeutic key: break the spiral early — restore systemic pressure (coronary perfusion), unload the RV, and avoid anything that raises afterload.
Confirm PH, characterise the RV
| Tool | Role |
|---|---|
| Echocardiography | First-line: RV size/function (TAPSE, S′), septal flattening ("D-sign"), estimated PA pressure, exclude LV cause & tamponade |
| Biomarkers | BNP/NT-proBNP and troponin track RV strain & prognosis |
| Right heart catheterisation | Confirms PH, distinguishes pre- vs post-capillary, guides vasodilator/inotrope titration |
| Find the trigger | CTPA (PE), ABG, sepsis screen, ECG (RV infarct), medication review |
The five levers
| Lever | What to do |
|---|---|
| 1. Treat the trigger | Reperfuse PE, treat sepsis, correct hypoxaemia/acidosis, resume PAH therapy |
| 2. Optimise preload | Avoid both over- and under-filling; if volume-overloaded (raised CVP, congestion) → diurese; give fluid only with proven fluid-responsiveness |
| 3. Perfusion pressure | Noradrenaline (± vasopressin) to keep MAP > PA pressure and protect RV coronary flow |
| 4. Reduce afterload | Correct hypoxaemia/hypercarbia/acidosis; inhaled pulmonary vasodilators (iNO, inhaled prostacyclin) — selective, no systemic hypotension |
| 5. Support contractility | Dobutamine or milrinone (watch systemic vasodilation — pair with a vasopressor) |
| Rescue | Early mechanical support (RVAD, VA-ECMO) — decide before arrest |
Powerful — and group-dependent
| Agent | Note |
|---|---|
| Inhaled nitric oxide (iNO) | Selective pulmonary vasodilation, improves V/Q; rebound on withdrawal — wean slowly |
| Inhaled prostacyclin (epoprostenol/iloprost) | Similar selective effect; useful bridge |
| IV prostacyclin | For established Group 1 PAH (specialist); systemic hypotension risk |
| PDE-5 inhibitors / ERAs / riociguat | Chronic PAH therapy — continue/resume; not first-line for acute rescue |
Avoid systemic vasodilators in acute RV failure — they drop the systemic pressure the RV depends on for its own coronary supply.
The ventilator can kill the RV
- Avoid intubation if you can — induction and positive pressure can precipitate arrest in severe PH. Optimise first; have vasopressor and pulmonary vasodilator ready.
- Both hypoxaemia and hypercarbia raise afterload — keep oxygenation up and CO₂ controlled.
- High PEEP and over-distension raise RV afterload — use modest tidal volumes and the lowest effective PEEP.
- Avoid acidosis (metabolic or respiratory) — it is a pulmonary vasoconstrictor.
Common mistakes
Filling a distended RV worsens septal bowing and drops output. Diurese the congested RV; give fluid only if truly responsive.
They harm Group 2 (flash oedema) and Group 3 (worse mismatch). Characterise first.
Dropping systemic pressure starves the RV coronary supply — use noradrenaline to protect it.
Peri-intubation arrest is common in severe PH — optimise, prepare, and involve seniors.
Consider mechanical support before cardiac arrest, not after.
Exam pearls
Q: Definition of PH?
Mean PA pressure >20 mmHg (with further pre-/post-capillary distinction on right heart catheterisation).
Q: Describe the RV death spiral.
↑ afterload → RV dilatation → septal bowing → LV underfilling → hypotension → RV coronary hypoperfusion → worsening RV failure.
Q: Vasopressor of choice in RV failure?
Noradrenaline (± vasopressin) to keep MAP > PA pressure and preserve RV coronary perfusion.
Q: Which PH groups should NOT get pulmonary vasodilators?
Group 2 (left heart — flash oedema) and Group 3 (lung disease — worse V/Q). Vasodilators are for Group 1 PAH.
Q: Inhaled vs IV pulmonary vasodilators?
Inhaled (iNO, prostacyclin) are selective without systemic hypotension — preferred in acute RV failure.
All the comparisons in one place
The distinctions that decide therapy and answers — gathered at the end.
Pre-capillary vs Post-capillary PH
| Feature | Pre-capillary (Groups 1,3,4) | Post-capillary (Group 2) |
|---|---|---|
| Problem | Pulmonary arterial disease | Raised left-heart filling pressures |
| PAWP | ≤15 mmHg | >15 mmHg |
| Pulmonary vasodilators | May help (esp. Group 1) | Harmful (flash oedema) |
RV failure vs LV failure
| Feature | RV failure | LV failure |
|---|---|---|
| Congestion | Systemic (raised JVP, oedema, hepatic) | Pulmonary (oedema, orthopnoea) |
| Preload handling | Very sensitive — easily over/under-filled | More tolerant |
| Pressor logic | Protect coronary perfusion, cut PVR | Reduce afterload, offload |
Inhaled vs Systemic vasodilators
| Feature | Inhaled (iNO/prostacyclin) | Systemic |
|---|---|---|
| Selectivity | Pulmonary only | Pulmonary + systemic |
| Systemic BP | Preserved | Falls (dangerous in RV failure) |
| V/Q | Improves (goes to ventilated lung) | May worsen mismatch |
References
- Irwin RS, Lilly CM, Mayo PH, Rippe JM (eds). Irwin & Rippe's Intensive Care Medicine. 9th ed. Wolters Kluwer; 2023.
- Marino PL. Marino's The ICU Book. 5th ed. Wolters Kluwer; 2025.
- Bersten AD, Handy JM (eds). Oh's Intensive Care Manual. Elsevier; 2026.
- Humbert M, Kovacs G, Hoeper MM, et al. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J. 2022;43:3618–3731.
- Simonneau G, Montani D, Celermajer DS, et al. Haemodynamic definitions and updated clinical classification of pulmonary hypertension. Eur Respir J. 2019;53:1801913.
- Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc. 2014;11:811–822.