📚 Guideline basis
2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism; ASE 2025 Right Heart Guideline; Rex et al. (Eur Heart J 2022, PMID 35778820); 2025 AHA Guidelines for CPR and ECC (intra-arrest considerations, Chapter 31).
Pathophysiology & Mechanisms
Mechanical obstruction of the pulmonary vascular bed is necessary but not sufficient to explain the haemodynamics. Three processes act together:
- Anatomical obstruction. Clinically significant pulmonary hypertension generally requires occlusion of a substantial proportion of the pulmonary vascular bed in a previously normal circulation.
- Neurohumoral vasoconstriction. Serotonin, thromboxane A₂ and endothelin released from platelet-rich thrombus, together with hypoxic vasoconstriction, amplify the resistance far beyond the mechanical obstruction — the reason a modest clot burden can produce severe haemodynamic compromise.
- RV afterload mismatch. A previously normal, thin-walled right ventricle cannot acutely generate a mean pulmonary artery pressure much above 40 mmHg. Beyond that, RV dilatation, wall stress and ischaemia begin, entering the RV spiral described in Chapter 9.
The final common pathway to death is not hypoxaemia but RV failure: RV dilatation → septal shift → reduced LV preload → falling cardiac output and systemic pressure → reduced RV coronary perfusion pressure → RV ischaemia → further RV failure.
Risk stratification and where echocardiography sits
The ESC framework combines haemodynamic status, the PESI score, RV dysfunction on imaging, and cardiac biomarkers.
Risk class | Haemodynamic instability | RV dysfunction (echo or CT) | Elevated troponin |
High | Yes | Yes (present by definition) | Usually |
Intermediate–high | No | Yes | Yes |
Intermediate–low | No | Either one positive, not both | Either |
Low | No | No | No |
RV dysfunction on echocardiography is what moves a normotensive patient into the intermediate-high category, and therefore what triggers monitored admission and consideration of rescue reperfusion. This is the principal clinical role of echocardiography in PE.
Echocardiography is also the appropriate first investigation in the unstable patient in whom CT pulmonary angiography is unsafe: RV dysfunction in a patient with shock and a compatible clinical picture supports emergency reperfusion when confirmatory imaging cannot be obtained.
Diagnostic Synthesis
Findings and their operating characteristics
Finding | Description | Interpretation |
RV dilatation, RV:LV ≥ 1.0 | RV-focused apical four-chamber, end-diastole | Sensitive for haemodynamically significant PE; not specific — occurs in ARDS, chronic lung disease, RV infarction, and after cardiac arrest of any cause |
Septal flattening / D-shaped LV | Parasternal short axis; flattening maximal in systole indicates pressure overload | Supports acute RV pressure overload |
McConnell's sign | Akinesia or hypokinesia of the RV mid free wall with preserved apical contraction | Suggestive of acute PE, but neither sensitive nor entirely specific — also described in RV infarction. Probably reflects apical tethering by the adjacent hypercontractile LV rather than regional sparing |
60/60 sign | RVOT acceleration time < 60 ms with a TR peak gradient ≤ 60 mmHg | Relatively specific: an acutely raised PVR that the RV has had no time to adapt to. In chronic pulmonary hypertension the gradient exceeds 60 mmHg |
RVOT mid-systolic notching | Notched RVOT PW envelope | High wave reflection from proximal obstruction; supports pre-capillary, acute physiology |
Thrombus-in-transit | Mobile echodense mass in the RA or RV, or straddling a PFO | Diagnostic when present; high mortality; changes management urgently |
TAPSE and TAPSE/PASP | Reduced TAPSE; TAPSE/PASP 0.3–0.4 mm/mmHg indicates RV–PA uncoupling | Prognostic; the most informative single RV index (ASE 2025) |
RV free wall strain | Less negative than −20% | Detects dysfunction before TAPSE falls |
RV free wall thickness | < 5 mm in genuinely acute disease | > 5 mm implies chronic pressure overload — reframes the diagnosis toward CTEPH or chronic PH |
Dilated non-collapsing IVC | Subcostal | Elevated RA pressure; supports RV failure |
Visible thrombus in the main or right pulmonary artery | Occasionally on TTE; better on TEE | Diagnostic |
Two rules that prevent the commonest errors
A normal right ventricle does not exclude pulmonary embolism. In a haemodynamically stable patient, a normal echocardiogram excludes RV strain, not PE. Segmental and subsegmental emboli routinely produce a normal study. Echocardiography is a risk-stratification tool in stable patients, not a rule-out test.
RV dilatation does not establish pulmonary embolism. This applies with particular force in two settings covered elsewhere in this book:
- In the ventilated ARDS patient, acute cor pulmonale from the disease and the ventilator is a far commoner explanation than embolism (Chapter 32).
- During cardiac arrest, RV dilatation develops as a consequence of arrest and CPR within minutes, in arrests of any cause. Thrombolysing on isolated intra-arrest RV dilatation is an error with major bleeding consequences (Chapter 31).
Specificity is raised by combining findings: the 60/60 sign, RVOT notching, thin RV free wall, thrombus-in-transit, and a compatible clinical prodrome each add to the case; isolated RV dilatation does not.
Adjunctive ultrasound
Compression ultrasonography for proximal deep vein thrombosis is high-yield and under-used at the bedside. A positive two-point or three-point compression study in a shocked patient with RV dysfunction and no alternative explanation raises the post-test probability of PE substantially and, in the patient too unstable for CT, can be sufficient to justify reperfusion.
Lung ultrasound contributes by exclusion: an A-line profile (dry lungs) with a dilated RV and a plethoric IVC is the classic composite of acute cor pulmonale or PE, and simultaneously argues against cardiogenic pulmonary oedema (Chapter 41). Subpleural wedge-shaped consolidations are described in PE but are neither sensitive nor specific.
ICU-Specific Limitations
Confounder | Effect | Response |
Mechanical ventilation | Independently raises RV afterload and can produce identical findings | Reduce driving pressure and correct hypercapnia, then rescan (Chapter 32) |
Pre-existing chronic PH or COPD | RV thickened and dilated at baseline | Measure RV free wall thickness; obtain prior imaging |
Cardiac arrest / recent CPR | RV dilatation is near-universal | Do not use as a stand-alone indication for thrombolysis |
Severe TR | PASP underestimated because the RV–RA gradient falls | Interpret PASP alongside TAPSE and RVOT VTI |
Failing RV | PASP falls as the RV decompensates | A falling PASP with worsening RV function is deterioration, not improvement |
Poor windows | RV assessment unreliable | Subcostal views; TEE, which also images the main and right pulmonary arteries |
Therapeutic Logic
Risk class | Management | Echocardiographic role |
High risk (shock/arrest) | Systemic thrombolysis; catheter-directed therapy or surgical embolectomy if thrombolysis is contraindicated or fails; VA-ECMO as a bridge | Establishes RV dysfunction when CT is unsafe; excludes alternative causes of shock |
Intermediate–high | Anticoagulation with monitoring for deterioration; rescue reperfusion if decompensation occurs | Defines the category; serial studies detect deterioration before hypotension |
Intermediate–low / low | Anticoagulation; consider early discharge in low-risk | Confirms absence of RV strain |
Haemodynamic support in high-risk PE
The principles are those of acute RV failure (Chapter 9):
- Vasopressor first. Noradrenaline restores systemic diastolic pressure and therefore RV coronary perfusion. This is the intervention that interrupts the spiral.
- Avoid aggressive volume loading. Beyond a small challenge (≤ 250 mL) in the clearly underfilled patient, fluid worsens RV dilatation, septal shift and LV filling.
- Inotropic support with dobutamine if RV contractility is the limiting factor, with vasopressor cover for its vasodilator effect.
- Reduce PVR — oxygenate, avoid hypercapnia and acidosis, consider inhaled nitric oxide or prostacyclin.
- Intubate with extreme caution. Induction agents cause vasodilatation, positive-pressure ventilation raises RV afterload, and both can precipitate arrest in a patient with obstructive shock. Optimise pressure first; use ketamine and a vasopressor bolus; avoid high tidal volumes and high PEEP.
Serial echocardiography documents the response: falling RV:LV ratio, resolving septal shift, rising TAPSE and TAPSE/PASP, and rising RVOT VTI.
Chronic thromboembolic pulmonary hypertension
Suspect when the "acute" presentation has RV free wall thickness > 5 mm, marked RV hypertrophy, PASP above roughly 60 mmHg (which an acutely stressed normal RV cannot generate), and RA dilatation out of proportion to the acute history. These patients require a different diagnostic and therapeutic pathway.
🛑 Critical pitfall: Thrombolysing on the basis of RV dilatation alone in a ventilated or peri-arrest patient. It is the least specific finding in the chapter and the one most likely to be over-interpreted under time pressure.
🛑 Critical pitfall: Reading a falling PASP as improvement. A decompensating RV cannot generate pressure.
🛑 Critical pitfall: Excluding PE on a normal echocardiogram in a stable patient. Echocardiography stratifies risk; it does not rule out embolism.
- 💡 Clinical pearl: Measure RV free wall thickness from the subcostal window in every patient with "acute" RV dilatation. A wall over 5 mm means the process is not acute and reframes the entire differential.
- 💡 Clinical pearl: The 60/60 sign takes under a minute — RVOT PW for acceleration time, CW for TR gradient — and is far more specific than RV dilatation.
- 💡 Clinical pearl: Add bilateral femoral vein compression to any focused study for suspected PE. It is quick, and a positive result in an unstable patient can justify treatment without CT.
References
- Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J 2020;41:543–603.
- American Society of Echocardiography. Guidelines for the echocardiographic assessment of the right heart in adults and special considerations in pulmonary hypertension. J Am Soc Echocardiogr 2025.
- Rex et al. Right heart assessment in the perioperative and critical care setting. Eur Heart J 2022. PMID 35778820.
- McConnell MV, Solomon SD, Rayan ME, et al. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol 1996;78:469–73.
- Vieillard-Baron A, Naeije R, Haddad F, et al. Diagnostic workup, etiologies and management of acute right ventricle failure. Intensive Care Med 2018;44:774–90.