Chapter 9 — The Right Ventricle and the Pulmonary Circulation

📚 Guideline basis

ASE 2025 — Guidelines for the Echocardiographic Assessment of the Right Heart in Adults and Special Considerations in Pulmonary Hypertension (J Am Soc Echocardiogr 2025), which supersedes Rudski et al. 2010 and introduces graded severity ranges in place of single cut-offs. Also: ESC/ERS pulmonary hypertension guidelines; Vieillard-Baron and Repessé work on acute cor pulmonale.

Pathophysiology & Mechanisms

The right ventricle is a thin-walled (normal free wall thickness < 5 mm), crescentic, volume-adapted pump ejecting into a low-impedance circuit. Three mechanical consequences define its behaviour in critical illness:

1. Afterload intolerance. RV stroke volume falls steeply with acute increases in pulmonary artery pressure. A previously normal RV cannot generate a mean PA pressure much above 40 mmHg acutely; a systolic pressure above ~60 mmHg in an acutely presenting patient implies chronic adaptation, not an acute event.
2. Series interdependence. RV output is LV preload. RV failure causes LV underfilling — the LV is small and hypercontractile while cardiac output is low.
3. Parallel (direct) interdependence. The ventricles share a septum inside a non-distensible pericardium. RV dilatation shifts the septum leftward, reducing LV end-diastolic volume and compliance. This is the mechanism by which "LV diastolic dysfunction" appears in a patient whose only disease is right-sided.

Contraction mechanics: ~80% of RV ejection is longitudinal (base-to-apex shortening) with the free wall moving toward the septum. This is why longitudinal indices (TAPSE, s′, free wall strain) dominate RV assessment, and why they become unreliable after pericardiotomy, when longitudinal motion falls acutely while global RV function is preserved.

Coronary perfusion: the normal RV is perfused in both systole and diastole because RV pressure is far below aortic pressure throughout. When RV systolic pressure rises toward systemic levels, systolic perfusion is lost and the RV becomes diastole-dependent — the basis of the RV spiral of death: RV dilatation → increased wall stress and decreased coronary perfusion pressure → RV ischaemia → worse RV function → further dilatation → septal shift → falling LV output and systemic pressure → further fall in RV coronary perfusion.

Interrupting that spiral is the entire therapeutic logic of RV failure: maintain systemic diastolic pressure (noradrenaline/vasopressin), reduce PVR (oxygenate, avoid hypercapnia and acidosis, consider inhaled pulmonary vasodilators), avoid volume loading a dilated RV, and reduce mean airway pressure.

Acquisition

RV assessment requires a dedicated RV-focused apical four-chamber view — rotate and tilt from the standard A4C to maximise RV free wall dimensions without foreshortening. Linear dimensions and TAPSE measured from a standard (LV-optimised) A4C are unreliable.

Diagnostic Synthesis — 2025 severity grading

The 2025 guideline replaces binary normal/abnormal with graded ranges.

Structure

Function

Strain values are reported as absolute magnitudes above; both RVFWS and RVGLS are normal when more negative than approximately −20% to −25%, with vendor dependence.

RV–PA coupling

RV–PA coupling index = TAPSE / PASP

A TAPSE/PASP ratio of 0.3–0.4 mm/mmHg indicates RV–PA uncoupling and is associated with increased mortality. This is the most useful single RV number in critical care because it expresses the RV's contractile response relative to the load it faces — a TAPSE of 1.5 cm against a PASP of 25 mmHg and against a PASP of 70 mmHg describe entirely different ventricles.

Pulmonary pressures

PASP = 4 v²(TR) + RAP     (absent RVOT obstruction or pulmonic stenosis)

RA pressure estimation from the IVC (subcostal, 1–2 cm from the cavo-atrial junction, spontaneously breathing patient):

This table is invalid under positive-pressure ventilation. In the ventilated patient the IVC distends with inspiration rather than collapsing, and the ASE RAP table does not apply. Hepatic vein Doppler and the interatrial septum are better guides (Chapter 13).

Mean PA pressure from pulmonary regurgitation early-diastolic velocity: mPAP = 4v²(PR early) + RAP. PA diastolic pressure from PR end-diastolic velocity: PADP = 4v²(PR end) + RAP.

Pulmonary vascular resistance estimate:

PVR (Wood units) ≈ (v_TR (m/s) / VTI_RVOT (cm)) × 10 + 0.16

Valid only in the mid range; unreliable when PVR is very high.

RVOT acceleration time and notching

RVOT acceleration time (onset of flow to peak velocity, PW in the RVOT):

• < 105 ms suggests pulmonary hypertension
• < 60 ms suggests markedly elevated PVR
• Mid-systolic notching of the RVOT envelope indicates high-PVR, high-wave-reflection physiology — characteristic of pre-capillary pulmonary hypertension and of acute pulmonary embolism, and rarely seen in purely post-capillary disease

The 60/60 sign (RVOT acceleration time < 60 ms with TR gradient ≤ 60 mmHg) is a specific sign of acute pulmonary embolism (Chapter 33): a sharply raised PVR that a normal RV has not had time to adapt to.

Acute cor pulmonale

The ICU-specific syndrome: acute RV pressure overload with dilatation and septal dysfunction. The operational echocardiographic definition used in the ARDS literature (Vieillard-Baron):

• RV end-diastolic area / LV end-diastolic area > 0.6 (severe if > 1.0), measured in the four-chamber view, plus
• Septal dyskinesia — paradoxical septal motion in systole, seen in the parasternal short axis

Septal motion distinguishes the mechanism

Mixed patterns are common in the ICU (an ARDS patient with severe functional TR has both).

ICU-Specific Limitations

🛑 Critical pitfall: Interpreting a falling PASP as improvement. As the RV fails it can no longer generate pressure; PASP falls while the patient deteriorates. TAPSE/PASP and RVOT VTI disambiguate.

🛑 Critical pitfall: Volume-loading a dilated, poorly contracting RV. Additional preload increases wall stress, worsens septal shift, further reduces LV filling, and lowers cardiac output. In acute cor pulmonale the correct response to hypotension is usually vasopressor plus afterload reduction, not fluid.

🛑 Critical pitfall: Using TAPSE alone in a post-cardiac-surgery patient. It will be low, and it will not mean what it means preoperatively.

• 💡 Clinical pearl: TAPSE/PASP is the single most informative RV number in the ICU. Record it explicitly.
• 💡 Clinical pearl: The ventilator is an RV drug. Before escalating inotropes for RV failure, reduce plateau pressure, driving pressure, and PaCO₂ — then rescan.
• 💡 Clinical pearl: A severely dilated RV with normal free wall thickness (< 5 mm) implies an acute process; free wall thickness > 5 mm implies weeks or more of pressure overload and reframes the differential entirely.
• 💡 Clinical pearl: McConnell's sign (akinetic RV free wall with preserved apical contraction) is suggestive of acute PE but is neither sensitive nor entirely specific — it is also described in RV infarction.

References

1. 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.
2. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults. J Am Soc Echocardiogr 2010;23:685–713.
3. 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.
4. Repessé X, Vieillard-Baron A. Right heart function during acute respiratory distress syndrome. PMID 30603577.
5. Rex et al. Right heart assessment. Eur Heart J 2022. PMID 35778820.