RVOT velocity–time integral

RVOT VTI · Pulsed Doppler, parasternal short axis at the aortic valve level (or subcostal), sample volume in the mid-RVOT just proximal to the pulmonary valve

Normal range & thresholds

Pathophysiology

Raised by

• High-output states — anaemia, sepsis, thyrotoxicosis, pregnancy, arteriovenous fistula
• Left-to-right shunt (atrial septal defect, VSD, PDA) — the pulmonary flow is genuinely greater than the systemic flow
• Bradycardia; exercise; inotropes
• Athletic conditioning

Lowered by

• RV systolic dysfunction of any cause
• Pulmonary hypertension with a failing RV — low VTI with a short acceleration time and a notch
• Hypovolaemia, tamponade, constriction
• Severe tricuspid regurgitation (forward output falls), pulmonary stenosis, RVOT obstruction
• Tachyarrhythmia; massive pulmonary embolism
• Positive-pressure ventilation with high PEEP

Technique & pitfalls

• Parasternal short axis at the aortic valve level, or the subcostal RVOT view when the parasternal window is poor; align the beam parallel to flow.
• Sample volume in the mid-RVOT, 0.5–1 cm proximal to the pulmonary valve, in the same location where the diameter was measured.
• Measure the RVOT diameter in mid-systole, inner edge to inner edge.
• Trace the modal velocity; note explicitly whether the envelope is notched, and where the notch falls (mid-systolic notching implies higher PVR and worse prognosis than late-systolic).
• Report acceleration time from the same envelope (card 29).
• RVOT diameter is the weakest link in every right-sided flow calculation — measure it carefully or use ratio-based indices instead.

Pseudo-change & artefact

• RVOT diameter error — squared in the stroke volume, so a 2 mm error changes RV stroke volume by ≈20%.
• Sample volume too close to the pulmonary valve (flow acceleration) or in the subvalvular muscular RVOT with dynamic obstruction.
• Angle error; poor parasternal windows in chronic lung disease — the very population in whom the measurement matters most.
• Positive-pressure ventilation and respiratory variation — measure at end-expiration.
• The Abbas PVR formula is unreliable at high resistance and in the presence of significant TR — do not report an echo PVR as if it were a catheter value.^[49]

Treatment thresholds

• Pulmonary hypertension: RV stroke volume and its surrogates are central to the ESC/ERS risk tables and hence to the choice between initial dual oral therapy and upfront triple therapy including parenteral prostacyclin, and to transplant referral.^[8]
• Shunt quantification: Qp:Qs = RV stroke volume / LV stroke volume; Qp:Qs ≥1.5 with right heart enlargement is the class I indication for atrial septal defect closure.^[25]
• Echo-estimated PVR is used as a screening triage tool — a high value prompts right heart catheterisation, which is the only acceptable basis for a haemodynamic diagnosis (mean PAP >20 mmHg with PVR >2 WU defines precapillary disease).^[8,49]
• Critical care: serial RVOT VTI tracks right-sided output during resuscitation and inotrope titration.
• No single RVOT VTI value triggers a specific therapy.

Next step

• Next: measure pulmonary artery acceleration time and inspect the envelope for notching; compute PVR as a screening estimate.
• Then: compare with LVOT stroke volume for Qp:Qs, and perform an agitated-saline study if a shunt is suspected.
• Then: V/Q scanning (not CT alone) to exclude chronic thromboembolic disease in any unexplained pulmonary hypertension — a missed CTEPH is a missed curable disease.^[8]
• Then: right heart catheterisation with vasoreactivity testing where appropriate.

Drugs

• Pulmonary vasodilators raise RVOT VTI in responders over weeks to months, and the rise is a marker of treatment response.^[8]
• Diuretics improve RV geometry and can raise forward output despite reducing preload.
• Inotropes raise it acutely.
• Beta-blockers, high PEEP and hypoxaemia lower it.
• Systemic vasodilators without pulmonary selectivity can be harmful in severe pulmonary arterial hypertension.

Reversibility