Pulmonary artery acceleration time
PAAcT (PAAT, AcT) · Pulsed Doppler in the RVOT, parasternal short axis; measure from onset of flow to peak velocity, sweep 100 mm/s
Normal range & thresholds
Normal >120–130 ms at a heart rate of 60–100/min. PAAT <105 ms suggests pulmonary hypertension; <60 ms with mid-systolic notching indicates markedly elevated pulmonary vascular resistance.[3,47]
Estimating mean pulmonary artery pressure: mPAP ≈ 79 − (0.45 × PAAT); when PAAT <120 ms, mPAP ≈ 90 − (0.62 × PAAT). These are population regressions, not measurements — report them as estimates.[47]
Estimating mean pulmonary artery pressure: mPAP ≈ 79 − (0.45 × PAAT); when PAAT <120 ms, mPAP ≈ 90 − (0.62 × PAAT). These are population regressions, not measurements — report them as estimates.[47]
Pathophysiology
The right ventricle ejects into a normally compliant, low-resistance pulmonary bed, so flow accelerates slowly and peaks late in systole. When the pulmonary arteries stiffen and resistance rises, the pressure wave reflected from the distal bed returns during systole rather than after it. That early reflected wave truncates acceleration — producing a short, early-peaking envelope and, when reflection is strong, a mid-systolic notch. PAAT is therefore a measure of pulmonary arterial impedance and stiffness, not simply of pressure, and it is available in patients who have no measurable tricuspid regurgitation jet at all — its main clinical value.[3,47]
Raised by
- Normal, compliant pulmonary circulation
- Bradycardia (PAAT lengthens as heart rate falls — correct for rate before interpreting)
- After successful treatment of pulmonary hypertension — a lengthening PAAT is a genuine response marker
Lowered by
- Pulmonary hypertension of any group — precapillary disease shortens it most
- Elevated pulmonary vascular resistance and proximal pulmonary artery stiffening
- Acute pulmonary embolism (short PAAT with the 60/60 sign: PAAT <60 ms with a TR gradient <60 mmHg — an acute, unadapted RV)
- Chronic thromboembolic disease; chronic lung disease
- Tachycardia (shortens PAAT independently of pressure)
- Low cardiac output states (misleadingly short)
Technique & pitfalls
- Pulsed Doppler with the sample volume in the mid-RVOT, beam parallel to flow; sweep speed 100 mm/s so the onset and peak can be timed accurately.
- Measure from the onset of systolic flow to the peak velocity — not to the end of ejection.
- Record the heart rate; if outside 60–100/min, correct or state the limitation, because PAAT is rate-dependent.
- Describe the envelope shape. Mid-systolic notching implies higher PVR and a worse prognosis than late-systolic notching, and it is not captured by any number.
- PAAT is the parameter to reach for when there is no adequate TR jet — roughly a quarter of patients — where it prevents an entirely missed diagnosis.[3]
Pseudo-change & artefact
- Heart rate is the dominant confounder: tachycardia shortens PAAT and can fabricate pulmonary hypertension.
- Angle error and a poorly defined onset of flow.
- Low sweep speed makes the measurement imprecise by 10–20 ms.
- Low cardiac output shortens the envelope without a rise in pressure.
- Poor parasternal windows in emphysema — use the subcostal RVOT view.
- Regression-derived pressure estimates carry wide confidence limits; never present them as measured pressures.
Treatment thresholds
- No treatment threshold is defined by PAAT. Its guideline role is as a supportive sign in the echocardiographic probability assessment of pulmonary hypertension — a short PAAT (<105 ms), mid-systolic notching, RV dilatation, septal flattening, a dilated pulmonary artery, a plethoric IVC and RA enlargement together raise the echocardiographic probability and drive the referral for right heart catheterisation.[8]
- Acute pulmonary embolism: the 60/60 sign supports RV strain from an acute obstruction rather than chronic disease — helpful when the clinical distinction is urgent.[8]
- A lengthening PAAT on treatment is a marker of therapeutic response in pulmonary arterial hypertension.
Next step
- Next: combine with TR velocity, RV size and function, septal shape, IVC and RA area to assign an echocardiographic probability of pulmonary hypertension.[8]
- Then: estimate PVR (TR Vmax/RVOT VTI); look for the cause — left heart disease (group 2, commonest), lung disease (group 3), thromboembolic disease (group 4).
- Then: V/Q scanning in every case of unexplained pulmonary hypertension.[8]
- Then: right heart catheterisation — the diagnosis of pulmonary hypertension (mean PAP >20 mmHg; PVR >2 WU for precapillary disease) is invasive by definition and cannot be made on echo.[8]
Drugs
- Lengthened by effective pulmonary vasodilator therapy in group 1 disease — endothelin receptor antagonists, PDE-5 inhibitors, riociguat, prostacyclin analogues, and by pulmonary endarterectomy or balloon pulmonary angioplasty in CTEPH.[8]
- Lengthened indirectly by treating left heart disease in group 2 — where pulmonary vasodilators are not indicated and may cause harm.[8]
- Shortened by hypoxaemia, acidosis, hypercapnia, and by anything raising pulmonary vascular tone.
- Shortened acutely by tachycardia from any cause, including drugs.
Reversibility
Reversible in proportion to the reversibility of pulmonary vascular resistance. Excellent recovery after treatment of acute pulmonary embolism and after pulmonary endarterectomy; substantial in vasodilator responders over 3–12 months; substantial after correction of a left-to-right shunt or successful treatment of left heart disease. Poor once the pulmonary vasculature is remodelled with fixed resistance — and the failure of PAAT to lengthen on treatment is itself a useful sign of that.[8]