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. 2022 Jun 20;14(1):26.
doi: 10.1186/s13089-022-00276-4.

Pulmonary artery acceleration time accuracy for systolic pulmonary artery pressure estimation in critically ill patients

Affiliations

Pulmonary artery acceleration time accuracy for systolic pulmonary artery pressure estimation in critically ill patients

Valentino Dammassa et al. Ultrasound J. .

Abstract

Background: Estimation of pulmonary pressures is of key importance in acute cardiovascular and respiratory failure. Pulmonary artery acceleration time (PAAT) has emerged as reliable parameter for the estimation of systolic pulmonary artery pressure (sPAP) in cardiological population with preserved right ventricular function. We sought to find whether PAAT correlates with sPAP in critically ill patients with and without right ventricular (RV) systolic dysfunction.

Methods: Observational study. We measured sPAP using continuous-wave Doppler analysis of tricuspid regurgitation velocity peak method and we assessed the validity of PAAT in estimating sPAP in patients admitted to adult intensive care unit (ICU) for acute cardiovascular and respiratory failure.

Results: We enrolled 236 patients admitted to cardiothoracic ICU for cardiovascular and respiratory failure (respectively: 129, 54.7% and 107, 45.3%). 114 (48.3%) had preserved RV systolic function (defined as TAPSE ≥ 17 mm), whilst 122 (51.7%) had RV systolic impairment (defined as TAPSE < 17 mm). A weak inverse correlation between PAAT and sPAP (ρ-0.189, p 0.0035) was observed in overall population, which was confirmed in those with preserved RV systolic PAAT and sPAP (ρ-0.361, p 0.0001). In patients with impaired RV systolic function no statistically significant correlation between PAAT and sPAP was demonstrated (p 0.2737). Adjusting PAAT values for log10, heart rate and RV ejection time did not modify the abovementioned correlations.

Conclusions: PAAT measurement to derive sPAP is not reliable in cardiothoracic critically ill patients, particularly in the coexistence of RV systolic impairment.

Keywords: Acute cardiovascular failure; Acute respiratory failure; Pulmonary artery acceleration time; Pulmonary artery pressure; Right ventricular dysfunction.

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Conflict of interest statement

FM received fees for lectures from GE Healthcare, Hamilton Medical, SEDA SpA, outside the present work. GT received fees for lectures from GE Healthcare, outside the present work.

Figures

Fig. 1
Fig. 1
Pulmonary artery acceleration time (PAAT, dashed red line) and right ventricular ejection time (RVET, yellow brace) measurement in parasternal short-axis view (A) and subcostal view (B). PAAT is calculated as the time interval between the onset of systolic pulmonary artery flow and its peak flow velocity; RVET is measured from the onset to the end of pulmonary artery Doppler spectrum. For further adjustment, sPAP was derived on the basis of the linear correlation linking PAAT to TRVmax as follows: log10(sPAP) = −0.004 (PAAT) + 2.1 [8]. Mean PAP (mPAP) can be estimated using the following formulae proposed by Dabestani et al. [28]: if PAAT ≥ 120 ms, mPAP = 79 – (0.45 * PAAT); if PAAT < 90 ms, mPAP = 90 – (0.62 * PAAT)
Fig. 2
Fig. 2
Scatter plot diagrams showing relationship between TR-derived sPAP and PAAT in overall population (left upper panel), preserved RV systolic function (right upper panel) and RV systolic dysfunction (lower panel)

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