scholarly journals Clinical applicability of monitoring pulmonary artery blood flow acceleration time variations inmonitoring fetal pulmonary artery pressure

2018 ◽  
Vol 27 (12) ◽  
pp. 1723-1727
Author(s):  
Hong-Yan Zhan ◽  
Feng-Qin Xu ◽  
Xi-Chuan Liu ◽  
Gang Zhao
2008 ◽  
Vol 108 (1) ◽  
pp. 55-62 ◽  
Author(s):  
Bélaïd Bouhemad ◽  
Fabio Ferrari ◽  
Kris Leleu ◽  
Charlotte Arbelot ◽  
Qin Lu ◽  
...  

Background In spontaneously breathing cardiac patients, pulmonary artery pressure (PAP) can be accurately estimated from the transthoracic Doppler study of pulmonary artery and tricuspid regurgitation blood flows. In critically ill patients on mechanical ventilation for acute lung injury, the interposition of gas between the probe and the heart renders the transthoracic approach problematic. This study was aimed at determining whether the transesophageal approach could offer an alternative. Methods Fifty-one consecutive sedated and ventilated patients with severe hypoxemia (arterial oxygen tension/fraction of inspired oxygen < 300) were prospectively studied. Mean PAP measured from the pulmonary artery catheter was compared with several indices characterizing pulmonary artery blood flow assessed using transesophageal echocardiography: preejection time, acceleration time, ejection duration, preejection time on ejection duration ratio, and acceleration time on ejection duration ratio. In a subgroup of 20 patients, systolic PAP measured from the pulmonary artery catheter immediately before withdrawal was compared with Doppler study of regurgitation tricuspid flow performed immediately after pulmonary artery catheter withdrawal using either the transthoracic or the transesophageal approach. Results Weak and clinically irrelevant correlations were found between mean PAP and indices of pulmonary artery flow. A statistically significant and clinically relevant correlation was found between systolic PAP and regurgitation tricuspid flow. In 3 patients (14%), pulmonary artery pressure could not be assessed echocardiographically. Conclusions In hypoxemic patients on mechanical ventilation, mean PAP cannot be reliably estimated from indices characterizing pulmonary artery blood flow. Systolic PAP can be estimated from regurgitation tricuspid flow using either transthoracic or transesophageal approach.


2008 ◽  
Vol 295 (5) ◽  
pp. L756-L766 ◽  
Author(s):  
Peter E. Oishi ◽  
Dean A. Wiseman ◽  
Shruti Sharma ◽  
Sanjiv Kumar ◽  
Yali Hou ◽  
...  

Cardiac defects associated with increased pulmonary blood flow result in pulmonary vascular dysfunction that may relate to a decrease in bioavailable nitric oxide (NO). An 8-mm graft (shunt) was placed between the aorta and pulmonary artery in 30 late gestation fetal lambs; 27 fetal lambs underwent a sham procedure. Hemodynamic responses to ACh (1 μg/kg) and inhaled NO (40 ppm) were assessed at 2, 4, and 8 wk of age. Lung tissue nitric oxide synthase (NOS) activity, endothelial NOS (eNOS), neuronal NOS (nNOS), inducible NOS (iNOS), and heat shock protein 90 (HSP90), lung tissue and plasma nitrate and nitrite (NOx), and lung tissue superoxide anion and nitrated eNOS levels were determined. In shunted lambs, ACh decreased pulmonary artery pressure at 2 wk ( P < 0.05) but not at 4 and 8 wk. Inhaled NO decreased pulmonary artery pressure at each age ( P < 0.05). In control lambs, ACh and inhaled NO decreased pulmonary artery pressure at each age ( P < 0.05). Total NOS activity did not change from 2 to 8 wk in control lambs but increased in shunted lambs (ANOVA, P < 0.05). Conversely, NOxlevels relative to NOS activity were lower in shunted lambs than controls at 4 and 8 wk ( P < 0.05). eNOS protein levels were greater in shunted lambs than controls at 4 wk of age ( P < 0.05). Superoxide levels increased from 2 to 8 wk in control and shunted lambs (ANOVA, P < 0.05) and were greater in shunted lambs than controls at all ages ( P < 0.05). Nitrated eNOS levels were greater in shunted lambs than controls at each age ( P < 0.05). We conclude that increased pulmonary blood flow results in progressive impairment of basal and agonist-induced NOS function, in part secondary to oxidative stress that decreases bioavailable NO.


2019 ◽  
Vol 41 (2) ◽  
pp. 265-271
Author(s):  
Bassel Mohammad Nijres ◽  
John Bokowski ◽  
Lamya Mubayed ◽  
Sabih H. Jafri ◽  
Alan T. Davis ◽  
...  

1961 ◽  
Vol 16 (2) ◽  
pp. 305-308 ◽  
Author(s):  
Lois T. Ellison ◽  
David P. Hall ◽  
Thomas Yeh ◽  
H. Mobarhan ◽  
Joseph Rossi ◽  
...  

Alterations in pulmonary function and in hemodynamics were studied in dogs with high pulmonary blood flow resulting from systemic pulmonary artery shunts. In order to facilitate elevation in pulmonary artery pressure, the vascular bed was reduced in some cases by obstructing branches of the pulmonary artery with Teflon clips or by lobectomy. Results in 30 control dogs and in 30 animals that survived 5–36 months (average 16) following creation of shunts indicated that pulmonary function was not significantly altered by increased pulmonary blood flow until pulmonary artery hypertension developed. When systolic pulmonary artery pressure exceeded 40 mm Hg, there was a decrease in arterial Po2, an increase in venous admixture percentage of cardiac output, and an increase in the A-a O2 difference during three levels of O2 breathing, indicating both abnormal venous admixture and abnormal diffusion. Possible explanations for these findings are presented. Evidence in one dog suggests that these alterations are reversible. Submitted on August 10, 1960


1958 ◽  
Vol 192 (3) ◽  
pp. 613-619 ◽  
Author(s):  
Michael T. Lategola

The relationship of pulmonary artery pressure to pulmonary blood flow was studied in the dog by means of occlusive shifting of blood flow within the pulmonary vascular bed. All experiments were performed using the closed-chest preparation. The range of blood flow increases studied was 25–388%. A graphical plot of the percentage change in blood flow versus the percentage change in mean pulmonary artery pressure is presented. A visually estimated curve of this latter data is presented, discussed and compared to four other curves from previous pulmonary vascular studies. A comparison of these curves suggests that the relative maximum capacity of the pulmonary vascular bed of man and dog are similar. These curves plus certain assumptions allow the speculative delineation of a graphical area representing the ‘active’ vasomotor component of exercise at different levels of pulmonary blood flow increase.


1989 ◽  
Vol 257 (2) ◽  
pp. H626-H634 ◽  
Author(s):  
S. H. Abman ◽  
F. J. Accurso

To determine the acute effects of increased pulmonary artery pressure and flow on the fetal pulmonary circulation, we studied the response of pulmonary blood flow and vascular reactivity to partial compression of the ductus arteriosus in 22 chronically prepared late-gestation fetal lambs. An inflatable occluder was placed loosely around the ductus arteriosus for compression. Partial compression of the ductus rapidly increased mean pulmonary artery pressure from 45 +/- 1 to 60 +/- 1 mmHg (mean +/- SE) and left pulmonary artery blood flow from 65 +/- 6 to 151 +/- 11 ml/min at 30 min (P less than 0.001; 12 animals). Despite keeping pulmonary artery pressure constant, pulmonary blood flow steadily declined and by 2 h was not different from base-line values. Pulmonary vascular resistance initially fell during the first 30 min of partial compression but then steadily increased and remained elevated above base-line values for at least 30 min after the release of the occluder (P less than 0.001). The decline of pulmonary vascular resistance during the first 30 min of compression was blunted after treatment with the cyclooxygenase inhibitor, meclofenamate (P less than 0.001; 6 animals). Rapid incremental ductus compressions demonstrated a decrease in the slope of the pressure-flow relationship from 3.30 +/- 0.27 (control) to 1.59 +/- 0.21 ml.min-1.mmHg-1 during the postcompression period (P less than 0.001; 12 animals). The vasodilation response to small increases of fetal PO2 was markedly blunted during the postcompression period (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)


Respirology ◽  
2005 ◽  
Vol 10 (5) ◽  
pp. 620-628 ◽  
Author(s):  
Robert J. PIERCE ◽  
Ken SHARPE ◽  
Jennifer JOHNS ◽  
Bruce THOMPSON

2017 ◽  
Vol 5 (1) ◽  
pp. 3-11
Author(s):  
Rajarajan Ganesan

ABSTRACT Background Pulmonary acceleration time (PAT) forms a valuable echocardiographic parameter in deriving the mean pulmonary artery pressure (MPAP). The present study aims to derive and validate a formula relating MPAP and PAT in an Indian population. Materials and methods Preoperative echocardiography was performed in 22 adult cardiac surgery patients undergoing coronary artery bypass grafting (CABG) and/or mitral valve replacement. The PAT, PAT/right ventricular ejection time (RVET), PAT corrected for heart rate [(HR) HRcPAT], and tricuspid regurgitation (TR) peak velocity were correlated with MPAP measured from pulmonary artery (PA) catheter, and a new formula relating MPAP and PAT was derived and subsequently validated in another cohort of 21 patients. Results The PAT, HRcPAT, and PAT/RVET correlated well (r2 = 0.69, 0.68 and 0.47 respectively, p < 0.0001), while TR velocity correlated poorly with MPAP (r2 = 0.20, p = 0.046). The cutoff values of PAT and HRcPAT for diagnosing pulmonary artery hypertension (PAH) (MPAP = 25 mm Hg) were 74 and 99 respectively, with 92% sensitivity and 100% specificity. The derived formula (MPAP = 62.4 - 0.3 PAT) correlated well with the standard formula (79-0.45 PAT) on applying in the validation cohort (Bland—Altman plot, bias <10%). In subgroup analysis, patients with severe PAH (MPAP = 50 mm Hg) showed better correlation than patients with less than severe PAH (r2 = 0.633, p =0.038 a nd r2 = 0.46, p = 0.108 respectively). Similarly, the formula for deriving pulmonary vascular resistance index (PVRI) from PAT [(PVRI = 14.9-0.09 pulmonary artery acceleration time (PAAT)] correlated well with the existing formula (PVRI = 9 - 0.07 PAAT). The inter- and intraobserver variabilities were not significant. Conclusion The indexed formula is better in predicting MPAP from PAT in Indian population, particularly in patients with severe PAH (MPAP = 50 mm Hg) and the cutoffs of PAT and HRcPAT in predicting PAH (MPAP = 25 mm Hg) in an Indian population are 74 and 99 msec respectively. How to cite this article Munirathinam GK, Kumar A, Ganesan R, Puri GD. Derivation and Validation of Formula relating Pulmonary Acceleration Time and Mean Pulmonary Artery Pressure in Indian Population. J Perioper Echocardiogr 2017;5(1):3-11.


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