Key result
Increased airway pressure and simulated branch pulmonary artery stenosis increased pulmonary regurgitation.
Why the study?
Does increased airway pressure or simulated branch pulmonary artery stenosis increase pulmonary regurgitation in patients after repair of tetralogy of Fallot?
Does increased airway pressure or simulated branch pulmonary artery stenosis increase pulmonary regurgitation in patients after repair of tetralogy of Fallot?
Increased airway pressure and branch pulmonary stenosis exacerbate pulmonary regurgitation, which has implications for the acute postoperative and long-term management of patients after tetralogy of Fallot repair.
Answers are grounded in this paper and cite their sources.
May inform perioperative ventilation and branch PA assessment after TOF repair; hypothesis-generating for modifiable factors worsening pulmonary regurgitation.
BACKGROUND: Pulmonary regurgitation (PR) is an important determinant of outcome after repair of tetralogy of Fallot. Baseline PR was measured by magnetic resonance (MR) phase velocity mapping and from real-time right ventricular pressure-volume loops with a conductance catheter. Subsequently, the impact of two loading maneuvers (increased airway pressure, simulated branch pulmonary artery stenosis) on PR was assessed by the conductance catheter method. METHODS AND RESULTS: Thirteen patients, 3 to 35 years after tetralogy of Fallot repair or pulmonary valvotomy, had PR measured by MR phase velocity mapping while breathing spontaneously. During catheterization under general anesthesia. PR was estimated from right ventricular pressure-volume loops generated by conductance and microtip pressure catheters. The effect of increased airway pressure (continuous positive airway pressure, 20 cm H2O; n = 12) and simulated branch pulmonary artery stenosis (transient balloon occlusion of a branch pulmonary artery, n = 7) was measured. Basal PR fraction derived by MR and from right ventricular pressure-volume loops had a correlation coefficient of .76 and mean of differences of 2.0 +/- 18.2% (95% limits of agreement). Increased airway pressure increased PR (16.3 +/- 11.4% to 25.7 +/- 17.3%, P < .01). Simulated branch pulmonary artery stenosis increased right ventricular end-systolic pressure (69.1 +/- 21.4 to 78.7 +/- 23.1 mm Hg, P < .05) and PR (27.5 +/- 11.3% to 36.9 +/- 12.8%, P < .05). CONCLUSIONS: There was reasonable agreement between MR phase velocity-derived PR fraction and that obtained from right ventricular pressure-volume loops generated by use of conductance and pressure-microtip catheters. Exacerbation of PR by increased airway pressure and branch pulmonary stenosis may be relevant to the acute postoperative and long-term management, respectively, of patients after repair of tetralogy of Fallot.
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Chaturvedi et al. (1997) studied Tetralogy of Fallot repair or pulmonary valvotomy (n=13). Increased airway pressure and simulated branch pulmonary artery stenosis vs. Baseline (spontaneous breathing/pre-maneuver) was evaluated on Pulmonary regurgitation fraction (p=<.01). Increased airway pressure and simulated branch pulmonary artery stenosis increased pulmonary regurgitation.
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