Acute effects of pulmonary artery banding in sheep on right ventricle pressure–volume relations: relevance to the arterial switch operation

Abstract

The first stage of the two-stage arterial switch operation (ASO) for transposition of the great arteries (TGA) is associated with depressed ventricular function and an unstable immediate post-operative course. It is unclear if this is because of the acute increase in afterload of the thin-walled, low-pressure ventricle by pulmonary artery banding (PAB). To determine the acute effects of afterload increase on the contractile function of thin-walled ventricles, we studied the right ventricular pressure-volume relations of seven sheep before and 30 min after PAB using combined pressure-conductance catheters during inflow reduction. Load independent indices of systolic and diastolic performance were derived from these relations. Pulmonary artery banding increased the mean ratio between right and left ventricular systolic pressure from 0.34 +/- 0.05 to 0.64 +/- 0.10, P < 0.05 (mean +/- SD). There were no significant changes in heart rate and end-systolic volume after banding although there was an incremental trend in the end-diastolic volume and stroke volume. Right ventricular output (530 +/- 163-713 +/- 295 mL min (-1), P < 0.05), slope of the end-systolic pressure-volume relation (ESPVR) (3.7 +/- 2.8-10.0 +/- 4.8 mmHg mL (-1), P < 0.05) and slope of the pre-load recruitable stroke work (PRSW) relation (9.6 +/- 1.8-15.0 +/- 3.1 mmHg, P < 0.05) were significantly increased indicating improved contractile state after banding. The diastolic function curve was unchanged after banding although the right ventricle (RV) was operating at a larger end-diastolic volume. Hence, the RV of sheep responded to acute pressure overload by demonstrating enhanced contractility and evidence of the Frank-Starling mechanism without associated change in right ventricular diastolic performance.

Effect of BM-573 [N-Terbutyl-N′-[2-(4′-methylphenylamino)-5-nitro-benzenesulfonyl]urea], a Dual Thromboxane Synthase Inhibitor and Thromboxane Receptor Antagonist, in a Porcine Model of Acute Pulmonary Embolism

“…In other words, increments in E a were coupled with preload recruitment to maintain RV performance. This feature is in agreement with previous studies suggesting the intervention of these two adaptive mechanisms in case of RV outflow obstruction (Rose et al, 1983;de Vroomen et al, 2000;Lopes Cardozo et al, 2000;Hon et al, 2001).…”

Effects of norepinephrine and dobutamine on pressure load-induced right ventricular failure*

“…Our results show that even in the absence of adrenergic blockade, RV contractility is profoundly and persistently altered after transient PA constriction (Ees change 1.1-0.4 mm Hg/mL), afterload remains increased (Ea change 0.8 -1.8 mm Hg/mL), and the combination of both factors results in a marked deterioration of RV-PA coupling efficiency (Ees/Ea change 1.2-0.3). The different degree of PA constriction explains why RV coupling was preserved in previous studies when pulmonary vascular resistance was increased about twofold (10,18,19) and why it deteriorated here when resistance was increased fourfold. The persistence of RV changes after PA release could result from RV myocardial stunning due to hypotension and RV ischemia (4) or to other yet undefined humoral, chemical, or mechanical factors (7,8).…”

Comparison of the Tei index with invasive measurements of right ventricular function

“…Hence, there was a low E wave (0.46 T 0.06 m/ s) and a high A wave (0.53 T 0.1 m/s), resulting in a lesser E / A ratio (0.9 T 0.27) ( P < 0.05). Hon et al, using a linear relation to describe the end-diastolic pressure -volume relationship, showed a highly significant increase in the chamber stiffness (b) (0.54 T 0.08 to 0.83 T 0.13 mm Hg ml À 1 ) with a slightly end-diastolic volume increase [34]. So that, although the slope of the end-diastolic pressurevolume relation increased significantly, there was probably no change in the position of the true non-linear/exponential fit of the end-diastolic pressure -volume relation.…”