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Alterations of right ventricular systolic time intervals by chronic pressure and volume overloading

Right ventricular (RV) systolic time intervals and hemodynamic parameters were determined by micromanometric techniques in 13 subjects with normal right ventricles (NRV). These data were compared to those of 16 patients with pulmonary hypertension (PH) or predominant pressure overloading and 13 indi...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1976-06, Vol.53 (6), p.997-1003
Main Authors: Curtiss, E I, Reddy, P S, O'Toole, J D, Shaver, J A
Format: Article
Language:English
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Summary:Right ventricular (RV) systolic time intervals and hemodynamic parameters were determined by micromanometric techniques in 13 subjects with normal right ventricles (NRV). These data were compared to those of 16 patients with pulmonary hypertension (PH) or predominant pressure overloading and 13 individuals with uncomplicated secundum atrial septal defects (ASD) or predominant volume overloading. In PH, the QP2 interval tends to remain within the normal range due to reciprocal changes in isovolumic contraction (ICT) and ejection (RVET) times. Elevations of pulmonary artery diastolic pressure are associated with increases in the mean rate of isovolumic pressure rise (MRIPR) (r = 0.84), but the latter change does not fully compensate for the widened ventriculoarterial diastolic pressure difference and ICT becomes prolonged (P less than 0.001). Factors other than stroke index depression which may contribute to the decreased duration of RVET (P less than 0.001) include tricuspid regurgitation and elevation of pulmonary vascular impedance. In ASD, QP2 is significantly prolonged (P less than 0.025) due to a significant increase in RVET (P less than 0.005). In contrast to NRV, a linear correlation of RVET and stroke index was not present, which suggested an alteration of ejection dynamics in this group. Despite a high incidence of complete or incomplete right bundle branch block the interval from QRS onset to rapid RV pressure upstroke was not prolonged. This is most probably the result of peripheral bundle branch block of genesis of the QRS pattern by right ventricular hypertrophy.
ISSN:0009-7322
1524-4539
DOI:10.1161/01.cir.53.6.997