Dlastolic Pressure-Volume Relationship in the Canine Left Ventricle
Journal - Circulation Research
Analysis of the passive pressure-volume filling curve of theleft ventricle demonstrates that heart size and ventriculargeometry exert major effects on the pressure-volume curve inthe absence of changes in intrinsic muscle stiffness. Becausethe pressure-volume relationship is curvilinear, both quantitativeand qualitative comparison of pressure-volume curves from differenthearts is difficult. In the fresh isolated canine left ventricle,the pressure-volume relation was found to be almost perfectlyexponential throughout a range of filling pressures from 5 to30 mm Hg. Therefore, a precise linear and quantitative expressionof the pressure-volume relation (dP/dV=aP+b) was developed (r=0.995).The effect of isolated changes in either initial ventricularvolume (mean a=3.1%) or ventricular geometry (mean a=27.1%)upon the slope, or a constant of this function was small incomparison to changes induced by rigor mortis (mean a =45%).It was concluded that the a constant was primarily affectedby changes in left ventricular wall stiffness. In this manner,comparison of the pressure-volume relationship from differenthearts is possible, and the contribution of changes in wallstiffness may be quantified.
|Keywords : ||compliance • ventricular geometry • ventricular volume • ventricular wall stiffness • ventricular end-diastolic pressure • rigor mortis • passive elastic modulus|
Journal - Circulation
His bundle recordings were obtained in three patients withhistories of recurrent supraventricular tachycardias and electrocardiogramsdemonstrating a short P-R interval with a normal QRS (the Lown-Ganong-Levinesyndrome). The His bundle electrograms obtained during sinusrhythm demonstrated a normal A-H (atrium-to-His bundle) timein one patient and a low normal A-H time in two patients. TheH-V (His bundle-to-ventricle) time was short in all three patients.Atrial pacing in two patients produced an attenuated degreeof prolongation of the A-H time without a change in conductiondistal to the proximal His bundle. The probable mechanisms ofaccelerated conduction in these three patients include: (1)partial A-V nodal bypass via (a) the posterior intenodal tractor (b) functional bypass fibers within the A-V node; and (2)accelerated conduction within the A-V conduction system distalto the A-V node.
|Keywords : ||Accelerated conduction • Arrhythmias • Posterior internodal tract • Right bundle branch • A-V node • Paraspecific fibers|