Sino-atrial node (SAN) function was evaluated in 46 patients, three of whom had the sick sinus syndrome. Patients were paced from the right atrium for 15 to 180 sec at rates of 90, 110, 130, and 150 beats/min. The rapid cessation of pacing was associated with suppression of the SAN at all paced rates and at all durations of pacing. The observed pause was terminated by a sinus beat in all instances. The duration of pacing had little influence on the duration of the observed pause. The pause increased as the pacing rate was increased until, at a rate of 150 beats/min, a marked decrease in the pause was noted. Atropine (1.5-3.0 mg iv) diminished but did not eliminate the SAN suppression. Subthreshold pacing did not suppress SAN function. Three patients with sick sinus syndrome had a greater degree of SAN suppression than normal patients (4732 ± 415 msec [SSS] M ± sem ; 1041 ± 56 msec for normal patients). The determination of the duration of the pause following cessation of atrial pacing provides a technique for recognition of abnormalities of SAN function.
Analysis of the passive pressure-volume filling curve of the left ventricle demonstrates that heart size and ventricular geometry exert major effects on the pressure-volume curve in the absence of changes in intrinsic muscle stiffness. Because the pressure-volume relationship is curvilinear, both quantitative and qualitative comparison of pressure-volume curves from different hearts is difficult. In the fresh isolated canine left ventricle, the pressure-volume relation was found to be almost perfectly exponential throughout a range of filling pressures from 5 to 30 mm Hg. Therefore, a precise linear and quantitative expression of the pressure-volume relation (dP/dV = aP + b) was developed ( r = 0.995). The effect of isolated changes in either initial ventricular volume (mean Aa = 3.1?) or ventricular geometry (mean Aa = 27.1%) upon the slope, or a constant of this function was small in comparison to changes induced by rigor mortis (mean Aa = 45^). It was concluded that the a constant was primarily affected by changes in left ventricular wall stiffness. In this manner, comparison of the pressure-volume relationship from different hearts is possible, and the contribution of changes in wall stiffness may be quantified. the ventricular P-V relationship. "Observed compliance," as determined by the ratio AV/AP, varies with the portion of the curve analyzed (9). In the range of normal ventricular filling pressure, the P-V curve is relatively flat, and therefore observed compliance is great. However, as ventricular filling pressure increases, the P-V curve becomes steeper, and observed compliance consequently decreases in the absence of any intrinsic change in muscle stiffness. It is thus impossible to compare P-V curves on the basis of the ratio AV/AP without specifying a discrete value for P. Any simple ratio of pressure to volume becomes inadequate, therefore, as an index of ventricular stiffness (10).Second, the stiffness of isolated muscle is only one of several determinants of the P-V relationship and overall ventricular compliance. Other factors-specifically, chamber size, geometry, and wall thickness-contribute to the final P-V relationship. Although these factors may remain relatively constant within
Thirty-one patients with symptomatic sinus node dysfunction were evaluated with electrocardiograms, Holter monitor recordings, exercise, isoproterenol infusions, atropine administration, Valsalva maneuvers, carotid sinus massage, and overdrive pacing. Four basic clinical subsets were recognized: (1) carotid sinus hypersensitivity (2) bradycardia-tachycardia syndrome, (3) episodic sinus arrest, and (4) persistent symptomatic sinus bradycardia. The study group demonstrated a normal heart rate response to exercise and isoproterenol infusion (%Δ = +95 exercise, +144 isoproterenol) in the face of diminished responsiveness to atropine administration (%Δ = +23). Marked carotid sinus hypersensitivity was demonstrated in eight patients, and four patients demonstrated slight abnormalities during performance of Valsalva maneuvers. Significant suppression of sinus node dysfunction was observed following atrial overdrive in the study group (postpacing pause = 3087 ± 464 msec) as compared to patients without significant sinus node function (postpacing pause = 1073 ± 63 msec) ( P < 0.001). In patients with intact V-A conduction, ventricular overdrive also resulted in sinus node suppression (postpacing pause = 1901 ± 357 msec). There was a marked decrease in the degree of sinus node depression following atropine administration. Ten of 31 patients demonstrated various degrees of A-V block following atrial pacing at rates less than 100 beats/min. It is concluded that the present methods of evaluation of sinus function, especially sinus node recovery time following overdrive pacing, may prove of value in the investigation of patients with syncope of unknown etiology.
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