The rate at which the ventricular pressure rises has been of interest to investigators for many years (1, 2). Wiggers demonstrated that when ventricular end-diastolic filling pressure was elevated by increasing the venous return to the heart or the resistance to ventricular ejection, the rate of rise of ventricular pressure also increased (3). When epinephrine (4) or digitalis (5) was administered the rate of pressure rise increased despite a fall in ventricular end-diastolic pressure. Conversely, when myocardial ischemia was induced, the slope of the ventricular pressure rise decreased in the face of a rising end-diastolic pressure (6). More recently, although further observations have been made in the dog on the determinants of the slope of the ventricular pressure pulse (7-11), there have been no systematic studies of the effects of physiologic stresses, pharmacologic agents, and various types of heart disease on the slope of the ventricular pressure pulse in man. Accurate determinations of the instantaneous rate of ventricular pressure change in intact human subjects have been prevented by the technical limitations imposed by the pressure-recording systems that are usually employed in cardiac catheterization. These systems, which consist of a fluid-filled catheter and an external manometer, have a very limited range in which the frequency response is uniform (usually to less than 15 cycles per second) and they are subject to frequent artifacts related to motion of the catheter within the heart. Such artifacts may be manifest as sudden changes in pressure and will therefore be greatly exaggerated when their first derivative is computed. These difficulties have been largely eliminated by obtaining the ventricular pressure tracings with a catheter that has a high-frequency micromanometer mounted at its tip, or by direct needle puncture of the ventricle. METHODS Percutaneous puncture of the left ventricle was carried out by the method of Brock, Milstein and Ross (12) as modified in this laboratory (13). All such tracings were obtained with a 3.5-inch no. 19 or 20 gage thin-walled needle attached directly to a Statham P23D pressure transducer without intervening tubing. All other studies from either the left or right ventricle were carried out with a Telco intracardiac manometer 1 (14, 15). This instrument consists of a double-lumen catheter, one lu-men of which carries the electrical connection to the micromanometer mounted at the tip, the other serving as a conventional fluid-filled catheter system which is attached to a Statham P23D manometer. The sensitivities of the micromanometer and the external manometer were equalized with an air-pressure calibrating system prior to the introduction of the catheter into the heart. The catheter tip was placed in the right or left ventricle and simultaneous pressure pulses were recorded from the two manometers. The baseline for the micromanometer was made equal to that of the external manometer by superimposing the diastolic portions of the two ventricu-lar pressure pulses...

The effect of heart rate on cardiac output and associated rate induced hemodynamic changes in dogs with chronic heart block is presented and discussed. At heart rates below 60/min., the stroke volume was maximum and relatively constant, and the cardiac output was largely rate-dependent. These relationships did not exist at ventricular rates above 60/min. Cinefluorographic evidence of decreased diastolic ventricular filling with increasing ventricular rates is presented. At very slow and very fast ventricular rates, the cardiac output decreased despite an increase in right atrial and right ventricular end-diastolic pressure. At slow rates the decreased output was due to rate alone, while at rapid rates it was attributed to the decreased diastolic filling period and resistance to ventricular distention, resulting in decreased diastolic filling.

The applicability of Starling's law of the heart to the circulation of intact human subjects was studied by means of serial biplane angiocardiography utilizing injections into the left ventricle in nine patients, four of whom were unanesthetized. The end-diastolic and end-systolic volumes of the left ventricle were determined from the angiocardiograms by the method described by Dodge, and stroke volumes were calculated by subtracting the end-systolic from the end-diastolic volumes. In four patients large beat-to-beat variations in left ventricular end-diastolic volume occurred. These were accompanied by changes in stroke volume which varied directly with the preceding left ventricular end-diastolic volume. In four patients the left ventricular end-diastolic volume remained about constant, and in these patients the stroke volume showed little or no change. From these observations it was concluded that the ventricular stroke volume is a function of the end-diastolic volume and that therefore Starling's law of the heart is applicable to man. In the ninth patient pulsus alternans occurred; this was accompanied by concordant alternation of the left ventricular end-diastolic volume; i.e., the larger end-diastolic volumes resulted in larger stroke volumes and higher systolic pressures than did the smaller end-diastolic volumes. These observations are compatible with the concept that alternation of ventricular contraction can be explained by alternation of end-diastolic volume.

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