Studies on the First Derivative of the Ventricular Pressure Pulse in Man

Abstract

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 catecholamine infusions on myocardial blood flow, metabolic heat production and on general haemodynamics, before and after alprenolol (H56/28), in anaesthetized cats

“…It was of interest to see whether this conclusion applied also to the heart in vivo. In fact, and as Gleason & Braunwald (1962) have demonstrated in man, there was a fairly good correlation between peak ventricular systolic pressure and dp/dt in the control animals and in those given isoprenaline, both before and after alprenolol (Fig. 12).…”

“…566 *.U".L rate of rise of the left ventricular pressure pulse (dp /dt), as suggested by Hamacher (1960Hamacher ( , 1963 and by Benfey, Greeff & Heeg (1967). The validity of this method has been reviewed by Gleason & Braunwald (1962), Wallace, Skinner & Mitchell (1963) and by Schaper, Lewi & Jageneau (1965). Provided LVEDP is adequately monitored, dp/dt max is a useful index of cardiac contractility which can be used in closed-chest, spontaneously breathing, preparations.…”

Efeitos do pós-condicionamento isquêmico na função ventricular esquerda de corações isolados de ratos

“…during periods of induced ischemia, that was maintained at zero. The effects on myocardial contractility and left ventricle relaxation was measured by calculating the first positive temporal derivative (+dP/dt max ) [12] and negative (-dP/dt max ) [13] of the left ventricular pressure, from measures obtained from the ventricular pressure curves, according to the method described by Gottschall [14].…”

Interleukin-6/soluble interleukin-6 receptor complex reduces infarct size via inhibiting myocardial apoptosis

“…Since LV dP/dt is very sensitive to inotrophic changes, it is considered to be a good marker which reflects LV function. [36][37][38] As shown in Table 3, trends towards higher positive dP/dt and negative dP/dt were observed at 30 min after occlusion and at 30 min after reperfusion in IL-6/sIL-6 complex group; however, these differences did not reach statistical significance.…”