Maximal negative dP/dt as an indicator of end of systole

1981 ◽  
Vol 240 (4) ◽  
pp. H676-H679 ◽  
Author(s):  
F. L. Abel
Keyword(s):  
Heart Rate ◽  
Correlation Coefficient ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Aortic Flow ◽  
Ventricular Pressure ◽  
First Derivative ◽  
Negative Peak ◽  
Anesthetized Dogs ◽  
Systolic Time

The maximal negative peak of the first derivative of left ventricular pressure was examined as an index of the end of ventricular ejection by comparing it with the end of aortic flow. Under varying heart rate and afterload situations in anesthetized dogs, a correlation coefficient of 0.982 was obtained with a mean error of less than 0.4 ms. This may be a useful end point for determining systolic time where only ventricular pressure is available.

Statistical analysis of effect of anoxia on rate of change of ventricular pressure

1982 ◽  
Vol 53 (3) ◽  
pp. 726-730 ◽  
Author(s):  
C. George ◽  
M. T. Kopetzky
Keyword(s):  
Heart Rate ◽  
Analysis Of Variance ◽  
Repeated Measures ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Aortic Flow ◽  
Ventricular Pressure ◽  
Ventricular Contractility ◽  
Sprague Dawley

Hearts from 32 male Sprague-Dawley rats were studied to determine effects of anoxia on ventricular contractility. Maximum rate of ventricular pressure changes with time (Pmax) were obtained from simultaneous recordings of right and left ventricular pressure curves. Peak aortic flow and heart rate were measured. Anoxia was produced by 100% N2 respiration. Statistical models were repeated-measures analysis of variance and randomized block factorial analysis of variance. Alpha was 0.05. Heart rate during anoxia was significantly lower than during the 1st min of recovery. Heart rate during both these periods was significantly lower than in preanoxia or the remainder of recovery. Peak aortic flow was not significantly altered. In left ventricles positive Pmax was significantly higher than negative Pmax. In right ventricles positive and negative Pmax were not significantly different. Left ventricular Pmax was significantly depressed during anoxia, whereas right ventricular Pmax was not. Significant differences in pressure developed per mass of tissue was a possible source of variation in right (0.12 +/- 0.002 mmHg/mg) and left (0.16 +/- 0.009 mmHg/mg) ventricular contractile maintenance.

scholarly journals Electrophysiological effects of right and left vagal nerve stimulation on the ventricular myocardium

2014 ◽  
Vol 307 (5) ◽  
pp. H722-H731 ◽  
Author(s):  
Kentaro Yamakawa ◽  
Eileen L. So ◽  
Pradeep S. Rajendran ◽  
Jonathan D. Hoang ◽  
Nupur Makkar ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nerve Stimulation ◽  
Regional Differences ◽  
Left Ventricular Pressure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Ventricular Pressure ◽  
Electrophysiological Effects

Vagal nerve stimulation (VNS) has been proposed as a cardioprotective intervention. However, regional ventricular electrophysiological effects of VNS are not well characterized. The purpose of this study was to evaluate effects of right and left VNS on electrophysiological properties of the ventricles and hemodynamic parameters. In Yorkshire pigs, a 56-electrode sock was used for epicardial ( n = 12) activation recovery interval (ARI) recordings and a 64-electrode catheter for endocardial ( n = 9) ARI recordings at baseline and during VNS. Hemodynamic recordings were obtained using a conductance catheter. Right and left VNS decreased heart rate (84 ± 5 to 71 ± 5 beats/min and 84 ± 4 to 73 ± 5 beats/min), left ventricular pressure (89 ± 9 to 77 ± 9 mmHg and 91 ± 9 to 83 ± 9 mmHg), and dP/d tmax (1,660 ± 154 to 1,490 ± 160 mmHg/s and 1,595 ± 155 to 1,416 ± 134 mmHg/s) and prolonged ARI (327 ± 18 to 350 ± 23 ms and 327 ± 16 to 347 ± 21 ms, P < 0.05 vs. baseline for all parameters and P = not significant for right VNS vs. left VNS). No anterior-posterior-lateral regional differences in the prolongation of ARI during right or left VNS were found. However, endocardial ARI prolonged more than epicardial ARI, and apical ARI prolonged more than basal ARI during both right and left VNS. Changes in dP/d tmax showed the strongest correlation with ventricular ARI effects ( R2 = 0.81, P < 0.0001) than either heart rate ( R2 = 0.58, P < 0.01) or left ventricular pressure ( R2 = 0.52, P < 0.05). Therefore, right and left VNS have similar effects on ventricular ARI, in contrast to sympathetic stimulation, which shows regional differences. The decrease in inotropy correlates best with ventricular electrophysiological effects.

Heart function after injection of small air bubbles in coronary artery of pigs

1993 ◽  
Vol 75 (3) ◽  
pp. 1201-1207 ◽  
Author(s):  
J. H. Van Blankenstein ◽  
C. J. Slager ◽  
J. C. Schuurbiers ◽  
S. Strikwerda ◽  
P. D. Verdouw
Keyword(s):  
Coronary Artery ◽  
Heart Function ◽  
Left Ventricular Pressure ◽  
Relative Increase ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Relative Reduction ◽  
Air Bubbles ◽  
First Derivative ◽  
A Minor

By its nature, vaporization of atherosclerotic plaques by laser irradiation or spark erosion may produce a substantial amount of gas. To evaluate the effect of gas embolism possibly caused by vaporization techniques, air bubbles with diameters of 75, 150, or 300 microns, each in a volume of 2 microliters/kg, were selectively injected subproximal in the left anterior descending coronary artery of seven anesthetized pigs (28 +/- 3 kg). Systemic hemodynamics such as heart rate, left ventricular pressure and its peak positive first derivative, and mean arterial pressure did not change after air injection, whereas there was a minor change in peak negative first derivative of left ventricular pressure. After injection of air bubbles there was a maximal relative reduction of systolic segment shortening (SS) in the myocardium supplied by the left anterior descending coronary artery of 27, 45, and 58% for 75-, 150-, and 300-microns bubbles, respectively, and a relative increase of postsystolic SS (PSS) of 148, 200, and 257% for 75-, 150-, and 300-microns bubbles, respectively. Recovery of SS and PSS started after 2 min and was completed after 10 min. A difference in SS and PSS changes between different bubble size injections could be demonstrated. From this study it is clear that depression of regional myocardial function after injection of air bubbles could pass unnoticed on the basis of global hemodynamic measurements.

Impairment of contraction increases sensitivity of epicardial lymph pressure for left ventricular pressure

1998 ◽  
Vol 274 (1) ◽  
pp. H187-H192 ◽  
Author(s):  
Jurgen W. G. E. Vanteeffelen ◽  
Daphne Merkus ◽  
Luc J. Bos ◽  
Isabelle Vergroesen ◽  
Jos A. E. Spaan
Keyword(s):  
Time Derivative ◽  
Left Ventricular Pressure ◽  
Relative Increase ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Ventricular Pressure ◽  
Local Contraction ◽  
Lymphatic Vasculature ◽  
Anesthetized Dogs ◽  
Lidocaine Administration

In the present study, cardiac contraction was regionally impaired to investigate the relationship between contractility [maximum first time derivative of left ventricular pressure (dPLV/d tmax)] and PLVon epicardial lymph pressure (Plymph) generation. Measurements were performed in open-chest anesthetized dogs under control conditions and while local contraction was abolished by intracoronary administration of lidocaine. Lidocaine significantly lowered dPLV/d tmaxand PLVpulse to 77 ± 9 (SD; n = 5) and 82 ± 5% of control, respectively, whereas Plymphpulse increased to 186 ± 101%. The relative increase of maximum Plymphto PLVrelated inversely to the change in dPLV/d tmaxafter lidocaine administration. Additional data were obtained when PLVwas transiently increased by constriction of the descending aorta. The ratio of pulse Plymphto PLVduring aortic clamping increased after lidocaine administration, from 0.063 ± 0.03 to 0.15 ± 0.09. The results suggest that transmission of PLVto the cardiac lymphatic vasculature is enhanced when regional contraction is impaired. These findings imply that during normal, unimpaired contraction lymph vessels are shielded from high systolic PLVby the myocardium itself.

scholarly journals Changes of left ventricular pressure-diameter-velocity relations by alterations of heart rate in conscious dogs.

1984 ◽  
Vol 48 (12) ◽  
pp. 1312-1321 ◽  
Author(s):  
MASUAKI FUJIYAMA ◽  
YOH-ICHIRO FURUTA ◽  
JUN MATSUMURA ◽  
AKIHIRO TANABE ◽  
JUN OHBAYASHI ◽  
...  
Keyword(s):  
Heart Rate ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Ventricular Pressure

Vagal stimulation decreases rate of left ventricular relaxation

1989 ◽  
Vol 256 (2) ◽  
pp. H428-H433 ◽  
Author(s):  
R. J. Henning ◽  
J. Cheng ◽  
M. N. Levy
Keyword(s):  
Vagal Stimulation ◽  
Left Ventricular Pressure ◽  
Pressure Change ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Maximal Rate ◽  
Left Ventricular Relaxation ◽  
Ventricular Relaxation ◽  
Anesthetized Dogs ◽  
Contraction And Relaxation

We determined the effects of vagal stimulation on the time constant (tau) of left ventricular isovolumic pressure decay and on the maximum rates of left ventricular pressure change (dP/dt) during contraction and relaxation in anesthetized dogs. In each dog, the atria were paced at a constant rate of 150 beats/min. We recorded left ventricular pressure waveforms in the absence (control) and in the presence of vagal stimulation at frequencies of 1, 2, and 3 Hz. During the control periods and during vagal stimulation at each frequency, we determined tau, the maximal rate of contraction, and the maximal rate of relaxation from left ventricular pressure waveforms recorded at medium (100 mmHg), high (130 mmHg), and low (73 mmHg) afterloads. Vagal stimulation at a frequency of 3 Hz increased tau by 23%. This effect of vagal stimulation on tau was most pronounced at the high afterload. Vagal stimulation at 3 Hz decreased the maximal rate of relaxation by 19%, but it decreased the maximal rate of contraction by only 8%. Thus vagal stimulation significantly decreased the rate of left ventricular relaxation and had a greater depressant effect on ventricular relaxation than on contraction.

Hemodynamic determinants of the maximal rate of rise of left ventricular pressure

1963 ◽  
Vol 205 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Andrew G. Wallace ◽  
N. Sheldon Skinner ◽  
Jere H. Mitchell
Keyword(s):  
Heart Rate ◽  
Diastolic Pressure ◽  
Complex Function ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Maximal Rate ◽  
Pressure Development ◽  
Ventricular Activation

The maximal rate of left ventricular pressure development (max. dp/dt) was measured in an areflexic preparation which permitted independent control of stroke volume, heart rate, and aortic pressure. Max. dp/dt increased as a result of elevating ventricular end-diastolic pressure. Elevating mean aortic pressure and increasing heart rate each resulted in a higher max. dp/dt without a change in ventricular end-diastolic pressure. Aortic diastolic pressure was shown to influence max. dp/dt in the absence of changes in ventricular end-diastolic pressure or contractility. Increasing contractility increased max. dp/dt while changing the manner of ventricular activation decreased max. dp/dt. These findings demonstrate that changes in max. dp/dt can and frequently do reflect changes in myocardial contractility. These data also indicate that max. dp/dt is a complex function, subject not only to extrinsically induced changes in contractility, but also to ventricular end-diastolic pressure, aortic diastolic pressure, the manner of ventricular activation, and intrinsic adjustments of contractility.

scholarly journals Why is the subendocardium more vulnerable to ischemia? A new paradigm

2011 ◽  
Vol 300 (3) ◽  
pp. H1090-H1100 ◽  
Author(s):  
Dotan Algranati ◽  
Ghassan S. Kassab ◽  
Yoram Lanir
Keyword(s):  
Heart Rate ◽  
Network Flow ◽  
Perfusion Pressure ◽  
Compressive Loading ◽  
Flow Simulation ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
New Paradigm ◽  
Vessel Wall Thickness

Myocardial ischemia is transmurally heterogeneous where the subendocardium is at higher risk. Stenosis induces reduced perfusion pressure, blood flow redistribution away from the subendocardium, and consequent subendocardial vulnerability. We propose that the flow redistribution stems from the higher compliance of the subendocardial vasculature. This new paradigm was tested using network flow simulation based on measured coronary anatomy, vessel flow and mechanics, and myocardium-vessel interactions. Flow redistribution was quantified by the relative change in the subendocardial-to-subepicardial perfusion ratio under a 60-mmHg perfusion pressure reduction. Myocardial contraction was found to induce the following: 1) more compressive loading and subsequent lower transvascular pressure in deeper vessels, 2) consequent higher compliance of the subendocardial vasculature, and 3) substantial flow redistribution, i.e., a 20% drop in the subendocardial-to-subepicardial flow ratio under the prescribed reduction in perfusion pressure. This flow redistribution was found to occur primarily because the vessel compliance is nonlinear (pressure dependent). The observed thinner subendocardial vessel walls were predicted to induce a higher compliance of the subendocardial vasculature and greater flow redistribution. Subendocardial perfusion was predicted to improve with a reduction of either heart rate or left ventricular pressure under low perfusion pressure. In conclusion, subendocardial vulnerability to a acute reduction in perfusion pressure stems primarily from differences in vascular compliance induced by transmural differences in both extravascular loading and vessel wall thickness. Subendocardial ischemia can be improved by a reduction of heart rate and left ventricular pressure.

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