Quantitative comparison of canine right and left ventricular isovolumic pressure waves

1987 ◽  
Vol 253 (2) ◽  
pp. H475-H479 ◽  
Author(s):  
D. Burkhoff ◽  
M. W. Kronenberg ◽  
D. T. Yue ◽  
W. L. Maughan ◽  
W. C. Hunter ◽  
...  
Keyword(s):  
Cardiac Cycle ◽  
Sampling Rate ◽  
Left Ventricular ◽  
Pressure Waves ◽  
Atrial Pacing ◽  
Maximum Value ◽  
Time Courses ◽  
Mean Square Difference ◽  
Developed Pressure ◽  
The Right

The mechanical properties of the right and left ventricles (RV and LV) have previously been studied separately. However, because of differences in RV and LV architecture, geometry, and muscle mass, it is not obvious how the properties of the two chambers would relate to each other. This study compared the time courses of RV and LV isovolumic pressure waves (LVP, RVP, respectively) measured simultaneously in the same heart. We compared RVP and LVP in each of five isolated, supported canine hearts after pentobarbital anesthesia. RV and LV volumes were varied independently so that on various beats peak LVP exceeded, equaled, or was less than peak RVP. There was a delay of approximately 35 ms between the onset of LV and RV pressure waves with atrial pacing, but only 5 ms with ventricular pacing. LVP and RVP were measured and digitized at a sampling rate of 200 Hz. Pressure waves were offset and rescaled by their respective amplitudes so that for each beat the pressure wave had a minimum value of 0% at end diastole and a maximum value of 100% at end systole. RVP was then shifted in time so that its upstroke was synchronous with that of the LVP at the point of 50% of maximal developed pressure. The rescaled, time-shifted RVP was plotted as a function of the rescaled LVP for each point of the cardiac cycle, and the relation between the two was quantified by their root mean square difference (Drms). Drms averaged 2.3 +/- 1.5% (SD) for the first half of contraction, 1.5 +/- 0.4% for the second half of contraction, and 4.6 +/- 1.6% during relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of responses of neonatal sinus and AV nodes to critically timed, brief vagal stimuli

1991 ◽  
Vol 260 (2) ◽  
pp. H459-H464 ◽  
Author(s):  
S. Yamasaki ◽  
A. Stolfi ◽  
A. S. Pickoff
Keyword(s):  
Cycle Length ◽  
Cardiac Cycle ◽  
Gradual Increase ◽  
Latency Period ◽  
Atrial Pacing ◽  
Response Curves ◽  
Stimulus Train ◽  
Sinus Cycle Length ◽  
The Right

We studied the responses of sinus cycle length and atrioventricular (AV) nodal conduction to brief, critically timed vagal stimuli in 25 neonatal (9.6 +/- 3.1 days) canines. Vagal stimuli were delivered to the right or left decentralized cervical vagosympathetic trunk as either a single, brief stimulus train or a repetitive, phase-coupled train with both stimulation paradigms programmed to scan the entire cardiac cycle. The effects of brief vagal stimuli on cardiac cycle length were measured while the heart was beating spontaneously, and the vagal effects on AV nodal conduction were measured while the cycle length was held constant by atrial pacing at 300 ms. Neither changes in sinus cycle length nor AV nodal conduction demonstrated classical phase dependency, i.e., a gradual increase in the magnitude of the vagal response as stimuli are delivered progressively later in the cardiac cycle until the latency period (that point in the cardiac cycle at which vagal stimulation no longer affects the next cardiac cycle) is reached. Phase-response curves (PRCs) to single and repetitive stimuli typically exhibited either a flat response or a small decrease in magnitude as the latency period of the PRC was approached. Thus the neonatal sinus and AV node PRCs exhibit a different configuration than that reported in the adult.

Influence of shock strength and timing on induction of ventricular arrhythmias in dogs

1988 ◽  
Vol 255 (4) ◽  
pp. H891-H901 ◽  
Author(s):  
N. Shibata ◽  
P. S. Chen ◽  
E. G. Dixon ◽  
P. D. Wolf ◽  
N. D. Danieley ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Atrial Pacing ◽  
Activation Patterns ◽  
T Wave ◽  
Vulnerable Period ◽  
Coupling Interval ◽  
Focal Pattern ◽  
Initial Activation ◽  
Left Ventricular Pacing ◽  
The Right

We delivered strong shocks via electrodes on the left ventricular apex and the right atrium in seven dogs during the T wave of atrial pacing while recordings were made from 56 epicardial electrodes. After shocks that induced arrhythmias were given, the earliest activation occurred in the middle of the ventricles for lower-energy shocks and in the base for higher-energy shocks. For shocks late in the vulnerable period, activation was recorded soon after the shock, whereas for shocks early in the vulnerable period activation was not recorded for a mean of 70 ms (+/- 17 ms SD) after the shock. We also gave 1-J shocks during right and left ventricular pacing. For shocks early in the vulnerable period, activation initiating fibrillation arose in a focal pattern from the paced region. For shocks during the midportion of the vulnerable period, fibrillation arose by two leading circle reentrant loops rotating in opposite directions, one on the left and the other on the right ventricle. For shocks at the end of the vulnerable period, the two reentrant loops fused on the side of the heart opposite the pacing site to again form a single focal activation pattern. Thus the initial activation patterns of arrhythmias initiated by shocks, the time from the shock until earliest postshock activation, and the site of earliest postshock activation are strongly influenced by the coupling interval and strength of the shock.

Electrical activation and mechanical asynchronism in the cardiac cycle of the dog

1959 ◽  
Vol 14 (3) ◽  
pp. 417-420 ◽  
Author(s):  
Philip Samet ◽  
William H. Bernstein ◽  
Robert S. Litwak ◽  
William H. Meyer ◽  
Louis Lemberg
Keyword(s):  
Left Ventricle ◽  
Isometric Contraction ◽  
Cardiac Cycle ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Electrical Activation ◽  
Qrs Complex ◽  
Simultaneous Registration ◽  
The Right ◽  
Premature Beats

Dissociation of electrical and mechanical asynchronism in the right and left ventricle of the dog has been studied by simultaneous registration of the precordial electrocardiogram and right and left ventricular pressure curves. Observations were made during sinus rhythm and during digitalis-induced ventricular premature beats with widened aberrant QRS complexes. Measurements were made of the time of onset of isometric contraction in the ventricles, relative to each other, and to the onset of the QRS complex. The results indicate that mechanical asynchronism in onset of isometric contraction is not a necessary consequence of the asynchronous electrical depolarization of ventricular premature systoles. Submitted on November 10, 1958

End-systolic pressure length relations of stunned right and left ventricles after inotropic stimulation

1993 ◽  
Vol 265 (6) ◽  
pp. H2099-H2109 ◽  
Author(s):  
R. Krams ◽  
L. K. Soei ◽  
E. O. McFalls ◽  
E. A. Winkler Prins ◽  
L. M. Sassen ◽  
...  
Keyword(s):  
Right Ventricle ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Segment Length ◽  
Atrial Pacing ◽  
Regression Equations ◽  
External Work ◽  
Left And Right ◽  
The Right

Regional end-systolic pressure-segment length relationships (ESPSLR) were used to compare the degree of right and left ventricular stunning induced by a 10-min occlusion of the left anterior descending coronary artery and the response to subsequent atrial pacing (50 beats/min above intrinsic heart rate) without and with dobutamine (2 micrograms.kg-1.min-1) in nine anesthetized open-chest pigs. From the ESPSLR, the slope (Ees) (at 100 mmHg for the left and 25 mmHg for the right ventricle) and the total area of the pressure-length relationship (PLA) were determined. From the latter, the distribution into external work (EW) and potential energy (PE) as well as the efficiency of energy transfer (EET = EW/PLA) were calculated. In both the stunned left and right ventricular myocardium Ees and EW were reduced according to the same linear regression equations (delta Ees = 0.7 Ees,baseline - 11.4, r2 = 0.86 and delta EW = 0.4 EWbaseline + 2.3, r2 = 0.67), where Ees,baseline and EWbaseline are Ees and EW at baseline, respectively. EET of the stunned left and right ventricular segments decreased as PLA remained unchanged, due to an increase in PE. EET decreased from 0.84 +/- 0.02 to 0.71 +/- 0.03 (P < 0.05) in the stunned right ventricular segment and from 0.71 +/- 0.02 to 0.44 +/- 0.03 (P < 0.05) in the stunned left ventricular segment. Atrial pacing did not affect EET with respect to stunning levels, whereas the additional infusion of dobutamine restored Ees, EW, and PE and consequently EET to baseline values. In conclusion, the right ventricle is susceptible to stunning. During atrial pacing the EET was lower than expected from the Ees, which could, in agreement with the time-varying elastance concept, be explained by an increase in afterload (a consequence of the decrease in stroke volume). Dobutamine not only increased Ees, EW, and EET but also restored the relationship between Ees and EET in both ventricular stunned segments.

scholarly journals Changes in regional myocardial volume during the cardiac cycle: implications for transmural blood flow and cardiac structure

2008 ◽  
Vol 295 (2) ◽  
pp. H610-H618 ◽  
Author(s):  
Hiroshi Ashikaga ◽  
Benjamin A. Coppola ◽  
Katrina G. Yamazaki ◽  
Francisco J. Villarreal ◽  
Jeffrey H. Omens ◽  
...  
Keyword(s):  
Blood Flow ◽  
Volume Change ◽  
Time Course ◽  
Cardiac Cycle ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Canine Heart ◽  
Spatiotemporal Resolution ◽  
Tissue Pressure

Although previous studies report a reduction in myocardial volume during systole, myocardial volume changes during the cardiac cycle have not been quantitatively analyzed with high spatiotemporal resolution. We studied the time course of myocardial volume in the anterior mid-left ventricular (LV) wall of normal canine heart in vivo ( n = 14) during atrial or LV pacing using transmurally implanted markers and biplane cineradiography (8 ms/frame). During atrial pacing, there was a significant transmural gradient in maximum volume decrease (4.1, 6.8, and 10.3% at subepi, midwall, and subendo layer, respectively, P = 0.002). The rate of myocardial volume increase during diastole was 4.7 ± 5.8, 6.8 ± 6.1, and 10.8 ± 7.7 ml·min−1·g−1, respectively, which is substantially larger than the average myocardial blood flow in the literature measured by the microsphere method (0.7–1.3 ml·min−1·g−1). In the early activated region during LV pacing, myocardial volume began to decrease before the LV pressure upstroke. We conclude that the volume change is greater than would be estimated from the known average transmural blood flow. This implies the existence of blood-filled spaces within the myocardium, which could communicate with the ventricular lumen. Our data in the early activated region also suggest that myocardial volume change is caused not by the intramyocardial tissue pressure but by direct impingement of the contracting myocytes on the microvasculature.

Distribution of fetal cardiac output: importance of pacemaker location

1976 ◽  
Vol 231 (1) ◽  
pp. 204-208 ◽  
Author(s):  
PT Pitlick ◽  
SE Kirkpatrick ◽  
WF Friedman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Left Atrial ◽  
Left Ventricular ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Foramen Ovale ◽  
Rate Versus ◽  
Left Ventricular Output ◽  
The Right

Important questions exist about the relative roles of changes in heart rate versus extent of myocardial shortening in regulating fetal cardiac output, because increases in heart rate created by left atrial pacing have been shown to increase right ventricular output and decrease left ventricular output. Since the pacemaker site could importantly influence foramen ovale flow and, hence, each ventricle's output, changes in individual ventricular outputs were examined when both the right and left atria were paced at a rate of 270 beats/min in five acute and in eight chronically instrumented fetal lamb studies. With pacing of either atrium, total cardiac output was unchanged compared to control values. However, the right ventricle contributed more to total cardiac output with left atrial pacing (73% acute, 65% chronic) than with right atrial pacing (51% acute, 57% chronic). Converse changes were observed in left atrial pacing (27% acute, 35% chronic) as compared to right atrial pacing (49% acute, 43% chronic). Thus the disparity that exists normally in the contributions of the right and left ventricles to total cardiac output is accentuated with left atrial pacing and minimized with right atrial pacing. Pressure measurements demonstrated changes in the atrial pressure relations that would be expected to alter flow across the foramen ovale depending on the chamber initially activated. Previous experimental differences can, therefore, be attributed to changes in the magnitude of shunting across the foramen ovale and depend on pacemaker location.

scholarly journals Time courses of central hemodynamics during rapid changes in posture

2014 ◽  
Vol 116 (9) ◽  
pp. 1182-1188 ◽  
Author(s):  
Patrik Sundblad ◽  
Jonas Spaak ◽  
Lennart Kaijser
Keyword(s):  
Left Ventricle ◽  
Stroke Volume ◽  
Pressure Difference ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Ventricular Filling Pressure ◽  
Leg Exercise ◽  
Time Courses ◽  
The Right ◽  
Ventricular Filling

Changes in posture cause blood volume redistribution, affecting cardiac filling and stroke volume (SV). We hypothesized that the time courses of ventricular filling would differ between the right and left ventricle during a rapid (2 s) tilt and that changes in right ventricular filling pressure would be more swift because of the direct coupling to the systemic circulation. We further hypothesized that the transient imbalance between right and left ventricular filling pressure would influence left ventricular SV changes. Right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP), left ventricular stroke volume, heart rate, and arterial pressure were recorded beat-by-beat during rapid tilts from supine to upright positions and back again, during rest and dynamic 100-W leg exercise. RAP changes had a faster time course than PCWP during down-tilts, both during rest and exercise (1 ± 1 vs. 6 ± 2 s and 2 ± 2 vs. 6 ± 2 s, respectively; P < 0.05). This discrepancy caused a transient decrease in the end-diastolic pressure difference between the right and left ventricle. The decreased pressure difference in diastole impeded left ventricular filling because of ventricular interdependence, causing SV to fall transiently. The mechanisms of ventricular interdependence were also involved in reverse during up-tilt, where SV was maintained for 2–3 s despite falling PCWP. Furthermore, the decrease in RAP during up-tilt in the resting condition was biphasic with an initial fast and a second slower component, which might suggest the effect of venous valves. This was not seen during dynamic leg exercise where blood pooling is prevented by the venous muscle pump.

Right ventricular TNF resistance during endotoxemia: the differential effects on ventricular function

2007 ◽  
Vol 293 (5) ◽  
pp. R1893-R1897 ◽  
Author(s):  
Troy A. Markel ◽  
Paul R. Crisostomo ◽  
Meijing Wang ◽  
Jeremy L. Herrmann ◽  
Aaron M. Abarbanell ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Ventricular Function ◽  
Ventricular Myocytes ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Endotoxin Exposure ◽  
Sprague Dawley Rats ◽  
Developed Pressure ◽  
The Right ◽  
Rv Function

Right and left ventricular myocytes originate from different cellular progenitors; however, it is unknown whether these cells differ in their response to endotoxemia. We hypothesized that 1) the percentage of endotoxemic functional depression within the right ventricle (RV) would be smaller than that of the left ventricle; and 2) that better RV function would correlate with lower levels of right ventricular TNF production. Adult Sprague-Dawley rats were divided into right and left control and endotoxin groups. Controls received vehicle, while endotoxin groups received LPS at 20 mg/kg ip. Hearts were excised either 2 or 6 h after injection. Hearts excised at 2 h were assayed for TNF, IL-6, TNF receptor 1 (TNFR1), TNFR2, and via ELISA, while hearts excised at 6 h were assayed via the Langendorff model. The percentage of cardiac functional depression, exhibited as developed pressure, contractility, and rate of relaxation (expressed as a percentage of control) was significantly smaller in right ventricles compared with left ventricles following endotoxin exposure. Tissue levels of TNF were significantly elevated in both right and left ventricles 2 h after endotoxin exposure, and right ventricular endotoxin groups expressed higher levels of TNF compared with their left ventricular counterparts. No significant differences in IL-6, TNFR1, or TNFR2 levels were noted between endotoxin-exposed ventricles. This is the first study to demonstrate that right and left ventricular function differs after endotoxin exposure.

Measurement of deformation of canine epicardium in vivo during cardiac cycle

1980 ◽  
Vol 239 (3) ◽  
pp. H432-H437 ◽  
Author(s):  
T. Arts ◽  
R. S. Reneman
Keyword(s):  
Magnetic Field ◽  
Cardiac Cycle ◽  
Experimental Situation ◽  
Accurate Method ◽  
Left Ventricular ◽  
Shear Angle ◽  
Left Ventricular Ejection ◽  
Natural Strain ◽  
The Right

A new accurate method to determine the deformation of the epicardial surface during the cardiac cycle in vivo is described. Epicardial deformation is determined by a circumferential strain, a base-to-apex strain, and a shear angle. In the measuring setup, one magnetic field-generating coil (MFGC) and two sensor coils are attached to the epicardium, thus forming an approximately right-angled triangle with the MFGC at the right-angled corner and the sides containing the right angle, parallel to the circumferential and base-to-apex direction, respectively. The MFGC generates a magnetic field that rotates around the axis of the coil. The strength of that field decreases with increasing distance. Both strains and the shear angle are derived from the amplitudes of the voltages induced in the sensor coils and their phase difference. In the experimental situation the accuracy of the measurement of strain and shear angle is +/- 0.005 and +/- 1 degree, respectively. The device has a frequency response of 100 Hz (-3 dB) and practically no zero drift. In four open-chest dogs during left ventricular ejection, circumferential natural strain, base-to-apex natural strain, and shear angle at the epicardium of the left ventricular free wall ranged from -0.06 to -0.13, from -0.02 to -0.08, and from 6.8 degrees to 11.5 degrees, respectively.

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