Pattern of function of left ventricle of mammals

1965 ◽  
Vol 209 (1) ◽  
pp. 22-32 ◽  
Author(s):  
J. P. Holt ◽  
Helga Kines ◽  
E. A. Rhode
Keyword(s):  
Left Ventricle ◽  
Stroke Volume ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Limited Range ◽  
Left Ventricular ◽  
Elasticity Constant ◽  
Systolic Volume ◽  
Total Potential ◽  
Internal Volume

Since, over a limited range, rubber has elastic properties similar to contracted cardiac muscle, a method for determining the elasticity constant of rubber left ventricle models has been developed and used to determine the elasticity constant of the contracted mammalian left ventricle. Serial determinations of left ventricular end-systolic pressure, enddiastolic volume, end-systolic volume, and stroke volume were carried out following increased blood volume and stepwise hemorrhages in rabbits, dogs, swine, horses, and cattle. The end-systolic pressure-volume relationship of the ventricle of these animals was found to be similar to that of rubber ventricle models, hemiprolate spheroids, and thick-walled spheres; evidence is presented that the contracted left ventricle, and rubber models of it, function as an equivalent thick-walled sphere having the same wall mass and internal volume. From the linear relationship between "average" wall stress and "average" circumference, equations are derived relating chamber internal volume and: systolic pressure, total potential energy, and energy dissipated in ejection of the stroke volume.

Preload reserve and mechanisms of afterload mismatch in normal conscious dog

1986 ◽  
Vol 250 (3) ◽  
pp. H464-H473
Author(s):  
J. D. Lee ◽  
T. Tajimi ◽  
J. Patritti ◽  
J. Ross
Keyword(s):  
Stroke Volume ◽  
Venous Return ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Left Ventricular ◽  
Pressure Loading ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
Volume Load ◽  
Average Maximum

Preload reserve and mechanisms of afterload mismatch were examined in 10 normal conscious dogs. The left ventricular (LV) pressure, wall thickness, and external major and minor axis diameters (sonomicrometry) were measured during sinus rhythm, and beat-averaged pressure-volume loops were generated. With maximum angiotensin II infusion, LV end-diastolic volume (EDV) increased by 13 +/- 2% (SEM), LV peak pressure (LVSP) increased by 44 +/- 6%, and stroke volume decreased by 12 +/- 3% (P less than 0.01), demonstrating an apparent descending limb of LV performance. With volume load alone, EDV increased by 9 +/- 2% from control (P less than 0.01), and stroke volume increased by 13 +/- 2%; mean wall stress during ejection was not increased, and heart rate and end-systolic pressure-volume relations showed no changes. To test whether the descending limb of function was due to maximum use of preload reserve or to inadequate venous return, angiotensin infusion was repeated during volume load. The descending limb relating LVEDV to stroke volume was always shifted upward and to the right after volume load, and the stroke volume at a comparable wall stress was 12 +/- 3% higher than during control angiotensin infusion (P less than 0.01). During pressure loading plus volume loading, the maximum EDV increase was 16 +/- 2%, and assuming unchanged afterload and end-systolic volume, an average maximum stroke volume reserve of 31 +/- 4% is calculated. 1) We conclude that sizable preload and stroke volume reserves exist in the normal resting dog; and 2) we describe a mechanism for the descending limb of LV performance curves produced by pressure loading in the intact circulation, which is related to inadequate venous return.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

Dimensional analysis of the left ventricle: effects of acute aortic regurgitation

1975 ◽  
Vol 228 (2) ◽  
pp. 536-542 ◽  
Author(s):  
SJ Leshin ◽  
LD Horwitz ◽  
JH Mitchell
Keyword(s):  
Left Ventricle ◽  
Aortic Regurgitation ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Systolic Volume ◽  
Severe Aortic Regurgitation ◽  
End Diastolic Volume ◽  
Catheter Technique ◽  
End Systolic Volume

The effects of acute severe aortic regurgitation on the left ventricle were investigated in conscious, chronically instrumented dogs. Left ventricular dimensions and volumes were measured from biplane cineradiographs of beads positioned near the endocardium. Data were collected before and after the production of aortic regurgitation by a catheter technique. The aortic regurgitation resulted in increases in mean aortic pulse pressure from 44 to 73 mmHg (P smaller than 0.001), heart rate from 87 to 122 beats/min (P smaller than 0.02), and left ventricular end-diastolic pressure from 11 to 25 mmHg (P smaller than 0.05). Mean end-diastolic volume rose from 61 to 69 cc (P smaller than 0.001), while end-systolic volume remained unchanged at 37 cc. The end-diastolic dilatation following regurgitation was asymmetrical in that the increase in size was due principally to an increase in the septal-lateral axis. The acute volume load of aortic regurgitation was accomplished by an increase in end-diastolic volume, i.e., the Frank-Starling mechanism. The tachycardia probably reflects augmented cardiac sympathetic activity, but the constant end-systolic volume at a similar mean systolic pressure suggests that the net contractile state was unchanged.

Left ventricular dysfunction induced by chronic alcohol ingestion in rats

1991 ◽  
Vol 261 (1) ◽  
pp. H212-H219 ◽  
Author(s):  
J. M. Capasso ◽  
P. Li ◽  
G. Guideri ◽  
P. Anversa
Keyword(s):  
Left Ventricle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Longitudinal Axis ◽  
Left Ventricular ◽  
Experimental Animals ◽  
Chamber Volume ◽  
The Right ◽  
Myocyte Damage

To determine whether moderate ingestion of alcohol for protracted periods of time affects normal cardiac performance and produces myocyte damage, male Fischer 344 rats at 4 mo of age were given 30% ethanol in their drinking water every day for a period of 8 mo. Experimental animals and age-matched controls were examined hemodynamically and morphometrically at 12 mo of age. Body and cardiac growth were depressed in alcoholic animals by 15 and 12%, respectively. Although left ventricular (LV) weight was reduced by 14% in alcoholic rats, no difference in right ventricular (RV) weight was noted, and consequently the ratio of RV weight to body weight increased by 12%. Systemic arterial pressures as well as LV peak systolic pressure decreased in alcoholic rats despite an unchanged heart rate. Myocardial contractility in alcoholic rats was further depressed as revealed by a significant decrease in the peak rate of ventricular pressure decay. Importantly, end-diastolic pressure was elevated 5.2-fold in the left ventricle and 2.9-fold in the right ventricle after 8 mo of ethanol consumption. LV diastolic chamber volume increased through myocardial remodeling as the longitudinal axis and transverse diameters from the base to the apex increased in experimental animals while the thickness of the LV diminished. Structural and hemodynamic alterations resulted in a 571% increase in the volume of diastolic circumferential wall stress on the left ventricle. Damage to the myocardium was increased in alcoholic animals with the volume percent of myocardial lesions increasing 342% in the wall of the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial perfusion in compensated and failing hypertrophied left ventricle

1985 ◽  
Vol 249 (3) ◽  
pp. H534-H539 ◽  
Author(s):  
D. G. Parrish ◽  
W. S. Ring ◽  
R. J. Bache
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Systolic Pressure ◽  
Weight Ratio ◽  
Wall Stress ◽  
Left Ventricular ◽  
Ventricular Systolic Pressure ◽  
Ventricular Wall Thickness ◽  
Left Ventricular Systolic Pressure ◽  
Increased Blood Flow

This study examined blood flow in the hypertrophied left ventricle with and without failure. Left ventricular hypertrophy was produced in 20 dogs by banding the ascending aorta at 6-7 wk of age; studies were performed after animals reached adulthood. Sixteen dogs had compensated hypertrophy, while four dogs had cardiac failure manifested by left ventricular dilatation and end-diastolic pressures greater than 18 mmHg. The degree of hypertrophy, assessed by left ventricular-to-body weight ratio, was similar in animals with compensated hypertrophy (7.29 +/- 0.26 g/kg) and failure (8.45 +/- 0.15); both were greater than control (4.50 +/- 0.15, P less than 0.01). Left ventricular systolic pressure was similar in compensated hypertrophy (184 +/- 9 mmHg) and failure (226 +/- 29), as compared with control (130 +/- 4; P less than 0.01). Left ventricular blood flow measured with microspheres was 0.89 +/- 0.07 ml X min-1 X g-1 in control animals, was increased to 1.34 +/- 0.05 with compensated hypertrophy (P less than 0.001), and was further increased with failure to 1.86 +/- 0.40 (P less than 0.05). The left ventricular wall thickness-to-cavity diameter ratio was increased to 0.63 +/- 0.04 with compensated hypertrophy but was only 0.40 +/- 0.05 in dogs with failure (P less than 0.01), suggesting that wall stress was greater in hearts with failure. These data suggest that increased blood flow rates in dogs with failure resulted from increased myocardial O2 requirements due to increased systolic wall stress. Need for increased blood flow during resting conditions in dogs with failure would impair the ability for further coronary vasodilation during periods of cardiac stress.

scholarly journals 2363

2017 ◽  
Vol 1 (S1) ◽  
pp. 36-36
Author(s):  
Leo Buckley ◽  
Justin Canada ◽  
Salvatore Carbone ◽  
Cory Trankle ◽  
Michele Mattia Viscusi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Stroke Volume ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Volume Index ◽  
Stroke Work ◽  
Systolic Volume ◽  
Arterial Blood ◽  
End Systolic Volume

OBJECTIVES/SPECIFIC AIMS: Our goal was to compare the ventriculo-arterial coupling and left ventricular mechanical work of patients with systolic and diastolic heart failure (SHF and DHF). METHODS/STUDY POPULATION: Patients with New York Heart Association Functional Class II-III HF symptoms were included. SHF was defined as left ventricular (LV) ejection fraction<50% and DHF as >50%. Analysis of the fingertip arterial blood pressure tracing captured with a finger plethysmography cuff according to device-specific algorithms provided brachial artery blood pressure and stroke volume. LV end-systolic volume was measured separately via transthoracic echocardiography. Arterial elastance (Ea), a measure of pulsatile and nonpulsatile LV afterload, was calculated as LV end-systolic pressure (ESP)/end-diastolic volume. End-systolic elastance (Ees), a measure of load-independent LV contractility, was calculated as LV ESP/end-systolic volume. Ventriculo-arterial coupling (VAC) ratio was defined as Ea/Ees. Stroke work (SWI) was calculated as stroke volume index×LV end-systolic pressure×0.0136 and potential energy index (PEI) as 1/2×(LV end-systolic volume×LV end-systolic pressure×0.0136). Total work index (TWI) was the sum of SWI+PEI. RESULTS/ANTICIPATED RESULTS: Patients with SHF (n=52) and DHF (n=29) were evaluated. Median (IQR) age was 57 (51–64) years. There were 48 (58%) and 59 (71%) patients were male and African American, respectively. Cardiac index was 2.8 (2.2–3.2) L/minute and 3.0 (2.8–3.3) L/minute in SHF and DHF, respectively (p=0.12). Self-reported activity levels (Duke Activity Status Index, p=0.48) and heart failure symptoms (Minnesota Living with Heart Failure Questionnaire, p=0.55) were not different between SHF and DHF. Ea was significantly lower in DHF compared with SHF patients [1.3 (1.2–1.6) vs. 1.7 (1.4–2.0) mmHg; p<0.001] whereas Ees was higher in DHF vs. SHF [2.8 (2.1–3.1) vs. 0.9 (0.7-1.3) mmHg; p<0.001). VAC was 1.8 (1.3–2.8) in SHF Versus 0.5 (0.4–0.7) in DHF (p<0.001). Compared with SHF, DHF patients had higher SWI [71 (57–83) vs. 48 (39–68) gm×m; p<0.001) and lower PEI [19 (12–26) vs. 44 (36–57) gm×m; p<0.001]. TWI did not differ between SHF and DHF (p=0.14). Work efficiency was higher in DHF than SHF [0.80 (0.74–0.84) vs. 0.53 (0.46–0.64); p<0.001]. DISCUSSION/SIGNIFICANCE OF IMPACT: The results underscore the differences in pathophysiology between SHF and DHF patients with similar symptom burden and exercise capacity. These results highlight the difference in myocardial energy utilization between SHF and DHF.

scholarly journals Mechanically Unloading the Left Ventricle Before Coronary Reperfusion Reduces Left Ventricular Wall Stress and Myocardial Infarct Size

Circulation ◽  
2013 ◽  
Vol 128 (4) ◽  
pp. 328-336 ◽  
Author(s):  
Navin K. Kapur ◽  
Vikram Paruchuri ◽  
Jose Angel Urbano-Morales ◽  
Emily E. Mackey ◽  
Gerard H. Daly ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Wall Stress ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Myocardial Infarct Size ◽  
Ventricular Wall ◽  
Coronary Reperfusion

Use of the Frank-Starling mechanism during submaximal versus maximal upright exercise

1986 ◽  
Vol 251 (6) ◽  
pp. H1101-H1105 ◽  
Author(s):  
G. D. Plotnick ◽  
L. C. Becker ◽  
M. L. Fisher ◽  
G. Gerstenblith ◽  
D. G. Renlund ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Blood Pool ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Vigorous Exercise ◽  
Systolic Volume ◽  
Early Exercise ◽  
End Diastolic Volume ◽  
Blood Pool Scintigraphy ◽  
End Systolic Volume

To evaluate the extent to which the Frank-Starling mechanism is utilized during successive stages of vigorous upright exercise, absolute left ventricular end-diastolic volume and ejection fraction were determined by gated blood pool scintigraphy at rest and during multilevel maximal upright bicycle exercise in 30 normal males aged 26-50 yr, who were able to exercise to 125 W or greater. Left ventricular end-systolic volume, stroke volume, and cardiac output were calculated at rest and during each successive 3-min stage of exercise [25, 50, 75, 100, and 125–225 W (peak)]. During early exercise (25 W), end-diastolic and stroke volumes increased (+17 +/- 1 and +31 +/- 4%, respectively), with no change in end-systolic volume. With further exercise (50–75 W) end-diastolic volume remained unchanged as end-systolic volume decreased (-12 +/- 4 and -24 + 5%, respectively). At peak exercise end-diastolic volume decreased to resting level, stroke volume remained at a plateau, and end-systolic volume further decreased (-48 +/- 7%). Thus the Frank-Starling mechanism is used early in exercise, perhaps because of a delay in sympathetic mobilization, and does not appear to play a role in the later stages of vigorous exercise.

Biplane ventriculography in the rat

1986 ◽  
Vol 250 (1) ◽  
pp. H131-H136
Author(s):  
J. L. Heckman ◽  
L. Garvin ◽  
T. Brown ◽  
W. Stevenson-Smith ◽  
W. P. Santamore ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Methyl Methacrylate ◽  
High Speed ◽  
Water Displacement ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume

Biplane ventriculography was performed on nine intact anesthetized rats. Images of the left ventricle large enough for analysis were obtained by placing the rats close to the radiographic tubes (direct enlargement). Sampling rates, adequate for heart rates of 500 beats/min, were obtained by filming at 500 frames/s. From the digitized silhouettes of the left ventricle the following information was obtained (means +/- SE): end-diastolic volume 0.60 +/- 0.03 ml, end-systolic volume 0.22 +/- 0.02 ml, stroke volume 0.38 +/- 0.02 ml, ejection fraction 0.63 +/- 0.02, cardiac output 118 +/- 7 ml/min, diastolic septolateral dimension 0.41 +/- 0.01 mm, diastolic anteroposterior dimension 0.40 +/- 0.01 mm, diastolic base-to-apex dimension 1.58 +/- 0.04 mm. To determine the accuracy with which the volume of the ventricle could be measured, 11 methyl methacrylate casts of the left ventricle were made. The correlation was high (r = 0.99 +/- 0.02 ml E) between the cast volumes determined by water displacement and by use of two monoplane methods (Simpson's rule of integration and the area-length method applied to the analysis of the anteroposterior films) and a biplane method (area-length). These results demonstrate that it is possible to obtain accurate dimensions and volumes of the rat left ventricle by use of high-speed ventriculography.

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