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.

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.

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.

Left ventricular-arterial coupling in conscious dogs

1991 ◽  
Vol 261 (1) ◽  
pp. H70-H76 ◽  
Author(s):  
W. C. Little ◽  
C. P. Cheng
Keyword(s):  
Stroke Volume ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Conscious Dogs ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Inotropic State ◽  
End Diastolic Volume ◽  
Wide Range

We investigated the criteria for the coupling of the left ventricle (LV) and the arterial system to maximize LV stroke work (SW) and the transformation of LV pressure-volume area (PVA) to SW. We studied eight conscious dogs that were instrumented to measure LV pressure and determine LV volume from three ultrasonically determined dimensions. The LV end-systolic pressure (PES)-volume (VES) relation was determined by caval occlusion. Its slope (EES) was compared with the arterial elastance (EA) and determined as PES per stroke volume. At rest, with intact reflexes, EES/EA was 0.96 +/- 0.20 EES/EA was varied over a wide range (0.18-2.59) by the infusion of graded doses of phenylephrine and nitroprusside before and during administration of dobutamine. Maximum LV SW, at constant inotropic state and end-diastolic volume (VED), occurred when EES/EA equaled 0.99 +/- 0.15. At constant VED and contractile state, SW was within 20% of its maximum value when EES/EA was between 0.56 and 2.29. The conversion of LV PVA to SW increased as EES/EA increased. The shape of the observed relations of the SW to EES/EA and SW/PVA to EES/EA was similar to that predicted by the theoretical consideration of LV PES-VES and arterial PES-stroke volume relations. We conclude that the LV and arterial system produce maximum SW at constant VED when EES and EA are equal; however, the relation of SW to EES/EA has a broad plateau. Only when EA greatly exceeds EES does the SW fall substantially. However, the conversion of PVA to SW increases as EES/EA increases. These observations support the utility of analyzing LV-arterial coupling in the pressure-volume plane.

Comparison of left ventricular volumes by dye dilution and angiographic methods in the dog

1963 ◽  
Vol 204 (3) ◽  
pp. 446-450 ◽  
Author(s):  
Franz J. Hallermann ◽  
G. C. Rastelli ◽  
H. J. C. Swan
Keyword(s):  
Stroke Volume ◽  
Left Ventricular ◽  
Dilution Method ◽  
Left Ventricular Volumes ◽  
Heart Rates ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
Fundamental Error ◽  
Indicator Dye

In each of 12 mongrel dogs, data for end-diastolic volume, end-systolic volume, and stroke volume of the left ventricle were obtained by two independent methods: the indicator dilution method and a radiographic method. While the values for stroke volume showed good agreement between the two methods, a significant and directionally constant difference was found between values for end-diastolic volume and end-systolic volume calculated by the two different methods. This was observed in dogs with fast heart rates (exceeding 150 beats/min), as well as in dogs with heart rates of about 100 beats/min. The findings strongly suggest that a fundamental error is present in estimations of volume based on the washout of an indicator dye.

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.

Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans

1997 ◽  
Vol 83 (3) ◽  
pp. 712-717 ◽  
Author(s):  
Antonio C. L. Nóbrega ◽  
Jon W. Williamson ◽  
Jorge A. Garcia ◽  
Jere H. Mitchell
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Knee Extension ◽  
Left Ventricular ◽  
Voluntary Contraction ◽  
Peak Exercise ◽  
Ventricular Contractility ◽  
Static Exercise ◽  
Systolic Volume ◽  
End Diastolic Volume

Nóbrega, Antonio C. L., Jon W. Williamson, Jorge A. Garcia, and Jere H. Mitchell. Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans. J. Appl. Physiol. 83(3): 712–717, 1997.—Ten patients with preserved inotropic function having a dual-chamber (right atrium and right ventricle) pacemaker placed for complete heart block were studied. They performed static one-legged knee extension at 20% of their maximal voluntary contraction for 5 min during three conditions: 1) atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HR fixed at the resting value (DOO-Rest; 73 ± 3 beats/min), and 3) HR fixed at peak exercise rate (DOO-Ex; 107 ± 4 beats/min). During control exercise (DDD mode), mean arterial pressure (MAP) increased by 25 mmHg with no change in stroke volume (SV) or systemic vascular resistance. During DOO-Rest and DOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of a SV-dependent increase in cardiac output (+1.3 and +1.8 l/min, respectively). The increase in SV during DOO-Rest utilized a combination of increased contractility and the Frank-Starling mechanism (end-diastolic volume 118–136 ml). However, during DOO-Ex, a greater left ventricular contractility (end-systolic volume 55–38 ml) mediated the increase in SV.

Effect of vasopressin on left ventricular performance

1993 ◽  
Vol 264 (1) ◽  
pp. H53-H60
Author(s):  
C. P. Cheng ◽  
Y. Igarashi ◽  
H. S. Klopfenstein ◽  
R. J. Applegate ◽  
Z. Shihabi ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Ventricular Performance ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
The Right

We assessed the effect of arginine vasopressin (AVP) on left ventricular (LV) performance in eight conscious dogs. Five minutes after AVP infusion (6 microns.kg-1 x min-1 for 2 min) the plasma AVP was elevated from 3.9 +/- 0.9 to 14.7 +/- 4.6 pg/ml (P < 0.05). With all reflexes intact, AVP caused significant increases in LV end-systolic pressure (P) (112 +/- 8 vs. 122 +/- 7 mmHg, P < 0.05) end-systolic volume (V) (30 +/- 5.8 vs. 38 +/- 7.7 ml, P < 0.05), total systemic resistance (6.2 +/- 1.8 vs. 10.6 +/- 4.0 mmHg.dl-1 x min, P < 0.01) and arterial elastance (Ea) (6.8 +/- 3.0 vs. 8.6 +/- 3.9 mmHg/ml, P < 0.05), while the heart rate (110 +/- 6 vs. 82 +/- 10 beats/min, P < 0.05) and stroke volume (16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml, P < 0.05) were decreased. There was no significant change in the coronary sinus blood flow (82 +/- 19 vs. 78 +/- 22 ml/min, P = not significant). AVP decreased the slopes of LV end-systolic P-V relation (10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml, P < 0.05), the maximal first derivative of LV pressure (dP/dtmax)-end-diastolic volume (VED) relation (135.2 +/- 18.7 vs. 63.1 +/- 7.7 mmHg.s-1 x ml-1, P < 0.05), and the stroke work-VED relation (81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg, P < 0.05) and shifted the relations to the right, indicating a depression of LV performance. A similar increase in Ea produced by methoxamine did not depress LV performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Ejecting deactivation does not affect O2 consumption-pressure-volume area relation in dog hearts

1993 ◽  
Vol 265 (3) ◽  
pp. H934-H942 ◽  
Author(s):  
O. Kawaguchi ◽  
Y. Goto ◽  
S. Futaki ◽  
Y. Ohgoshi ◽  
H. Yaku ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Generation Process ◽  
Ejection Velocity ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume

We studied the effects of ejection velocity and resistive properties of the left ventricle (LV) on myocardial oxygen consumption (VO2) in 13 excised cross-circulated dog hearts. Increases in peak ejection velocity (-dV/dt) from 4.0 +/- 1.3 (SD) end-diastolic volume (EDV)/s to 12.7 +/- 5.3 EDV/s with constant EDV and end-systolic volume (velocity run) induced systolic pressure deficit. This decreased pressure-volume area (PVA; a measure of ventricular mechanical energy) and LV end-systolic elastance (Emax) by 47 +/- 14 and 38 +/- 15%, respectively. Unchanged maximum rate of left ventricular pressure rise and time-varying elastance during the isovolumic contraction period at the same EDV indicated that these contractions started with the same contractile state although the quicker ejection caused the greater deactivation. If the PVA deficit due to systolic pressure deficit is attributable to an internal energy-dissipating resistive element, VO2 in the velocity run will not as much decrease in proportion to PVA as in the isovolumic or slowly ejecting control run. However, the decreases in PVA due to increased -dV/dt decreased VO2 to the same extent as in the control run. This result negated the possibility that the pressure and PVA deficits would be caused by a mechanical energy-losing process. The same results were obtained whether or not Emax was decreased by quick ejection. We conclude that the pressure and PVA deficits and the proportionally decreased VO2 during quick ejection are mainly attributable to suppression of a ventricular mechanical energy generation process, but not of mechanical energy-losing process, by ejecting deactivation.

Cardiac performance: independence of adrenergic inotropic and chronotropic effects

1978 ◽  
Vol 234 (5) ◽  
pp. H525-H532
Author(s):  
A. Ilebekk ◽  
J. Lekven ◽  
F. Kiil
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Right Atrial ◽  
Diastolic Filling ◽  
Atrial Pacing ◽  
Heart Rates ◽  
Systolic Volume ◽  
End Diastolic Volume

During right atrial pacing in open-chest anesthetized dogs, the relationships between reduction in stroke volume and rise in heart rate were identical in control experiments, during intravenous infusion of isoproterenol, and after blockade of adrenergic beta-receptors by propranolol. To examine the mechanism of this constant relationship, left ventricular volume was estimated by continuous recordings of myocardial chord length (MCL) between ultrasonic elements inserted into the anterior ventricular wall. Diastolic filling curves were curtailed by raising heart rate and end-diastolic MCL was reduced. At constant heart rate, end-diastolic MCL was not altered by isoproterenol infusion, except for a slight rise at heart rates exceeding 220 beats/min. End-systolic MCL, however, was reduced, accounting for larger stroke volume during isoproterenol than during propranolol infusion. The reduction in end-systolic MCL was constant at all heart rates examined. Hence, chronotropic changes influence end-diastolic volume and inotropic changes influence end-systolic volume; their effects on stroke volume regulation are, therefore, virtually independent.

scholarly journals Cardiac structure and function in schizophrenia: a cardiac MR imaging study

2019 ◽  
Author(s):  
Emanuele F. Osimo ◽  
Stefan P. Brugger ◽  
Antonio de Marvao ◽  
Toby Pillinger ◽  
Thomas Whitehurst ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Imaging Study ◽  
Left Ventricular ◽  
Structure And Function ◽  
Cardiac Structure ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
Cardiac Structure And Function ◽  
And Function

AbstractBackgroundHeart disease is the leading cause of death in schizophrenia.AimsWe investigated cardiac structure and function in patients with schizophrenia using cardiac magnetic resonance imaging (CMR) after excluding medical and metabolic comorbidity.Methods80 participants underwent CMR to determine biventricular volumes and function and measures of blood pressure, physical activity, and glycated haemoglobin levels. Patients and controls were matched for age, sex, ethnicity, and body surface area.ResultsPatients with schizophrenia had significantly smaller indexed left ventricular (LV) end-diastolic volume, end-systolic volume, stroke volume, right ventricular (RV) end-diastolic volume, end-systolic volume, and stroke volume but unaltered ejection fractions relative to controls. LV concentricity and septal thickness were significantly larger in schizophrenia. The findings were largely unchanged after adjusting for smoking or exercise levels and were independent of medication dose and duration.ConclusionsPatients with schizophrenia show evidence of prognostically-adverse cardiac remodelling compared to matched controls, independent of conventional risk factors.

Sign in / Sign up

Export Citation Format

Share Document