Cardiac output by MR imaging: An experimental study comparing right ventricle and left ventricle with thermodilution

1989 ◽  
Vol 13 (2) ◽  
pp. 172
Keyword(s):  
Experimental Study ◽  
Cardiac Output ◽  
Left Ventricle ◽  
Mr Imaging ◽  
Right Ventricle

Concomitant Pulsatile and Continuous Flow VAD in Biventricular and Univentricular Physiology: A Comparison Study with a Numerical Model

2017 ◽  
Vol 40 (2) ◽  
pp. 74-81 ◽  
Author(s):  
Arianna Di Molfetta ◽  
Gianfranco Ferrari ◽  
Roberta Iacobelli ◽  
Sergio Filippelli ◽  
Paolo Guccione ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Numerical Model ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Continuous Flow ◽  
Single Ventricle ◽  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Fontan Physiology ◽  
The Right

Introduction To develop and test a lumped parameter model to simulate and compare the effects of the simultaneous use of continuous flow (CF) and pulsatile flow (PF) ventricular assist devices (VADs) to assist biventricular circulation vs. single ventricle circulation in pediatrics. Methods Baseline data of 5 patients with biventricular circulation eligible for LVAD and of 5 patients with Fontan physiology were retrospectively collected and used to simulate patient baselines. Then, for each patient the following simulations were performed: (a) CF VAD to assist the left ventricle (single ventricle) + a PF VAD to assist the right ventricle (cavo-pulmonary connection) (LCF + RPF); (b) PF VAD to assist the left ventricle (single ventricle) + a CF VAD to assist the right ventricle (cavo-pulmonary connection) (RCF + LPF) Results In biventricular circulation, the following results were found: cardiac output (17% RCF + LPF, 21% LCF + RPF), artero-ventricular coupling (-36% for the left ventricle and -21.6% for the right ventricle), pulsatility index (+6.4% RCF + LPF, p = 0.02; -8.5% LCF + RPF, p = 0.00009). Right (left) atrial pressure and right (left) ventricular volumes are decreased by the RCF + LPF (by RPF + LCF). Pulmonary arterial pressure decreases in the LCF + RPF configuration. In Fontan physiology: cardiac output (LCF + RPF 35% vs. 8% in RCF + LPF), ventricular preload (+4% RCF + LPF, -10% LCF + RPF), Fontan conduit pressure (-5% RCF + LPF, +7% LCF + RPF), artero-ventricular coupling (-14% RCF + LPF vs. -41% LCF + RPF) and pulsatility (+13% RCF + LPF, - 8% LCF + RPF). Conclusions A numerical model supports clinicians in defining and innovating the VAD implantation strategy to maximize the hemodynamic benefits. Results suggest that the hemodynamic benefits are maximized by the LCF + RPF configuration.

Cardiac function and morphology with aging in the spontaneously hypertensive rat

1979 ◽  
Vol 237 (4) ◽  
pp. H461-H468 ◽  
Author(s):  
J. M. Pfeffer ◽  
M. A. Pfeffer ◽  
M. C. Fishbein ◽  
E. D. Frohlich
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Stroke Volume ◽  
Right Ventricle ◽  
Cardiac Function ◽  
Spontaneously Hypertensive Rat ◽  
Left Ventricular ◽  
Ether Anesthesia ◽  
Spontaneously Hypertensive ◽  
The Right

To determine the effects of a chronic pressure load on cardiac function and morphology, spontaneously hypertensive rats (SHR) and two normotensive strains of Wistar rats (WKY and NWR) were studied under ether anesthesia at 13, 25, 52, and 90 wk of age. Although resting cardiac index of the SHR was comparable to that of WKY and NWR at all ages, the peak cardiac output and peak stroke volume per gram of left ventricle determined during a rapid intravenous infusion of Tyrode solution was markedly reduced in the SHR only at 90 wk of age. Autonomic inhibition did not alter the peak stroke volume attained, but reduced peak cardiac output at all ages in each of the strains. Absolute left ventricular dimensions in the SHR increased out of proportion to body growth, consistent with concentric hypertrophy. As peak pumping ability markedly declined from 52 to 90 wk of age in the SHR, the free wall of the left ventricle greatly thickened whereas the septum remained unchanged. At this time the right ventricle also hypertrophied. This disproportionate thickening of the walls of the left ventricle and the hypertrophy of the right ventricle were reflected in measurements of their fiber diameters. These alterations in ventricular architecture may contribute to the decrease in pumping ability observed in long-standing hypertension.

MECHANISMS OF ADAPTATION OF THE LEFT VENTRICLE TO MUSCULAR EXERCISE

PEDIATRICS ◽  
1963 ◽  
Vol 32 (4) ◽  
pp. 660-670
Author(s):  
Jere H. Mitchell
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Stroke Volume ◽  
Pulse Rate ◽  
Individual Factors ◽  
Normal Male ◽  
Oxygen Intake ◽  
Mechanisms Of Adaptation ◽  
Male Subjects ◽  
Oxygen Difference

THE mechanisms of adaptation of the left ventricle to the demands of muscular exercise have intrigued cardiovascular physiologists for many years. Although highly complex, these adaptive mechanisms are more and more susceptible to analysis and quantification. In this presentation I will attempt to identify some of the individual factors which appear to be important in the response of the left ventricle to exercise, beginning with data obtained from experiments on conscious normal male subjects and proceeding to experiments performed on dog preparations in which individual factors were controlled and analyzed. The changes in oxygen intake, cardiac output, estimated arteriovenous oxygen difference, pulse rate and estimated mean stroke volume were determined in 15 normal male subjects during rest in the standing position and during treadmill exercise at the maximal oxygen intake level. Oxygen intake was obtained from the volume and composition of expired air, cardiac output by the dye dilution technique, and pulse rate from the electrocardiogram. Estimated arteriovenous oxygen difference was obtained by dividing the oxygen intake by the cardiac output (Fick principle) and estimated mean stroke volume by dividing the cardiac output by the heart rate. The data are shown in Figure 1. Oxygen intake increased from a mean value of 0.34 at rest to a maximal value of 3.22 L./min. The corresponding mean values for cardiac output were 5.4 and 23.4 L./min. and for arteriovenous oxygen difference were 6.5 and 14.3 ml./100 ml. Thus, as oxygen intake increased 9.5 times, the cardiac output increased 4.3 times and the arterio venous oxygen difference 2.2 times.

Impact of sickle cell anaemia on cardiac chamber size in the paediatric population

2016 ◽  
Vol 27 (5) ◽  
pp. 918-924 ◽  
Author(s):  
Philippe M. Adjagba ◽  
Gaston Habib ◽  
Nancy Robitaille ◽  
Yves Pastore ◽  
Marie-Josée Raboisson ◽  
...  
Keyword(s):  
Lactate Dehydrogenase ◽  
Sickle Cell Disease ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Sickle Cell ◽  
Myocardial Performance ◽  
Cell Disease ◽  
Left Ventricle Mass ◽  
Cardiac Chamber ◽  
Chamber Size

AbstractPurposeSickle cell disease is known to cause various degrees of vasculopathy, including impact on heart function. The aims of this single-centre, retrospective study were to assess cardiac chamber size and function and the relationship with haematological indices such as haemoglobin, aspartate aminotransferase, reticulocytosis and bilirubin, lactate dehydrogenase in sickle cell disease.MethodsRight ventricle and left ventricle diastolic diameters, left ventricle mass estimate, left ventricle shortening fraction, myocardial performance index, and an index of myocardial relaxation (E/E’) were calculated and correlated with haematological parameters.ResultsA total of 110 patients (65% haemoglobin SS, 29% haemoglobin SC) were studied at a mean age of 12.14±5.26 years. Right ventricle dilatation and left ventricle dilatation were present in 61.5 and 42.9%, respectively. Left ventricle mass was abnormal in 21.9%; all patients had normal myocardial performance index, 31.4% had abnormal E/E’, and left ventricle shortening fraction was low in 38.1%. Cardiac dilatation was best correlated with haemoglobin, aspartate aminotransferase, reticulocytosis and bilirubin. Best subset regression analysis yielded significant additional prediction for right ventricle or left ventricle dilatation with haemoglobin, bilirubin, and lactate dehydrogenase. Abnormal E/E’ was solely predictable with haemoglobin level. Hydroxyurea-treated patients had improved diastolic function.ConclusionRight ventricle dilatation was more prevalent than left ventricle dilatation. The long-term consequences of right ventricular dilatation, clinical consequences, and association with pulmonary vasculopathy need to be further determined.

Regulation of K+ and Ca2+ channels in experimental cardiac failure

1991 ◽  
Vol 261 (6) ◽  
pp. H1979-H1987 ◽  
Author(s):  
M. Gopalakrishnan ◽  
D. J. Triggle ◽  
A. Rutledge ◽  
Y. W. Kwon ◽  
J. A. Bauer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Cardiac Failure ◽  
Radioligand Binding ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
The Right

To examine the status of ATP-sensitive K+ (K+ATP) channels and 1,4-dihydropyridine-sensitive Ca2+ (Ca2+DHP) channels during experimental cardiac failure, we have measured the radioligand binding properties of [3H]glyburide and [3H]PN 200 110, respectively, in tissue homogenates from the rat cardiac left ventricle, right ventricle, and brain 4 wk after myocardial infarction induced by left coronary artery ligation. The maximal values (Bmax) for [3H]glyburide and [3H]PN 200 110 binding were reduced by 39 and 40%, respectively, in the left ventricle, and these reductions showed a good correlation with the right ventricle-to-body weight ratio in heart-failure rats. The ligand binding affinities were not altered. In the hypertrophied right ventricle, Bmax values for both the ligands were not significantly different when data were normalized to DNA content or right ventricle weights but showed an apparent reduction when normalized to unit protein or tissue weight. Moderate reductions in channel densities were observed also in whole brain homogenates from heart failure rats. Assessment of muscarinic receptors, beta-adrenoceptors and alpha 1-adrenoceptors by [3H]quinuclidinyl benzilate, [3H]dihydroalprenolol, and [3H]prazosin showed reductions in left ventricular muscarinic and beta-adrenoceptor densities but not in alpha 1-adrenoceptor densities, consistent with earlier observations. It is suggested that these changes may in part contribute to the pathology of cardiac failure.

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.

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