Left ventricular force-length relations of isovolumic and ejecting contractions

1976 ◽  
Vol 231 (2) ◽  
pp. 337-343 ◽  
Author(s):  
KT Weber ◽  
JS Janicki ◽  
LL Hefner

To determine the interrelationships between ejecting and isovolumic force-length relations and the extent to which the left ventricle will shorten, data obtained in 27 isolated, servo-regulated hearts were examined. For each heart a series of contractions, variably loaded (delta L) were derived for a thickwalled sphere and normalized by the cross-sectional area of muscle and length at zero end-diastolic pressure. It was found that within the physiological range examined total and active force were essentially a linear function of initial L with respective increments or reductions in slope produced by positive or negative shifts in contractile state. The force-L relations obtained isovolumically and at end ejection were virtually identical. For a given ejection pressure, end-systolic L was constant, despite variations in filling and therefore independent of initial L and deltaL; moreover, the L to which the ventricle shortened was determined by the course of the systolic force L-relation. Thus, irrespective of loading, delta L occurs within the confines of the contractile state-dependent isovolumic force-L relation and where the latter is equivalent to the end-systolic force-length relation.


2001 ◽  
Vol 91 (6) ◽  
pp. 2531-2536 ◽  
Author(s):  
Jiun-Jr Wang ◽  
Kim H. Parker ◽  
John V. Tyberg

Left ventricular (LV) wave speed (LVWS) was studied experimentally and confirmed in theory. Combining the definition of elastance (E) with the equations for the conservation of mass and momentum shows that LVWS is proportional to the square root of E LA, where L is long-axis length and A is the cross-sectional area, and the density of the blood. (We defined E LA = γ, where γ is compressibility.) We studied nine open chest, anesthetized dogs, three of which were studied during caval constriction when LV end-diastolic pressure was ≤0 mmHg. The hearts were paced at ∼90 beats/min, and LV cross-sectional area was measured by using two pairs of ultrasonic crystals; E was calculated from the LV pressure-area loop. A pulse generator was connected to the LV apex, and LVWS was measured by using two pressure transducers: one near the apex and the other near the base. Their distance was measured roentgenographically and compared with the diameter of a reference ball. LVWS ranged from ∼1 m/s during diastole to ∼10 m/s during systole. The slope of the log c(where c is wave speed) vs. log γ was 0.546, which is in agreement with theory (0.5). When γ ≤ 0, LVWS was ∼1.5 m/s.



Author(s):  
Casandra L. Niebel ◽  
Kelley C. Stewart ◽  
Takahiro Ohara ◽  
John J. Charonko ◽  
Pavlos P. Vlachos ◽  
...  

Left ventricular diastolic dysfunction (LVDD) is any abnormality in the filling of the left ventricle and is conventionally evaluated by analysis of the relaxation driven phase, or early diastole. LVDD has been shown to be a precursor to heart failure and the diagnosis and treatment for diastolic failure is less understood than for systolic failure. Diastole consists of two filling waves, early and late and is primarily dependent on ventricular relaxation and wall stiffness.



2014 ◽  
Vol 2014 ◽  
pp. 1-3
Author(s):  
Murat Yuksel ◽  
Abdulkadir Yildiz ◽  
Mustafa Oylumlu ◽  
Nihat Polat ◽  
Halit Acet ◽  
...  

Coronary cameral fistulas are abnormal communications between a coronary artery and a heart chamber or a great vessel which are reported in less than 0.1% of patients undergoing diagnostic coronary angiography. All three major coronary arteries are even less frequently involved in fistula formation as it is the case in our patient. A 68-year-old woman was admitted to cardiology clinic with complaints of exertional dyspnea and angina for two years and a new onset palpitation. Standard 12-lead electrocardiogram revealed atrial fibrillation (AF) with a ventricular rate of 114 beat/minute and accompanying T wave abnormalities and minimal ST-depression on lateral derivations. Transthoracic echocardiographic examination was normal except for diastolic dysfunction, minimally mitral regurgitation, and mild to moderate enlargement of the left atrium. Sinus rhythm was achieved by medical cardioversion with amiodarone infusion. Coronary angiography revealed diffuse and multiple coronary-left ventricle fistulas originating from the distal segments of both left and right coronary arterial systems without any stenosis in epicardial coronary arteries. The patient’s symptoms resolved almost completely with medical therapy. High volume shunts via coronary artery to left ventricular microfistulas may lead to increased volume overload and subsequent increase in end-diastolic pressure of the left ventricle and may cause left atrial enlargement.



PEDIATRICS ◽  
1966 ◽  
Vol 38 (3) ◽  
pp. 457-464
Author(s):  
Norman S. Talner ◽  
Thomas H. Gardner ◽  
S. Evans Downing

The performance of the left ventricle in 20 newborn lambs was examined in a preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. Reduction of arterial pH from a normal range (7.35 to 7.5) to severe acidemia (6.8 to 7.0) by hydrochloric or lactic acid infusion resulted in no significant impairment of left ventricular function. Prolonged acidemia (over 2 hours) failed to produce a reduction in left ventricular stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure. Responsiveness of the left ventricle of the lamb to catecholamine stimulation was not diminished over the pH range 7.5 to 6.8. Under conditions of these investigations the apparent resistance of the myocardium of the newborn lamb, as well as the adult cat, to wide variations in pH may reflect a buffering capacity of cardiac muscle which would allow minimal change in intracellular pH, even though extracellular pH may indicate the presence of severe metabolic acidosis.



1990 ◽  
Vol 20 (4) ◽  
pp. 748
Author(s):  
Doo Hong Choi ◽  
Hak Sun Kim ◽  
Sun Ho Chang ◽  
Joo Young Cho ◽  
Sung Gu Kim ◽  
...  


1990 ◽  
Vol 259 (4) ◽  
pp. H1086-H1096 ◽  
Author(s):  
J. M. Capasso ◽  
T. Palackal ◽  
G. Olivetti ◽  
P. Anversa

To determine if aging engenders alterations in the functional properties of the myocardium and ventricular remodeling, the hemodynamic performance and structural characteristics of the left ventricle of male Fischer 344 rats at 4, 12, 20, and 29 mo of age were studied by quantitative physiology and morphology. In vivo assessment of cardiac pump function showed no change up to 20 mo, whereas left ventricular end-diastolic pressure was increased at 29 mo. Moreover, peak rates of pressure rise and decay, stroke volume, ejection fraction, and cardiac output were depressed at the later age interval, demonstrating the presence of ventricular failure at this time. The measurements of chamber size and wall thickness showed that ventricular end-diastolic and end-systolic volumes progressively increased with age with the greatest change occurring at 20-29 mo. Aging was also accompanied by a marked augmentation in the volume fraction of fibrotic areas in the ventricular myocardium that was due to an increase in their number and cross-sectional area with time. These architectural rearrangements, in combination with the abnormalities in ventricular function, resulted in an elevation in the volume of wall stress throughout the cardiac cycle. Wall stress increased by 64, 44, and 50% from 4 to 12, 12 to 20, and 20 to 29 mo of age. In conclusion, aging leads to a continuous rise in wall stress that is not normalized by ventricular remodeling. These two independent processes appear to be responsible for the onset of heart failure in the senescent rat.



1979 ◽  
Vol 236 (2) ◽  
pp. H323-H330 ◽  
Author(s):  
D. Ling ◽  
J. S. Rankin ◽  
C. H. Edwards ◽  
P. A. McHale ◽  
R. W. Anderson

In eight chronically instrumented conscious dogs, apical and middle left ventricular transverse diameters were measured with pulse-transit ultrasonic dimension transducers. Intracavitary apical and midventricular pressures and intrapleural pressure were measured with micromanometers. Both diameters were normalized as a percent extension from the dimension at zero transmural pressure, determined during a transient vena caval occlusion. During the rapid phase of diastolic filling, there was a 2--5 mmHg pressure gradient from the midventricle to the apex. During late rapid filling, the apical transmural pressure and diameter increased more rapidly and reached diastasis 17 +/- 4 ms earlier than the corresponding midventricular measurements (P less than 0.01). The static diastolic pressure-dimension characteristics at the apical and midventricular levels were not significantly different (P greater than 0.30). The dynamic diastolic pressure-dimension relationship was also similar at the two levels and could be represented by a model incorporating parallel viscous properties. Because of regional differences in pressures and dimensions, however, the dynamic relationship could not be modeled when pressure was compared to the dimension at a different level. Thus, diastolic pressures should be measured at the same level as dimensions when assessing left ventricular diastolic mechanics.



2021 ◽  
Vol 3 (2) ◽  
pp. 01-07
Author(s):  
Mariela Céspedes Almira ◽  
Adel Eladio González Morejón ◽  
Giselle Serrano Ricardo ◽  
Tania Rosa González Rodríguez ◽  
Judith Escobar Bermúdez

ALCAPA syndrome was characterized by anomalous origin of left coronary artery from pulmonary artery. Its clinical presentation is varied and although it is an anomaly of congenital origin, it is not exclusive to pediatric ages. Its epidemiological documentation is difficult. We aimed to make the non-invasive diagnosis of the ALCAPA syndrome and its variants. An observational, prospective and cross-sectional study was conducted with 31 patients with a positive echocardiographic diagnosis of ALCAPA syndrome at Pediatric Cardio Center “William Soler” from 2005 to 2018. The variables with significance for diagnosis were the echocardiographic visualization of the anomalous connection and the reversed flow in the left coronary artery. The variables with significance for typing were age at diagnosis, ischemia in the electrocardiogram, echocardiographic visualization of left ventricle papillary muscles fibrosis, presence of severe mitral regurgitation, left ventricle spheroidal remodeling, left ventricle ejection fraction, left ventricular end-diastolic volume index, and left ventricular end-diastolic diameter index. An algorithm integrated by various diagnostic modalities associated with echocardiography as a tool for the detection of ALCAPA was developed. The documentation of the diagnostic and classificatory aspects of the syndrome is possible by detecting echocardiographic elements in conjunction with electrocardiographic and radiological aspects.



1988 ◽  
Vol 255 (2) ◽  
pp. H366-H374 ◽  
Author(s):  
Y. Goto ◽  
B. K. Slinker ◽  
M. M. LeWinter

The end-systolic pressure-volume relation (ESPVR), a measure of ventricular contractile state, and systolic pressure-volume area (PVA), a primary determinant of cardiac oxygen consumption per beat (VO2), have been derived from the pressure-volume diagram of the cross-circulated dog left ventricle. The slope of the PVA-VO2 relation represents the efficiency of chemomechanical energy transduction of the contractile machinery. To see whether these relationships were similar in other animals, we studied the isovolumic ESPVR and the VO2-PVA relation in nine excised, cross-circulated rabbit left ventricles. The base-line ESPVR was linear (r = 0.94-0.99) with the slope (Emax) and volume-axis intercept (V0) equal to 83.4 +/- 18.3 mmHg/ml and 0.43 +/- 0.17 ml, respectively. When normalized for left ventricular weight, Emax (4.1 +/- 1.1 mmHg.ml-1.100 g) and V0 (8.9 +/- 3.7 ml/100 g) were similar to values reported for the dog left ventricle. The correlation between PVA and VO2 was linear (r = 0.93-1.00), and the slope (1.90 X 10(-5) +/- 0.44 X 10(-5) ml O2.mmHg-1.ml-1) and VO2-axis intercept (0.040 +/- 0.009 ml O2.beat-1.100 g-1) were similar to values found in the dog left ventricle. Hence, despite the greatly different heart size, the base-line contractile state and chemomechanical energy conversion efficiency of the excised, cross-circulated rabbit left ventricle are similar to those of the dog left ventricle.



2012 ◽  
Vol 303 (9) ◽  
pp. H1135-H1142 ◽  
Author(s):  
Sarah Mahne ◽  
Gin C. Chuang ◽  
Edward Pankey ◽  
Lucy Kiruri ◽  
Philip J. Kadowitz ◽  
...  

Epidemiological studies have consistently linked inhalation of particulate matter (PM) to increased cardiac morbidity and mortality, especially in at risk populations. However, few studies have examined the effect of PM on baseline cardiac function in otherwise healthy individuals. In addition, airborne PM contain environmentally persistent free radicals (EPFR) capable of redox cycling in biological systems. The purpose of this study was to determine whether nose-only inhalation of EPFRs (20 min/day for 7 days) could decrease baseline left ventricular function in healthy male Sprague-Dawley rats. The model EPFR tested was 1,2-dichlorobenzene chemisorbed to 0.2-μm-diameter silica/CuO particles at 230°C (DCB230). Inhalation of vehicle or silica particles served as controls. Twenty-four hours after the last exposure, rats were anesthetized (isoflurane) and ventilated (3 l/min), and left ventricular function was assessed using pressure-volume catheters. Compared with controls, inhalation of DCB230 significantly decreased baseline stroke volume, cardiac output, and stroke work. End-diastolic volume and end-diastolic pressure were also significantly reduced; however, ventricular contractility and relaxation were not changed. DCB230 also significantly increased pulmonary arterial pressure and produced hyperplasia in small pulmonary arteries. Plasma levels of C-reactive protein were significantly increased by exposure to DCB230, as were levels of heme oxygenase-1 and SOD2 in the left ventricle. Together, these data show that inhalation of EPFRs, but not silica particles, decreases baseline cardiac function in healthy rats by decreasing cardiac filling, secondary to increased pulmonary resistance. These EPFRs also produced systemic inflammation and increased oxidative stress markers in the left ventricle.



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