Biomedical subjects

Israel Belenkie

Publications and source records attributed to Israel Belenkie.

10 recordsLinked to original sources

PubMed2006

Wave intensity analysis of left atrial mechanics and energetics in anesthetized dogs.

The left atrium (LA) acts as a booster pump during late diastole, generating the Doppler transmitral A wave and contributing incrementally to left ventricular (LV) filling. However, after volume loading and in certain disease states, LA contraction fills the LV less effectively, and retrograde flow (i.e., the Doppler Ar wave) into the pulmonary veins increases. The purpose of this study was to provide an energetic analysis of LA contraction to clarify the mechanisms responsible for changes in forward and backward flow. Wave intensity analysis was performed at the mitral valve and a pulmonary vein orifice. As operative LV stiffness increased with progressive volume loading, the reflection coefficient (i.e., energy of reflected wave/energy of incident wave) also increased. This reflected wave decelerated the forward movement of blood through the mitral valve and was transmitted through the LA, accelerating retrograde blood flow in the pulmonary veins. Although total LA work increased with volume loading, the forward hydraulic work decreased and backward hydraulic work increased. Thus wave reflection due to increased LV stiffness accounts for the decrease in the A wave and the increase in the Ar wave measured by Doppler.

Animals↗

PubMed2006

Assessment of right ventricular diastolic suction in dogs with the use of wave intensity analysis.

Diastolic suction (DS) can be defined as that property of the ventricle by means of which it tends to refill itself during early diastole, independent of any force from the atrium. Although thought to be significant in the left ventricle (LV), DS in the right ventricle (RV) has received little attention, probably because of RV geometry. Our recent LV studies have shown that DS is related to both decreased elastance (i.e., tau, the relaxation time constant) and end-systolic volume (V(LVES)), thus reconciling the two mechanisms that have been used to explain the concept of DS. We hypothesized that RV DS would similarly depend on tau and V(RVES). In six anesthetized open-chest dogs, aortic, RV, right atrial (RA), pulmonary arterial (PA), and RV pericardial pressure, tricuspid velocity, and PA flow were measured. V(RVES) was calculated by measuring distances between eight ultrasonic crystals. An empirical index of relaxation, tau', and V(RVES) were manipulated by volume loading/caval constriction and isoproterenol/esmolol. We calculated the total energy (I(W-)) of the backward expansion wave generated during RV relaxation and that component causing DS [I(W-(DS))]; i.e., the energy remaining after tricuspid valve opening. I(W-) [I(W-(DS)) also] was found to be inversely related to tau' and to V(RVES) {i.e., I(W-) = -8.85.e((-0.0423tau')).e([-0.0665(%V(RVES))])}. Thus, as for the LV, the energy of the backward-going wave generated by the RV during relaxation depends on both the rate at which elastance decreases and the completeness of ejection. Despite the thin wall and nonspherical shape of the RV, DS appears to be an important mechanism.

Animals↗

PubMed2005

Continuous positive airway pressure for central sleep apnea and heart failure.

BACKGROUND: The Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure trial tested the hypothesis that continuous positive airway pressure (CPAP) would improve the survival rate without heart transplantation of patients who have central sleep apnea and heart failure. METHODS: After medical therapy was optimized, 258 patients who had heart failure (mean age [+/-SD], 63+/-10 years; ejection fraction, 24.5+/-7.7 percent) and central sleep apnea (number of episodes of apnea and hypopnea per hour of sleep, 40+/-16) were randomly assigned to receive CPAP (128 patients) or no CPAP (130 patients) and were followed for a mean of two years. During follow-up, sleep studies were conducted and measurements of the ejection fraction, exercise capacity, quality of life, and neurohormones were obtained. RESULTS: Three months after undergoing randomization, the CPAP group, as compared with the control group, had greater reductions in the frequency of episodes of apnea and hypopnea (-21+/-16 vs. -2+/-18 per hour, P<0.001) and in norepinephrine levels (-1.03+/-1.84 vs. 0.02+/-0.99 nmol per liter, P=0.009), and greater increases in the mean nocturnal oxygen saturation (1.6+/-2.8 percent vs. 0.4+/-2.5 percent, P<0.001), ejection fraction (2.2+/-5.4 percent vs. 0.4+/-5.3 percent, P=0.02), and the distance walked in six minutes (20.0+/-55 vs. -0.8+/-64.8 m, P=0.016). There were no differences between the control group and the CPAP group in the number of hospitalizations, quality of life, or atrial natriuretic peptide levels. An early divergence in survival rates without heart transplantation favored the control group, but after 18 months the divergence favored the CPAP group, yet the overall event rates (death and heart transplantation) did not differ (32 vs. 32 events, respectively; P=0.54). CONCLUSIONS: Although CPAP attenuated central sleep apnea, improved nocturnal oxygenation, increased the ejection fraction, lowered norepinephrine levels, and increased the distance walked in six minutes, it did not affect survival. Our data do not support the use of CPAP to extend life in patients who have central sleep apnea and heart failure.

Aged↗

PubMed2005

RV filling modulates LV function by direct ventricular interaction during mechanical ventilation.

During mechanical ventilation, phasic changes in systemic venous return modulate right ventricular output but may also affect left ventricular function by direct ventricular interaction. In 13 anesthetized, closed-chest, normal dogs, we measured inferior vena cava flow and left and right ventricular dimensions and output during mechanical ventilation, during an inspiratory hold, and (during apnea) vena caval constriction and abdominal compression. During a single ventilation cycle preceded by apnea, positive pressure inspiration decreased caval flow and right ventricular dimension; the transseptal pressure gradient increased, the septum shifted rightward, reflecting an increased left ventricular volume (the anteroposterior diameter did not change); and stroke volume increased. The opposite occurred during expiration. Similarly, the maneuvers that decreased venous return shifted the septum rightward, and left ventricular volume and stroke volume increased. Increased venous return had opposite effects. Changes in left ventricular function caused by changes in venous return alone were similar to those during mechanical ventilation except for minor quantitative differences. We conclude that phasic changes in systemic venous return during mechanical ventilation modulate left ventricular function by direct ventricular interaction.

Abdomen↗

PubMed2005

Ventricular interaction during mechanical ventilation in closed-chest anesthetized dogs.

The cardiac effects of positive pressure ventilation and positive end-expiratory pressure are incompletely understood. External constraint due to increased intrathoracic pressure decreases left ventricular end-diastolic volume; the effects on venous return and ventricular interaction are less clear. Phasic changes in inferior vena caval flow, end-diastolic ventricular dimensions and output were measured in seven anesthetized, ventilated normal dogs. During inspiration, caval flow, right ventricular diameter and output decreased; end-diastolic transseptal pressure gradient, septum-to-left ventricular free wall diameter, left ventricular area (ie, left ventricular volume index) and output increased despite the decreased sum of the septum-to-free wall diameters. The reverse occurred during expiration. Increased positive end-expiratory pressure decreased the left ventricular area, but the end-expiratory right ventricular diameter was unchanged. At given airway pressures, right ventricular diameter was greater at higher positive end-expiratory pressures, suggesting that a leftward septal shift (direct ventricular interaction) added to the effect of external constraint on left ventricular end-diastolic volume. In conclusion, positive pressure ventilation reduced right ventricular end-diastolic volume during inspiration and increased the transseptal pressure gradient, which shifted the septum rightward, increasing left ventricular end-diastolic volume and output. The reverse occurred during expiration. Positive end-expiratory pressure constrained left ventricular filling and decreased left ventricular end-diastolic volume further by a leftward septal shift.

Anesthesia↗

PubMed2003

Opening the pericardium during pulmonary artery constriction improves cardiac function.

During acute pulmonary hypertension, both the pericardium and the right ventricle (RV) constrain left ventricular (LV) filling; therefore, pericardiotomy should improve LV function. LV, RV, and pericardial pressures and RV and LV dimensions and LV stroke volume (SV) were measured in six anesthetized dogs. The pericardium was closed, the chest was left open, and the lungs were held away from the heart. Data were collected at baseline, during pulmonary artery constriction (PAC), and after pericardiotomy with PAC maintained. PAC decreased SV by one-half. RV diameter increased, and septum-to-LV free wall diameter and LV area (our index of LV end-diastolic volume) decreased. Compared with during PAC, pericardiotomy increased LV area and SV increased 35%. LV and RV compliance (pressure-dimension relations) and LV contractility (stroke work-LV area relations) were unchanged. Although series interaction accounts for much of the decreased cardiac output during acute pulmonary hypertension, pericardial constraint and leftward septal shift are also important. Pericardiotomy can improve LV function in the absence of other sources of external constraint to LV filling.

Animals↗

PubMed2003

Pericardium modulates left and right ventricular stroke volumes to compensate for sudden changes in atrial volume.

The pericardium may modulate acute compensatory changes in stroke volumes seen with sudden changes in cardiac volume, but such a mechanism has never been clearly demonstrated. In eight open-chest dogs, we measured left and right ventricular pressures, diameters, stroke volumes, and pericardial pressures during rapid (approximately 300 ms) systolic infusions or withdrawals of approximately 25 ml blood into and out of the left atrium and right atrium. Control beats, the infusion/withdrawal beat, and 4-10 subsequent beats were studied. With infusions, ipsilateral ventricular end-diastolic transmural pressure, diameter, and stroke volume increased. With the pericardium closed, there was a compensatory decrease in contralateral transmural pressure, diameter, and stroke volume, mediated by opposite changes in transmural end-diastolic pressures. The sum of the ipsilateral increase and contralateral decrease in stroke volume approximated the infused volume. Corresponding changes were seen with blood withdrawals. This direct ventricular interaction was diminished when pericardial pressure was <5 mmHg and absent when the pericardium was opened. Pericardial constraint appears essential for immediate biventricular compensatory responses to acute atrial volume changes.

Animals↗

PubMed2002

Evidence for left ventricular constraint during open heart surgery.

BACKGROUND: The degree to which the lungs and other mediastinal structures constrain the heart during cardiac surgery is uncertain. OBJECTIVES: To assess the degree of constraint to left ventricular (LV) filling that is present during cardiac surgery. PATIENTS AND METHODS: Central venous (CVP) and pulmonary capillary wedge pressures (PCWP), and an index of LV end-diastolic volume (LVEDV) - LV area, transesophageal echocardiography - were measured before and after sternotomy, after volume loading, after pericardiotomy, and before and after sternal closure following the clinically indicated procedure in 12 patients undergoing cardiac surgery. PCWP and estimated transmural LVEDP (PCWP-CVP) were plotted against the LV area. RESULTS: In all patients, the difference between PCWP and estimated transmural LVEDP-LV area relations over the full range of LV areas was substantial, indicating the presence of important constraint to filling. Even at small LV areas, when transmural LVEDP approached zero, PCWP was almost always greater than 10 mmHg. Because transmural LVEDP approached zero when areas were smallest, transmural LVEDP-LV area relations were judged to be more plausible than the corresponding PCWP-LV area relations. CONCLUSIONS: Considerable constraint to cardiac filling is effected by the lungs and other mediastinal structures. This constraint must be considered when assessing LV filling pressure - PCWP is not a reliable measure of LV preload in these circumstances.

Aged↗

PubMedDate not supplied

The cardiovascular effects of arteriovenous fistulas in chronic kidney disease: a cause for concern?

Arteriovenous fistulas (AVFs) are the preferred type of vascular access, but relatively little is known regarding their effects on cardiovascular remodeling and cardiac function. The following is a review regarding the immediate and long-term complications associated with AVF creation, including the development of left ventricular hypertrophy, high-output cardiac failure, exacerbation of coronary ischemia, and the possible contribution to the development of central vein stenosis.

Arteriovenous Shunt, Surgical↗

PubMedDate not supplied

Relationship between right ventricular wave speed and elastance in dogs.

Wave speed (c) must be known to separate forward- and backward-going waves during wave-intensity analysis, which measures the energy transported by the waves in the circulation. c is related to elastance; the present study was performed to measure right ventricular (RV) c during the cardiac cycle and to compare c with RV elastance. In 7 dogs, we measured right atrial, pulmonary arterial, pericardial and 2 RV pressures, and pulmonary arterial flow. A pulse generator was connected to the RV apex, and c was measured by determining the transit time between the 2 high-fidelity RV pressure transducers; the distance was measured roentgenographically. Eight sonomicrometry crystals were implanted in the RV endocardium to calculate RV volume and, thereby, elastance. RV c ranged from approximately 1 m/s during diastole to approximately 4 m/s during systole. Log-log plots of c vs. elastance were linear. These slopes represent the power relationships between c and elastance and ranged from 0.30 to 0.56; for the combined data, it was 0.31. Given knowledge of c, forward- and backward-going waves can be identified and their energy quantitated. In the canine RV, c is approximately proportional to 1/3 the power of elastance: log c = 0.31.log E - 2.05.

Animals↗