scholarly journals Static and dynamic operating characteristics of a pericardial balloon

2001 ◽  
Vol 90 (4) ◽  
pp. 1481-1488 ◽  
Author(s):  
Douglas R. Hamilton ◽  
Gwyneth Devries ◽  
John V. Tyberg

Previously, we developed a balloon transducer to measure the constraint of the pericardium (i.e., pericardial pressure) on the surface of the heart. It was validated physiologically in that it was shown to measure a pressure equal to the difference between the left ventricular end-diastolic pressure measured before and after pericardiectomy at the same left ventricular volume. To define its static operating characteristics, we loaded the balloon nonuniformly with weights that covered fractions of the balloon surface and found that the balloon accurately recorded the average stress if the stress was applied over at least 23% of its surface. To test its performance when curved, we placed it in large and small cylinders (minimum diameter 31 mm) and found that the balloon accurately recorded the stress. To define its dynamic operating characteristics, we applied sinusoidal stresses and found that its frequency response was limited only by that of the connecting catheter. When better dynamic response is required, we introduce a micromanometer-tipped catheter to obtain a unity-gain frequency response that is flat to 200 Hz.

1990 ◽  
Vol 258 (4) ◽  
pp. H1079-H1086 ◽  
Author(s):  
R. J. Applegate ◽  
W. P. Santamore ◽  
H. S. Klopfenstein ◽  
W. C. Little

We evaluated the contribution of the thorax and the undisturbed pericardium to the external pressure of the euvolemic left ventricle in thirteen anesthetized dogs. Left ventricular (LV) end-diastolic pressure (EDP) in the euvolemic state was 7 +/- 2 mmHg initially and increased to 10 +/- 2 mmHg after the chest and pericardium were opened. LV end-diastolic volume (conductance catheter) was 43 +/- 20 ml initially and did not change after the chest or the pericardium was opened. Intrathoracic (PIT) and pericardial (PPER) pressures were calculated as the difference in LV chamber pressure before and after opening these spaces. Thus for the LV, PIT was -3 +/- 1 mmHg, and PPER was 0 +/- 2 mmHg. Isovolumic relaxation, early diastolic filling, and total diastolic filling were not significantly altered after the chest or pericardium was opened. Thus under euvolemic conditions in this model pericardial pressure is negligible, and the external pressure of the undisturbed left ventricle is negative and equal to intrathoracic pressure.


2001 ◽  
Vol 281 (5) ◽  
pp. H1938-H1945 ◽  
Author(s):  
Chari Y. T. Hart ◽  
John C. Burnett ◽  
Margaret M. Redfield

Anesthetic regimens commonly administered during studies that assess cardiac structure and function in mice are xylazine-ketamine (XK) and avertin (AV). While it is known that XK anesthesia produces more bradycardia in the mouse, the effects of XK and AV on cardiac function have not been compared. We anesthetized normal adult male Swiss Webster mice with XK or AV. Transthoracic echocardiography and closed-chest cardiac catheterization were performed to assess heart rate (HR), left ventricular (LV) dimensions at end diastole and end systole (LVDd and LVDs, respectively), fractional shortening (FS), LV end-diastolic pressure (LVEDP), the time constant of isovolumic relaxation (τ), and the first derivatives of LV pressure rise and fall (dP/d t max and dP/d t min, respectively). During echocardiography, HR was lower in XK than AV mice (250 ± 14 beats/min in XK vs. 453 ± 24 beats/min in AV, P < 0.05). Preload was increased in XK mice (LVDd: 4.1 ± 0.08 mm in XK vs. 3.8 ± 0.09 mm in AV, P < 0.05). FS, a load-dependent index of systolic function, was increased in XK mice (45 ± 1.2% in XK vs. 40 ± 0.8% in AV, P < 0.05). At LV catheterization, the difference in HR with AV (453 ± 24 beats/min) and XK (342 ± 30 beats/min, P < 0.05) anesthesia was more variable, and no significant differences in systolic or diastolic function were seen in the group as a whole. However, in XK mice with HR <300 beats/min, LVEDP was increased (28 ± 5 vs. 6.2 ± 2 mmHg in mice with HR >300 beats/min, P < 0.05), whereas systolic (LV dP/d t max: 4,402 ± 798 vs. 8,250 ± 415 mmHg/s in mice with HR >300 beats/min, P < 0.05) and diastolic (τ: 23 ± 2 vs. 14 ± 1 ms in mice with HR >300 beats/min, P < 0.05) function were impaired. Compared with AV, XK produces profound bradycardia with effects on loading conditions and ventricular function. The disparate findings at echocardiography and LV catheterization underscore the importance of comprehensive assessment of LV function in the mouse.


1997 ◽  
Vol 273 (2) ◽  
pp. H583-H592 ◽  
Author(s):  
S. Yasuda ◽  
T. Shishido ◽  
Y. Goto

The left ventricular (LV) mechanical performance and the LV myocardial oxygen consumption (VO2)-to-pressure-volume area (PVA; LV total mechanical energy index) relationship were measured in isovolumic contraction of isolated blood-perfused dog hearts before and after direct current (DC) countershocks. At a constant LV volume, DC shocks increased LV end-diastolic pressure progressively and strikingly with the progression of myocardial edema and a marked prolongation of the time constant of LV pressure decay. In contrast, DC shocks changed neither the slope of the LV end-systolic pressure-volume relationship nor the contractile efficiency (the slope of the Vo2-PVA relationship). The oxygen cost of contractility (the slope of the relationship between PVA-independent VO2 and LV contractility) increased 27% after DC shocks. However, the magnitude of this change was considerably smaller than that previously reported in postischemic stunned myocardium (123%), suggesting that the adverse effect of DC shocks on the energy cost of excitation-contraction coupling is relatively minor. Thus, despite the severe diastolic dysfunction, DC shocks do not substantially impair either the efficiency of cross-bridge cycling or calcium cycling. Myocardial interstitial edema is more likely a potential mechanism of diastolic dysfunction after DC shocks.


1989 ◽  
Vol 256 (2) ◽  
pp. H567-H573 ◽  
Author(s):  
B. K. Slinker ◽  
Y. Goto ◽  
M. M. LeWinter

Changes in right ventricular volume affect left ventricular function via direct ventricular interaction mediated by the septum, common myocardial fibers in the free wall, and the pericardium, and also via series interaction mediated by changes in right ventricular output reaching the left ventricle through the pulmonary circulation. To study direct interaction, series interaction must be held constant or removed from the experimental preparation. Because there has been no way to directly measure direct ventricular interaction in the intact circulation, we developed a new method to experimentally separate these two components of ventricular interaction by combining abrupt occlusion of both venae cavae and quick withdrawal of 10-15 ml of blood from the right ventricle. This procedure decreased right ventricular end-diastolic pressure (RVEDP) on the next beat without changing pulmonary venous flow, left ventricular end-diastolic segment lengths, or left ventricular systolic function. The direct interaction gains, quantified as delta LVEDP/delta RVEDP, where LVEDP is left ventricular end-diastolic pressure, and delta refers to the change between the beats before and after reducing right ventricular volume, were (means +/- SD) 0.32 +/- 0.32 at steady-state LVEDP = 5 mmHg, 0.38 +/- 0.23 at LVEDP = 10 mmHg, and 0.28 +/- 0.32 at LVEDP = 15 mmHg. These gains were not significantly different (P greater than 0.50). Therefore, we calculated an overall average gain by pooling data from the three base-line LVEDP conditions. This value is 0.33 with 95% confidence interval 0.16-0.51. This 95% confidence interval indicates our data are consistent with many previous reports of diastolic direct interaction.


1961 ◽  
Vol 201 (1) ◽  
pp. 102-108 ◽  
Author(s):  
Cecil E. Cross ◽  
P. Andre Rieben ◽  
Peter F. Salisbury

Pressure-volume diagrams of paced, isolated hearts were derived from isovolumic contractions and auxotonic contractions (simultaneous changes of pressure and volume). Coronary perfusion, fluid accumulation in heart muscle, and left ventricular volume and pressure were measured and controlled. Pressure-volume diagrams from isovolumic and auxotonic contractions were virtually identical in the same heart and were influenced by the same factors to a similar degree. At equal diastolic volumes the magnitude of systolic, as well as of diastolic pressures, and the occurrence of a systolic descending limb were directly related to coronary perfusion pressure. At equal diastolic volumes, other factors being constant, myocardial edema did not influence the contractile strength (i.e., maximum contractile tension development) of a ventricle, but did decrease its distensibility (i.e., increase diastolic pressure) in proportion to fluid accumulation. Myocardial water content and coronary factors (coronary arterial and venous pressures, coronary blood volume and flow) therefore constitute intrinsic mechanisms which can regulate the performance of a ventricle by changing its contractile strength, its distensibility, or both. The effects of coronary factors and of myocardial edema on the distensibility of a ventricle are sufficient in magnitude to explain hemodynamic abnormalities which characterize certain types of congestive heart failure.


1978 ◽  
Vol 234 (3) ◽  
pp. H260-H265
Author(s):  
A. C. Kralios ◽  
T. J. Tsagaris

In pentobarbital-anesthetized, open-chest dogs with fixed heart rate, cardiac output, and systemic arterial pressure, ectopic ventricular activation originating from apical as compared to basilar regions of either ventricle was associated with small (3--5%) but significantly (P less than 0.005) lower myocardial O2 consumption (MVO2) and thus higher left ventricular (LV) efficiency without change in LV end-diastolic pressure (LVEDP), work index (LVWI), and LV dP/dt. Data obtained during epicardial and corresponding endocardial activation did not differ. During normal ventricular activation, MVO2 remained unchanged but LVEDP was significantly (P less than 0.005) lower, thus yielding higher LVWI and efficiency. MVO2 differences among ectopic sites were abolished after coronary artery occlusion, whereas data obtained during endocardial and epicardial on normal and ectopic activation were not affected. Thus, normal activation resulting in lower LVEDP is most efficient; apical ventricular activation is less efficient at the same MVO2P basilar is the least efficient, because both MVO2 and LVEDP are higher. Ventricular activation sequence changes do not constitute a substantial determinant of MVO2.


Author(s):  
Andreas Schaefer ◽  
Harun Sarwari ◽  
Niklas Schofer ◽  
Yvonne Schneeberger ◽  
Dirk Westermann ◽  
...  

Abstract Background We herein aimed for analysis of influence of mitral annular calcification (MAC) and mitral stenosis (MS) on outcomes in transcatheter aortic valve implantation (TAVI). Methods Between 11/2009 and 06/2017, 1,058 patients underwent TAVI in the presence of concomitant MAC or MS at our center. Subgroups were built and multivariate logistic regression, COX regression, Kaplan–Meier survival analyses, and receiver operating characteristics method were performed. Results Thirty-day mortality was 7.5% (79/1,058) with highest mortality in patients severe MS (MAC: 3.4% vs. mild MS: 5.9% vs. moderate MS: 15.0% vs. severe MS: 72.7%; p < 0.001). Moderate-to-severe MS (odds ratio [OR]: 7.75, confidence interval [CI]: 3.94–16.26, p < 0.001), impaired left ventricular ejection fraction (OR: 1.38, CI: 1.10–1.72, p < 0.01), and coronary artery disease (OR: 1.36, CI: 1.11–1.67, p < 0.01) were predictive of 30-day survival. Left ventricular systolic/end-diastolic pressure drop of <59.5 mm Hg / <19.5 mm Hg was associated with increased mortality. Conclusions TAVI in the presence of MAC and mild MS is associated with acceptable acute outcomes but should be considered high-risk procedures in patients with moderate and especially those with severe MS. Our results suggest adverse hemodynamics after TAVI with concomitant MS, which may be caused by underfilling of the left ventricle leading to low-cardiac output.


2013 ◽  
Vol 11 (3) ◽  
pp. 40-49
Author(s):  
Aleksandr Sergeyevich Radchenko ◽  
N. S. Borisenko ◽  
A. I. Kalinichenko ◽  
Yu Yu Rodionova ◽  
Yuriy Nikolayevich Korolev ◽  
...  

The study wThe left ventricular end diastolic pressure (EDP) fluctuations, specific peripheral vascular resistance (SPR) and cardiointervals (RR) on the respiration frequency under hard normobaric hypoxia (FIO2 = 0.1) were studied. 7 young men (volunteers) were subject to series of hard hypoxic exposures (6 weeks, every other day, intermittently by 6 × 5 min – FIO2 = 0.1). The hypoxic tests (HT1 and HT2) – FIO2 = 0.1, 15 min continuously) were performed before and after each series. SаO2 at the last 3 m of the tests on average was 82.5 % and 92.0 % respectively (Р < 0.05). During HT1 and HT2 (in comparison with inactivity) were increased: angle of max QRS vector (VQRS) in the frontal plain (68.5° ± 16.68 and 72.94° ± 15.32; 69.62° ± 22.4 and 74.45° ± 17.98 respectively), minutes blood flow (MBF) (6.41 ± 1.98 l/min and 6.87 ± 1.27 l/min; 5,27 ± 1,02 l/min and 5.67 ± 1.19 l/min respectively) (Р < 0.05). SPR was decreased too (27.39 ± 5.45 s.u. and 25.62 ± 4.96 s.u.; 30.59 ± 6.34 s.u. and 27.93 ± 5.77 s.u. respectively) (Р < 0.05). By means of transfer function analysis was shown that EDP fluctuations at HT2 significantly outpace by time (phase) the SPR and RR fluctuations on the respiration frequency (1.19 s ± 0.64 and 1.99 s ± 0.63 or 94.39° ± 43.3 and 125.4° ± 7.54; 1.65 s ± 1.28 and 2.22 s ± 0.87 or 101.4° ± 59.6 and 152.7° ± 21.26 respectively) (Р < 0.05). The increased oxyhemoglobin saturation is a trigger of artery wall smooth muscle relaxation mechanisms and this one is changes the background for beat to beat baroreflex realization on the respiration frequency.


2005 ◽  
Vol 289 (2) ◽  
pp. H501-H512 ◽  
Author(s):  
Daniel Burkhoff ◽  
Israel Mirsky ◽  
Hiroyuki Suga

Assessment of left ventricular systolic and diastolic pump properties is fundamental to advancing the understanding of cardiovascular pathophysiology and therapeutics, especially for heart failure. The use of end-systolic and end-diastolic pressure-volume relationships derived from measurements of instantaneous left ventricular pressure-volume loops emerged in the 1970s as a comprehensive approach for this purpose. As invasive and noninvasive techniques for measuring ventricular volume improved over the past decades, these relations have become commonly used by basic, translational, and clinical researchers. This review summarizes 1) the basic concepts underlying pressure-volume analysis of ventricular and myocardial systolic and diastolic properties, 2) deviations from ideal conditions typically encountered in real-life applications, 3) how these relationships are appropriately analyzed, including statistical analyses, and 4) the most common problems encountered by investigators and the appropriate remedies. The goal is to provide practical information and simple guidelines for accurate application and interpretation of pressure-volume data as they pertain to characterization of ventricular and myocardial properties in health and disease.


1990 ◽  
Vol 29 (03) ◽  
pp. 109-112
Author(s):  
J. Mester ◽  
E. Henze ◽  
R. Ochsenkühn ◽  
R. Lietzenmayer ◽  
R. Weller ◽  
...  

The suitability of a 3-dimensional filter in diminishing the statistical noise of left ventricular volume curves without any systematical error in the left ventricular ejection fraction (EF) was investigated. The EF values were compared in 50 studies on 24 patients. There was no significant systematical difference between the EFs before and after filtering. The filter diminishes the statistical uncertainty of the EF by a factor of 0.47. Therefore, the method may possibly be employed in processing the left ventricular volume curves.


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