Beat-to-Beat Analysis of Left Ventricular Pressure-Volume Relation and Stroke Volume by Conductance Catheter and Aortic Modelflow in Cardiomyoplasty Patients

Circulation ◽  
1995 ◽  
Vol 91 (7) ◽  
pp. 2010-2017 ◽  
Author(s):  
J.J. Schreuder ◽  
F.H. van der Veen ◽  
E.T. van der Velde ◽  
F. Delahaye ◽  
O. Alfieri ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Conductance Catheter ◽  
Volume Relation

scholarly journals Quantitative effects of myocardial edema on the left ventricular pressure-volume relation

1993 ◽  
Vol 106 (4) ◽  
pp. 651-657 ◽  
Author(s):  
Daphne T. Hsu ◽  
Zen-Chung Weng ◽  
Alfred C. Nicolosi ◽  
Paul W. Detwiler ◽  
Robert Sciacca ◽  
...  
Keyword(s):  
Left Ventricular Pressure ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Volume Relation

scholarly journals Synergistic Model of Cardiac Function with a Heart Assist Device

2019 ◽  
Vol 7 (1) ◽  
pp. 1
Author(s):  
Eun-jin Kim ◽  
Massimo Capoccia
Keyword(s):  
Cardiac Function ◽  
Heart Diseases ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Self Organization ◽  
Ventricular Pressure ◽  
Time Varying ◽  
Assist Device ◽  
Clinical Scenarios ◽  
Volume Relation

The breakdown of cardiac self-organization leads to heart diseases and failure, the number one cause of death worldwide. The left ventricular pressure–volume relation plays a key role in the diagnosis and treatment of heart diseases. Lumped-parameter models combined with pressure–volume loop analysis are very effective in simulating clinical scenarios with a view to treatment optimization and outcome prediction. Unfortunately, often invoked in this analysis is the traditional, time-varying elastance concept, in which the ratio of the ventricular pressure to its volume is prescribed by a periodic function of time, instead of being calculated consistently according to the change in feedback mechanisms (e.g., the lack or breakdown of self-organization) in heart diseases. Therefore, the application of the time-varying elastance for the analysis of left ventricular assist device (LVAD)–heart interactions has been questioned. We propose a paradigm shift from the time-varying elastance concept to a synergistic model of cardiac function by integrating the mechanical, electric, and chemical activity on microscale sarcomere and macroscale heart levels and investigating the effect of an axial rotary pump on a failing heart. We show that our synergistic model works better than the time-varying elastance model in reproducing LVAD–heart interactions with sufficient accuracy to describe the left ventricular pressure–volume relation.

scholarly journals Acute effect of clonidine on left ventricular pressure-volume relation in hypertensive patients with diastolic heart dysfunction

2001 ◽  
Vol 15 (9) ◽  
pp. 635-642 ◽  
Author(s):  
C Stefanadis ◽  
A Manolis ◽  
J Dernellis ◽  
C Tsioufis ◽  
E Tsiamis ◽  
...  
Keyword(s):  
Left Ventricular Pressure ◽  
Acute Effect ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Hypertensive Patients ◽  
Heart Dysfunction ◽  
Volume Relation

Effects of vasoactive intestinal peptide on myocardial performance

1994 ◽  
Vol 266 (2) ◽  
pp. H399-H405 ◽  
Author(s):  
N. P. Xenopoulos ◽  
R. J. Applegate
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Contractile Function ◽  
Time Derivative ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Adrenergic Blockade ◽  
Volume Relation ◽  
First Time

It is now recognized that stimulation of the vagus releases both acetylcholine (ACh) and vasoactive intestinal peptide (VIP). Whereas ACh depresses cardiac function, recent data indicate that VIP may have a cardiostimulatory effect. Exogenously administered VIP appears to enhance left ventricular (LV) contractile function; however, whether endogenously released VIP alters LV performance is not known. Accordingly, we evaluated the effects of exogenous VIP and endogenously released VIP during vagal stimulation after muscarinic and beta-adrenergic blockade (VS-B) on LV performance using pressure-volume analysis. Eight anesthetized open-chest dogs instrumented to measure LV pressure and volume (conductance catheter) were pretreated with atropine (0.1 mg/kg) and propranolol (1 mg/kg). The cervical vagi were transected. Hemodynamic data were obtained at steady state and during transient vena caval occlusion. Exogenous intravenous VIP (0.05 microgram/kg-1 x min-1) increased HR minimally [2.1 +/- 0.9% increase; P = not significant (NS)] but significantly increased maximum first time derivative of left ventricular pressure (dP/dtmax; 29.4 +/- 19.9% increase; P < 0.05) and the slope of the end-systolic pressure-volume relation (Ees; 3.1 +/- 1.3 to 8.9 +/- 4.2 mmHg/ml; P < 0.05). Minimum first time derivative of left ventricular pressure (dP/dtmin) decreased 22 +/- 16.2% (P < 0.05), and the time constant of isovolumic relaxation (tau) decreased 38 +/- 18% (P < 0.05). During VS-B (20 Hz, 15 v, 5 min), HR increased significantly (98 +/- 11 to 130 +/- 26 beats/min; P < 0.05). Ees also increased significantly (3.3 +/- 1.6 vs. 5.2 +/- 2.8 mmHg/ml; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of lactic acidosis on canine hemodynamics and left ventricular function

1990 ◽  
Vol 258 (4) ◽  
pp. H1193-H1199 ◽  
Author(s):  
K. Teplinsky ◽  
M. O'Toole ◽  
M. Olman ◽  
K. R. Walley ◽  
L. D. Wood
Keyword(s):  
Cardiac Output ◽  
Lactic Acidosis ◽  
Stroke Volume ◽  
Venous Return ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Right Atrial ◽  
Lactic Acidemia

Hypoperfusion states cause lactic acidosis, and the acidemia further reduces the inadequate cardiac output. Conceivably, the adverse effect of lactic acidemia on cardiac output is due to depressed contractility demonstrated in isolated myocardium. Alternatively, factors governing venous return cause a relative hypovolemic state and/or acidemic pulmonary vasoconstriction-induced right ventricular dysfunction. We reasoned that examination of left ventricular pressure-volume relationships at end systole and end diastole would determine which of these potential mechanisms accounted for reduced cardiac output during progressive lactic acidosis in anesthetized, mechanically ventilated dogs. Left ventricular (LV) volume was estimated from two pairs of epicardial ultrasonic crystals placed in the anterior-posterior and longitudinal planes, and LV pressure was obtained rom a catheter-tipped transducer. During progressive acidemia induced by a continuous intravenous infusion of 0.5 N lactic acid, cardiac output, stroke volume, and mean systemic arterial pressure fell significantly while mean pulmonary artery pressure and right atrial pressure increased significantly. These variables did not change with time in control (no-acid infusion) dogs. Lactic acidemia caused a 40% reduction in stroke volume, which could be attributed to depressed LV contractility, characterized by a decrease in maximum dP/dt as well as a fall in slope (Emax) with no change in volume intercept (Vo) of the left ventricular pressure-volume relationship at end systole. Neither the measured left ventricular end-diastolic pressure nor the estimated left ventricular end-diastolic volume (LVEDV) decreased with acidemia, suggesting that the reduced venous return did not result from relative hypovolemia. However, acidemic pulmonary hypertension may have interfered with the expected response to myocardial depression, which is an increase in LVEDV.

Cardiac Output Derived From Left Ventricular Pressure During Conductance Catheter Evaluations: An Extended Modelflow Method

2007 ◽  
Vol 21 (4) ◽  
pp. 227-235
Author(s):  
Sergio Valsecchi ◽  
Giovanni B. Perego ◽  
Jan J. Schreuder ◽  
Federica Censi ◽  
Jos R. C. Jansen
Keyword(s):  
Cardiac Output ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Conductance Catheter

A self-calibrating telemetry system for measurement of ventricular pressure-volume relations in conscious, freely moving rats

2004 ◽  
Vol 287 (6) ◽  
pp. H2906-H2913 ◽  
Author(s):  
Kazunori Uemura ◽  
Toru Kawada ◽  
Masaru Sugimachi ◽  
Can Zheng ◽  
Koji Kashihara ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Ventricular Pressure ◽  
Telemetry System ◽  
Conductance Catheter ◽  
Dual Frequency ◽  
Blood Resistivity ◽  
Freely Moving Rats ◽  
Freely Moving ◽  
Volume Relation ◽  
Parallel Conductance

Using Bluetooth wireless technology, we developed an implantable telemetry system for measurement of the left ventricular pressure-volume relation in conscious, freely moving rats. The telemetry system consisted of a pressure-conductance catheter (1.8-Fr) connected to a small (14-g) fully implantable signal transmitter. To make the system fully telemetric, calibrations such as blood resistivity and parallel conductance were also conducted telemetrically. To estimate blood resistivity, we used four electrodes arranged 0.2 mm apart on the pressure-conductance catheter. To estimate parallel conductance, we used a dual-frequency method. We examined the accuracy of calibrations, stroke volume (SV) measurements, and the reproducibility of the telemetry. The blood resistivity estimated telemetrically agreed with that measured using an ex vivo cuvette method ( y = 1.09 x − 11.9, r2 = 0.88, n = 10). Parallel conductance estimated by the dual-frequency (2 and 20 kHz) method correlated well with that measured by a conventional saline injection method ( y = 1.59 x − 1.77, r2 = 0.87, n = 13). The telemetric SV closely correlated with the flowmetric SV during inferior vena cava occlusions ( y = 0.96 x + 7.5, r2 = 0.96, n = 4). In six conscious rats, differences between the repeated telemetries on different days (3 days apart on average) were reasonably small: 13% for end-diastolic volume, 20% for end-systolic volume, 28% for end-diastolic pressure, and 6% for end-systolic pressure. We conclude that the developed telemetry system enables us to estimate the pressure-volume relation with reasonable accuracy and reproducibility in conscious, untethered rats.

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