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Biomedical subjects

R H Pichel

Publications and source records attributed to R H Pichel.

33 records · Page 2Linked to original sources

Detection of left ventricular regional myocardial ischaemia in dogs by intraventricular conductance catheter.

Nine adult mongrel dogs were instrumented with ultrasonic microcrystals to measure left ventricular basal anteroposterior diameter and midwall myocardial segment length near the cardiac apex. Pneumatic cuff occluders were positioned around the left circumflex coronary artery near its origin and around the left anterior descending coronary artery two thirds of the way along its length. A pressure microtransducer was implanted into the left ventricle. Ten days after instrumentation the animals were anaesthetised with morphine chlorhydrate and pentobarbital sodium. An eight electrode catheter was advanced into the left ventricle to measure ventricular apical and basal regional and total electrical conductance. Minor ischaemia caused by occlusion of the left anterior descending artery was detected only by the electrode pair located near the apex, as decreased local ejection fraction. Major ischaemia caused by left circumflex artery occlusion was detected by both apical and basal electrode pairs and by total conductance, the three conductance signals indicating reduced ejection fractions compared with control values. The basal diameter signal indicated that basal regional motility changed only during major ischaemia, thus confirming the specificity of the changes in the basal conductance signals. The apical segment length signal confirmed the altered motility indicated by the apical conductance signal. These results suggest that regional wall motion abnormalities may be detected by the use of a multielectrode conductance catheter.

Animals↗

End-systolic pressure-volume relationships in dogs during ventilation with PEEP.

Whether left ventricular (LV) contractility changes during ventilation with positive end-expiratory pressure (PEEP) remains controversial. To assess LV inotropic state during PEEP using a load-independent index, we generated end-systolic pressure-volume relationships (ESPVRs) in eight closed-chest, chronically instrumented, anesthetized dogs undergoing 0 [zero end-expiratory pressure for the 1st time (ZEEP1)], 5 (PEEP-5), 10 (PEEP-10), and again 0 (ZEEP2) cmH2O PEEP. LV volume was calculated from three orthogonal internal diameters (sonomicrometry), and LV pressure was measured using an implanted transducer. ESPVRs at each level of PEEP were generated by transient inflation of a vena caval occluder. Despite significant decreases in cardiac output with PEEP-5 (1.81 +/- 0.38 l/min, means +/- SE; P less than 0.05) and PEEP-10 (1.70 +/- 0.46; P less than 0.01) with respect to ZEEP1 (2.12 +/- 0.41), no change was found in the slope (ZEEP1: 6.99 +/- 1.03 mmHg/ml; PEEP-5: 7.48 +/- 1.20; PEEP-10: 7.17 +/- 1.02; ZEEP2: 7.38 +/- 1.02), the volume intercept (ZEEP1: 7.4 +/- 3.4 ml; PEEP-5: 6.6 +/- 3.0; PEEP-10: 7.2 +/- 4.0; ZEEP2: 6.6 +/- 3.6), or the new index area beneath the ESPVR (ZEEP1: 304 +/- 98; PEEP-5: 329 +/- 104; PEEP-10: 310 +/- 98; ZEEP2: 343 +/- 114). We conclude that these levels of PEEP do not affect LV contractility as assessed by the ESPVR.

Animals↗

A computer study of the relation between chamber mechanical properties and mean pressure-mean flow of the left ventricle.

Computer simulation of left ventricular contraction was used to analyze the mean left ventricular pressure-mean flow relation with changes of parameter values: end-diastolic volume, contractile state, internal resistance, characteristic resistance, capacitance, end-diastolic stiffness, and heart rate and with changes of experimental conditions: filling kinetics (constant atrial pressure as opposed to constant end-diastolic volume) and coronary perfusion pressure (constant or varying with atrial pressure, i.e., self-perfused). The chamber mechanical properties used in the simulation were defined in terms of a modified purely elastic behavior model with a flow-dependent resistive component. Computed results showed that at constant end-diastolic volume and constant ventricular perfusion pressure the mean pressure-mean flow relation was linear, except for changes in internal resistance where a cubic fit of points was more appropriate. In these conditions, parameter variations in the accepted linear relation produced changes in the slope and mean pressure axis intercept. Imposition of changes in experimental conditions gave rise to nonlinear mean pressure-mean flow relations. The results indicate that with elastic-resistive chamber mechanical properties as a starting point, the experimental conditions would be responsible for the different shapes of the mean pressure-mean flow relation obtained in isolated heart experiments. However, a more complete description of chamber properties (such as the addition of a deactivation component) could also give rise to nonlinear pump function graphs.

Biomechanical Phenomena↗

Relationship between chamber mechanical properties and mean pressure-mean flow diagram of the left ventricle.

We undertook a theoretical analysis of the source resistance of the left ventricle represented in a mean pressure-mean flow (P-Q) diagram, using the chamber properties established in terms of the pressure-volume relationship. This analysis showed that P-Q pairs of points should lie above the linear function proposed by Elzinga and Westerhof. A third-order polynomial function would theoretically explain better than a linear relation or a parabolic fit the curved shape of experimentally obtained P-Q relationships. The analysis resolves the discrepancy between Elzinga and Westerhof's theoretical concept of linear source resistance and the actual nonlinear P-Q relationship.

Animals↗

Inconsistency of the slope and the volume intercept of the end-systolic pressure-volume relationship as individual indexes of inotropic state in conscious dogs: presentation of an index combining both variables.

We tested the ability of the slope (Emax) and the volume intercept (Vo) of the end-systolic pressure-volume relationship (ESPVR) to indicate contractility changes in conscious dogs instrumented with sonomicrometers measuring left ventricular diameter in three orthogonal axes and a left ventricular pressure microtransducer. ESPVRs were generated by inferior vena caval occlusion under control conditions (C1 and C2) and during enhanced (I+) and depressed (I-) inotropic states achieved by infusion of dobutamine and injection of propranolol, respectively. No significant difference between the first control (C1) and I+ or between the second control (C2) and I- were found for either Emax (C1, 5.31 +/- 1.68 mm Hg/ml, mean +/- SD; I+, 5.37 +/- 1.44; C2, 5.20 +/- 1.62; I-, 4.18 +/- 1.32) or Vo (C1, 10.3 +/- 9.6 ml; I+, 7.3 +/- 9.1; C2, 9.9 +/- 9.0; I-, 12.7 +/- 12.5), despite significant changes in other indexes of contractility. Comparison of changes in Emax in individual animals in response to I+ and I- revealed that 63% were nonsignificant, 28% were significant and expected, and 9% were significant and paradoxical. Within defined volume limits and irrespective of individual changes in Emax and Vo, in all animals I+ shifted the ESPVR above and to the left of C1 and I- shifted the ESPVR below and to the right of C2. We thus integrated the changes in Emax and Vo by measuring the area beneath each ESPVR between defined limits of end-systolic volume. The values for area were: C1, 612 +/- 150 mm Hg.ml; I+, 745 +/- 191 (p less than .001); C2, 520 +/- 198; I-, 420 +/- 139 (p less than .001). We conclude that (1) neither Emax nor Vo are individually reliable indexes of changed contractility, and (2) the area beneath the ESPVR between defined end-systolic volume limits is a consistent indicator of variations in inotropic state.

Animals↗

Animal model of acute pulmonary thromboembolism treated by local recirculation of streptokinase through the lung.

Massive acute pulmonary thromboembolism has a high mortality within the first few hours. Surgical intervention can remove only larger thrombi. Systemic fibrinolytic administration requires many hours for adequate treatment. We describe an anesthetized dog model of acute, massive, disseminated pulmonary thromboembolism achieved by injection of 1.7 ml/kg of 1-hour-old thrombi directly into the pulmonary artery. The emboli were lysed with 50,000 IU streptokinase recirculated for 20 minutes through the isolated pulmonary vascular bed by use of a roller pump while the systemic bed was supported by conventional cardiopulmonary bypass. On reestablishing natural circulation all hemodynamic parameters returned to preembolism values. Success of lysis was histologically confirmed. Perfusion of the pulmonary vascular bed without inclusion of streptokinase in the perfusate worsened the hemodynamic state of the animals compared with an untreated nonperfused control group.

Acute Disease↗

A comparative in vitro study of the closing characteristics of Björk-Shiley and Bicer-Val tilting disc mitral valve prostheses.

The replacement of mitral valves has become a relatively common procedure in cardiac surgery. Information concerning losses due to backflow through the valve may be used to assess and compare the physical characteristics of commercially available prostheses. A simple apparatus based on an artificial ventricle was used to measure closing volume, leakage volume, total volume, leakage rate and closing time on a beat by beat basis for Björk-Shiley and Bicer Val prosthetic mitral valves. The Björk-Shiley valve opened to 60 degrees and displayed a smaller closing volume than the Bicer Val, which opened to 75 degrees; and the Björk-Shiley displayed higher leakage than the Bicer Val, thus reducing its advantage in terms of closing volume. Overall, the Bicer-Val showed about 1 ml greater reflux per beat than the Björk-Shiley. Study of a Bicer-Val, modified to have an opening angle of 80 degrees, confirmed that valve closing volume was a function of opening angle.

Cardiac Output↗

Left intraventricular pressure-impedance diagrams (DPZ) to assess cardiac function. Part I: morphology and potential sources of artifacts.

Left ventricular function can be assessed with pressure-volume diagrams (DPV). Since there exists a relationship between ventricular volume changes and changes in intraventricular impedance (ZIV), we propose a diagram, DPZ, obtained from the intraventricular pressure (PIV) and the ZIV signals. This method was tested in 10 anesthetized mongrel dogs (morphine, sc, 30 mg/kg, and pentobarbital, sc, 5-7 mg/kg). PIV was measured with a Millar microtip catheter advanced under fluoroscopy via the femoral artery. ZIV was measured with a laboratory impedance meter (100 microA rms constant current, 12 kHz) in a tetrapolar configuration using another intraventricular catheter. ECG, aortic pressure and basal ZIV were also recorded to help identification of the different cardiac cycle phases on the diagram. Single-beat and multiple-beat loops were obtained in bradycardia and tachycardia to test for repeatability. These loops were always of a quadrangular-like shape with clockwise rotation. No attempt was made to calibrate the impedance axis in terms of volume. Apparent small volume changes in the isovolumic phases were probably due to ZIV catheter bending and/or movement. It is suggested that DPZ can serve in itself as a complementary evaluation tool of ventricular function by application of different maneuvers (physical, physiological of pharmacological).

Animals↗

Left intraventricular pressure-impedance diagrams (DPZ) to assess cardiac function. Part II: determination of end-systolic loci.

UNLABELLED: By means of tetrapolar intraventricular impedancimetric measurements and by modifying the aortic impedance with a brief volume unit step afterload increase, with a balloon catheter, we obtained the geometric locus of the end-systolic pressure-admittance points (PES-YES) from the beat to beat pressure-impedance diagram (DPZ), usually three or four beats after inflation. Six experiments in five anesthetized mongrel dogs (average weight 21.6 kg, SD 2.5) were carried out under control conditions and after a slow infusion (4 micrograms/kg/min) of epinephrine to change the myocardial inotropic state. In control, the PES-YES points fell in all cases on a straight line (average correlation 0.968, SD 0.033). After epinephrine, linearity was still good in four experiments (average correlation 0.938, SD 0.059). All animals showed displacements of the regression lines after epinephrine with respect to control. However, the direction of the shifts was not always consistent: three dogs yielded an upward-leftward shift; one showed a crossing point between the two regression lines with an increase in slope after epinephrine; in the remaining two experiments (same dog in different days), the post-epinephrine regression lines of the pressure-admittance end-systolic points were displaced downwards and rightwards. Five out of the six experiments increased the slopes of the lines after infusion of epinephrine. IN CONCLUSION: the method supplied the end-systolic point locus obtained from simple cardiac catheterization and this locus was altered by inotropic intervention.

Animals↗

Multichannel tetrapolar admittance meter (MY) for intracardiac volume measurements in animals.

With an 8-electrode catheter, this instrument measures simultaneously five intraventricular sections of admittance and, also, total admittance, the latter obtained as the sum of five component sections. It injects through the two outermost electrodes of the catheter a constant current (828 microA rms) of high frequency (14 kHz). Actually, the instrument measures the mathematical inverse of the resistive component (conductance) of the impedance seen by the voltage sensing electrodes. The sensitivity per channel was adjusted to 25 V/mho, resulting in an overall sensitivity of 5.28 V/mho for the total intraventricular admittance. Nonlinearity in any single channel was less than or equal to 3.4% while, for the total admittance, it was less than or equal to 1.5%. The difference between any two individual channels when the same calibration resistor was connected, relative to the expected value, was less than or equal to 4.8%. The equipment demonstrated good performance in animal experiments and showed the possibility of detecting localized dysfunctions. Human applications still remain to be done.

Animals↗

Characterization of ventricular dynamics in dogs using computerized variables and their statistical treatment.

To improve the analysis of mechanical events of the cardiac cycle and the selection of indexes of cardiac function, it is necessary to obtain the most probable time course of a given variable or of the shape of a loop. With this objective, a special program has been devised to obtain mean time tracings of left ventricular pressure (LVP) and posterior wall thickness (PWTH). The time scale can be normalized or beats with small variation in duration can be chosen. Mean loops are obtained in dogs by relating mean LVP and PWTH values. The distribution of pairs of individual values is assumed as normal bivariate with respect to its corresponding mean value, yielding confidence and tolerance ellipses. Results show that for a 95% confidence limit the loop is open in normal conditions. We postulate that this statistical treatment, by giving a more precise course of a mechanical signal allows a more accurate comparison between different experimental or clinical situations in the whole cardiac cycle, as well as the development of cardiac indexes.

Animals↗

The effect of the new calcium antagonist nisoldipine (BAY k-5552) on myocardial infarct size limitation in conscious dogs.

The effect of the new calcium antagonist nisoldipine (BAY k-5552) on myocardial infarct size was studied in four groups of conscious dogs undergoing acute left anterior descending coronary artery occlusion. Group I received placebo for 48 hours before and for 24 hours after occlusion; group II received placebo before and nisoldipine (0.3 mg/kg orally every 6 hours) after occlusion; group III received nisoldipine before and placebo after occlusion; and group IV received nisoldipine before and after occlusion. Infarct size was quantified with the tetrazolium red staining technique. Infarcted ventricular mass was 24.5 +/- 6.6% (mean +/- SD) for group I (control), 21.4 +/- 4.4% for group II (p = NS against control), 13.9 +/- 4.5% for group III (p less than 0.05), and 14.1 +/- 4.0% for group IV (p less than 0.05). Post occlusion sudden death was 30% in non-pretreated dogs and 0% in pretreated dogs (p less than 0.001). We conclude that prophylactic oral treatment with nisoldipine decreases infarct size and lowers the incidence of sudden death in conscious dogs undergoing acute coronary occlusion.

Animals↗

Experimental acute right ventricular failure and right ventricular assist in the dog.

We describe a technique for the production of acute progressive right ventricular failure in experimental animals that mimics the hemodynamic characteristics of right ventricular failure found in some patients being weaned from extracorporeal circulation after surgical repair of left ventricular abnormalities. The technique combines three alterations of right ventricular state: excision of the tricuspid valve, ventriculotomy, and ligation of the right coronary artery. Seven control dogs died within 3 hours after this intervention. Death was due to low cardiac output as a result of low left atrial and pulmonary arterial pressures. Right atrial pressure was high. Use of a right ventricular assist device in an additional seven dogs to pump blood from the right atrium to the pulmonary artery confirmed good preservation of left ventricular function by reestablishing adequate left ventricular filling pressure. All seven dogs survived for more than 3 hours. The validity of the technique in restricting failure principally to the right ventricle was thus demonstrated.

Animals↗

A cardiac output monitor and diagnostic unit for pneumatically driven artificial hearts.

The pneumatic artificial heart uses a flexible diaphragm to separate blood from air. The air space behind the diaphragm is connected to the atmosphere during diastole. Blood entering the heart during diastole displaces an equal volume of air into the atmosphere. A pneumotachograph is used to sense this flow of air. Integration of the airflow signal with respect to time yields the volume of air displaced during diastole, which is equal to the volume of blood entering the heart over the same period. This measured filling volume is equal to the cardiac output when averaged over a number of cardiac cycles. Allowance is made for regurgitant losses owing to the prosthetic heart valves. The output of the pneumotachograph is independent of absolute pressure, and so the device may also be used during the systolic (air compression) phase of the cardiac cycle. Analysis of the display of the airflow curves during diastole and systole has great diagnostic value. This device is accurate, easy to calibrate, stable, noninvasive, and does not require modification of any existing air-driven artificial hearts.

Air↗