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At least 19 recordsLinked to original sources
PubMed1988

A new multisensor pacing system using stroke volume, respiratory rate, mixed venous oxygen saturation, and temperature, right atrial pressure, right ventricular pressure, and dP/dt.

A new multisensor pacing device using respiratory rate (RR), stroke volume (SV), oxygen saturation (SO2), temperature (T), right atrial pressure (RAP), right ventricular pressure (RVP) and right ventricular dP/dt, has been developed. It consists of a 7F multisensor catheter and an external pacing unit. It allows simultaneous recording of the input signals and the corresponding data can be compared among the different parameters under identical conditions. Furthermore, several parameters can be combined in such a way as to form a new combination better suitable for rate responsive pacing. The response of each parameter to exercise was studied in 12 healthy volunteers (mean age: 28 years). Exercise testing was carried out using a bicycle ergometer, with workloads up to 200 W. The dynamic characteristics, response and sensitivity to changes of workloads of each parameter were analyzed and compared to one another. SO2 proved to be a quick responding parameter (less than 10 sec) with higher sensitivity in the low exercise range (less than 75 W), T, on the other hand, responded slowly (greater than 30 sec) to exercise changes and had the highest sensitivity in the exercise range beyond 75 W. RR displayed a slow response (greater than 30 sec) and an adequate sensitivity was only found in the upper exercise range (greater than 100 W). SV reacted rapidly to workload changes (less than 10 sec) but showed poor sensitivity at all exercise levels. RAP, RVP and dP/dt displayed quick responses and constantly good sensitivity throughout the workload range. Furthermore, respiratory rate was easily derived from the RAP curve. Special algorithms were developed for each parameter so that pacing rate would reproduce sinus rate behavior. We found that SO2 and all pressure parameter imitated sinus rate response quite well. When using parameter combinations, SO2 and T proved to be superior. Five patients (mean age 68 years) with third degree AV-block were stimulated temporarily using this system. Compared to fixed rate stimulation (VVI 70), exercise performance improved, using SO2 as the input parameter for rate response, by 25% to 50%.

Adult↗
PubMed1990

Right ventricular pressure during ventricular arrhythmias in humans: potential implications for implantable antitachycardia devices.

Implantable defibrillators use algorithms based on ventricular electrographic data to detect the onset and termination of arrhythmias, but these algorithms do not always differentiate hemodynamically stable from unstable arrhythmias. Although, ideally, left ventricular function should be used to assess the hemodynamic state, right ventricular pulse pressure can be assessed in humans on a long-term basis with a transvenous lead. The potential utility of right ventricular pulse pressure to assess hemodynamic stability was studied in 22 patients with induced ventricular arrhythmias. Right ventricular pressure was measured with use of a transvenous right ventricular endocardial pacing lead with a piezoelectric bender pressure sensor 3 cm from its tip. Single ventricular premature paced beats administered in up to a bigeminal frequency did not alter the mean right ventricular pulse pressure (control 33.7 +/- 26, bigeminy 35.7 +/- 26 mm Hg). Twenty-one episodes of induced ventricular tachycardia were studied in the electrophysiology laboratory. Five seconds after tachycardia induction, hemodynamically stable ventricular tachycardia had a longer cycle length (294 +/- 41 ms) and the right ventricular pulse pressure ratio was higher (0.55 +/- 0.26) than that in unstable ventricular tachycardia (cycle length 256 +/- 55 ms, p = 0.06; pulse pressure ratio 0.26 +/- 0.09, p less than 0.05). Twenty episodes of ventricular fibrillation were induced in eight patients. One second after induction, right ventricular pulse pressure decreased from 25 +/- 5 to 6 +/- 3 mm Hg (p less than 0.05). On the first beat after defibrillation, right ventricular pulse pressure increased to 24 +/- 14 mm Hg, a level not significantly different from that before the induction of ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Coronary oscillatory flow amplitude is more affected by perfusion pressure than ventricular pressure.

In this study on the isolated, maximally vasodilated, blood-perfused cat heart we investigated the relation between left ventricular developed pressure (delta Piv) and coronary oscillatory flow amplitude (diastolic minus systolic flow, delta F) at different levels of constant perfusion pressure (Pp). We hypothesized that the effect of cardiac contraction on the phasic flow results from the changing elastic properties of cardiac muscle. The coronary vessel compartment can, as can the left ventricular lumen compartment, be described by a time-varying elastance. This concept predicts that the effect of left ventricular pressure on delta F is small, whereas the effect of Pp is considerable. Both the waterfall model and the intramyocardial pump model predict the inverse. The relation between delta Piv and delta F at a Pp of 10 kPa is delta F = (4.71 +/- 3.08).delta Piv + 337 +/- 75 (slope in ml.min-1.100 g-1.kPa-1 and intercept in ml.min-1.100 g-1; n = 7); the relation between (constant levels of) Pp and delta F at a constant delta Piv of 10 kPa is delta F = 51.Pp + 211 (slope in ml.min-1.100 g-1.kPa-1 and intercept in ml.min-1.100 g-1; n = 6). The differences in slope are best predicted by the time-varying elastance concept.

Animals↗
PubMed1990

Left ventricular pressure effects on right ventricular pressure and volume outflow.

Massive destruction of the right ventricular free wall has been shown to cause only mild hemodynamic alterations. Further, the derivative of right ventricular (RV) pressure (P) is broad or double peaked, with one peak occurring coincidentally with peak left ventricular (LV) dP/dt. Both observations suggest a direct LV assistance to RV function. Since the ventricles contract nearly simultaneously, the relative contribution of LV to RV pump function has been difficult to determine. This LV assistance was quantified in six canine experiments using a unique electrically isolated RV preparation. While on total cardiopulmonary bypass, the RV free wall was electrically isolated from the remainder of the heart. This preparation allowed for wide variations in the timing interval between RV and LV contractions. Double-peaked waveforms for RVP and pulmonary flow (RVF) occurred over a wide range (0 to 300 ms) of pacing intervals between the RV and LV. One derivative peak always followed RV contraction for RVP and RVF (r = 0.971 +/- .011, P less than 0.01: r = 0.972 +/- .012, p less than 0.01; respectively). The second derivative peak was unrelated to the RA-RV pacing interval (r = 0.297 +/- .191, P greater than 0.5 RVP; 4 = 0.237 +/- .278, P greater than 0.5 RVF), but corresponded to the maximal LVP rise. Additionally, the magnitude of the two derivative peaks was similar when the ventricles contracted synchronously. When RV contraction preceded or followed LV contraction, the derivative peak associated with LV contraction was significantly greater (P less than 0.05, range 2.1 +/- 0.6 to 6.7 +/- 1.6 for RVP; P less than 0.05 range 1.9 +/- 0.4 to 6.7 +/- 1.5 for RVF) than the derivative associated with RV contraction. These data demonstrate a normally present, large LV assistance to RV contraction and may help to explain the RV response to myocardial infarction.

Animals↗
PubMed1984

Effect of right ventricular pressure on the end-diastolic left ventricular pressure-volume relationship before and after chronic right ventricular pressure overload in dogs without pericardia.

We studied the effect of chronic right ventricular pressure overload on diastolic ventricular interdependence in dogs without pericardia, instrumented to measure left ventricular pressure, right ventricular pressure, and 3 left ventricular dimensions. We studied 12 dogs before (control) and nine dogs after 6 weeks of pulmonary artery constriction producing systolic right ventricular pressure greater than or equal to 70 mm Hg. Compared to control, following pulmonary artery band there was greater (P less than 0.01) interventricular septal mass (53 +/- 15 vs. 35 +/- 7 mg, mean +/- SD), thickness (15 +/- 2 vs. 10 +/- 1 mm), and ratio of the surface area of the interventricular septal to total left ventricular surface area (0.38 +/- 0.03 vs. 0.33 +/- 0.02), but unchanged left ventricular free wall mass (81 +/- 12 vs. 84 +/- 14 mg) and thickness (11 +/- 2 vs. 11 +/- 2 mm). End-diastolic right and left ventricular pressures and left ventricular volume were varied by vena cava and pulmonary artery occlusions and releases. Volume was calculated as an ellipsoid and the data in each dog fit to: left ventricular pressure = a0 + a1V + a2V2 + a3V3 + a4V4 + bPRV, r greater than or equal to 0.91 in each dog. During control, b was similar, whether calculated from both pulmonary artery and vena cava occlusions (0.47 +/- 0.09) or from vena cava occlusions alone (0.43 +/- 0.11), and was greater than the ratio of the interventricular septal surface area to left ventricular surface area (0.33 +/- 0.02, P less than 0.05). Following the pulmonary artery band, b decreased to 0.21 +/- 0.10 (P less than 0.05) and was less than the ratio of interventricular septal surface area to the left ventricular surface area which increased to 0.38 +/- 0.03 (P less than 0.05). We conclude that the effect of alterations in right ventricular pressure on the end-diastolic left ventricular pressure volume relationship, independent of the pericardium, is reduced following the pulmonary artery band that produces interventricular septal hypertrophy. These results are consistent with the hypothesis that the effect of alterations of right ventricular pressure on the diastolic left ventricular pressure-volume relationship depends on the relative elastance of the interventricular septum and left ventricular free wall, and not simply on the ratio of the interventricular septal surface area to the left ventricular surface area.

Animals↗
PubMed1995

[The evaluation of systolic right ventricular pressure and right ventricular hypertrophy using body surface mapping (isointegral map, isochrone map)].

We studied QRS and QRST isointegral maps, and isochrone map for the diagnosis of right ventricular hypertrophy and its severity in atrial septal defects and primary pulmonary hypertensions. The discriminant analysis in QRS isointegral map showed better results for differential diagnosis between atrial septal defects and both normal subjects and incomplete right bundle branch block patients than these in QRST isointegral map and isochrone map. Three parameters (Qp/Qs, systolic right ventricular pressure, right ventricular ejection fraction) for right ventricular overload showed significant correlation with QRS isointegral map and QRS isopotential map. Thus body surface map was an useful method for the evaluation of right ventricular hypertrophy.

Body Surface Potential Mapping↗
PubMed1985

Halothane effects on subendocardial oxygen supply-demand balance: estimation from intramyocardial tissue pressure and left ventricular pressure.

We evaluated the effect of halothane on the balance of subendocardial oxygen supply and demand in six dogs by estimating the endocardial viability ratio (EVR) based on the pressure generated within the subendocardium (ENDO-IMP). Concurrently, the conventional EVR based on left ventricular pressure (LVP) was estimated and compared with the EVR based on ENDO-IMP. The subendocardial oxygen supply-demand ratio based on ENDO-IMP (IMP-EVR) was significantly less than EVR based on LVP (LVP-EVR) (0.87 +/- 0.03 vs 1.07 +/- 0.06, P less than 0.05) during the control period. With 0.5% halothane administration, IMP-EVR improved significantly (1.04 +/- 0.07, P less than 0.05) while LVP-EVR remained unchanged (1.08 +/- 0.09). No further changes in EVR (either IMP-EVR or LVP-EVR) were observed with increasing halothane concentrations up to 2%. The relationship between the two indices was weak (r2 = 0.44, P less than 0.001) but statistically significant. Because an estimate of EVR based on direct measurement of subendocardial tissue pressure (IMP-EVR) would reflect more accurately the oxygen supply-demand balance of this region than the LVP-EVR, our results suggest that the oxygen balance of the subendocardium improves with halothane administration. The use of LVP-EVR as a hemodynamic index of subendocardial oxygen balance during halothane anesthesia, therefore, is questionable.

Anesthesia↗
PubMed1990

[Non-invasive Doppler echocardiography assessment of right ventricular pressure in patients with ventricular septal defect].

In patients with VSD right ventricular pressure can be determined noninvasivly by subtracting the VSD-gradient from the systolic blood pressure. Using a stand-alone continuous-wave Doppler the VSD-gradient may be underestimated due to a large angle theta caused by the various VSD locations and the often atypical VSD-jet directions. Therefore Color-Doppler was used to visualize the VSD-jet and to align (angle less than 15 degrees) the continuous-wave Doppler beam. 37 patients, who underwent catheterization were studied. By VSD-jet visualization 3 patients were correctly identified in whom the VSD gradient would have been underestimated due to a large angle 0. They were excluded from this study because of the resulting error. In the remaining 34 patients VSD-gradients up to 105 mmHg were measured. A good correlation was found between the noninvasively an invasively determined right ventricular pressures: r = 0.93; y = 1.06x -2.4. One source of error in this method is the difference between the maximal instantaneous and the peak to peak VSD-gradient. Differences of up to 39 mmHg were found when the maximal instantaneous gradient occurred either very early or very late in systole. In these cases the midsystolic gradient should be used. It is concluded that the presented method is easy to perform and permits a reliable noninvasive estimation of the right ventricular pressure in patients with VSD.

Adolescent↗
PubMed1995

Effect of negative intrathoracic pressure on left ventricular pressure dynamics and relaxation.

To investigate the effect of a fall of intrathoracic pressure on left ventricular (LV) hemodynamics and relaxation, simultaneous micromanometric recordings of LV and aortic pressures were performed at rest and during two graded Mueller maneuvers in 16 patients undergoing cardiac catheterization for aortic valve stenosis (n = 8) or chest pain (n = 8). The reductions (means +/- SE) of airway pressure during the lesser and greater maneuvers were 26 +/- 1 and 42 +/- 1 mmHg, respectively. Simultaneously, LV isovolumic-developed pressure increased by 9 +/- 3 and 21 +/- 4 mmHg, respectively (P < 0.03 for both). During the greater maneuver, the individual changes of the time constant of LV isovolumic relaxation (tau) correlated with the changes of LV isovolumic-developed pressure (r = 0.73; P = 0.002). In patients with a > 20-mmHg rise in isovolumic-developed pressure, tau increased by 10.3 +/- 4.6 ms. By multiple-regression analysis, the change of tau was related directly to the change of isovolumic-developed pressure (standardized coefficient beta = 0.80; P = 0.001) and inversely related to the resting systolic LV-aortic pressure gradient (beta = -0.37; P = 0.050). The other hemodynamic changes were independent of aortic valve stenosis. In conclusion, during the Mueller maneuver, the LV isovolumic contraction load increases and tau lengthens, particularly with higher elevations of LV systolic load.

Adult↗
PubMed1989

Effects of left ventricular pressure reductions on right ventricular systolic performance.

Reductions in left ventricular pressure (LVP) have been shown to produce a leftward shift of the interventricular septum and to reduce left ventricular contribution to right ventricular performance. To evaluate the magnitude of this contribution in the intact heart, five anesthetized pigs were implanted with a left prosthetic ventricle to gradually decrease LVP while maintaining arterial systemic pressure. Three descriptors of RV global and regional systolic function were studied in the septum to free wall (RVSFW) and anterior to posterior (RVAP) dimensions and in an outflow tract segment length (RVSL), during both steady state and transient inferior vena cava occlusion. LVP gradual reduction from 102 +/- 4 to 11 +/- 3 mmHg (90% decrease in peak systolic pressure) produced no changes in the RV global stroke work curve or in the RVAP and RVSL pressure-dimension relationships. However, the reduction in LVP resulted in parallel shifts in the RVSFW dimension, with 16.6 +/- 6.7% increase in the intercept D(o) of the end-systolic relationship and 16.5 +/- 2.5% increase in D(o) of the dimensional stroke work relationship, with no significant changes in their respective slopes as calculated by linear regression. Therefore, in the normal intact heart, large reductions in left ventricular pressure affect the geometry of the right ventricle because of septal shifting, but there is a negligible net effect of this anatomic ventricular interaction on overall right ventricular performance.

Animals↗
PubMed1992

[Left ventricular behavior following acute right ventricular pressure overload: an experimental study].

Relationships between biventricular pressures, left ventricular shape and paradoxical septal motion in patients with right ventricular pressure overload (RVPO) are unknown. To clarify these relationships, we measured left and right ventricular short-axis dimensions and ventricular pressures using anesthetized open-chest dogs with pulmonary embolizations. With repeated microembolization, right ventricular systolic pressure (RVSP) increased stepwise from a level of 27 mmHg to the maximum value of 72 mmHg. This elevation caused gradual leftward shift of the interventricular septum (IVS) both at end-diastole and end-systole. Further embolization caused collapse (shock: left ventricular systolic pressure: LVSP < 70 mmHg) with a fall in RVSP. In the state of shock, the rise in right ventricular end-diastolic pressure (RVEDP) and fall in left ventricular end-diastolic pressure (LVEDP) were prominent, and the degree of shift of the IVS became significantly greater at end-diastole than at end-systole, resulting in paradoxical motion of the IVS. There were significant linear relationships between the degree of end-diastolic IVS displacement and end-diastolic transseptal pressure (LVEDP-RVEDP), and between the degree of end-systolic IVS displacement and end-systolic transseptal pressure (LVESP-RVESP) throughout the course of repeated pulmonary microembolization even in the state of shock. In conclusion, abnormal movements of the IVS in RVPO patients indicate the presence of a marked decrease in end-diastolic transseptal pressure due to right ventricular failure.

Animals↗
PubMed1983

A clinical comparison of subdural screw pressure measurements with ventricular pressure.

Simultaneous recordings of intracranial pressure (ICP) from a single-lumen subdural screw and a ventricular catheter were compared in 10 patients with severe head injury. Forty-one percent of the readings corresponded within the same 10 mm Hg ranges, while 13% of the screw pressure measurements were higher and 46% were lower than the associated ventricular catheter measurements. In 10 other patients, also with severe head injury, pressure measurements obtained with the Leeds-type screw were similarly compared with ventricular fluid pressure. Fifty-eight percent of the dual pressure readings corresponded, while 15% of the screw measurements were higher and 27% were lower than the ventricular fluid pressure, within 10-mm Hg ranges. It is concluded that subdural screws may give unreliable results, particularly by underestimating the occurrence of high ICP.

Cerebral Ventricles↗
PubMed1993

Interpretation of cardiac pathophysiology from pressure waveform analysis: simultaneous left and right ventricular pressure measurements.

In addition to demonstrating constrictive and restrictive cardiac physiology, simultaneous right and left ventricular pressure measurements can be helpful to identify various aspects of myocardial dysfunction. Intracardiac conduction defects will displace the right ventricular pressure under the left ventricular pressure upstroke and identify differences in the timing of ventricular contraction. Right ventricular dysfunction will also produce abnormal right ventricular pressure waveforms which may overlap left ventricular pressure and contribute to abnormalities in right atrial and ventricular pressure waveforms.

Adult↗
PubMed1993

Left ventricular pressure transmission to myocardial lymph vessels is different during systole and diastole.

In six open-thorax-anaesthetized dogs with paced hearts and a retrogradely cannulated epicardial lymph vessel, the sensitivity of myocardial lymph pressure to left ventricular pressure during systole and during diastole was determined. The lymph vessels were cannulated using PE-90 tubing, and lymph pressure was measured by connecting the cannula to a microtip pressure transducer. To obtain the systolic sensitivity, left ventricular pressure was changed by clamping the descending aorta, which caused left ventricular pressure to increase. The diastolic sensitivity was obtained from natural variation to left ventricular pressure caused by atrial contractions during induced long diastoles. The mean ratio of the pulse in lymph pressure to the pulse in left ventricular pressure was determined: systole: 0.069 +/- 0.013, n = 213, diastole: 0.76 +/- 0.16, n = 249 and, if possible, linear regression analysis between lymph and left ventricular pressure was performed. The systolic regression coefficients could be determined in six dogs and the diastolic coefficients in three dogs. During long diastoles lymph pressure variations are on average 76 per cent of those in the left ventricle. However, during systole, the sensitivity of lymph pressure to left ventricular pressure is more than ten times lower. It is not unlikely that the structural embedment of lymph vessels within the myocardium is such that volume variations by cardiac contraction are limited.

Animals↗
PubMed1975

[Measurement of mean pulmonary pressures and right systolic ventricular pressure by radiocardiography].

Computer exploitation of some parameters of the radiocardiogram and of the pressures measured by catheterization in a series of 678 subjects, studied both in Paris and in Prague, has made it possible to establish regression equations providing the rates of mean pulmonary arterial and wedge pressures together with the systolic right ventricular pressure on the basis of the radiocardiogram data. The latter was obtained by the conventional technique of the isotope dilution curves or by gamma-angiocardiography. Easy repetition of radiocardiography makes it an interesting investigation for the haemodynamic follow-up of the patients with heart disease.

Barium↗
PubMed1992

Doppler echocardiographic demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling.

To compare the effects of isolated right ventricular pressure and volume overload on left ventricular diastolic geometry and filling, 11 patients with primary pulmonary hypertension, 11 patients with severe tricuspid regurgitation due to tricuspid valve resection and 11 normal subjects were studied with use of Doppler echocardiographic techniques. Right ventricular systolic overload in primary pulmonary hypertension resulted in substantial leftward ventricular septal shift that was most marked at end-systole and early diastole and decreased substantially by end-diastole. Right ventricular diastolic overload after tricuspid valve resection resulted in maximal leftward ventricular septal shift at end-diastole sparing end-systole and early diastole. The early diastolic distortion of left ventricular geometry associated with right ventricular pressure overload resulted in prolongation of isovolumetric relaxation of the left ventricle (129 +/- 39 ms) and a reduction in early diastolic filling compared with values in normal subjects. Late diastolic distortion of left ventricular geometry associated with right ventricular volume overload had no influence on the duration of left ventricular isovolumetric relaxation (52 +/- 32 ms) but caused a reduction in the atrial systolic contribution to late diastolic filling of the left ventricle compared with values in normal subjects. In patients with right ventricular pressure overload, 52 +/- 16% of left ventricular filling occurred in early diastole compared with 78 +/- 11% in patients with right ventricular volume overload (p less than 0.001). The differential effects of systolic and diastolic right ventricular overload on the pattern of left ventricular filling appear to be related to the timing of leftward ventricular septal displacement.

Adult↗
PubMed1996

Measurement of pulmonary artery diastolic pressure from a right ventricular pressure transducer in patients with heart failure.

Recent studies have demonstrated that pulmonary artery diastolic (PAD) pressure can be measured from a transducer positioned in the right ventricle (RV) based on the finding that PAD and RV pressures are equal at the time of pulmonary valve opening, which is associated with the time of maximum positive rate of pressure development (dP/dtmax) in the ventricle. The objective of this study was to assess the correlation between estimated PAD (ePAD) pressure, obtained through a RV transducer, and actual PAD (aPAD) pressure in patients with heart failure who have abnormal hemodynamics, reduced systolic function, and variable degrees of mitral regurgitation (MR) and tricuspid regurgitation (TR). Simultaneous measurements of pulmonary artery and RV pressures were obtained with a high-fidelity Millar catheter (Millar Instruments, Houston, TX) in 10 patients with New York Heart Association class III-IV heart failure who were being evaluated for cardiac transplantation. The overall correlation between ePAD and aPAD pressures was .92 (R2 = .878). This was not significantly different during the Valsalva maneuver (r = .96, R2 = .943), submaximal bicycle exercise (r = .87, R2 = .756), or infusions of dobutamine and nitroglycerin (r = .82, R2 = .730). The overall average difference between the average ePAD (24.6 +/- 7.0 mmHg) and aPAD (23.6 +/- 7.0 mmHg) pressures was 1.0 +/- 3.4 mmHg. The average difference between the two pressures in patients with mild to severe MR or TR was not different compared to those patients with no or trace MR or TR. The estimation of PAD pressure from an RV transducer is valid in patients with heart failure who have abnormal hemodynamics, reduced systolic function, and variable degrees of MR and TR. This correlation was observed at rest and during several provocative maneuvers. These data will be important for the development of a chronic, implantable hemodynamic monitor for patients with heart failure.

Adult↗