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Biomedical subjects

R W Salo

Publications and source records attributed to R W Salo.

9 recordsLinked to original sources
PubMed1997

Acute hemodynamic improvement by pacing in patients with severe congestive heart failure.

Since the first report on dual chamber pacing for congestive heart failure (CHF) in 1991, a number of investigators have explored the topic with conflicting results. These conflicts may arise from an incomplete understanding of the mechanisms by which pacing improves cardiac function. Potential mechanisms include: (1) increase in filling time; (2) decrease in mitral regurgitation; (3) optimization of left heart mechanical atrioventricular delay (left heart MAVD); and (4) normalization of ventricular activation. One or more of these mechanisms may be operative in an individual patients, implying that patients may require individual optimization. Acute pacing studies were conducted on nine CHF patients, NYHA Class II-III to Class IV. Measurements of conduction times in sinus rhythm revealed: (1) normal interatrial conduction times (59 +/- 5 ms) in all patients, with wide variations in interventricular conduction times (range, -5-105 ms); and (2) a wide range of left heart MAVD (range, 97-388 ms). While pacing the right, left, or both ventricles, measurement of high fidelity aortic pressure and mitral and aortic velocities revealed the following: (1) 6 of 9 patients increased mean pulse pressure over sinus during RV or LV pacing at an optimal AV delay; (2) the maximum aortic pulse pressure was achieved when the atrium was not paced: an 8% increase over sinus pulse pressure with paced RV versus a 5% decrease for paced atrium and RV at optimum AV delay (paired Student's t-test, P = 0.01), and a 0% increase over sinus with paced LV versus 7% decrease for paced atrium and LV at optimum AV delay, P < 0.05; (3) significant dependence on pacing site was noted, with 4 patients doing best with RV pacing, 3 patients achieving a maximum with LV pacing, and 2 patients showing no preference; and (4) 2 of 4 patients with restrictive filling patterns were converted to nonrestrictive patterns with optimum pacing. Patient hemodynamics appear to benefit acutely from individually optimized pacing. Increases in filling time, optimization of left heart MAVD, and normalization of intraventricular activation are the most significant mechanisms. Atrial pacing is inferior to atrial sensed modes if the patient has a functional sinus node.

Cardiac Pacing, Artificial↗
PubMed1997

Problems and pitfalls in evaluating studies for pacing in heart failure.

Pacing therapy has been recently proposed as a new non-pharmacological approach to patients suffering from congestive heart failure refractory to medical therapy (refractory CHF), but the extention and the real benefit of this method remains to be defined. Although pacing therapy for refractory CHF has been restricted to patients in sinus rhythm presenting atrial, atrioventricular or interventricular conduction disturbances, considerable conflicting results have been published. The contradictory data is most likely due to large heterogeneity of the investigated study population (ie etiology of CHF, NYHA class, duration of follow-up, end-points of the study, etc.), to difference in study methology as well as in the site and modality of acute and chronic pacing. Although several empirical data indicates, at least in some individuals, major improvement in CHF symptoms by properly coordinating the atria and the ventricles thus reducing pre-systolic mitral and/or tricuspidal regurgitation or finally, prolonging the diastolic filling time, a lack of understanding of the mechanisms responsible for acute and chronic benefit persists. In evaluating pacemaker therapy as a new supportive treatment for CHF, the clinical investigator must consider that each study protocol embodies assumptions and methodological limitations and thus provides an incomplete analysis of potential benefit. Relying solely on noninvasive measures is risky due to problems of sensitivity and repeatability.

Cardiac Pacing, Artificial↗
PubMed1993

Improvement of cardiac function in patients with severe congestive heart failure and coronary artery disease by dual chamber pacing with shortened AV delay.

Medical therapy often fails to control symptoms of severe heart failure. The possibility of modifying to some degree the global ventricular performance with the implantation of a physiological dual chamber pacemaker, set with a short atrioventricular delay (100 msec), has been adopted in two patients with severe heart failure due to coronary artery disease. The baseline clinical condition of both patients was characterized by leg edema, ascites, dyspnea at rest, or even orthopnea with a functional New York Heart Association (NYHA) class III-IV. Acute measurements of hemodynamic and echocardiographic parameters during stepwise shortening of AV interval guided the pacemaker implantation and setting of AV delay in the chronic phase. Within a few days after pacemaker implantation, both patients considerably improved their clinical status as well as their functional NYHA class, improving to class II in one patient and to class II-III in the other patient. In addition, modification of systolic and diastolic parameters paralleled these improvements functional class and clinical condition. Pacemaker therapy in severe heart failure refractory to medical therapy can be of considerable benefit in patients whose quality-of-life is severely compromised when pharmacological therapy is no longer effective. Acute hemodynamic and echocardiographic testing is useful in assessing the most appropriate AV delay and pacing mode.

Aged↗
PubMed1992

Improvement in intracardiac impedance volumes by field extrapolation.

The measurement of volume by electrical impedance is complicated by non-homogeneous current distribution resulting from small current sources, by the irregular shape of the ventricle, and by loss of current to surrounding anatomical structures. A mathematical technique, field extrapolation, was developed to partially correct the current distribution. The technique mathematically transforms measured potentials into the potential distribution which would result from infinitely distant current sources. The linear correlation coefficient between impedance stroke volume or cardiac output using field extrapolation and thermodilution stroke volume or cardiac output was 0.83 (n = 86) in 11 dogs and 0.76 (n = 92) in 12 patients. The average linear correlation coefficient between impedance stroke volume and integrated aortic flow in four dogs was 0.83 +/- 0.09 (n = 49) using field extrapolation.

Animals↗
PubMed1986

The effect of VVI pacing and resultant atrioventricular dyssynchrony on segmental volumes.

Left and right ventricular volumes were monitored simultaneously in four anesthetized dogs by intracardiac impedance ventriculography during normal sinus rhythm, spontaneous ventricular rhythm, and VVI and VDD pacing. Cardiac output was found to increase with VVI pacing rate but remained somewhat lower than normal sinus or VDD values. The dissynchronous atrial contraction was found to distort the volume waveforms but had little effect on right ventricular volumes. Left atrial contraction had the greatest impact on left ventricular filling at near normal AV delays. Cardiac output during VDD pacing was found to be a maximum at 170 msec and decreased in three of four dogs at 220 msec. Examination of volume waveforms during "filling" indicates that the right ventricle is dominated by passive filling while the left ventricle demonstrates a large active or "fast" filling phase.

Animals↗
PubMed1984

Continuous ventricular volume assessment for diagnosis and pacemaker control.

Stroke volume measurements made by a catheter-based, right ventricular, intracardiac impedance system at rest and during upright bicycle ergometry were found to compare favorably with measurements made by acetylene rebreathing (r = 0.96, n = 13) and by radionuclide ventriculography (r = 0.96, n = 13) in a 46-year-old male pacemaker-dependent subject. The impedance information was then used to control the ventricular pacing rate during bicycle exercise, utilizing an algorithm that attempts to maintain a constant stroke volume. This resulted in a 23% increase in cardiac output accompanied by a 70% decrease in stroke volume as compared to the values measured during the same exercise at 70 pulses per minute (ppm).

Cardiac Output↗
PubMed1984

Instantaneous measurement of left and right ventricular stroke volume and pressure-volume relationships with an impedance catheter.

The feasibility of using continuous on-line recording of intraventricular electrical impedance to measure ventricular stroke volume was assessed in 12 patients at cardiac catheterization with a multielectrode impedance catheter and a 1.3 kHz measuring current of 4 microA. Stroke volumes determined by electrical impedance were compared with stroke volumes determined by the thermodilution technique in 10 patients and correlated with an r value of .95. Directional changes in impedance recordings throughout the cardiac cycle were also compared with volume curves obtained from six patients by radionuclide ventriculography, and in all instances the agreement between the two volume recordings was excellent. For all patients, on-line measurements of impedance showed a beat-by-beat decrease in stroke volume with the Valsalva maneuver and the administration of amyl nitrite, as well as an immediate increase in stroke volume in the contraction following an extra-systolic beat. Similar directional changes in stroke volume were recorded in both left and right ventricles. Left ventricular pressure-volume relationships were assessed with simultaneous left ventricular pressure recordings and volume signals recorded from the impedance catheter to determine if impedance measurements of volume can be used clinically. Pressure-volume diagrams were subsequently plotted, and for all patients these diagrams showed characteristic isovolumetric contraction and relaxation phases as well as typical ejection and filling periods. Moreover, beat-by-beat sequential pressure-volume diagrams constructed for patients during the administration of amyl nitrite revealed a linear end-systolic pressure-volume relationship.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMedDate not supplied

Effects of acute changes in canine LV-chamber volume and shape on accuracy of impedance catheter estimates of LV-chamber volume.

The accuracy with which a multiple-electrode impedance catheter (IC) tracks instantaneous global, in-situ left ventricular (LV) volumes was tested in 13 anesthetized dogs scanned in the Dynamic Spatial Reconstructor (DSR), a fast volumetric computed tomographic (CT) scanner. All dogs were scanned during control conditions and during an acute hemodynamic intervention. Hypertonic saline calibrations were performed for the IC prior to each DSR scan. In six of the dogs the IC-derived LV end-diastolic volume (Y) correlated with the DSR-derived global LV end-diastolic volume (X) as follows: end-diastolic volume, Y = 1.01X - 9.9, r = 0.812. The IC-derived LV end-diastolic volume, under control conditions, correlated with the DSR-derived truncated (i.e., that region of the LV chamber between the proximal and distal electrodes of the IC catheter) LV end-diastolic volume, Y = 1.00X + 17.4, r = 0.803. Under reduced preload the relation was Y = 1.3X - 15.26, r = 0.911. The segmental volume (between adjacent sensing electrodes on the IC) at the basal portion of the LV correlated poorly (Y = 1.88X + 3.3, r = 0.459 etc.), but correlated better at mid- and more apical LV levels (Y = 0.97X + 2.7, r = 0.762). Correlations between segmental stroke volumes were similar at basal (Y = 1.31X + 1.60, r = 0.815) and mid- and more apical levels (Y = 1.42X + 0.11, r = 0.763). Stroke volume during acute ischemia (two dogs) was Y = 1.33X - 1.41, r = 0.717; during acutely decreased preload (four dogs) it was Y = 1.24X - 2.88, r = 0.572). Thus, the IC tracks the changes in LV-chamber volume throughout a cardiac cycle quite well under a variety of conditions, but accuracy deteriorates as the shape of the LV chamber changes in response to changes in hemodynamic loading or local myocardial ischemia.

Animals↗