PubMed Health⌕ Search

Biomedical subjects

R Fletcher

Publications and source records attributed to R Fletcher.

At least 73 records · Page 4Linked to original sources

Ejection fraction, peak exercise oxygen consumption, cardiothoracic ratio, ventricular arrhythmias, and plasma norepinephrine as determinants of prognosis in heart failure. The V-HeFT VA Cooperative Studies Group.

BACKGROUND: Recognition of the complex pathophysiology of heart failure and its high mortality has emphasized the need for prognostic markers that can be used in clinical assessment as well as in the design of mortality trials. Data from the Department of Veterans Affairs Cooperative Vasodilator-Heart Failure Trials (V-HeFT I, 642 patients; V-HeFT II, 804 patients) were therefore examined to determine the influence of prerandomization measurements on subsequent mortality. METHODS AND RESULTS: Patients entered into these trials were men with cardiac dysfunction and reduced peak exercise capacity. Measurements included in this analysis were left ventricular ejection fraction (EF) measured by radionuclide angiography, peak bicycle exercise oxygen consumption (VO2), cardiothoracic ratio (CTR) measured on a chest x-ray, ventricular arrhythmias assessed in a core laboratory by short-term Holter monitoring, plasma norepinephrine and plasma renin activity measured in a core laboratory only in V-HeFT II, and a variety of diagnostic and demographic data. The variables related only weakly to each other. EF, VO2, and CTR were powerful independent predictors of all-cause mortality in both studies. Ventricular arrhythmia was a significant independent predictor in V-HeFT II but not in V-HeFT I. Plasma norepinephrine but not plasma renin activity measured in V-HeFT II also had independent prognostic value. Other variables did not exert an independent effect on mortality. CONCLUSIONS: Optimal assessment of the mortality risk in an individual or a group of individuals with heart failure uses measurement of EF, peak VO2, CTR, plasma norepinephrine, and the presence of ventricular arrhythmias.

Arrhythmias, Cardiac↗

The relationship between the arterial to end-tidal PCO2 difference and hemoglobin saturation in patients with congenital heart disease.

In right-to-left (RL) intracardiac shunting, the venous blood that is added to the oxygenated blood in the left heart is both poor in oxygen and rich in carbon dioxide. Thus, any given degree of arterial desaturation is associated with an obligatory arterial to end-tidal carbon dioxide tension difference (PaCO2--PETCO2). This paper presents a theoretical analysis of the relationship between PaCO2-PETCO2 and arterial hemoglobin saturation (SaO2) in cyanotic heart disease. Using the shunt equation as a starting point, a curvilinear, negative correlation between PaCO2-PETCO2 and SaO2 can be demonstrated. The slope of the regression of PaCO2--PETCO2 against SaO2 is shown to be positively correlated to Hb concentration, PaCO2, and the respiratory quotient R. The slope of the regression is also slightly increased at relatively high SaO2s and at high inspired oxygen fractions, although these latter factors are of lesser significance. However, in addition to the above primary effects of RL shunting, secondary effects may occur if pulmonary perfusion is reduced sufficiently to cause "alveolar hypoperfusion," which also creates an alveolar dead space. Primary and secondary effects are additive. This theoretical analysis is illustrated with a study of 27 children with congenital heart disease. Their lungs were ventilated with a Servoventilator 900 C, and carbon dioxide single-breath tests were obtained on-line with the use of a computerized system based on the Siemens-Elema carbon dioxide analyzer 930. Blood was sampled for PaCO2 measurement and arterial Hb saturation was measured by pulse oximetry (SpO2).(ABSTRACT TRUNCATED AT 250 WORDS)

Bicarbonates↗

Isocapnic high frequency jet ventilation: dead space depends on frequency, inspiratory time and entrainment.

Twelve healthy pigs were ventilated with high frequency jet ventilation via a Mallinckrodt HiLo jet tube. The expired gas was led to a conventional ventilator and CO2 analyzer which were used to measure CO2 elimination. There was no bias flow, so that the jet entrained only expired gas, i.e. rebreathing occurred. Frequency was varied between 2 and 11 Hz and the duration of inspiration, as a fraction of the ventilatory cycle (Ti/Ttot), from 5 to 20%. The minute ventilation, Vjet, delivered by the jet ventilator was adjusted to maintain a constant PaCO2. At 2 Hz and a Ti/Ttot of 5%, Vjet was of the same magnitude as ventilation during conventional intermittent positive pressure ventilation, and the total dead space fraction, VD/VT was 0.32. Both increasing frequency at a constant Ti/Ttot, and increasing Ti/Ttot at a constant frequency, increased VD/VT which was maximal (0.8) at 11 Hz and a Ti/Ttot of 20%. When entrainment was blocked, tidal jet volume had to be greatly increased. The continuous measurement of CO2 elimination was found to be useful for maintaining isocapnia when the jet ventilator setting was changed.

Animals↗

Evaluation of the effects of a pyrophosphate-fluoride anticalculus dentifrice on remineralization and fluoride uptake in situ.

Enamel slabs and thin sections with artificially formed caries lesions were placed in the removable dentures of 15 subjects who brushed them three times daily for 2 weeks with a 1.3% pyrophosphate/1,100 ppm F/1.5% Gantrez dentifrice, a 1,100-ppm F dentifrice without pyrophosphate or Gantrez, or a placebo dentifrice in a double-blind, crossover study. Analysis of the thin sections by quantitative microradiography showed that the pyrophosphate/F dentifrice remineralized the lesions 15.9% (p less than 0.05) and the fluoride dentifrice 11.2%, whereas the placebo produced 4.4% demineralization. Fluoride uptake by the enamel slabs was similar for both fluoride dentifrices and significantly greater from the placebo dentifrice (p less than 0.05). The findings suggest that the anticaries mechanisms of fluoride include not only the prevention of demineralization, but also the promotion of remineralization.

Adult↗

Effect of a steel mesh and human dental plaque on fluoride uptake in vitro.

Blocks of bovine enamel, covered with a steel mesh or a steel mesh plus plaque or with neither, were treated in vitro with a 20% slurry of a fluoride dentifrice for 1 h. An initial experiment showed that fluoride in blocks without mesh or plaque increased significantly, whereas fluoride in blocks covered with a steel mesh harboring intraorally accumulated plaque did not. A follow-up experiment showed that enamel blocks covered with the mesh but without plaque acquired a small amount of fluoride, but significantly less than the blocks without mesh. These experiments indicate that covering enamel specimens with mesh, as is done during in situ experiments, may significantly influence the transport of fluoride to the enamel and, therefore, the amount of fluoride acquired by the specimens and perhaps the degree of de- or remineralization. They also suggest that the fluoride distribution to some areas of the natural dentition may be inadequate.

Animals↗

Conditioning prepulse of biphasic defibrillator waveforms enhances refractoriness to fibrillation wavefronts.

The mechanism of biphasic waveform defibrillation threshold reduction is unknown. We tested the hypothesis that, during refractory period stimulation, sarcolemmal hyperpolarization by the first pulse of biphasic waveforms facilitates excitation channel recovery, which enhances graded responses produced by the second depolarizing pulse. This prolongs cellular refractoriness to fibrillation wavefronts when compared with a monophasic depolarizing stimulus. Monophasic (10 msec, rectangular wave) or symmetrical biphasic (10 msec, each pulse) current injection S2 stimuli at 1.5 and two times S1 threshold were used to scan the S1 action potential refractory period (S1 cycle length, 600 msec) in myocardial cell aggregates. S2 waveforms were delivered with normal and reversed polarity to test the hyperpolarizing action of biphasic waveforms. Responses to an S3 stimulus, which simulated a potential incoming fibrillation wavefront, were also determined. Results showed that biphasic S2 waveforms produced longer graded responses during and immediately after the S1 refractory period than did corresponding monophasic S2 waveforms. The maximum difference in response duration produced by the biphasic and monophasic waveforms was 58.6 +/- 10.0 msec (p less than 0.001). This maximum difference occurred 10 msec before the end of the S1 refractory period. The longer response durations produced by biphasic S2 also produced longer refractoriness to the S3 stimulus. The maximum difference in total refractoriness to S3 of 51.8 +/- 2.8 msec (p less than 0.002) occurred at the same S1S2 coupling interval as the maximum difference in S2 response duration. Prolonged refractoriness may protect ventricular cells from refibrillation wavefronts and act as the cellular basis for greater biphasic waveform defibrillation efficacy.

Animals↗