[Molecular genetic tests are not yet useful for diagnosis of malignant hyperthermia].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R Fletcher.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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)
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.
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.
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.
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.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Deadspace is defined in terms of the efficiency of the lung in eliminating carbon dioxide. The airway deadspace is the volume of the airway in which gas moves chiefly by convection. The alveolar deadspace is caused by ventilation/perfusion inequalities at the alveolar level. The commonest causes of increased alveolar deadspace are airways disease--smoking, bronchitis, emphysema, and asthma. Other causes include pulmonary embolism, pulmonary hypotension, and ARDS. In addition, right-to-left shunting (cyanotic heart disease, atelectasis) causes an apparent or virtual deadspace, which, although not representing non-perfusion of any compartment, nevertheless reduces the efficiency of ventilation.
There is little data directly comparing steroid-tipped permanent pacemaker leads to otherwise state-of-the-art porous platinum leads. Eighteen patients receiving unipolar generators capable of low voltage outputs were randomized at the time of implant to receive either steroid-tipped leads or porous platinum leads. All leads were unipolar, tined, passive fixation, and placed in the right ventricular apex or atrial appendage. This study is single center. At implant, threshold pulse width was determined at 3 voltages (2.5, 1.5, and 0.8 V). Follow-up thresholds were determined at weeks 1, 2, 3, and 4, and at 3 and 6 months. There was no difference in implant thresholds or amplitudes for sensing. By 2 weeks postimplant, lower thresholds were noted for the steroid leads, and this discrepancy grew more significant with time. There was no significant postimplant rise in threshold for steroid-tipped leads. At 6 months, the average threshold pulse width for ventricular steroid leads at 0.8 V was 0.3 +/- 0.1 msec. In contrast, five patients with standard leads did not capture at maximum pulse width at 0.8 V (P less than 0.0001). There was no significant difference in the amplitude of the chronic atrial electrogram. This study shows steroid-tipped leads to offer a significant advantage in reducing thresholds early postimplant and chronically.
The effect of a strontium-polyacrylate complex on fluoride uptake by bovine enamel was determined. A salivary pellicle was formed on sound enamel and enamel with artificially formed caries lesions. Ten specimens of each were treated with solutions containing (A) 225 ppm F, (B) 225 ppm F plus Sr complex, (C) 200 ppm F, 0.1 M phosphate, pH 4.5 or (D) placebo for 1 h and then washed 24 h to remove labile fluoride. Analysis of ten thin layers of enamel showed that, on both enamel types, solution (C) deposited the largest amount of fluoride. The strontium complex decreased fluoride deposition, particularly in the outermost layer.
Biphasic waveforms reduce defibrillation threshold compared with corresponding monophasic waveforms. However, effects of fibrillation duration on relative efficacy of monophasic and biphasic waveforms are unknown. This study used a newly developed defibrillation model, the isolated right- and left-sided working rabbit heart, with epicardial defibrillation electrodes, to compare threshold for a monophasic waveform (5 msec rectangular) and an asymmetrical biphasic waveform (5 msec each pulse, V2 = 50% V1). Mean voltage defibrillation threshold (V50) was determined from sigmoidal probability of successful defibrillation versus shock intensity curves after 5, 15, and 30 seconds of fibrillation in a paired study with 10 hearts. Results showed that biphasic waveforms had significantly lower voltage and energy thresholds at all fibrillation durations and that their relative efficacy improved with increasing fibrillation duration. Biphasic voltage threshold was 38.2 +/- 2.2, 44.7 +/- 4.8, and 46.6 +/- 3.2 V after 5, 15, and 30 seconds of fibrillation compared with monophasic thresholds of 51.7 +/- 4.4 (p less than 0.002), 63.0 +/- 7.6 (p less than 0.05), and 72.1 +/- 3.9 V (p less than 0.005). Biphasic waveform energy threshold was 0.67 that for the monophasic waveform after 5 seconds of fibrillation (0.12 +/- 0.01 versus 0.18 +/- 0.03 J, p less than 0.05). The ratio between biphasic waveform threshold and monophasic waveform threshold (B/M) decreased to 0.62 at 15 seconds. At 30 seconds, B/M was 0.52 (0.17 +/- 0.02 versus 0.33 +/- 0.04 J, p less than 0.02). This study also showed that biphasic waveform threshold was a nonlinear function of monophasic waveform threshold so that improved biphasic defibrillator waveform efficacy was greatest for hearts having higher monophasic thresholds.(ABSTRACT TRUNCATED AT 250 WORDS)
It has been previously demonstrated that patients can maintain consciousness by vigorously coughing during episodes of prolonged ventricular asystole or ventricular fibrillation. Using two-dimensional Doppler echocardiography and arterial blood pressure recordings, we evaluated the changes that occur during coughing in nine patients who were dependent on pacemakers and in whom periods of asystole could be induced. During asystole in each patient the mitral valve stayed partially open and the left ventricular area comprised 87% and 90% (apical four-chamber view, short-axis view, respectively) of the area during diastole of paced rhythm. Peak arterial pressure during coughing and asystole was 80% of peak systolic pressure of paced rhythm (P = 0.001). Left ventricular area during coughing was 110% (both apical four-chamber view and short-axis views) of the area during asystole when patients were not coughing. Both the mitral and aortic valves showed no appreciable motion during coughing. During coughing the mean flow velocity across the mitral valve was 0.06 +/- 0.03 m/sec and the flow velocity integral was 0.03 +/- 0.02 cm. Thus coughing during asystole produced minimal flow despite a rise in brachial arterial pressure.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Although hypertension is the major cause of left ventricular hypertrophy (LVH), numerous studies failed to demonstrate a close correlation between resting blood pressure (BP) and degree of LVH. Some authors have shown better correlation between BP at work and left ventricular mass (LV mass), whereas other studies supported an association between catecholamines or angiotensin II and LV mass. In this study we investigated the relationship of resting and exercise BP and catecholamines to the degree of LVH. Nineteen patients with established mild to moderate hypertension were studied. Blood pressure was measured following a ten-minute rest and every three minutes during exercise using a Bruce protocol. Electrolytes, epinephrine (EP), and norepinephrine (NE) were measured at rest, at peak exercise, and at ten-minutes postexercise. Resting BP averaged 154 +/- 24/99 +/- 9 mm Hg and at three minutes of exercise 195 +/- 30/101 +/- 6 (P less than .001). Resting EP was 51 +/- 20 pg/mL, NE 314 +/- 187, and at peak exercise EP was 107 +/- 61 (P less than .001) and NE 1016 +/- 566 (P less than .001). The average LV mass was 277 +/- 85 g. A significant correlation was found only between systolic BP at three minutes of exercise and LV mass (r = .479, P less than .04). No other variable correlated significantly with LV mass. These data suggest that systolic BP achieved at low level of exercise (5 mets), corresponding to usual daily activities, may be the most important determinant of LVH in patients with hypertension.