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Biomedical subjects

L A Geddes

Publications and source records attributed to L A Geddes.

At least 127 records · Page 7Linked to original sources

Loss of diffusible indicator in the pulmonary vascular circuit.

In this study, the loss of a diffusible indicator in the pulmonary vascular circuit was quantitated by comparing cardiac output values obtained by measuring paired dilution curves, one from the pulmonary artery (PA) and the other from the aorta, resulting from the injection of a few ml of 5% saline in the right atrium. Cardiac outputs were calculated from the PA and aortic dilution curves from the same indicator injection in 10 anesthetized dogs. From 43 paired trials, the cardiac output values derived from the aortic dilution curves exceeded those obtained from the PA, indicating loss of this diffusible indicator in the pulmonary vascular circuit.

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Right-side cardiac output determined with a newly developed catheter-tip resistivity probe using saline indicator.

Right-heart cardiac output was determined in 10 dogs using a newly developed, highly accurate catheter-tip resistivity probe. A saline indicator was injected into the right atrium and the blood resistivity was monitored at the catheter tip in the pulmonary artery. The resulting dilution curves were calibrated electrically according to the manner in which blood resistivity changes with saline concentration and cardiac output values were calculated. Cardiac output values determined simultaneously by the direct Fick method were used as a reference.

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Functional cardiac depression caused by defibrillator shocks. Quantitation of the safety factor for electrical defibrillation.

The overdose shock strengths required to depress ventricular contraction were determined for damped sinusoidal current in 7 metabolically supported, isolated contracting canine hearts. Each heart was suspended in an isoresistive and isotonic solution-through which the defibrillating shocks were delivered. Defibrillation thresholds were determined with standard damped sine wave shocks of 4.4-5.5 msec duration. Then overdose shocks were delivered and the depressant effect on systolic left ventricular pressure was measured for shocks of 3-12 times threshold current. The minimum (threshold) current and energy densities required to defibrillate were 59.5 +/- 4.6 mA/cm2 (average) and 3.12 +/- 0.2 mJ/cm3. Increasing the shock strength above threshold produced a concomitant reduction of postshock left ventricular systolic pressure. The current and energy densities required to produce 50% depression (TD50) of left ventricular systolic pressure were 5.0 and 24.1 times the threshold current and energy densities respectively, indicating a wide safety margin using this criterion.

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Electrical stimulation on skin wound healing in the horse: preliminary studies.

The effect of low-level direct-current stimulation on skin wound healing in the horse was assessed. Self-sustaining electrical circuits with electrodes were implanted subcutaneously in or near the wound. Stimulation by direct current (10 or 20 microA) was used to determine the effect on equine skin healing. The efficacy of electrotherapy was evaluated by sequentially comparing the clinical appearance of the wound and measuring the size of the granulating wound bed. The histologic appearance of the healing stimulated wounds was compared with that in nonstimulated control wounds created on 9 horses. Seemingly, electrical stimulation had no discernible effect on experimentally created skin wounds. Clinical observation and histologic examination of the wounds indicated that severe tissue reaction from the implanted electrodes and concurrent local infection produced local detrimental effects to wound healing.

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Alterations induced by a single defibrillating shock applied through a chronically implanted catheter electrode.

In ten beagles ranging in weight from 7.4 to 13.0 kg, a defibrillating shock of 10 A (three dogs), 20 A (four dogs), or 30 A (three dogs) intensity was applied through a chronically implanted right ventricular catheter electrode. Ten-lead ECG, right ventricular electrogram, and right ventricular impedance were recorded prior to, immediately following, and 48 hours post-shock. A single shock of 10 A, 20 A, and 30 A intensity succeeded in defibrillating nine of ten dogs. One dog required two 20 A shocks to defibrillate. No shock was fatal. Post-shock arrhythmias increased in duration and severity as the shock strength increased. ECG vector analysis suggested damage to the right ventricle in eight of ten dogs. The impedance signal amplitude increased directly after the shock, but dropped below control level by 200 seconds post-shock and remained below control by 48 hours post-shock. Pale areas of shock-induced myocardial necrosis were concentrated in the right ventricular walls adjacent to the distal electrode. The mean weight of necrotic myocardium was 0.043 + 0.006 grams at 10 A, 1.203 + 0.268 grams at 20 A, and 1.397 + 1.218 grams at 30 A (mean + sd). Defibrillation was effective after long-term implantation. The alterations sustained from defibrillation were minimized by using a low intensity shock.

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Relationship of blood pressure and flow during CPR to chest compression amplitude: evidence for an effective compression threshold.

This study was conducted to investigate the importance of the depth of chest compression in producing effective cardiopulmonary resuscitation (CPR) in animals, as indicated by cardiac output and mean arterial blood pressure. Cardiac output was measured by a modified indicator dilution technique in 8 anesthetized dogs, 6 to 12 kg body weight, during repeated 2-minute episodes of electrically induced ventricular fibrillation and CPR provided by a mechanical chest compressor and ventilator (Thumper). Chest compression exceeding a threshold value (xo) between 1.5 and 3.0 cm was required in each animal to produce measurable cardiac output. In particular, cardiac output (CO) was linearly related to chest compression depth (x) by an expression of the form CO = a(x-xo) for x greater than xo. The mean value of xo was 2.3 cm. A similar threshold for measurable blood pressure was observed in 7 of the 8 dogs, with a mean value of 1.8 cm. For chest compression of 2.5 cm or greater, relatively modest increases in chest compression depth caused relatively large changes in cardiac output.

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Efficacy and safety of defibrillation with rectangular waves of 2- to 20-milliseconds duration.

The effect of suprathreshold defibrillator shocks on cardiac function was compared in 8 isolated, perfused, contracting canine hearts using 4 durations of rectangular electrical waveforms. Defibrillation threshold was first determined for each duration; then overdose shocks of 3, 4.5, 6, and 9 times threshold current density were delivered. Left ventricular isovolumic systolic pressure decreased immediately after the shocks in proportion to the overdose shock strength. The mean defibrillation current density thresholds for the 2-, 5-, 10-, and 20-msec durations were 101, 63, 47, and 39 mA/cm2, respectively. The corresponding energy density thresholds were 4.6, 3.5, 4.4, and 6.4 mJ/cm3, respectively. The safety factor for defibrillation was defined as the current overdose ratio (delivered current density/threshold current density) required to produce a 50% decrease in isovolumic systolic pressure immediately after the shock. This dose was determined by interpolation of the curve for depression versus overdose of shock strength. The mean current safety factors for the 2-, 5-, 10-, and 20-msec durations were 3.9, 5.1, 5.4, and 5.2, respectively. The corresponding mean energy safety factors were 15, 25, 28, and 27. The margin of safety for functional depression of the heart was significantly less (p less than 0.05) for the 2 msec rectangular wave then for the 5-, 10-, and 20-msec rectangular waves.

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Thermographic evaluation of horses with podotrochlosis.

The distal forelimbs of 10 clinically normal horses with hair clipped on 1 limb were thermographically scanned before and after exercise. The thermal patterns, temperature distribution, and temperature changes after exercise were determined and compared with those of 8 horses with podotrochlosis. Clipping the hair did not cause changes in the thermal patterns, but the clipped limbs were warmer than the unclipped limbs. The temperature of the limbs of horses with podotrochlosis did not increase as much after exercise as did the limbs of normal horses. The failure of skin temperature increase correlated with the radiographic evidence of enlarged vascular foramina in the navicular bone. Because the failure to increase skin temperature after exercise is the result of low blood flow, the enlarged vascular foramen can be related to a state of low blood flow.

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Myocardial stimulation with ultrashort duration current pulses.

In order to identify a practical short-duration limit for stimulating myocardium, theoretical and experimental studies were carried out using dog and turtle hearts. The strength-duration curves for current, charge and energy were derived from the standard excitable membrane model which employs a parallel resistance and capacitance. From these derivations, the predicted duration for minimum energy was identified. The experimentally measured strength-duration curves for two types of myocardium followed the predicted values closely. The duration for minimum energy was calculated to be 1.25 times the membrane time constant. The practical short-duration limit for a pacemaking stimulus is about 10% of the membrane time constant. For dog myocardium the average time constant was 2.4 ms. Therefore, a practical stimulus duration for minimum charge in the dog should be no longer than about two-tenths of a millisecond, although shorter duration stimuli are equally effective. This minimum charge criterion provides the minimum drain on the stimulator power supply.

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