Search PubMed⌕ Search

Biomedical subjects

L A Geddes

Publications and source records attributed to L A Geddes.

At least 163 records · Page 9Linked to original sources
PubMed1979

Electrocardiographic and serum enzymic alterations associated with cardiac alterations induced in dogs by single transthoracic damped sinusoidal defibrillator shocks of various strengths.

The safety margin between the strength of shock needed to defibrillate the ventricle and shocks which produce cardiac damage has not previously been reported. This study quantitates the shock intensity required to produce ECG alterations, serum alpha-1LDH and MB CPK isoenzyme elevation and myocardial damage using single transchest damped sinusoidal defibrillator shocks. Shocks of 1 to 20 amperes per Kg. of body weight were applied. Fifty-six dog weighing 2.4 to 15 kilograms were shocked with defibrillator pulses via 10 centimeter diameter electrodes applied to the thorax. Electrocardiograms were taken to be analyzed for arrhythmias, S-T segment changes, and T wave changes. Serum enzyme levels were determined in 25 dogs. Macroscopic and histopathologic studies were conducted on the hearts. Transchest single damped sine wave shocks did not produce microscopically detectable cardiac damage until at least a threefold current overdose was applied. No macroscopic morphologic alterations were observed until at least a sixfold current overdose was applied and no deaths occurred until a twelvefold or greater current overdose was delivered. Incidence and severity of ECG changes, increase in serum enzyme activity, incidence and severity of cardiac damage, and incidence of mortality all correlated positively with shock strength. However, these four adverse effects did not correlate well with each other. Transient ECG changes were very frequent following shock application regardless of the morphologic damage produced, and hence the transient changes have little value as indicators or predictors of damage. Persistent ECG changes were predictive of morphologic changes but were not sensitive enough to detect damage in mildly injured hearts. Likewise, elevated serum cardiac isoenzyme activity was a reliable but insensitive indicator of damage.

Animals↗
PubMed1979

Indirect measurement of mean blood pressure in the normotensive and hypotensive horse.

Indirect mean arterial pressure was obtained from the tails of 78 anaesthetised and unanaesthetised normotensive and hypotensive horses. Data were obtained to determine the optimum cuff width in relation to tail circumference. A cuff that is too wide under-estimates and a cuff that is too narrow over-estimates blood pressure. With the optimum cuff width, which is slightly in excess of about one-fifth of the tail circumference, indirect mean blood pressure was obtained consistently in normotensive and hypotensive animals with mean blood pressures of 40 mmHg and frequently in animals with pressure as low as 30 mmHg.

Animals↗
PubMed1978

Active cables for use with dry electrodes for electrocardiography.

With the active cables described in this paper, it is possible to record the electrocardiogram with dry electrodes. Simultaneous recordings of the ECG from dry electrodes via the active cables and from conventional electrodes with electrode paste demonstrate that there is no discernible difference in the electrocardiographic waveforms.

Electrocardiography↗
PubMed1978

The electrical dose for direct ventricular defibrillation in man.

The threshold electrical energy for direct ventricular defibrillation was measured in 100 patients whose hypothermic hearts were fibrillated for cardiac operations. In 93 cases 10 joules or less was sufficient, and in 48 of these cases 5 joules or less defibrillated the ventricles. Because a shock of 10 joules defibrillated the heart of most of our patients, we recommend an initial shock of 5 to 10 joules rather than the 20 joules used more commonly. Until the safety margin between defibrillation threshold and damage threshold is established for direct defibrillation, use of shocks with adequate but not excessive strength may avoid unnecessary damage to the myocardium. When hearts refibrillate after defibrillation, it is unnecessary to use higher energy settings for subsequent defibrillation attempts. Instead, an antiarrhythmic drug should be administered and another shock of the same intensity that defibrillated the first time should be applied.

Adult↗
PubMed1978

Effect of shock strength on survival and acute cardiac damage induced by open-thorax defibrillation of dogs.

The safety of open thorax defibrillation with single damped sine-wave shocks and 6-cm-diameter electrodes was evaluated in healthy anesthetized dogs. Twenty-one dogs were allotted to 6 groups: Group A were nonshocked controls and groups B through F were given single shocks of 4-, 7-, 12-, 19-, or 32-fold, respectively, greater than a defibrillation threshold dose (30 mA/g of heart). Immediate postshock death resulted in group F dogs; group A through E dogs survived and were killed after 2 days. The incidence and severity of cardiac morphologic damage increased with shock strength (mild damage occurred in 1 of 3 dogs in group C and in 3 of 4 dogs in group D and severe damage occurred in 2 of 3 dogs in group E). The cardiac lesions were characterized grossly and microscopically. In dogs that died immediately after shocking, damage was apparent as pale circular zones of edema and myofibrillar degeneration in the ventricular free walls beneath the electrode placement sites on the cardiac surface. In the dogs that survived 2 days, the defibrillator-induced areas of myocardial necrosis and calcification were concentrated in arc or ringlike patterns beneath the periphery of the electrode placement sites. All dogs that were studied 2 days after shocking had mild fibrinous pericarditis. Postshock electrocardiographic changes were not good indicators of cardiac damage because the mild epicardial inflammatory reaction associated with the surgical procedure produced large ST and T wave changes which masked any changes associated with myocardial necrosis induced by the electric shocks. It was concluded that a substantial safety margin exists between the required defibrillation threshold shock dose and the large shocks required to produce marked cardiac damage or death in healthy dogs.

Animals↗
PubMed1977

The thoracic windows for electrical ventricular defibrillation current.

The thoraces of dogs were mapped out to identify those areas where defibrillating current gains easiest access to the heart. Of all of the transchest and chest-to-back electrode locations, the lowest current dose (0.6 amp. per kilogram of body weight) was found with one electrode over the apex-beat area with transchest electrodes and slightly anterior to the apex-beat area with chest-to-back electrodes.

Animals↗
PubMed1976

Electrical ventricular defibrillation.

Ventricular fibrillation is the condition in which all of the muscle fibers in the ventricles of the heart contract and relax randomly and do not propel blood from the heart. This condition, which is the major cause of sudden death from a heart attack, can be reversed by passage of a single pulse of current through the heart using electrodes applied to the chest wall; this technique is known as ventricular defibrillation. World-wide clinical experience has shown that with existing defibrillators, successful defibrillation of subjects weighing over 100 kg is infrequent. It should not be concluded, however, that defibrillation cannot be achieved in such subjects. To illustrate this point, data will be presented to show that it is possible to establish a dose concept in which the output required from a defibrillator can be specified in terms of the weight of the subject. This dose concept evolved slowly from studies reported by investigators in various countries. For example, the present-day techniques of ventricular defibrillation are due to the investigations of researchers all over the world. Prevost and Battelli (1898) in Switzerland first showed that electric current can both induce ventricular fibrillation and achieve defibrillation. The studies of Kouwenhoven in the 1930's in the USA showed that 60 Hz alternating current can be used for defibrillation. The first human defibrillations in 1947 and 1952 used this type of current; these studies were reported by Beck and Zoll in the USA. The present-day technique for defibrillation derives from the animal studies reported by Gurvich and Yuniev 1946 in Russia. Finally, Lown et al. in the early 1960's applied the technique to man. Exciting new developments are underway in ventricular defibrillation. Not only are higher output defibrillators beginning to appear, but automatic and fully implantable defibrillators are being involved. In this paper, the present state of the art of defibrillation will be reported and future trends will be described.

Animals↗