Search PubMed⌕ Search

Biomedical subjects

W A Tacker

Publications and source records attributed to W A Tacker.

At least 73 records · Page 4Linked to original sources
PubMed1983

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.

Animals↗
PubMed1982

CPR with simultaneous compression and ventilation at high airway pressure in 4 animal models.

CPR with simultaneous chest compression and ventilation at high airway pressure (SCV-CPR) improves blood flow in some studies but not in others, perhaps because of differences in the animal models employed. To resolve such discrepancies, we compared SCV-CPR to standard CPR in 4 mechanically different canine models, using both small and large dogs and small and large compression pads. The 4 groups were: large dogs receiving chest compression through a large pad (model A), large dogs receiving chest compression through a small pad (model B), small dogs receiving chest compression through a large pad (model C), and small dogs receiving chest compression through a small pad (model D). Cardiac output (CO) during CPR was determined by a specially modified indicator dilution method. Models A, B, and C all had similar mean COs of 14 ml/min . kg body weight during standard CPR, and 27 ml/min . kg during SCV-CPR. However, in model D, there was no significant difference during standard vs. SCV-CPR, and the mean output was 33 ml/min . kg. We conclude that in models A, B, and C, little direct heart compression occurred and the higher intrathoracic pressure pulses produced by SCV-CPR improved blood flow. However it seems likely that there was effective cardiac compression in model D. In the absence of direct cardiac compression, SCV-CPR provides an alternative means of generating satisfactory flow in a mechanically appropriate animal model.

Animals↗
PubMed1981

Cardiovascular alterations induced by chronic transvenous implantation of an automatic defibrillator electrode catheter in dogs.

Six dogs (three large, three small) had defibrillator electrode catheters implanted transvenously via the right jugular vein for 17 weeks. The dogs remained healthy throughout the study. At necropsy, the lead-induced cardiovascular alterations were characterized by (1) formation of a thin white fibrous sheath over portions of the lead along its course in the veins, right atrium and right ventricle; (2) adhesion of parts of the sheathed segments of the lead to the adjacent venous intima or endocardium of the right atrium, tricuspid valve and right ventricle; (3) endocardial fibrosis with foci of cartilaginous metaplasia in areas traumatized by the lead; (4) thrombus formation at ends of sheathed segments of the lead but lack of pulmonary embolism; and (5) partial penetration of the myocardium at the apex of the right ventricle by the end of the lead in two of the small dogs. The lead-induced lesions were similar in type and severity to those produced by chronically-implanted pacemaker leads.

Animals↗
PubMed1980

Therapeutic indices for transchest defibrillator shocks: effective, damaging, and lethal electrical doses.

Although prospective studies of defibrillator shock overdose cannot be performed in man, the therapeutic indices of various defibrillating current waveforms can be measured in animals. We determined the ratios TD50/ED50 and LD50/ED50 (where TD50 = median "toxic" or damage-inducing dose, ED50 = median effective or defibrillating dose, and LD50 = median lethal dose) as measures of the therapeutic index for damped sine wave defibrillator shocks in dogs. Death of an animal and/or any degree of cardiac damage found by gross or microscopic examination were defined as harmful effects of shock, analogous to drug toxicity. In terms of peak current, the ED50, TD50, and LD50 were 1.1, 5.8, and 24 amperes/kg.; the therapeutic indices were TD50/ED50 = 5 for morphologic damage and LD50/ED50 = 22 for death. In terms of delivered energy the ED50, TD50, and LD50 were 1.5, 30, and 470 joules/kg.; the therapeutic indices were TD50/ED50 = 20 for damage and LD50/ED50 = 320 for death. These data indicate a reasonable margin of safety for damped sine wave defibrillator shocks in dogs, and are consistent with reported incidences of suspected shock-induced damage in humans.

Animals↗
PubMed1980

Dependence of defibrillation threshold upon extracellular/intracellular K+ concentrations.

The effect of increasing extracellular potassium concentration (Ko) upon electrical ventricular defibrillation threshold was investigated in pentobarbital anesthetized dogs treated with intravenous potassium chloride. Defibrillation threshold fell duirng potassium intoxication. The percent decrease in defibrillation threshold was linearly related to the logarithm of Ko and to the potassium equilibrium potential (Ek), calculated from measured extracellular and intracellular potassium concentrations of ventricular muscle. In dogs supported by left ventricular bypass in order to maintain the circulation during potassium intoxication, the values of Ko and Ek required for spontaneous, K+ induced defibrillation (electrical defibrillation threshold = zero) were 16.6 mEq/L and -46 mV compared to the normal values of 3.9 mEq/L and -84 mV. Changes in defibrillation threshold related to changes in Ek may be significant events in digitalis intoxication and in myocardial anoxia during prolonged fibrillation.

Animals↗
PubMed1980

Bipolar catheter defibrillation in dogs using trapezoidal waveforms of various tilts.

The choice of defibrillating waveform is critical in determining the size, battery life, and effectiveness of an automatic implantable defibrillator (AID). The trapezoidal (truncated exponential) waveform is well suited for the AID and its use can be optimized by the selection of appropriate values of pulse duration and tilt. The purpose of this study was to determine the dependence of the threshold peak current (the minimum peak current necessary to defibrillate the ventricles) on pulse duration and tilt for a bipolar catheter electrode configuration. Successive fibrillation-defibrillation trials were performed in 30 dogs anesthetized with sodium pentobarbital (30 mg/kg). The defibrillating pulse was applied via a bipolar-electrode catheter positioned such that the electrodes were located in the right ventricle at the apex and in the superior vena cava. The threshold peak current was determined in each dog for trapezoidal waveforms with 80%, 65%, 50%, and less than 5% tilt and with pulse durations of 2, 5, 10, 15, and 20 milliseconds. From a total of 600 threshold peak-current values, a strength-duration curve was derived for each value of tilt. The threshold peak current dose (peak current divided by body weight) increased with increasing tilt and decreasing duration. The threshold average current dose (average current over the duration of the defibrillating pulse divided by body weight) was IAV = 0.26 + 0.47/d, where d is the pulse duration in milliseconds and IAV is the average current in amperes per kilogram. If catheter apparent impedance is known, the minimum capacitance and output voltage necessary for defibrillation can be inferred from the strength-duration curves. From these data one can quantitatively assess the effect of trapezoidal waveform shape on the design criteria for the AID.

Animals↗
PubMed1980

Regional blood flow during cardiopulmonary resuscitation in dogs.

To determine differences in regional blood flow during CPR versus normal cardiac function, the authors measured regional blood flow to several organs in 19 pentobarbital-anesthetized dogs (6--12 kg). Regional blood flow was measured during sinus rhythm in five dogs and during electrically induced ventricular fibrillation with CPR in the other 14 dogs. Regional blood flow and cardiac output were measured using radioactively labeled polystyrene microspheres of 15 +/- 3 mu diameter, injected into the left ventricle. Adequacy of microsphere mixing at low cardiac outputs was verified by comparing flow rates to paired organs. Cardiac output was 175 ml/kg . min during sinus rhythm versus 47 ml/kg . min during CPR. Flow to all organs sampled was less during CPR, but the relative decrease varied widely. The ratios of regional blood flow during CPR to regional blood flow during sinus rhythm were 90% for brain, 35% for heart, 15% for kidneys, 17% for adrenal glands, 14% for pancreas, 3% for spleen, and 33% for small intestine. These results provide baseline values for regional blood flow during CPR which can be used to evaluate alternative CPR techniques and/or drugs which may improve perfusion of vital organs during CPR.

Animals↗
PubMed1980

Influence of adrenergic drugs upon vital organ perfusion during CPR.

To determine whether adrenergic drugs administered during CPR alter the distribution of artificial cardiac output, the authors measured regional blood flow and cardiac output using radioactive microspheres in 12 dogs. Ventricular fibrillation was induced electrically and CPR was immediately begun with a mechanical chest compressor and ventilator (Thumper) at 60 compressions/min, with a ventilation: compression ratio of 1:5, a compression duration of 0.5 sec, and a ventilation pressure of 20 cm H2O. Compression force was sufficient to develop 40--50 mm Hg peak intraesophageal pressure. After 30 sec of CPR, either 0.9% saline vehicle or 50 micrograms/kg of epinephrine, phenylephrine, or isoproterenol was administered through a central venous catheter. One min later, microspheres were injected into the left ventricle. After 250 sec of CPR, the ventricles were defibrillated electrically. Between each drug injection, 20-min recovery periods were interposed. Each dog received all three drugs and saline according to a predetermined sequence. After saline, epinephrine, phenylephrine, and isoproterenol treatment, respective, cardiac output averaged 392, 319, 255, and 475 ml/min; brain blood flow averaged 37, 54, 29, and 28 ml/min; coronary blood flow averaged 25, 79, 26, and 15 ml/min; and kidney blood flow averaged 44, 4, 16, and 29 ml/min. Epinephrine improved blood flow to the brain, probably because of its alpha-adrenergic activity. Epinephrine improved blood flow to the heart during CPR much more than the other agents, probably because of its combined alpha- and beta-adrenergic activity. This effect may explain its superiority in restoring circulation after prolonged arrest and resuscitation. Isoproterenol should not be used in CPR because it shunts blood away from vital organs.

Animals↗
PubMed1980

The effect of newer antiarrhythmic drugs on defibrillation threshold.

This study was conducted to determine the effects of clofilium phosphate and bretylium tosylate on ventricular defibrillation threshold. Dogs were anesthetized with pentobarbital and subjected to repeated fibrillation-defibrillation episodes. Defibrillation thresholds were determined at 15-min intervals, using underdamped 5--6 msec sinusoidal current shocks, from 30 min before drug injection to 120 min after injection. Eight dogs were given clofilium phosphate (0.34 mg/kg, iv). Another 10 dogs were given bretylium tosylate (10.0 mg/kg, iv). Both drugs lowered defibrillation threshold from 15--90 min after injection. The maximum clofilium effect was a 31% decrease in threshold current and a 54% decrease in threshold energy. The greatest decrease in defibrillation threshold produced by bretylium was 16% for current and 31% for energy. These drug induced changes in defibrillation threshold are of potential clinical benefit if they occur in human subjects at doses which are effective for control of ventricular arrhythmias.

Animals↗
PubMed1980

Energy and current requirements for ventricular defibrillation using trapezoidal waves.

The threshold energy and current required for ventricular defibrillation was determined in dogs ranging in weight from 6.4 to 38 kg and in ponies ranging in weight from 40 to 101 kg. Trapezoidal waves, 10 ms in duration, with 10%, 50%, 70%, and 90% tilt were applied to transchest electrodes. For all values of tilt, the energy and current required increased with body weight. The energy dose (joules per kilogram of body weight) was higher for the heavier animals, whereas the current dose (peak amperes per kilogram of body weight) was essentially the same for dogs and ponies. In both species and for all four waveforms, the percent success increased with increasing energy and current dose. For all four waveforms and for both species, the threshold average current required for defibrillation was between 0.38 and 0.48 A/kg, indicating that average current may be a convenient unit to compare the efficacy of different waveforms.

Animals↗
PubMed1979

Elevation of ventricular defibrillation threshold in dogs by antiarrhythmic drugs.

Effects of antiarrhythmic drugs upon the threshold delivered energy (TDE) and threshold peak current (TPC) for electrical ventricular defibrillation by damped sinusoidal shocks were investigated in 25 pentobarbital-anesthetized dogs. TDE and TPC were increased by the three antiarrhytmic drugs tested. Bolus injections produced a transient rise and continuous infusions produced a steady rise in difibrillation threshold. The maximal percent elevations in mean defibrillation threshold during the 60 minutes after intravenous drug treatment in groups of n = 5 dogs were: (formula: see text). Accordingly, individuals receiving antiarrhythmic drugs who nonetheless fibrillate may require greater electric shock strength for defibrillation.

Animals↗
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↗