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Biomedical subjects

C F Babbs

Publications and source records attributed to C F Babbs.

At least 127 records · Page 7Linked to original sources
PubMed1981

Cardiac output during cardiopulmonary resuscitation at various compression rates and durations.

Cardiac output during cardiopulmonary resuscitation (CPR) was measured by a modified indicator-dilution technique in 20 anesthetized dogs (6-12 kg), during repeated 1- to 2-min episodes of electrically induced ventricular fibrillation, by a mechanical chest compressor and ventilator. With compression rates from 20 to 140/min and compression durations (duty cycles) from 10 to 90% of cycle time, cardiac output (CO) was predicted by the equation: CO = CR . SVmax . [DC/(k1 . CR + DC)] . [(1 -- DC)/k2 . CR + 1 - DC)], where CR is compression rate, DC is duty cycle, SVmax (19 ml) is the effective capacity of the pumping chamber, and k1 (0.00207 min) and k2 (0.00707 min) are ejection and filling constants. This expression predicts maximal CO for DC = 0.40 and cR = 126/min and 90-100% of maximal CO for 0.3 less than DC less than 0.5 and 70 less than CR less than 150/min. Such mathematical analysis may prove useful in the optimization of CPR.

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

INfluence of interposed ventilation pressure upon artificial cardiac output during cardiopulmonary resuscitation in dogs.

This study was conducted to determine the effects of high pressure interposed ventilations during cardiopulmonary resuscitation (CPR). Cardiac output was measured by a modified indicator dilution technique in eight anesthetized, intubated mongrel dogs. Positive pressure ventilations (12/min, 80% O2) were interposed after every five chest compressions (performed at 62/min) by a mechanical chest compressor (Thumper). On repeated trials in the same animal, ventilation pressures from 10--50 cm of H2O were tested in randomized sequence, while the technique of chest compression was held constant. Arterial blood gases immediately after resuscitation were monitored. Increasing ventilation pressure had surprisingly little effect on cardiac output curing CPR, although blood gases were profoundly altered. For ventilation pressures of 10, 20, 30, 40, and 50 cm of H2O, producing mean tidal volumes 23, 38, 61, 83, and 94 ml/kg; cardiac output remained nearly constant, averaging 21, 25, 23, 26, and 24 ml/min . kg. Corresponding mean postresuscitation pH was 7.24, 7.41, 7.51, 7.56, and 7.53; PCO2 was 41, 26, 18, 16, and 15 torr. The postresuscitation arterial oxygen tension was greater than 100 torr at all ventilation pressures except 10 cm of H2O. Interposed ventilations of pressure and volume more than adequate to prevent acidosis during CPR did not impair artificial cardiac output. If anything, cardiac output was slightly improved by more forceful ventilation.

Animals↗
PubMed1980

A new technique for repeated measurement of cardiac output during cardiopulmonary resuscitation.

The authors have developed a method for measurement of cardiac output during CPR with ventricular fibrillation. The method avoids the problems encountered when conventional techniques are used under the conditions of very low cardiac output. The method consists of injecting 5% saline as the indicator into the left ventricular and detecting its appearance in the descending aorta by withdrawing aortic blood through an electrically calibrated conductivity cell. The adequacy of indicator mixing has been verified by obtaining dilutions curves simultaneously from the brachial and femoral arteries. Cardiac output can be determined even when output is as low as 7 ml/min . kg during CPR with ventricular fibrillation. Repeated determinations can be made as often as every min. This method offers promise as a practical research tool which can also be used with dye indicators.

Cardiac Output↗
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↗
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↗