Antonio Boba

The effects of atropine on the heart rate

SummaryThe cardiac-accelerating effects of 0.6 mgm of atropine administered intravenously were tested in 111 patients (three groups of 37 patients each). The patients in Group “A” received pentobarbitone and diphenhydramine orally before the atropine injection; those in Group “B” received no medications and those in Group “C” received pentobarbitone orally and meperidine intramuscularly. For the purpose of greater precision the time elapsed between ten consecutive electrical systoles was taken as the measure of the heart rate. Measurements were carried out before and two minutes after atropine injection.The control mean heart rate was slower in Group “C” and faster in Group “A”. Atropine increased the heart rate of all patients, most of those in Group “C” and least of those in Group “A” and in such a manner that, after atropine, the means for the three groups were nearly identical.There is very poor correlation between the weight-adjusted dose and the cardiac accelerating effects of 0.6 mg atropine administered intravenously. The highest correlation coefficient (0.680) is found between the heart rate before and after atropine; i.e., the slower hearts are those that accelerated the most and the fastest hearts accelerated the least, irrespective of weight-adjusted dose or concomitant premedication routine.RésuméLes effets d’une dose de 0.6 mg d’Atropine sur la fréquence cardiaque ont fait l’objet d’une étude chez 111 patients répartis en trois groupes de 37 sujets. Pour fins de mesures et de comparaison dans ce travail, on a défini la fréquence comme la durée de dix systoles électriques consécutives.Les malades du premier groupe (A) ont recu 100 mg de Pentobarbital et 100 mg de Diphrenhydramine par la bouche deux heures avant l’injection d’Atropine; ceux du groupe B n’ont pas recu de prémédication; enfin, les patients du Groupe C ont reçu 100 mg de Pentobarbital et 125 mg de Meperidine par voie intramusculaire deux heures avant l’injection d’Atropine. On a calculé la fréquence immédiatement avant l’injection d’Atropine et deux minutes après son injection par voie intraveineuse.En mesurant, comme mentionné plus haut, la durée de 10 systoles électriques consécutives, on a obtenu les résultats moyens suivants. Groupe A: avant Atropine: 7.5 sec. (déviation standard 1.4); après Atropine: 6 sec. (1.1). Groupe B: avant Atropine: 7.9 sec. (1.7); après: 6.2 sec. (1.4). Groupe C: avant: 8.2 sec. (1.5); après: 6.3 sec. (1.2).L’on a établi la relation entre la dose d’Atropine (0.6 mg) et la poids des patients chez les malades du groupe C et Ton a réalisé que les malades qui ont recu la plus petite dose d’Atropine ( en fonction du poids ) ont démontré la plus grande accélération de fréquence. Sur la base de cette observation Ton a établi un graphique tenant compte du pourcentage d’accéléVation de fréquence et de la dose d’Atropine en fonction du poids, et ceci pour tous les sujets de l’étude. Sur la base de ce graphique il n’y a pas de bonne corrélation.Finalement, le pourcentage d’accé1ération de la fréquence après Atropine a été inscrit sur un graphique en fonction de la fréquence cardiaque avant Atropine. L’on obtient de cette façon le plus haut coéfficient de corrélation ( + 0.680 ).L’auteur conclut que les effets de 1’Atropine sur la fréquence cardiaque sont difficiles à prédire et conseille d’administrer cet agent en petites doses répétées jusqu’à ce que l’effet désiré soit obtenu.

Significant Effects on the Blood Pressure of an Apparently Trivial Atrial Dysrhythmia

Continuous automatic monitoring and recording, at slow paper speed, of the intra-arterial blood pressure revealed serious disturbances in blood pressure in a small number of patients undergoing general anesthesia. In all instances, the underlying mechanism was found to be a rhythm disturbance so trivial as to have escaped earlier detection by means of conventional audio-visual monitoring. The practice of routine monitoring and recording of the intra-arterial blood pressure would appear to receive support from these findings.

An abnormal electrocardiographic pattern and its relation to ventricular fibrillation (observations during clinical and experimental hypothermia)

Abstract Under the conditions of the experiment it has been possible to produce the appearance of a peculiar wave in the electrocardiogram of hypothermic dogs. This wave is very similar morphologically to a wave which is seen in human beings at comparable hypothermic levels. A numerical correlation exists between the appearance of this wave and the incidence of ventricular fibrillation, so that the hypothesis that this wave should be considered as a premonitory sign of ventricular fibrillation seems justified. Hyperventilation does not affect significantly the temperature at which the wave appears, but it increases the margin between this temperature and the temperature at which ventricular fibrillation eventually supervenes. Possible clinical implications of these findings are discussed.

Fetal responses to maternal oxygen inhalation during hemorrhagic stress

Abstract Experiments were carried out in 25 pregnant dogs at or near term in order to determine the effect of maternal oxygen inhalation on fetal arterial oxygen tension and fetal heart rate under various experimental conditions. In normovolemic mothers, an increase in maternal arterial oxygen tension induced by 100 per cent oxygen inhalation resulted in a prompt and similar increase in fetal arterial oxygen tension. When hypovolemia and hypotension were induced by repeated maternal hemorrhage, the inhalation of 100 per cent oxygen by the mother did not significantly influence low fetal arterial tension level or fetal bradycardia. When 100 per cent oxygen was administered to hypovolemic mothers who had received a vasopressor drug for restoration of blood pressure, fetal arterial oxygen tension persisted at a low level in three of five experiments. The inhalation of 100 per cent oxygen prior to, during, and after hemorrhage and administration of vasopressor drugs did not prevent the usual decline of fetal arterial oxygen tension and bradycardia which is invariably observed following hemorrhage and the use of vasopressor drugs.

Mannitol-vasopressin interactions in the splenectomized dog

Summary Experiments were carried out in 46 splenectomized dogs demonstrating that the intravenous administration of mannitol will produce an increase in urinary flow under all conditions of water loading. It was also demonstrated that the intramuscular administration of vasopressin will not significantly alter the expected course of events except when high water loading has been carried out; in that case a significant increase in urinary flow is noted. Further experiments have indicated that the renal blood flow, measured directly, is consistently greater in the high water load, mannitol- and vasopressin-treated dog than in the high water load, mannitol- but not vasopressin-treated animal. A very high urinary excretion of chlorides was also noted in the vasopressin-treated, mannitolized, high water load animals.

Experimental hypothermia in the pregnant mouse

Abstract The results of controlled laboratory experiments indicate that hypothermia, if administered during the first third of gestation, may adversely affect the continuation of pregnancy in mice. These findings are discussed in their possible relation to the administration of hypothermia to a pregnant woman.

Effects of halothane on life expectancy of mice

SummaryAn investigation of the effects of repeated halothane administration to mice during the early period of their adult life has shown that at high concentrations the drug is immediately lethal to a significant number, and that at very low concentrations it has no significant immediate lethal effects. In the intermediate concentration range the drug has a moderate lethal effect which does not disappear with cessation of administration of the drug but continues to exert its effects for an additional three- to six-week period.Once an animal has reached the expected median of life, as determined in the control group, its life expectancy is not affected any longer by previous exposure to halothane in any concentration.Some considerations about the assessment and evaluation of the toxicity of certain drugs, implicit in these results, have been discussed.RésuméOn a administré de l’halothane à trois groupes de 96 souris. On a utilisé comme contrô1e un quatrième groupe de 96 souris.Toutes les souris étaient nées le même jour et on les avait identifiéers avec precision à 1’age de douze semaines. De la treiziéme a la dix-huitiéme semaine d’âge, on a anesthésié trois fois par semaine, durant trois heures chaque fois, les animaux des groupes servant à I’expérience. Un groupe a reç,u l’halothane à 0.2 pour cent, un groupe 1’halothane à 0.8 pour cent et un groupe 1’halothane à 1.8 pour cent. Le groupe de contrôole n’à regu aucune anesthésie.Chaque jour, on a visite les cages et on a enlevé les animaux morts. A la 48e semaine on a terminé l’expérience, et à l’aide des données receuillies, on a préparé les tables de survie.Ces tables ont réVélé qu’il n’y a aucune différence de survie entre les animaux qui n’ont rien reçu et ceux qui ont reçu 1’halothane à 0.2 pour cent. Parmi les animaux anesthésiés à 1’halothane à 1.8 pour cent, plusieurs sont morts au début de l’expérience. Par la suite, la survie se compare à celle des animaux de contrô1e. Les animaux qui ont inhalé de 1’halothane à 0.8 pour cent ont présenté une singulière augmentation du taux de mortalité durant les quatre ou cinq semaines qui ont suivi le temps des expériences.L’orsqu’un animal survivait aussi longtemps que la moyenne des animaux de contrôle, le nombre des jours qui lui restaient à vivre n’était pas influencé par l’administration antérieure du médicament, quelle qu’en ait été la concentration.D’aprés ces résultats, on peut supposer qu’une étude de toxicité aigue ou qu’une épreuve fonctionnelle isolée, durant la période aigue, peuvent être peu significatives quant aux propriétés toxiques d’un produit.