Ivan Dimich

Evaluation of oxygen saturation monitoring by pulse oximetry in neonates in the delivery system

The pulse oximeter was evaluated for use in neonates in the delivery room. One hundred neonates, delivered vaginally or by Caesarean section with general or epidural anaesthesia, were studied. After delivery, pulse oximetry probes were placed simultaneously on the ulnar side of the right hand and on the right Achilles tendon to determine whether there was a difference in arterial oxygenation (SpO2)-Measurements of SpO2 were taken at 1,5,10 min, and 24 hr after delivery. At one and five minutes, SpO2 recorded from the right hand was higher than that recorded from the lower extremities (71.9% ± 6.5% vs 63.4% ± 4.3% and 83.3% ± 4.2% vs 76% ± 4.1%, mean ± SD, respectively). At ten minutes these differences diminished, and had almost completely disappeared after 24 hr. These results can be explained by the presence of R-L shunting at the ductus arteriosus level, producing reduced SaO2 in the lower extremities. Oxygen saturation did not differ between neonates delivered vaginally or by Caesarean section, regardless of the presence or type of anaesthesia. We concluded that neonates remain relatively desaturated in the immediate postpartum period and that the SpO2 obtained from the right hand is a better index of neonatal oxygenation than that obtained from the heel.RésuméLe saturomètre de pouls fut évalué chez des nouveaux-nés dans la salle d’accouchement. Cent nouveau-nés après accouchement vaginal ou césarienne avec une anesthésie générate ou épidurale, ont été étudiés. Après l’accouchement les sondes de saturomètre de pouls ont été simultanément placées sur le côté cubital de la main droite et à droite du tendon d’achille afin de déterminer s’il y a une différence dans l’oxygénation artérielle. Les mesures de la (SPO2) furent prises à une, cinq, dix minutes et 24 heures après l’accouchement. A une et cinq minutes, la SPO2 enregistrée dans la main droite a été supérieure à celle enrégistrée dans les membres inférieurs (71, 9% ± 6,5% vs 63,4% ± 4,3% et 83,3% ± 4,2% vs 76% ± 4,1%, moyenne ± SD respectivement). A dix minutes ces différences ont diminué et ont presque complètement disparu après 24 heures. Ces résultats pourraient être expliqués par la présence d’un shunt droitgauche au niveau du canal artériel produisant une diminution de la saturation d’oxygène dans les membres inférieurs. La saturation d’oxygène n’était pas différente entre les nouveau-nés accouchés par voie vaginale ou par césarienne indépendamment de l’anesthésie utilisée. On conclut que le nouveauné demeure relativement désaturé à la période immédiate après l’accouchement et que la SPO2 obtenue de la main droite étant un meilleur indice de l’oxygénation néonatale obtenue du talon.

Intraoperative pulmonary oedema in a young cocaine smoker

This is a case of a 28-yr-old man who underwent general anaesthesia for emergency repair of a right lid laceration and lacrimal apparatus. Following induction of anaesthesia and local nasal application of phenylephrine (0.25%) he developed transient elevation of blood pressure, which was treated immediately with labetalol. Subsequently the patient developed acute pulmonary oedema which responded to treatment with morphine and furosemide. The diagnosis of pulmonary oedema was confirmed by blood gas studies, chest x-ray and serial echocardiograms. Subsequent investigation revealed that he was a cocaine user, as the urine tested positive for cocaine. Considering that the patient was young and otherwise healthy and that the hypertension was transient, it is unlikely that phenylephrine was the main cause of pulmonary oedema. Cardiac morbidity was most likely precipitated by the interaction of phenylephrine-induced hypertension with a cocaine-depressed myocardium.RésuméIl s agit d’un homme de 28 ans soumis à une anesthésie générale pour la réparation d’une lacération de la paupière et des voies lacrymales du côté droit. Après l’induction de l’anesthésie et l’application locale de phényléphrine (0,25%), il présente une élévation transitoire de la pression artérielle traitée immédiatement avec du labétalol. Par la suite, il développe un oedème pulmonaire aigu qui répond au traitement à (a morphine et au furosémide. Les diagnostic d’oedème pulmonaire est confirmé par l’analyse de gaz artériels, la radiographie pulmonaire et des échocardiographies séquentielles. L’investigation subséquente révèle qu’il est un habitué de la cocaïne laquelle est détectée dans son urine. Comme le patient est jeune et que son état de santé est bon, il est peu plausible que la phényléphrine ait été la principale cause de l’oedème pulmonaire. L’incident cardiaque a plutôt été précipité par l’action de l’hypertension induite par la phényléphrine sur un myocarde déjà déprimé par la cocaïne.

A comparison of esmolol and labetalol for the treatment of perioperative hypertension in geriatric ambulatory surgical patients

This is an open randomized study comparing the efficacy and safety of iv esmolol and labetalol in the treatment of perioperative hypertension in ambulatory surgery. Twenty-two elderly patients undergoing cataract surgery under local anaesthesia were studied. The main inclusion criteria were development of systolic blood pressure > 200 mmHg or diastolic > 100 mmHg. Esmolol was given as a bolus 500 μg · kg−1 iv followed by a maintenance infusion (150–300 μg · kg−1 · min−1). Labetalol was given as a bolus of 5 mg iv followed by 5 mg increments as needed up to a maximum of 1 mg · kg−1. Esmolol and labetalol both produced reductions in systolic and diastolic blood pressure (P < 0.05) within ten minutes of administration which lasted for at least two hours. Reduction of blood pressure by esmolol was accompanied by a decrease in HR (P < 0.05). Two patients developed extreme bradycardia (HR < 50 beats · min−1) and esmolol had to be discontinued. Labetalol, in contrast, induced only a moderate decrease in HR. None of the patients treated with labetalol experienced any prolonged side effects such as orthostatic hypotension. In conclusion, esmolol may produce considerable bradycardia in elderly patients when hypertension is not accompanied by tachycardia. Labetalol was easier to administer in the ambulatory setting and one-tenth the cost of esmolol.RésuméIl s’agit d’une étude randomisée comparant l’efficacité et la sécurité du traitement avec esmolol et labétalol iv de l’hypertension peropératoire lors de la chirurgie ambulatoire. Nous avons étudié 22 patients âgés subissant une chirurgie pour cataracte sous anesthésie locale. Les critères d’inclusion principaux étaient l’apparition d’une tension artérielle systolique plus grande que 200 mmHg ou diastolique plus grande que 100 mmHg. Le traitement à l’esmolol comprenait un bolus de 500 μg · kg−1 iv suivi d’une perfusion de 150 a 300 μg · kg−1 · min−1. Le traitement au labétalol comprenait un bolus de 5 mg iv suivi d’une dose de 5 mg selon les besoins jusqu’à un maximum de 1 mg · kg−1. L’esmolol et le labétalol ont diminué les tensions artérielle systoliques et diastoliques (P < 0,05) en dedans de dix minutes après leur administration, effet qui a persisté pour au moins deux heures. La diminution de la tension artérielle par l’esmolol était accompagnée par une diminution de la fréquence cardiaque (P < 0,05). Deux patients ont présenté une bradycardie sévère (fréquence cardiaque < 50 battements · min−1) et l’esmolol a du être cessé. Le labétalol ne causait qu’une diminution modérée de la fréquence cardiaque. Aucun des patients traités avec labétalol n’a montré d’effets secondaires prolongés importants tel que l’hypotension orthostatique. En conclusion, l’esmolol peut causer une bradycardie importante chez les patients âgés lorsque Vhypertension n’est pas accompagnée de tachycardie. Le labétalol est plus facile à administrer dans le contexte ambulatoire, et ce à un coût dix fois moins important que l’esmolol.

Milrinone is superior to epinephrine as treatment of myocardial depression due to ropivacaine in pigs.

Purpose: To determine whether milrinone is more effective than epinephrine in the resuscitation of ropivacaine induced cardiotoxicity in pigs.Methods: Arterial, pulmonary, and LVdP/dt catheters were placed in 12 anesthetized, intubated and mechanically ventilated pigs. They received ropivacaineiv to cardiovascular toxicity: 50% decrease in LVdP/dt, cardiac output and mean arterial pressure (MAP). Group 1 (n=6) was treated with 100 µg·kg−1 milrinoneiv, and Group II (n=6) received 0.5 mg epinephrineiv. Resuscitation was successful if cardiac output returned to baseline, and MAP reached 80% of baseline.Results: After ropivacaine, MAP decreased from 88±7 to 49±8 mmHg (P<0.05), CO decreased from 2.8±0.4 to 1.2±0.2 L·min−1 (P<.05), HR decreased from 103±8 to 74±7 beats·min (P<0.05) and LVdp/dt decreased from 1950±130 to 755±125 mmHg (P<0.05). The LV EDP increased from 5±1 to 8±1 mmHg (P<0.05) and SVR from 2317 to 3000±120 dynes·sec−1·cm−5. Electrocardiogram changes included increases in the QTU interval and QRS duration. In all animals, milrinone restored MAP, CO, SV, HR, and dP/dt to baseline and no animal developed arrhythmias. In contrast, epinephrine produced severe hypertension and tachycardia. There was no improvement in CO or SV, and SVR increased. Epinephrine caused A-V dissociation and ventricular arrhythmias in three animals.Conclusion: Milrinone, was more successful than epinephrine in resuscitating anesthetized pigs from ropivacaine-induced cardiovascular toxicity.RésuméObjectif: Déterminer si la milrinone est plus efficace que l’épinéphrine au moment de réanimer des porcs victimes d’une cardiotoxicité induite par la ropivacaïne.Méthode: Des cathéters artériels, pulmonaires et ventriculaires gauches (dP/dtVG) ont été mis en place chez 12 porcs anesthésiés, intubés et sous ventilation mécanique. Ils ont reçu de la ropivacaïneiv qui a provoqué la cardiotoxicité manifestée par: une baisse de 50 % dP/dtVG, du débit cardiaque (DC) et de la pression artérielle moyenne (PAM). Le groupe I (n=6) a été traité avec 100µg·kg−1 de milrinoneiv et le groupe II (n=6) avec 0,5 mg d’épinéphrineiv. La réanimation était réussie lorsque le DC revenait aux valeurs de base et que la PAM atteignait 80 % des valeurs de base.Résultats: Après l’administration de la ropivacaïne, la PAM a chuté de 88±7 à 49±8 mmHg (P<0,05), le DC de 2,8±0,4 à 1,2±0,2 L·min−1 (P<0,05), la FC de 103±8 to 74±7 battements·min (P<0,05) et dP/dtVG de 1950±130 à 755±125 mmHg (P<0,05). La pression télédiastolique du VG a augmenté, passant de 5±1 à 8±1 mmHg (P<0,05) et la résistance vasculaire périphérique (RVP) de 2317 à 3000±120 dynes·s−1·cm−5. Les changements à l’électrocardiogramme comprenaient des augmentations de l’intervalle QTU et de la durée de QRS. Chez tous les animaux, la milrinone a ramené la PAM, le DC, le débit systolique (DS), la FC et dP/dt aux valeurs de base et aucun animal n’a présenté d’arythmie. Par ailleurs, l’épinéphrine a produit une sévère hypertension et de la tachycardie. Il n’y a pas eu d’amélioration du DC ou du DS et la RVP a augmenté. L’épinéphrine a aussi causé une dissociation AV et des arythmies ventriculaires chez trois animaux.Conclusion: La milrinone a été plus efficace que l’épinéphrine pour la réanimation de porcs anesthésiés qui ont subi une cardiotoxicité provoquée par de la ropivacaïne.

Congestive heart failure in neonatal thyrotoxicosis. A curable casue of heart failure in the newborn.

A 3,250 g white infant was born after an unremarkable pregnancy and delivery to a 2~-yearxad old mother with a history of exophthalmia and goiter for four years. She was currently under therapy for hyperthyroidism with tapazole and potassium iodide. The infant was well until ten days of age when he developed severe congestive heart failure associated with diarrhea. At that time, his temperature was 99.6 F, pulse 210/minute, and respiratory rate 64/minute. The thyroid was diffu~ely enlarged with a bruit heard on auscultation. The precordium was moving and a grade II/VI systolic murmur was heard at the left sternal

Treatment of recurrent paroxysmal ventricular tachycardia

Abstract This case report demonstrates the therapeutic effect of the combination of propranolol and procainamide upon recurrent paroxysmal ventricular tachycardia in a 10-year-old boy. When used as a single agent, procainamide, diphenylhydantoin, and propranolol proved ineffective in suppressing the arrhythmia. The child has been in normal sinus rhythm for 20 months without side effects, while receiving a combination of propranolol and procainamide. The etiology and therapy of this condition was discussed.

Cardiovascular consequences of the concomitant administration of nifedipine and magnesium sulfate in pigs.

There is concern regarding the interaction of magnesium sulfate and nifedipine used concomitantly in obstetrical patients, because both are calcium channel antagonists and may induce myocardial depression as well as peripheral vasodilatation. The objective of this study was to determine the hemodynamic consequences of concomitant administration of nifedipine and magnesium sulfate in anesthetized pigs. Twelve pigs were anesthetized with sodium pentobarbital, intubated mechanically ventilated. Following placement of invasive monitors, baseline hemodynamic measurements were made. Animals were randomized to one of two groups. Group I received nifedipine first, and then magnesium sulfate. Group II received magnesium sulfate first, and then nifedipine. Hemodynamic measurements were recorded. Hypotension was treated with calcium chloride, ephedrine and phenylephrine. Nifedipine alone (Group I) decreased peripheral vascular resistance and mean arterial pressure (MAP) (P<0.05). Magnesium sulfate alone in group II decreased the first derivative of left ventricular pressure (LVdP/dt) and increased left ventricular end-diastolic pressure (LVEDP) (P<0.05). Magnesium sulfate also decreased peripheral vascular resistance and MAP The concomitant administration of nifedipine and magnesium sulfate in both groups I and 11 led to a further decrease in myocardial contractility, as evidenced by a decrease in LVdP/dt and increase in LVEDP (P<0.05). Treatment with calcium chloride or ephedrine was only partially successful in improving myocardial contractility. Phenylephrine increased peripheral vascular resistance and MAP, but did not improve myocardial function. In conclusion, the depressive effects of nifedipine and magnesium sulfate on the cardiovascular system are potentiated when administered concomitantly.

Role of zatebradine and propranolol in attenuation of tachycardia produced by dobutamine in pigs

Background: Zatebradine is a new specific bradycardic agent that selectively slows the depolarization in the pacemaker cells of the sinoatrial node. The purpose of our investigation was to determine whether the tachycardia induced by dobutamine can be attenuated by the administration of zatebradine. The results were compared with those produced by propranolol, which is used in the treatment of sinus tachycardia.

Diltiazem in the prevention and treatment of cocaine-induced cardiotoxicity in dogs

Abstract Cocaine can induce serious cardiovascular sequelae, including myocardial depression and coronary artery constriction. The objective of this study was to determine, in the experimental canine model, whether the calcium channel blocker diltiazem, administered intravenously, can ameliorate cocaine-induced cardiotoxicity. The study was conducted in two parts. In the first part of the study, the protective effect of diltiazem against cocaine-induced cardiotoxicity was evaluated. Dogs given pentobarbital were pretreated with either diltiazem 0.25 mg/kg or saline, and then given a 10-mg/kg intravenous bolus of cocaine. In the second part of the study, the role of diltiazem in the treatment of cocaine-induced left ventricular myocardial dysfunction was evaluated. All dogs received a 10-mg/kg intravenous bolus of cocaine. The dogs then received either diltiazem 0.25 mg/kg intravenously or saline. Administration or diltiazem before cocaine reduced the cardiotoxic effects of cocaine. Compared with the control group, there was less depression of the first derivative of left ventricular pressure (LV dP/dt), cardiac output, and left ventricular end diastolic pressure. ST segment elevation occurred in the majority of the control animals after cocaine injection but in none of the animals pretreated with diltiazem. In the second part of the study, cocaine produced left ventricular dysfunction in all animals and ST segment elevation on the electrocardiogram in a majority of the animals. Treatment with diltiazem after the onset of cocaine-induced myocardial dysfunction did reverse the ST segment elevation. It did not, however, improve the hemodynamics significantly compared with the control group. Partial recovery of left ventricular function occurred at 15 minutes in both groups. It was concluded that, in the canine model, administration of diltiazem before injection of cocaine prevents myocardial depression and ST segment elevation. Diltiazem is also effective as treatment to reverse cocaine-induced ST segment elevation but not cocaine-induced myocardial depression.