Parada cardíaca inesperada durante colecistectomia: relato de caso

JUSTIFICATIVA E OBJETIVOS: A parada cardíaca per-operatória é um evento grave, e sua incidência em nosso serviço é de 31:10.000 anestesias. O objetivo deste relato é apresentar um caso de parada cardíaca durante anestesia geral em uma paciente submetida a colecistectomia. RELATO do CASO: Paciente feminina, 16 anos, 62 kg, estado físico ASA I, submetida à colecistectomia por via aberta. Midazolam (15 mg) por via oral foi a medicação pré-anestésica. Foi realizadas indução anestésica com sufentanil (50 µg), propofol (150 mg) e atracúrio (30 mg). A anestesia foi mantida com isoflurano e N2O. Após trinta minutos de cirurgia ocorreu bradicardia sinusal revertida com atropina (0,5 mg). Vinte minutos depois, ocorreu outra bradicardia com bloqueio átrio-ventricular de 3º grau evoluindo rapidamente para parada cardíaca (PCR) em assistolia, apesar da administração de atropina (1 mg). As manobras de reanimação foram iniciadas imediatamente, juntamente com a administração de adrenalina (1 mg), com retorno dos batimentos cardíacos espontâneos após aproximadamente cinco minutos da PCR. A cirurgia foi concluída e a paciente manteve-se estável hemodinami- camente. A paciente foi extubada duas horas após o término da cirurgia apresentando-se sonolenta, não contactante, com bom padrão ventilatório e hemodinâmico. Após doze horas de observação na unidade de terapia intensiva (UTI) a paciente apresentava-se agitada e desconexa. Vinte e quatro horas após a PCR a paciente recebeu alta da UTI consciente, orientada, sem queixas e sem déficit neurológico. Recebeu alta hospitalar no 4º dia do pós-operatório. CONCLUSÕES: Diversos fatores podem contribuir para a ocorrência de disritmias e parada cardíaca no per-operatório, destacando-se a estimulação vagal secundária às manobras cirúrgicas. O diagnóstico precoce e o rápido início das manobras de reanimação são de fundamental importância para a boa evolução neurológica desses pacientes

Effects of experimental amitraz intoxication in cats

Este trabalho estudou os efeitos da intoxicação experimental por amitraz em 16 gatos, distribuídos, aleatoriamente, em dois grupos: grupo amitraz - animais receberam amitraz a 1,5% na dose de 1,0 mg/kg IV; e grupo controle - animais sem amitraz. Parâmetros fisiológicos sangüíneos, do sistema cardiorespiratório e de sedação foram aferidos até 360min. Perfil sangüíneo, uréia, creatinina, alanina aminotransferase e aspartato aminotransferase não foram afetados pelo amitraz. Sedação, perda de reflexos, hipotermia, bradicardia, bradiarritmias, hipotensão, bradipnéia, midríase, além de transitória hiperglicemia, hipoinsulinemia e diminuição dos níveis de cortisol, foram observados nos gatos experimentalmente expostos ao amitraz. Os efeitos alfa 2-adrenérgicos induzidos pela intoxicação por amitraz em gatos são muito similares aos mesmos efeitos relatados em outras espécies, contribuindo com mais informações dessa intoxicação para a toxicologia veterinária.

Uso de dexmedetomidina em anestesiologia

JUSTIFICATIVA E OBJETIVOS: A dexmedetomidina é um novo agonista alfa2-adrenérgico que apresenta relação de seletividade entre os receptores alfa2:alfa1 de 1600:1, com importante ação sedativa e analgésica, bom controle hemodinâmico frente ao estresse e que pode produzir, por si só, anestesia. Este agente tem sido empregado para promover analgesia e sedação no período pós-operatório e nas unidades de tratamento intensivo. Devido à suas propriedades, recentemente, a dexmedetomidina passou a ser utilizada também na sala de operações, como fármaco coadjuvante em anestesia. Assim, este artigo faz uma revisão da literatura com relação ao uso da dexmedetomidina na prática anestésica. CONTEÚDO: São apresentados os principais trabalhos com o emprego da dexmedetomidina em Anestesiologia, seja como medicação pré-anestésica, ou durante o ato anestésico-cirúrgico. O mecanismo de ação dos fármacos alfa2-agonistas e as propriedades farmacocinéticas e farmacodinâmicas da dexmedetomidina também são revistos neste artigo. CONCLUSÕES: O uso da dexmedetomidina como medicação pré-anestésica, durante anestesia, ou no período pós-operatório, promove boa estabilidade hemodinâmica. Há redução do consumo de anestésicos durante a anestesia. Os pacientes sedados com a dexmedetomidina podem ser despertados, quando solicitados, e tornarem-se cooperativos. Mesmo doses elevadas do fármaco não provocam depressão respiratória. Bradicardia é um efeito adverso observado com freqüência, problema amenizado pela administração lenta da droga. Assim, a dexmedetomidina torna-se importante recurso adicional para a prática clínica da Anestesiologia, com possibilidade de uso em diversos tipos de pacientes e procedimentos cirúrgicos.

Efeitos da associação da clonidina à bupivacaína hiperbárica na anestesia subaracnóidea alta

JUSTIFICATIVA E OBJETIVOS: Dados da literatura sugerem que a clonidina, um agonista alfa2-adrenérgico, em associação com a bupivacaína, na anestesia subaracnóidea alta pode aumentar a incidência de hipotensão e bradicardia. O objetivo desta pesquisa foi verificar o potencial sinergismo entre diferentes doses de clonidina, de 45 e 75 µg, e bupivacaína hiperbárica nas características e nos efeitos hemodinâmicos do bloqueio subaracnóideo alto (T4). MÉTODO: em estudo aleatório e duplamente encoberto, foram avaliados 60 pacientes estado físico ASA I, submetidos à cirurgia do abdômen inferior e membros inferiores. Os pacientes foram submetidos à anestesia subaracnóidea, com bupivacaína hiperbárica a 0,5% (17,5 mg - 3,5 ml) mais a associação das seguintes drogas: grupo Controle (n = 20) - solução fisiológica (0,5 ml); grupo Clon 45 (n = 20) - clonidina, na dose de 45 µg (0,3 ml), associada à solução fisiológica (0,2 ml); grupo Clon 75 (n = 20) - clonidina, na dose de 75 µg (0,5 ml). A cirurgia somente foi realizada quando o nível do dermátomo atingido pelo bloqueio analgésico foi de T4. RESULTADOS: A latência dos bloqueios analgésico e motor da anestesia subaracnóidea não diferiu significativamente entre os grupos (p > 0,05). Ambas as doses de clonidina prolongaram, de maneira significativa, a duração do bloqueio analgésico em T8 e do bloqueio motor grau 3 (determinado pela escala modificada de Bromage) (p < 0,05). A incidência de hipotensão arterial no per-operatório foi evidente somente no grupo Clon 75, em relação ao grupo Controle (p < 0,05), com o Clon 45 apresentando incidência intermediária entre os demais grupos. Não houve diferença significante entre os grupos em relação à bradicardia (p > 0,05). Ambas as doses de clonidina prolongaram a analgesia pós-operatória (intervalo de tempo decorrido entre o bloqueio subaracnóideo e a primeira solicitação de analgésico pelo paciente no pós-operatório) (p < 0,05). CONCLUSÕES: A clonidina na maior dose (75 µg) em associação com a bupivacaína durante anestesia subaracnóidea alta (T4) determina maior incidência de hipotensão arterial, mas prolonga o bloqueio analgésico e a analgesia pós-operatória igualmente como a menor dose (45 µg).

Parametric evaluation of methotrimeprazine-midazolam-ketamine and methotrimeprazine-midazolam-ketamine-xylazine combination in dogs

OBJETIVO: Avaliar os parâmetros de cães anestesiados com diferentes protocolos de fármacos dissociativos por infusão intravenosa contínua. MÉTODOS: Foram utilizados 30 cães, machos e fêmeas, clinicamente sadios, distribuídos aleatoriamente em três grupos (G1,G2 e G3) (*)). em G1 utilizou-se levomepromazina como medicação pré-anestésica (MPA), midazolam-cetamina pela via intravenosa em bolus para indução e midazolam-cetamina em infusão intravenosa contínua por 60 minutos para manutenção. em G2 procedeu-se da mesma forma que em G1 elevando-se, porém, a dose de midazolam durante a manutenção. em G3 repetiu-se o tratamento empregado em G2, acrescentando-se a xilazina à manutenção. Após a indução, iniciou-se imediatamente a manutenção anestésica, realizando-se aferições, 15 minutos depois da MPA, em intervalos de 10 minutos, durante a manutenção (M0 a M7). RESULTADOS: em G3 ocorreu bradicardia, bloqueio átrio-ventricular, bradipnéia e hipoxemia e em G1 e G2, discreta hipotensão. CONCLUSÃO: A via intravenosa contínua apresentou vantagens quanto a: não oscilação dos parâmetros e redução no período de recuperação anestésica. A elevação da dose de midazolam resultou em discretas variações paramétricas, estas, acentuadas pelo uso da xilazina, que causou hipoxemia, bradiarritmia, diminuição da freqüência respiratória e volume minuto.

Evaluation of the effect of hyoscine-N-butyl bromide on the cardiovascular actions of detomidine in the horse

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Gill chemoreceptors and cardio-respiratory reflexes in the neotropical teleost pacu, Piaractus mesopotamicus

This study examined the location and distribution of O-2 chemoreceptors involved in cardio-respiratory responses to hypoxia in the neotropical teleost, the pacu (Piaractus mesopotamicus). Intact fish and fish experiencing progressive gill denervation by selective transection of cranial nerves IX and X were exposed to gradual hypoxia and submitted to intrabuccal and intravenous injections of NaCN while their heart rate, ventilation rate and ventilation amplitude were measured. The chemoreceptors producing reflex bradycardia were confined to, but distributed along all gill arches, and were sensitive to O-2 levels in the water and the blood. Ventilatory responses to all stimuli, though modified, continued following gill denervation, however, indicating the presence of internally and externally oriented receptors along all gill arches and either in the pseudobranch or at extra-branchial sites. Chemoreceptors located on the first pair of gill arches and innervated by the glossopharyngeal nerve appeared to attenuate the cardiac and respiratory responses to hypoxia. The data indicate that the location and distribution of cardio-respiratory O-2 receptors are not identical to those in tambaqui (Colossoma macropomum) despite their similar habitats and close phylogenetic lineage, although the differences between the two species could reduce to nothing more than the presence or absence of the pseudobranch.

DEVELOPMENT OF BLOOD-PRESSURE AND CARDIAC REFLEXES IN THE FROG PSEUDIS-PARADOXSUS

Systemic arterial blood pressure and heart rate (f(H)) were measured in unanesthetized, unrestrained larvae and adults of the paradoxical frog, Pseudis paradoxus from São Paulo State in Brazil. Four developmental groups were used, representing the complete transition from aquatic larvae to primarily air-breathing adults. f(H) (49-66 beats/min) was not significantly affected by development, whereas mean arterial blood pressure was strongly affected, being lowest in the stage 37-39 larvae (10 mmHg), intermediate in the stage 44-45 larvae (18 mmHg), and highest in the juveniles and adults (31 and 30 mmHg, respectively). Blood pressure was not significantly correlated with body mass, which was greatest in the youngest larvae and smallest in the juveniles. In the youngest larvae studied (stages 37-39), lung ventilation was infrequent, causing a slight decrease in arterial blood pressure but no change in heart rate. Lung ventilation was more frequent in stages 44-45 larvae and nearly continuous in juveniles and adults floating at the surface. Bradycardia during both forced and voluntary diving was observed in almost every advanced larva, juvenile, and adult but in only one of four young larvae. Developmentally related changes in blood pressure were not complete until metamorphosis, whereas diving bradycardia was present at an earlier stage.

The role of branchial and orobranchial O-2 chemoreceptors in the control of aquatic surface respiration in the neotropical fish tambaqui (Colossoma macropomum): progressive responses to prolonged hypoxia

The present study examined the role of branchial and orobranchial O-2 chemoreceptors in the cardiorespiratory responses, aquatic surface respiration (ASR), and the development of inferior lip swelling in tambaqui during prolonged (6 h) exposure to hypoxia. Intact fish (control) and three groups of denervated fish (bilateral denervation of cranial nerves IX+X (to the gills), of cranial nerves V+VII (to the orobranchial cavity) or of cranial nerves V alone), were exposed to severe hypoxia (Pw(O2) = 10 mmHg) for 360 min. Respiratory frequency (fR) and heart rate (fH) were recorded simultaneously with ASR. Intact (control) fish increased fR, ventilation amplitude (V-AMP) and developed hypoxic bradycardia in the first 60 min of hypoxia. The bradycardia, however, abated progressively and had returned to normoxic levels by the last hour of exposure to hypoxia. The changes in respiratory frequency and the hypoxic bradycardia were eliminated by denervation of cranial nerves IX and X but were not affected by denervation of cranial nerves V or V+VII. The VAMP was not abolished by the various denervation protocols. The fH in fish with denervation of cranial nerves V or V+VII, however, did not recover to control values as in intact fish. After 360 min of exposure to hypoxia only the intact and IX+X denervated fish performed ASR. Denervation of cranial nerve V abolished the ASR behavior. However, all (control and denervated (IX+X, V and V+VII) fish developed inferior lip swelling. These results indicate that ASR is triggered by O-2 chemoreceptors innervated by cranial nerve V but that other mechanisms, such as a direct effect of hypoxia on the lip tissue, trigger lip swelling.

CARDIOVASCULAR EFFECTS OF CENTRAL CLONIDINE IN CONSCIOUS RATS AFTER HYPOTHALAMIC-LESIONS

The central injection of clonidine (an alpha-2-adrenoceptor agonist) in conscious normotensive rats produces hypertensive responses and bradycardia. The present study was performed to investigate the effect of electrolytic lesions in the anteroventral third ventricle (AV3V) region or in the lateral hypothalamus (LH) on the pressor and bradycardic responses induced by central clonidine in rats. Mean arterial pressure and heart rate were recorded in sham or AV3V-lesioned rats with cerebral stainless steel cannulae implanted into the lateral cerebral ventricle (ICV) or LH. and in sham or bilateral LH-lesioned rats with cannulae-implanted ICV. The injection of clonidine (40 nmol) ICV or into the LH of sham rats produced a pressor response (37 +/- 2-48 +/- 3 mmHg) and bradycardia (-45 +/- 10--93 +/- 6 bpm). After AV3V-lesion (3 and 12 days) or LH-lesion (3 days) the pressor response was abolished and a small hypotensive response was induced by the injection of clonidine (-1 +/- 3--16 +/- 3 mmHg). The bradycardia (-27 +/- 6--57 +/- 11 bpm) was reduced, but not abolished by the lesions. These results show that the AV3V region and LH are important cerebral structures that participate in the excitatory pathways involved in the pressor response to central clonidine in rats. They also suggest that, in the absence of these pressor pathways, the hypotensive responses to central clonidine may appear in conscious rats.

LESIONS OF THE LATERAL HYPOTHALAMUS IMPAIR THE PRESSOR-RESPONSE TO CLONIDINE INJECTED INTO THE MEDIAL SEPTAL AREA OF CONSCIOUS RATS

The central injection of clonidine (an alpha-2-adrenoceptor agonist) in conscious normotensive rats produces hypertensive responses and bradycardia. The present study was performed to investigate the effect of electrolytic lesions of the lateral hypothalamus (LH) on the pressor and bradycardic responses induced by clonidine injected into the medial septal area (MSA) in conscious and unrestrained rats. Male Holtzman rats weighing 250-300 g were used. Mean arterial pressure and heart rate were recorded in sham- or bilateral LH-lesioned rats with a cerebral stainless steel cannula implanted into the MSA. The injection of clonidine (40 nmol/mu-l) into the MSA of sham rats (N = 8) produced a pressor response (36 +/- 7 mmHg, P<0.05) and bradycardia (-70 +/- 13 bpm, P<0.05) compared to saline. Fourteen days after LH-lesion (N = 9) the pressor response was reduced (9 +/- 10 mmHg, P<0.05) but no change was observed in the bradycardia (-107 +/- 24 bpm). These results show that LH is an important area involved in the pressor response to clonidine injected into the MSA of rats.

AV3V-LESION IMPAIRS RESPONSES INDUCED BY CHOLINERGIC ACTIVATION OF SFO IN RATS

This study was performed to investigate the effect of lesion of the anteroventral third ventricle (AV3V) region on the pressor, bradycardic, dipsogenic, natriuretic, kaliuretic, and antidiuretic responses induced by cholinergic activation of the subfornical organ (SFO) in rats. Male Holtzman rats with sham or electrolytic AV3V lesion were implanted with a stainless steel cannula directly into the SFO. Microinjection of the cholinergic agonist carbachol (2 nmol) into the SFO of sham rats induced natriuresis (563 +/- 70 mueq/120 min), kaliuresis (205 +/- 13 mueq/120 min), antidiuresis (10.4 +/- 0.5 ml/120 min), water intake (9.3 +/-1.4 ml/h), bradycardia (-42 +/- 11 beats/min), and increased mean arterial pressure (53 +/- 3 mmHg). In AV3V-lesioned rats (1-5 and 14-18 days), there was a reduction of natriuresis (23 +/-11 and 105 +/- 26 mueq/120 min, respectively), kaliuresis (92 +/- 16 and 100 +/- 17 mueq/120 min), water intake (2.5 +/- 0.9 and 1.8 +/- 1.0 ml/h), and arterial pressure increase (17 +/- 2 and 16 +/- 2 mmHg) induced by carbachol into the SFO. Increased antidiuresis (6.0 +/- 1.0 and 5.2 +/- 0.7 ml/120 min, respectively) and tachycardia (39 +/- 4 and 15 +/- 12 beats/min) instead of bradycardia were also observed in both groups of AV3V-lesioned rats. These results show that cholinergic activation of the rat SFO produces marked natriuresis and kaliuresis in addition to the well-known pressor and dipsogenic responses. They also show that the AV3V region plays an important role in the cardiovascular, fluid, and electrolytic changes induced by cholinergic activation of the SFO in rats.

EFFECT OF LATERAL HYPOTHALAMUS LESIONS ON THE WATER AND SALT INTAKE, AND SODIUM AND URINE EXCRETION INDUCED BY ACTIVATION OF THE MEDIAN PREOPTIC NUCLEUS IN CONSCIOUS RATS

In this-study we investigated the influence of electrolytic lesion of the lateral hypothalamus (LH) on the water and salt appetite, and the natriuretic, diuretic and cardiovascular effects induced by angiotensinergic, cholinergic and noradrenergic stimulation of the median preoptic nucleus (MnPO) in rats. Male Holtzman rats were implanted with a cannula into the MnPO. Other groups of sham- and LH-lesioned rats received a stainless steel cannula implanted into the MnPO. ANGII injection into the MnPO induced water and sodium intake, and natriuretic, diuretic, presser and tachycardic responses. Carbachol induced water intake, and natriuretic, presser and bradycardic responses, whereas noradrenaline increased urine, sodium excretion and blood pressure, and induced bradycardia. In rats submitted to LH-lesion only, water and sodium intake was reduced compared with sham rats. LH lesion also reduced the sodium ingestion induced by ANGII (12 ng) into the MnPO. In LH-lesioned rats, the dipsogenic, diuretic and presser responses induced by ANGII (12 ng), carbachol (2 nmol) and noradrenaline (20 nmol) injection into the MnPO were reduced. The same occurred with sodium excretion when carbachol (2 nmol) and noradrenaline (20 nmol) were injected into the MnPO of LH-lesioned rats, whereas ANGII(12 ng) induced an increase in sodium excretion. These data show that electrolytic lesion of the LH reduces fluid and sodium intake, and presser responses to angiotensinergic, cholinergic and noradrenergic activation of the MnPO. LH involvement with MnPO excitatory and inhibitory mechanisms related to water and sodium intake, sodium excretion and cardiovascular control is suggested.

Maximal lactate steady state in running mice: Effect of exercise training

1. Maximal lactate steady state (MLSS) corresponds to the highest blood lactate concentration (MLSSc) and workload (MLSSw) that can be maintained over time without continual blood lactate accumulation and is considered an important marker of endurance exercise capacity. The present study was undertaken to determine MLSSw and MLSSc in running mice. In addition, we provide an exercise training protocol for mice based on MLSSw.2. Maximal lactate steady state was determined by blood sampling during multiple sessions of constant-load exercise varying from 9 to 21 m/min in adult male C57BL/6J mice. The constant-load test lasted at least 21 min. The blood lactate concentration was analysed at rest and then at 7 min intervals during exercise.3. The MLSSw was found to be 15.1 +/- 0.7 m/min and corresponded to 60 +/- 2% of maximal speed achieved during the incremental exercise testing. Intra- and interobserver variability of MLSSc showed reproducible findings. Exercise training was performed at MLSSw over a period of 8 weeks for 1 h/day and 5 days/week. Exercise training led to resting bradycardia (21%) and increased running performance (28%). of interest, the MLSSw of trained mice was significantly higher than that in sedentary littermates (19.0 +/- 0.5 vs 14.2 +/- 0.5 m/min; P = 0.05), whereas MLSSc remained unchanged (3.0 mmol/L).4. Altogether, we provide a valid and reliable protocol to improve endurance exercise capacity in mice performed at highest workload with predominant aerobic metabolism based on MLSS assessment.

DIFFERENT EFFECTS ON RAT ARTERIAL-PRESSURE AND HEART-RATE WHEN LOSARTAN IS INJECTED INTO THE 3RD-VENTRICLE OR 4TH-VENTRICLE

Cardiovascular responses to central losartan (LOS), a non-peptide angiotensin II (ANG II) receptor antagonist, were investigated by comparing the effects of LOS injection into the 3rd and 4th cerebral ventricles (3rdV, 4thV) on mean arterial pressure (MAP) and heart rate (HR). Adult male Holtzman rats were used (N = 6 animals per group). Average basal MAP and HR were 114 +/- 3 mmHg and 343 +/- 9 bpm (N = 23), respectively. LOS (50, 100 or 200 nmol/2 mu l) injected into the 3rdV induced presser (peak of 25 +/- 3 mmHg) and tachycardic (peak of 60 +/- 25 bpm) responses. LOS injected into the 4thV had no effect on MAP, but it induced bradycardia (peak of -35 +/- 15 bpm). KCl (200 nmol/2 mu l) injected into the 3rdV or into the 4thV had no effect on either MAP or HR compared to 0.9% saline injection. The results indicate that LOS injected into the third ventricle acts on forebrain structures to induce its presser and tachycardic effects and that bradycardia, likely dependent on hindbrain structures, is obtained when LOS is injected into the fourth ventricle.