Diferentes frações inspiradas de oxigênio em coelhos hipovolêmicos anestesiados com propofol e submetidos à ventilação mecânica

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Ventilação mandatória intermitente sincronizada versus ventilação com suporte pressórico e volume garantido em coelhos induzidos à hemorragia aguda

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Parâmetros eletrocardiográficos e cardiovasculares em cães anestesiados pelo isofluorano e submetidos à hipovolemia aguda

Avaliaram-se os efeitos da hipovolemia aguda em cães anestesiados pelo isofluorano sobre a eletrocardiografia com a duração e amplitude da onda P (Pms e PmV, respectivamente); intervalo entre as ondas P e R (P-R); duração do complexo QRS (QRS); amplitude da onda R (RmV); intervalo entre as ondas Q e T (Q-T) e intervalo entre as duas ondas (R-R), freqüência cardíaca (FC), índice cardíaco (IC), índice sistólico (IS) e pressões arteriais sistólica (PAS), diastólica (PAD) e média (PAM). Verificou-se também a possível influência do anestésico sobre a resposta compensatória à hipovolemia aguda. Para tal, foram utilizados 20 cães hígidos, sem raça definida, adultos, machos e fêmeas. Induziu-se a anestesia geral com isofluorano por meio de máscara naso-oral a 2,5 CAM e, após a intubação orotraqueal, o vaporizador foi ajustado em 1,5 CAM. Induziu-se a hipovolemia nos animais retirando-se volume total de 35 mlkg-1 de sangue. As mensurações foram realizadas antes da hipovolemia (M0), imediatamente após a retirada do volume total de sangue calculado (M1), e aos dez (M2), trinta (M3) e sessenta (M4) minutos. A avaliação estatística das variáveis foi efetuada por meio de Análise de Variância (ANOVA), seguida pelo teste de Tukey, considerando nível de significância de 5% (P<0,05). Houve redução do tempo de condução elétrica átrio-ventricular, aumento da impedância da musculatura ventricular, redução da freqüência cardíaca, dos índices cardíacos e sistólico, porém sem alteração na despolarização ventricular, sendo que o isofluorano não influenciou no desencadeamento da resposta compensatória à hipovolemia aguda.

Efeitos cardiovasculares e respiratórios da infusão contínua ne naloxona ou tramadol, em coelhos anestesiados com isofluorano e submetidos à hipovolemia aguda

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Estudo de diferentes frações inspiradas de oxigênio em coelhos submetidos à hipovolemia aguda e anestesiados com isofluorano, associado ou não à infusão contínua de tramadol

Pós-graduação em Cirurgia Veterinária - FCAV

Estudo comparativo entre as ventilações espontânea, mandatória intermitente sincronizada, pressão de suporte e volume garantido e suporte pressórico, em coelhos anestesiados com propofol e induzidos à hipovolemia aguda

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Estudo de diferentes frações inspiradas de oxigênio em coelhos induzidos à hipovolemia aguda, anestesiados com propofol e submetidos à ventilação controlada a pressão

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Hemodynamic parameters change earlier than tissue oxygen tension in hemorrhage

BACKGROUND: Untreated hypovolemia results in impaired outcome. This study tests our hypothesis whether general hemodynamic parameters detect acute blood loss earlier than monitoring parameters of regional tissue beds. MATERIALS AND METHODS: Eight pigs (23-25 kg) were anesthetized and mechanically ventilated. A pulmonary artery catheter and an arterial catheter were inserted. Tissue oxygen tension was measured with Clark-type electrodes in the jejunal and colonic wall, in the liver, and subcutaneously. Jejunal microcirculation was assessed by laser Doppler flowmetry (LDF). Intravascular volume was optimized using difference in pulse pressure (dPP) to keep dPP below 13%. Sixty minutes after preparation, baseline measurements were taken. At first, 5% of total blood volume was withdrawn, followed by another 5% increment, and then in 10% increments until death. RESULTS: After withdrawal of 5% of estimated blood volume, dPP increased from 6.1% +/- 3.0% to 20.8% +/- 2.7% (P < 0.01). Mean arterial pressure (MAP), mean pulmonary artery pressure (PAP) and pulmonary artery occlusion pressure (PAOP) decreased with a blood loss of 10% (P < 0.01). Cardiac output (CO) changed after a blood loss of 20% (P < 0.05). Tissue oxygen tension in central organs, and blood flow in the jejunal muscularis decreased (P < 0.05) after a blood loss of 20%. Tissue oxygen tension in the skin, and jejunal mucosa blood flow decreased (P < 0.05) after a blood loss of 40% and 50%, respectively. CONCLUSIONS: In this hemorrhagic pig model systemic hemodynamic parameters were more sensitive to detect acute hypovolemia than tissue oxygen tension measurements or jejunal LDF measurements. Acute blood loss was detected first by dPP.

Cardiovascular effects of desflurane following acute hemorrhage in dogs

Objective: To determine the cardiovascular effects of desflurane in dogs following acute hemorrhage.Design: Experimental study.Animals: Eight mix breed dogs.Interventions: Hemorrhage was induced by withdrawal of blood until mean arterial pressure (MAP) dropped to 60 mmHg in conscious dogs. Blood pressure was maintained at 60 mmHg for 1 hour by further removal or replacement of blood. Desflurane was delivered by facemask until endotracheal intubation could be performed and a desflurane expiratory end-tidal concentration of 10.5 V% was maintained.Measurements and main results: Systolic, diastolic, and mean arterial blood pressure (SAP, DAP and MAP), central venous pressure (CVP), cardiac output (CO), stroke volume (SV), cardiac index (0), systemic vascular resistance (SVR), heart rate (HR), respiratory rate (RR), partial pressure of carbon dioxide in arterial blood (PaCO2), and arterial pH were recorded before and 60 minutes after hemorrhage, and 5, 15, 30, 45 and 60 minutes after intubation. Sixty minutes after hemorrhage, SAP, DAP, MAP, CVP, CO, Cl, SV, PaCO2, and arterial pH decreased, and HR and RR increased when compared with baselines values. Immediately after intubation, MAP and arterial pH decreased, and PaCO2 increased. Fifteen minutes after intubation SAP, DAP, MAP, arterial pH, and SVR decreased. At 30 and 45 minutes, MAP and DAP remained decreased and PaCO2 increased, compared with values measured after hemorrhage. Arterial pH increased after 30 minutes of desflurane administration compared with values measured 5 minutes after intubation.Conclusions: Desflurane induced significant changes in blood pressure and arterial pH when administered to dogs following acute hemorrhage.

Glibenclamide effects on renal function and histology after acute hemorrhage in rats under sevoflurane anesthesia

Introduction. Hypovolemia from hemorrhage evokes protective compensatory reactions, such as the renin-angiotensin system, which interferes in the clearance function and can lead to ischemia. This study was designed to evaluate the effects of glibenclamide, a K-ATP(+) channel blocker, on renal function and histology in rats in a state of hemorrhagic shock under sevoflurane anesthesia. Material and Methods. Twenty Wistar rats were randomized into two groups of 10 animals each (G1 and G2), only one of which (G2) received intravenous glibenclamide (1 mu g.g(-1)), 60 min before bleeding was begun. Both groups were anesthetized with sevoflurane and kept on spontaneous respiration with oxygen-air, while being bled of 30% of volemia in three stages with 10 min intervals. There was an evaluation of renal function-sodium para-aminohippurate and iothalamate clearances, filtration fraction, renal blood flow, renal vascular resistance-and renal histology. Renal function attributes were evaluated at three moments: M1 and M2, coinciding with the first and third stages of bleeding; and M3, 30 min after M2, when the animals were subjected to bilateral nephrectomy before being sacrificed. Results. Significant differences were found in para-aminohippurate clearance, G1 < G2, and higher renal vascular resistance values were observed in G1. Histological examination showed the greater vulnerability of kidneys exposed to sevoflurane alone (G1) with higher scores of vascular and tubular dilatation. There were vascular congestion and tubular vacuolization only in G1. Necrosis and signs of tubular regeneration did not differ in both groups. Conclusion. Treatment with glibenclamide attenuated acutely the renal histological changes after hemorrhage in rats under sevoflurane anesthesia.

Renal histology and immunohistochemistry after acute hemorrhage in rats under sevoflurane and ketoprofen effect

OBJETIVO: Investigar a influência do inibidor não-seletivo da ciclooxigenase, cetoprofeno (ceto) intravenoso, em alterações histológicas e dos níveis das citocinas renais - fator α de necrose tumoral (TNF- α) e interleucina 1 (IL-1) - após hemorragia de 30% da volemia (10%, três vezes, em intervalos de 10 min). MÉTODOS: Sob anestesia com sevoflurano (sevo), os grupos sevo e sevo+ceto (10 ratos cada) foram preparados cirurgicamente para leitura de pressão arterial média (PAM) e administração de solução de Ringer (5 mL/kg/h) e de cetoprofeno (1,5 mg/kg), no início da anestesia, no grupo sevo+ceto. Mediu-se temperatura retal continuamente. Os valores de temperatura e PAM foram observados antes da primeira hemorragia (T1), após a terceira hemorragia (T2) e 30 min após T2 (T3). Realizada nefrectomia bilateral nos dois grupos para análise histológica e imuno-histoquímica. RESULTADOS: Nos dois grupos, temperatura e PAM diminuíram com relação aos valores basais. Hipotermia foi mais acentuada no grupo sevo (p=0,0002). Necrose tubular foi mais frequente no grupo sevo (p=0,02). As citocinas estiveram igualmente presentes nos rins dos dois grupos. CONCLUSÃO: Cetoprofeno foi mais protetor no rim de rato durante anestesia com sevoflurano e hipovolemia, porém parece que TNF- α e IL-1 não estão envolvidas nessa proteção.

[Acute asthma attacks in childhood]

The diagnosis of an acute asthmatic attack in a child is made on a clinical basis. The severity of the exacerbation can be assessed by physical examination and measurement of the transcutaneous oxygenation saturation. A blood gas analysis can be helpful in this assessment. A child with a severe asthma exacerbation should be promptly referred to an emergency department of a hospital. Oxygen should be given to keep the oxygen saturation above 92% and short-acting, selective beta-2 agonists should be administered. Beta-2 agonists can be delivered by intermittent nebulization, continuous nebulization or by metered dose inhaler (MDI) with a spacer They can also be given intravenously in patients who are unresponsive to escalating therapy. The early administration of systemic corticosteroids is essential for the management of acute asthma in children. When tolerated, systemic corticoseroids can be given orally but inhaled corticosteroids are not recommended. Oxygen delivery, beta-2 agonists and steroid therapy are the mainstay of emergency treatment. Hypovolemia should be corrected either intravenously or orally. Administration of multiple doses of ipratropium bromide has been shown to decrease the hospitalization rate in children and adolescents with severe asthma. Clinical response to initial treatment is the main criterion for hospital admission. Patients with failure to respond to treatment should be transferred to an intensive care unit. A critical aspect of management of the acute asthma attack in a child is the prevention of similar attacks in the future.

Hypotension and hypovolemia during hemodialysis: is the usual suspect innocent?

Hypotension during intermittent hemodialysis is common, and has been attributed to acute volume shifts, shifts in osmolarity, electrolyte imbalance, temperature changes, altered vasoregulation, and sheer hypovolemia. Although hypovolemia may intuitively seem a likely cause for hypotension in intensive care patients, its role in the pathogenesis of intradialytic hypotension may be overestimated.