Efeitos hemodinâmicos da anestesia em plano profundo com infusão intravenosa contínua de propofol ou propofol associado à lidocaína em cães / Hemodynamic effects of deep anesthesia with a constant rate infusion of propopol or propofol combined with lidocaine in dogs

Os efeitos hemodinâmicos da anestesia total intravenosa com propofol ou propofol associado à lidocaína foram estudados em 12 cães. No grupo P (n=6), os animais receberam bolus de 6mg kg-1 de propofol e infusão contínua de 1,25mg kg-1 min-1. No grupo PL (n=6), os animais receberam bolus de 6mg kg-1 de propofol e 1,5mg kg-1 de lidocaína, seguido de infusão de 1,0mg kg-1 min-1 e 0,25mg kg-1 min-1, dos mesmos fármacos, respectivamente. Os animais foram instrumentados para mensuração das variáveis hemodinâmicas e do índice bispectral (BIS), aos 75, 90, 105 e 120 minutos de anestesia. Foram observados valores menores de índice cardíaco, índice sistólico, pressões arteriais sistólica, diastólica e média no grupo P do que no grupo PL (P<0,05). Não foram observadas diferenças entre os grupos na frequência cardíaca, índice de resistência vascular sistêmica e BIS. As concentrações plasmáticas de propofol foram menores no grupo PL do que no grupo P (medianas de 5,7 a 6,1µg mL-1 no grupo P versus 3,1 a 3,7µg mL-1 no grupo PL). As concentrações plasmáticas de lidocaína (medianas de 2,27 a 2,51µg mL-1) mensuradas encontram-se na faixa que resulta em analgesia e abaixo de valores que resultam em toxicidade em cães. Os valores de BIS obtidos nos dois grupos foram compatíveis com plano profundo de anestesia (médias de 43 a 46 e 45 a 49 nos grupos P e PL, respectivamente). A manutenção da anestesia em plano profundo com lidocaína-propofol causa menor depressão cardiovascular do que a anestesia com dose equipotente de propofol isoladamente.

The hemodynamic effects of total intravenous anesthesia with propofol or propofol in combination with lidocaine were investigated in 12 dogs. In the P group (n=6), the dogs received a loading dose (LD) of 6mg kg-1 of propofol followed by a constant rate infusion (CRI) of 1.25mg kg-1 min-1. In the PL group (n=6), dogs received a LD of 6mg kg-1 of propofol and 1.5mg kg-1 of lidocaine followed by CRIs of 1.0mg kg-1 min-1 and 0.25mg kg-1 min-1 of propofol and lidocaine, respectively. The animals were instrumented for measurement of hemodynamic variables and bispectral index (BIS), recorded at 75, 90, 105 and 120 minutes during anesthesia. Cardiac index, stroke index, systolic, diastolic and mean arterial blood pressures were lower in the P group compared to the PL group (P<0.05). There were no significant differences between groups in heart rate, systemic vascular resistance index and BIS. Plasma concentrations of propofol were lower in group PL than in group P (medians of 5.7 to 6.1mg mL-1 in the P group versus 3.1 to 3.7mg mL-1 in the PL group). Measured lidocaine plasma concentrations (medians of 2.27 to 2.51mg mL-1) were in the range that result in analgesia and were below values that result in toxicity in dogs. The BIS values observed in the two groups of dogs were compatible with deep anesthesia (mean values of 43-46 and 45-49 in groups P and PL, respectively). Maintenance of deep anesthesia with lidocaine-propofol causes less cardiovascular depression than equipotent doses of propofol alone.

Minimum infusion rate and hemodynamic effects of propofol, propofol-lidocaine and propofol-lidocaine-ketamine in dogs.

OBJECTIVE: To evaluate the effects of a constant rate infusion (CRI) of lidocaine alone or in combination with ketamine on the minimum infusion rate (MIR) of propofol in dogs and to compare the hemodynamic effects produced by propofol, propofol-lidocaine or propofol-lidocaine-ketamine anesthesia. STUDY DESIGN: Prospective, randomized cross-over experimental design. ANIMALS: Fourteen adult mixed-breed dogs weighing 15.8 ± 3.5 kg. METHODS: Eight dogs were anesthetized on different occasions to determine the MIR of propofol alone and propofol in combination with lidocaine (loading dose [LD] 1.5 mg kg(-1), CRI 0.25 mg kg(-1) minute(-1)) or lidocaine (LD 1.5 mg kg(-1), CRI 0.25 mg kg(-1) minute(-1)) and ketamine (LD 1 mg kg(-1), CRI 0.1 mg kg(-1) minute(-1)). In six other dogs, the hemodynamic effects and bispectral index (BIS) were investigated. Each animal received each treatment (propofol, propofol-lidocaine or propofol-lidocaine-ketamine) on the basis of the MIR of propofol determined in the first set of experiments. RESULTS: Mean ± SD MIR of propofol was 0.51 ± 0.08 mg kg(-1) minute(-1). Lidocaine-ketamine significantly decreased the MIR of propofol to 0.31 ± 0.07 mg kg(-1) minute(-1) (37 ± 18% reduction), although lidocaine alone did not (0.42 ± 0.08 mg kg(-1) minute(-1), 18 ± 7% reduction). Hemodynamic effects were similar in all treatments. Compared with the conscious state, in all treatments, heart rate, cardiac index, mean arterial blood pressure, stroke index and oxygen delivery index decreased significantly, whereas systemic vascular resistance index increased. Stroke index was lower in dogs treated with propofol-lidocaine-ketamine at 30 minutes compared with propofol alone. The BIS was lower during anesthesia with propofol-lidocaine-ketamine compared to propofol alone. CONCLUSIONS AND CLINICAL RELEVANCE: Lidocaine-ketamine, but not lidocaine alone, reduced the MIR of propofol in dogs. Neither lidocaine nor lidocaine in combination with ketamine attenuated cardiovascular depression produced by a continuous rate infusion of propofol.

Comparison of a sidestream capnograph and a mainstream capnograph in mechanically ventilated dogs.

OBJECTIVE: To compare the ability of a sidestream capnograph and a mainstream capnograph to measure end-tidal CO2 (ETCO2) and provide accurate estimates of PaCO2 in mechanically ventilated dogs. DESIGN: Randomized, double Latin square. ANIMALS: 6 healthy adult dogs. PROCEDURE: Anesthesia was induced and neuromuscular blockade achieved by IV administration of pancuronium bromide. Mechanical ventilation was used to induce conditions of standard ventilation, hyperventilation, and hypoventilation. While tidal volume was held constant, changes in minute volume ventilation and PaCO2 were made by changing the respiratory rate. Arterial blood gas analysis was performed and ETCO2 measurements were obtained by use of either a mainstream or a sidestream capnographic analyzer. RESULTS: A linear regression model and bias analysis were used to compare PaCO2 and ETCO2 measurements; ETCO2 measurements obtained by both capnographs correlated well with PaCO2. Compared with PaCO2, mainstream ETCO2 values differed by 3.15 +/- 4.89 mm Hg (mean bias +/- SD), whereas the bias observed with the sidestream ETCO2 system was significantly higher (5.65 +/- 5.57 mm Hg). Regardless of the device used to measure ETCO2, bias increased as PaCO2 exceeded 60 mm Hg. CONCLUSIONS AND CLINICAL RELEVANCE: RelevancehAlthough the mainstream cas slightly more accurate, both methods of ETCO2 measurement correlated well with PaCO2 and reflected changes in the ventilatory status. However, ETCO2 values > 45 mm Hg may inaccurately reflect the severity of hypoventilation as PaCO2 may be underestimated during conditions of hypercapnia (PaCO2 > 60 mm Hg).