Sergio Gregoretti

Hemodynamic changes and oxygen consumption in burned patients during enflurane or isoflurane anesthesia

The effects of enflurane or isoflurane anesthesia on the systemic circulation and whole-body oxygen (O2) uptake (Vo2) of 15 burn patients undergoing wound excision and skin grafting procedures were studied. The possibility that burn wound excision might adversely affect pulmonary circulation was also investigated. The patients were prean-esthetically in a hyperdynamic-hypermetabolic state, characterized by a resting cardiac index (Cl) of 6.2 ± 0.9 L·min−1 · m(mean ± −2 (mean ± SD), a Vo2 (calculated using the Fick principle) of 213 ± 44 mL·min−1 ·m−2, a normal mean systemic arterial pressure (MAP) (92 ± 15 mm Hg), and markedly decreased systemic vascular resistance (SVR) (570 ± 162 dynes·ec·cm−5). Mean pulmonary arterial pressure (MPAP) prean-esthetically was slightly increased (21 ± 3 mm Hg), while pulmonary vascular resistance (PVR) was in the low-normal range (59 ± 16 dynes·sec·m−5). No difference among the effects of enflurane and isoflurane on systemic and pulmonary hemodynamics and metabolic rate was detected. Induction of anesthesia was associated with a decrease in Vo2, CI, MAP, and MPAP (P < 0.001), while SVR and PVR did not change. The decrease in CI paralleled the decrease in Vo2, thereby maintaining whole-body O2, supply-demand balance. Vo2 decreased most likely because of lessened tissue O2 requirements. When anesthesia was discontinued, all metabolic and hemodynamic variables promptly returned to prean-esthetic values. No effect of burn wound excision on pulmonary circulation was detected.

Haemodynamic changes and oxygen uptake during crossclamping of the thoracic aorta in dexmedetomidine pretreated dogs

This study was designed to test the hypothesis that the a2 adrenergic agonist, dexmedetomidine (DEX), decreases tissue oxygen demand thereby increasing tolerance to hypoxic insult. In 17 anaesthetized dogs, cardiac output was measured with thermodilution, blood flow through the inferior caval vein was determined using an electromagnetic flowmeter, and oxygen consumption was calculated by the Fick principle. The animals were divided into three groups: control group (n = 5), D3 and D30 groups (n = 6 for each group) treated with two doses of DEX (3 μg · kg−1 and 30 μg · kg−1, respectively) prior to aortic crossclamping. Upon crossclamping of the thoracic aorta, the cardiac index decreased in all three groups with the largest decrease in the D30 group, and the smallest decrease in the control group. Blood flow through the inferior vena cava decreased in all three groups of animals while blood flow through the superior caval vein increased in the control group, did not change in the D3 group, and decreased in the D30 group. Oxygen saturation in mixed venous blood increased in the control group, did not change in the D3 group and decreased in D30 group. Blood flow and oxygen uptake in the lower part of the body decreased in all groups. Oxygen consumption in the upper part of the body decreased equally in all three groups. Arterial lactate concentrations increased almost two-fold in the control group while it increased by only 30% in animals treated with DEX. A lesser increase in lactate concentrations and oxygen extraction in tissues below aortic crossclamping is consistent with the hypothesis that DEX decreases tissue oxygen requirement which might prove particularly useful in clinical situations where tissue hypoxia is expected.RésuméCette étude a pour but de déterminer si la dexmédétomidine, un agoniste alpha2 adrénergique, diminue la demande tissulaire en oxygène et augmente ainsi la tolérance à l’hypoxie. Dix-sept chiens sous anesthésie régionale sont étudiés. Le débit cardiaque est mesuré par thermodilution. Le débit sanguin de la veine cave inférieure est déterminé a l’aide d’un débitmètre électromagnétique et la consommation en oxygène est calculée à partir du principe de Fick. Les animaux sont divisés en trois groupes: un groupe contrôle (n = 5), un groupe D3 traité avec dexmédétomidine 3 μg · kg−1 (n = 6) et un groupe D30 traité avec dexmédétomidine 30 μg · kg−1 (n = 6) administrée avant le clampage aortique. À la suite du clampage de l’aorte thoracique, les trois groupes d’animaux présentent une chute de l’index cardiaque: la plus grande diminution est retrouvée dans le groupe D30 et la plus petite dans le groupe contrôle. Le débit sanguin dans la veine cave inférieure diminue dans les trois groupes, alors que le débit dans la veine cave supérieure augmente dans le groupe contrôle, ne change pas dans le groupe D3 et diminue dans le groupe D30. La saturation en oxygène du sang veineux mêlé augmente dans le groupe contrôle, ne change pas dans le groupe D3 et diminue dans le groupe D30. Le débit sanguin et la consommation en oxygène dans l’hémicorps situés sous le clampage aortique diminuent dans tous les groupes d’animaux. La consommation en oxygène dans l’hémicorps au-dessus du clampage aortique diminue egalement dans les trois groupes. La concentration artérielle de lactate est presque doublee dans le groupe controle alors qu’elle n’augmente que de 30% chez les animaux traités avec dexmédétomidine. Cette plus faible production de lactate accompagnant une moins grande demande tissulaire en oxygène pour les organes sous le clampage aortique chez les animaux traités avec la dexmédétomidine, suggère que ce médicament peut être utile dans les situations cliniques d’hypoxie tissulaire.

Simultaneous cardiac output measurements by transtracheal Doppler, electromagnetic flow meter, and thermodilution during various hemodynamic states in pigs.

The transtracheal Doppler (TTD) method of cardiac output (CO) measurement was compared with thermodilution (TDL) and aortic electromagnetic flow meter (EFM). Simultaneous CO measurements with the three methods were obtained during various hemodynamic states in eight pigs. Cardiac output ranged from 1 to 3 L/min during the study. For 128 measurements, the mean difference +/- SD between TTD-TDL and TTD-EFM measurements was -0.037 +/- 0.24 L/min and -0.055 +/- 0.23 L/min, respectively. TDL-EFM mean difference +/- SD was -0.017 +/- 0.15 L/min. The limits of the agreement between TTD and the reference methods were 0.4 to -0.5 L/min. The limits of agreement between the reference methods were 0.3 to -0.3 L/min. Regression analysis yielded TTD = 0.383 + 0.779 TDL (r = 0.86); TTD = 0.351 + 0.788 EFM (r = 0.87); TDL = 0.077 + 0.95 EFM (r = 0.95). Only a change greater than 0.6 L/min in TTD CO could predict with 95% confidence a change in TDL or EFM CO. These results suggest that, in the CO range of this study, the TTD method does not accurately reproduce the CO measurements obtained by TDL or EFM.

Lack of immediate effects of wound excision on the hyperdynamic circulation of burned patients.

The high cardiac output (CO) observed during the chronic phase in burned patients has been ascribed, among other factors, to the elevated blood flow in the burn wound. The hemodynamic effects of wound excision to fascia have been studied in eight patients with second- and third-degree burns ranging from 42% to 70% total body surface area (TBSA) undergoing debridement and skin-grafting procedures. The study was performed on the 4th to the 51st postburn day when all patients were in a hyperdynamic state. Serial hemodynamic measurements, including arterial and mixed-venous blood O2 saturation and content, were made before induction of anesthesia, during surgery both before and after wound excision, and in the recovery room a few hours after surgery. During anesthesia, the elevated CO decreased probably as a consequence of decreased metabolic requirements, but no further hemodynamic change was observed following wound excision. The size of burn wound excised to fascia averaged 24% TBSA and ranged from one-third to more than one-half of the initial burn. With discontinuation of anesthesia, CO rose rapidly above preoperative values, apparently to meet a similar increase in oxygen consumption. The excision of large areas of burned tissue did not attenuate the hyperdynamic circulation in burned patients, at least during and immediately after surgery. The data suggest that the elevated blood flow in the burn wound does not play a significant role in the pathogenesis of the hyperdynamic state.

Total Body Oxygen Supply-Demand Balance in Burned Patients Under Enflurane Anesthesia

The effects of enflurane anesthesia on the oxygen supply-demand balance have been studied in nine hypermetabolic-hyperdynamic burned patients undergoing debridement and skin-grafting procedures. Mean burn size was 55% of total body surface area. The patients were without cardiac, lung, hepatic, and kidney dysfunction and were not septic. Anesthesia was induced with sodium pentothal and maintained with enflurane and nitrous oxide in oxygen. Ventilation was controlled to maintain PaCO2 within normal limits. Crystalloid solutions and blood were administered to maintain adequate heart filling pressures. Serial measurements of cardiac output, arterial and mixed venous blood gases, and oxygen content were made before, during, and after anesthesia. Following induction of anesthesia and enflurane administration, cardiac output, oxygen delivery, and oxygen consumption decreased in a parallel fashion to approximately 60% of control. These variables did not change significantly throughout the procedure and returned to control values when enflurane was discontinued. Arteriovenous oxygen content difference did not increase and metabolic acidosis did not develop, suggesting that tissue perfusion remained adequate. Under anesthesia, oxygen consumption in burned patients was similar to that observed in normal subjects, indicating that enflurane blunts the hypermetabolic effects of thermal injury. It is concluded that in burned patients enflurane decreases metabolic rate and cardiac output, and maintains an adequate oxygen supply-demand balance.

Uneventful extradural analgesia after unrecognized dural perforation

SummaryA case is reported of an uneventful continuous extradural block in spite of unrecognized durai perforation. Although the perforation was recognized later during the block, the dura was probably pierced during the insertion of the catheter and only later the terminal hole came to lie in the subarachnoid space. Consequently both extradural and subarachnoid spread of the injected local anaesthetic occurred, preventing an extensive subarachnoid block.R & #x00E9;SUM & #x00E9;Ľauteur rapporte un cas ďanalgésie péridurale sans complications cliniques, malgré une perforation non reconnue de la dure-mère. Bien que ľon se soit rendu compte de la perforation tardivement en cours ďintervention, celle-ci est probablement survenue au cours de ľinsertion du cathéter. Ce dernier est vraisemblablement venu se placervis-à-vis ľouverture dure-méridienne à la suite des doses de rappel ďanesthésique, la solution se distribuant dans les deux espaces (sousdural et péridural), ce qui explique ľabsence ďun bloc sous-arachnoïdien total.