Case 1-1995. Anesthetic management for resection of a giant pulmonary arteriovenous malformation.
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Biomedical subjects
Publications and source records attributed to W J Greeley.
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OBJECTIVES: To answer the following questions: a) Does jugular venous ligation (simulating venovenous extracorporeal life support) alter proximal jugular venous pressure, intracranial pressure, hemispheric cerebral blood flow, or cerebral metabolism? b) Does release of ligation reverse these effects? and c) What are the comparative effects of venous ligation alone vs. venous ligation in combination with arterial ligation? DESIGN: Prospective, randomized, laboratory investigation. SETTING: Multidisciplinary laboratory setting. SUBJECTS: Sixteen swine, weighing 8.1 to 12.1 kg, 3 to 4 wks of age. INTERVENTIONS: Sixteen swine were randomly assigned to two groups, utilizing a random sequence of vessel ligation. Nine swine underwent occlusion of the right internal and external jugular veins alone (venovenous ligation) followed by release of the occlusion and then occlusion of the right common carotid artery and the right internal and external jugular veins together (venoarterial ligation). The remaining seven swine underwent venoarterial ligation, followed by release of the occlusion and then venovenous ligation. In the experimental group in which venovenous ligation was performed first, the 5, and 30-min release periods after ligation were taken to represent the effects of draining the right jugular vein during venovenous extracorporeal life support. MEASUREMENTS AND MAIN RESULTS: Data were obtained at baseline, 5, and 30 mins after each ligation/release period. Intracranial pressure, right and left internal jugular pressures/flow rates, and cerebral sinus lactate concentrations were measured. Cerebral blood flow was determined using 133Xe clearance methodology, and the cerebral metabolic rate was calculated. There were no significant differences between the ipsilateral internal jugular pressure or extracorporeal life support at 5 or 30 mins after venovenous or venoarterial ligation compared with baseline values or compared with the release of the ligation at 5 or 30 mins. There was a significant increase in right-side (44.7 +/- 2.0 vs. 38.8 +/- 2.4 mL/kg/min; p < .05) and left-side (42.9 +/- 2.3 vs. 38.7 +/- 1.9 mL/kg/min; p < .05) cerebral blood flow 5 mins after venovenous ligation when compared with baseline values. Similarly, after venoarterial ligation, there was a significant increase in right-side (44.6 +/- 2.2 vs. 38.8 +/- 2.4 mL/kg/min; p < .05) and left-side (43.9 +/- 1.5 vs. 38.7 +/- 1.9 mL/kg/min; p < .05) and cerebral blood flow. Cerebral oxygen consumption was significantly increased after venovenous (2.7 +/- 0.2 to 3.2 +/- 0.2 mL/kg/min; p < .05) and venoarterial (2.7 +/- 0.2 to 3.1 +/- 0.2 mL/kg/min; p < .05) ligation at 5 mins after ligation. This increase persisted at the 30-min period and after release of ligation. CONCLUSIONS: Ligation of the right jugular veins alone (venovenous ligation) or jugular veins and right carotid artery (venoarterial ligation) does not increase jugular venous pressures or intracranial pressure. However, this procedure does increase cerebral blood flow and cerebral oxygen consumption. These findings demonstrate that there is adequate decompression of the venous system by the cerebrovascular system and retrograde decompression during extracorporeal life support appears unwarranted.
OBJECTIVES: To correlate the initial and maximal lactate levels with the occurrence of intracranial hemorrhage (ICH) and survival in patients treated with extracorporeal life support (ECLS). DESIGN: Retrospective chart review. SETTING: Pediatric intensive care unit. PATIENTS: Eighty-two neonatal patients placed on ECLS for respiratory failure due to sepsis, meconium aspiration, or persistent pulmonary hypertension of the newborn. MEASUREMENTS: The initial lactate level measured within 6 hours of initiating ECLS and the maximal lactate level measured throughout the ECLS course were collected. Lactate levels were described as mean lactate +/- SE (mM). Head ultrasound reports and survival were reviewed. Platelet counts and activated clotting times (ACTs) were examined. RESULTS: The mean initial and maximal lactate levels were higher in ECLS patients who developed ICH (initial: 10 +/- 1.7 mM vs 6.4 +/- 0.8 mM, p = .05 and maximal: 12.4 +/- 2.5 mM vs 7.9 +/- 0.8 mM, p = .04). Initial and maximal lactate levels were also elevated in nonsurvivors (initial: 11.7 +/- 3 mM vs 6.4 +/- 0.7 mM, p = .01 and maximal: 14.8 +/- 3.3 mM vs 7.8 +/- 0.8 mM, P < .01). Platelet counts and ACT did not differ in patients with and without ICH. CONCLUSIONS: Lactate is a useful marker for the development of ICH in ECLS patients. In addition, elevated lactates during ECLS identify a subgroup of patients with poor outcome. Prospective studies are needed to determine whether the incorporation of this information into pre-ECLS and ECLS management will decrease the occurrence of ICH and improve survival.
During repair of congenital heart defects, extended periods of hypothermic circulatory arrest (CA) have been shown to cause short-term cerebral metabolic and flow abnormalities as well as long-term neuropsychologic dysfunction. Occasionally, a second period of CA is required during the same operative setting to revise a complicated repair. However, the metabolic effects of two consecutive periods of CA on the brain are unclear. In this study, we compared the recovery of cerebral metabolism after 60 minutes of CA with that after two sequential 30-minute periods of CA separated by a brief period of rewarming (30'SEQ). Fifteen neonatal piglets (2 to 3 kg) were placed on cardiopulmonary bypass at 100 mL.kg-1 x min-1 and cooled to 18 degrees C. Each animal then underwent either 60 minutes of uninterrupted cardiopulmonary bypass at 18 degrees C, 60 minutes of CA, or two 30-minute periods of CA separated by a brief period of rewarming. After these experimental periods, animals were rewarmed to 37 degrees C and weaned from cardiopulmonary bypass. Data were obtained before cardiopulmonary bypass and after cardiopulmonary bypass at 37 degrees C and included measurements of cerebral blood flow by xenon 133 clearance, arterial and sagittal sinus blood gases, and cerebral metabolism (mL O2.100 g-1 x min-1). Our results demonstrated that acute recovery of cerebral metabolism was significantly impaired after 60 minutes of CA and that recovery of cerebral metabolism after two sequential 30-minute periods of CA was significantly better than after 60 minutes of continuous CA.(ABSTRACT TRUNCATED AT 250 WORDS)
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BACKGROUND: This prospective study was intended to determine in a homogeneous population of children whether hemofiltration, performed during cardiopulmonary bypass rewarming, is able to improve hemodynamics and biologic hemostasis variables, to reduce postoperative blood loss, time to extubation, and plasma cytokines, and complement fragments. METHODS: Thirty-two children undergoing surgical correction of tetralogy of Fallot were randomly assigned to a hemofiltration or control group. Hemofiltration was performed with a polysulphone hemofilter during rewarming of cardiopulmonary bypass. Plasma clotting factors, D-dimers, antithrombin-III, complement fragments C3a and C5a, interleukin-1 beta, interleukin-6, interleukin-8, and tumor necrosis factor-alpha were measured before and after hemofiltration. Systemic mean arterial pressure, left atrial pressure, time to extubation, and postoperative blood loss were monitored. RESULTS: In the hemofiltration group, significant reductions in 24-h blood loss (250 (176-356) vs. 319 (182-500) ml/m2, median (minimum-maximum), time to extubation (15 (9-22) vs. 19 (11-24) h), plasma concentrations of C3a, C5a, interleukin-6, and tumor necrosis factor-alpha were observed compared to control. Arterial oxygen tension on admission to the intensive care unit was significantly greater in the hemofiltration group (136 +/- 20 vs. 103 +/- 25 mmHg, mean +/- SD). Significant increases in mean arterial pressure, clotting factors, and antithrombin-III were noted for the hemofiltration group. No intergroup difference was observed in left atrial pressure, platelets count, D-dimers, interleukin-8, and duration of stay in the intensive care unit. CONCLUSIONS: Hemofiltration during cardiopulmonary bypass in children improves hemodynamics and early postoperative oxygenation and reduces postoperative blood loss and duration of mechanical ventilation. Hemofiltration is able to remove some major mediators of the inflammatory response.
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Hypothermic total circulatory arrest (CA) is commonly used to facilitate repair of complex congenital heart defects. However, the "safe" period of CA remains to be defined. Extended periods of hypothermic total circulatory arrest may impair cerebral metabolism and cause ischemic brain injury. This study defines the relationship between increasing durations of CA at 18 degrees C and cerebral metabolism, and examines the protective value of topical cooling of the head or continuous "trickle" flow (5 to 10 mL.kg-1.min-1). Thirty-three 1-week-old piglets were randomized to six experimental groups: control; 15, 30, or 60 minutes of CA; 60 minutes of CA with topical cooling of the head; and 60 minutes of trickle flow. Animals were placed on cardiopulmonary bypass (CPB) at 100 mL.kg-1.min-1 and cooled to 18 degrees C. After the experimental period of CA or trickle flow (or 60 minutes of CPB at normal flow for the control group), animals were rewarmed to 37 degrees C and weaned from CPB. Data were obtained before and immediately after CPB at 37 degrees C, and before and immediately after the experimental period at 18 degrees C. Parameters measured included cerebral blood flow by xenon 133 clearance, arterial and sagittal sinus blood gases, and cerebral metabolism. Hypothermic total circulatory arrest caused an impairment of cerebral metabolism that was directly proportional to CA duration (r2 = 0.73; p = 0.0001), and recovery of metabolic function after 60 minutes of CA improved more than 50% if the head was packed in ice.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of reduced pump flow rate (PFR) on cerebral blood flow, cerebral oxygen consumption (CMRO2), oxygen extraction, cerebral vascular resistance, and total body vascular resistance were examined in 27 pediatric patients during hypothermic cardiopulmonary bypass (hCPB). During steady state hCPB the extracorporeal flows were randomly adjusted to a conventional PFR and a reduced PFR for each patient. The reduced pump flow rates were dictated by surgical needs. Cerebral blood flow measured using Xenon 133 clearance, and CMRO2 and oxygen extraction were calculated. Our results demonstrated that cerebral blood flow and CMRO2 are unchanged if pump flow rates are reduced by 35% to 45% of conventional PFRs at moderate and deep hypothermic temperatures. Reductions in PFR of 45%-70% from conventional PFRs affect the brain differently during either moderate or deep hCPB. At moderate hCPB (26 degrees to 29 degrees C), reductions in PFRs of 45% to 70% resulted in a significant decrease in cerebral blood flow and CMRO2, whereas oxygen extraction increased in a compensatory manner. During deep hCPB (18 degrees to 22 degrees C), PFR reductions of 45% to 70% of conventional PFR significantly reduced cerebral blood flow and CMRO2 but did not increase oxygen extraction, suggesting that at deep hypothermic temperatures, cerebral blood flow and CMRO2 exceed cerebral metabolic needs. Cerebral vascular resistance increased significantly with decreasing temperature but was not affected by pump flow reductions. We have derived indices for minimal acceptable low-flow cardiopulmonary bypass based on the known effects of temperature on cerebral metabolism and have speculated on its utility based on our limited data and a literature review.
The primary goal of monitoring cerebral blood flow and metabolism is to improve our understanding of the association with cardiopulmonary bypass and deep hypothermic circulatory arrest so that effective brain protection strategies can be developed and employed. A review of our cerebral blood flow/cardiopulmonary bypass database, presently totaling 275 neonates and infants, for the purposes of this publication, reveals certain trends and some conclusions that can be drawn. Deep hypothermic circulatory arrest continues to be a factor in the delayed recovery of cerebral blood flow and metabolism in these patients. Examining flow and metabolism serially in the postoperative period shows that in the majority of patients, flow, metabolism and autoregulation return to normal within 24 hours after operation. Some patients' cerebral oxygen metabolism is unable to exert a protective response of increasing extraction in the setting of low cerebral blood flow. We have also observed that in the setting of low cardiac output after cardiac repair, cerebral blood flow is low. It is therefore likely that low cardiac output and pressure-passive cerebral blood flow potentiate brain ischemia after cardiopulmonary bypass and operation in some patients. We have also examined in our series of 275 patients selective neuroprotection strategies for their potential for improving recovery of cerebral blood flow and cerebral metabolism. Duration of cooling on cardiopulmonary bypass correlates directly with suppression of metabolism due to hypothermia. Low-flow cardiopulmonary bypass instead of deep hypothermic circulatory arrest, and topical brain cooling with ice during deep hypothermic circulatory arrest, improve cerebral blood flow and cerebral metabolic recovery.
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Although cerebral monitoring during CPB remains primarily investigational, recent data support its clinical utility. In particular, it is cerebral metabolic monitoring that provides meaningful information in terms of preparing the brain for dhCPB and dhCA. Cerebral blood flow or cerebral blood flow velocity monitoring is less beneficial due to the presence of luxuriant cerebral blood flow at deep hypothermic temperatures. Conventional temperature monitoring can be improved upon by adding jugular venous oxygen saturation monitoring to satisfy the primary goal of cerebral protection--uniform cerebral cooling and metabolic suppression. Although online measures of cerebral cellular metabolism are not widely available, early experience with near infrared technology suggests that it is a feasible and reliable monitor of cerebral metabolic activity and is likely to represent an important noninvasive continuous monitor in the near future. CMRO2 recovery data have suggested that cerebral metabolic suppression is more severe the longer the period of dhCA. Cerebral protection strategies, such as intermittent cerebral perfusion have demonstrated less metabolic suppression of dhCA in animal models and are currently undergoing clinical evaluation in our institution. Finally, the postoperative period remains a high-risk period for neurologic injury because temperatures are normothermic, cardiac output is reduced, cerebral autoregulation is impaired, and management strategies, such as hyperventilation, are commonly used to increase pulmonary blood flow with little knowledge on its effects on cerebral perfusion.
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Although much has been learned about cerebral physiology during CPB in the past decade, the role of alterations in CBF and CMRO2 during CPB and the unfortunately common occurrence of neuropsychologic injury still is understood incompletely. It is apparent that during CPB temperature, anesthetic depth, CMRO2, and PaCO2 are the major factors that effect CBF. The systemic pressure, pump flow, and flow character (pulsatile versus nonpulsatile) have little influence on CBF within the bounds of usual clinical practice. Although cerebral autoregulation is characteristically preserved during CPB, untreated hypertension, profound hypothermia, pH-stat blood gas management, diabetes, and certain neurologic disorders may impair this important link between cerebral blood flow nutrient supply and metabolic demand (Figure 5). During stable moderate hypothermic CPB with alpha-stat management of arterial blood gases, hypothermia is the most important factor altering cerebral metabolic parameters. Autoregulation is intact and CBF follows cerebral metabolism. Despite wide variations in perfusion flow and systemic arterial pressure, CBF is unchanged. Populations of patients have been identified with altered cerebral autoregulation. To what degree the impairment of cerebral autoregulation contributes to postoperative neuropsychologic dysfunction is unknown. It must be emphasized that not the absolute level of CBF, but the appropriateness of oxygen delivery to demand is paramount. However, the assumption that the control of cerebral oxygen and nutrient supply and demand will prevent neurologic injury during CPB is simplistic. A better understanding of CBF, CMRO2, autoregulation and mechanism(s) of cerebral injury during CPB has lead to a scientific basis for many of the decisions made regarding extracorporeal perfusion.
Our group has previously reported a large prospective experience with the use of intraoperative echocardiography with Doppler color-flow imaging (IE-DCFI) during the repair of congenital heart defects. We have now performed IE-DCFI in 621 patients and have observed a major change in the impact of this technology, which has stabilized during our most recent experience (the last 207 patients). To evaluate the surgical learning curve with IE-DCFI, we divided patients into three groups: group 1, patients 1 through 207; group 2, patients 208 through 414; and group 3, patients 415 through 621. There were no major differences between groups with respect to age or disease entities. The average time needed to perform an IE-DCFI examination decreased from 3.75 +/- 1.77 minutes in group 1 to 3.35 +/- 1.52 minutes in group 2 and has remained stable. The number of patients requiring revisions in the operating room (based on IE-DCFI findings) decreased from 17 (8%) in group 1 to 7 (3%) in group 2 to 5 (2%) in group 3. Furthermore, revisions were 100% successful in correcting the problem in groups 2 and 3, whereas 18% of group 1 patients left the operating room with persistent residual defects by IE-DCFI. Surgeons can acquire the ability to interpret the results of IE-DCFI themselves and use it to enhance their operative repair of congenital heart defects, but this requires an experience of at least 200 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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