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• W2019993149 abstract "During open heart surgery, entrapment and systemic arterial embolization of air has long been recognized as a potentially fatal danger [1]. For prevention of air embolism, flooding of the surgical field with carbon dioxide (CO2), which is heavier and more soluble than air and whose embolism is relatively benign, was advocated [2,3], and, at our institution, has been used for a number of years. We present a case in which the use of CO2 flooding led to inadvertent hypercarbia in the patient during cardiopulmonary bypass (CPB). Case Report A 35-yr-old, 65-kg woman with a history of childhood rheumatic fever and mitral valve annuloplasty 5 yr before admission presented in congestive heart failure. Echocardiography and cardiac catheterization revealed severe mitral regurgitation and moderate aortic insufficiency with a left ventricular ejection fraction of 0.40. Her medical history was otherwise unremarkable. She was referred for replacement of her mitral and aortic valves. On the day of surgery, invasive monitoring including a pulmonary artery catheter, and a systemic arterial catheter was instituted. General anesthesia was induced with IV midazolam 5 mg and fentanyl 30 micro g/kg; endotracheal intubation was facilitated with pancuronium. Baseline arterial blood gas (ABG) analysis with a fraction of inspired oxygen (FIO2) of 1.0 and minute ventilation of 5.6 L/min were PaO2 444 mm Hg, PaCO2 38 mm Hg, pH 7.40, and calculated base excess (BE) of 0. For the remainder of surgery, additional fentanyl and isoflurane were administered as needed, pancuronium was intermittently administered to maintain complete muscle relaxation, and lorazepam 2 mg was given during CPB. After median sternotomy, the aorta was cannulated with a 7-mm aortic perfuser (Sarns, Ann Arbor, MI). Two 36-French Sarns venous cannulae were placed in the superior and inferior vena cavae. The CPB circuit consisted of a membrane oxygenator with a hard shell venous reservoir and integral cardiotomy reservoir (Excel; COBE, Arvada, CO), a centrifugal pump (Delphin; Sarns/3M), and a bridged single-pass cardioplegia administration set (Myotherm; Avecor, Minneapolis, MN) (Figure 1).Figure 1: A schematic of the cardiopulmonary bypass circuit, demonstrating how CO (2) flooding the surgical field may have been collected into the venous reservoir. CO2 from the cylinder was brought to the surgical field, from which the field suction and left ventricular sump drainage brought the gas into the venous reservoir, from which air was displaced out by CO2. CO2 then mixed with the venous blood. The CO2-enriched venous blood was pumped into the membrane oxygenator, in which gas exchange with the ventilatory gases from the air-oxygen blender took place before blood was returned to the aorta. Water ports for heat exchange are also shown.CPB was initiated and normothermia was maintained while the surgeon dissected adhesions to mobilize the heart. The patient was ventilated at an FIO2 of 0.6 and a sweep gas flow of 2.0 L/min. Fourteen minutes later, the patient was cooled to a nasopharyngeal temperature of 27[degree sign]C. The FIO2 was reduced to 0.4 and the gas flow was maintained at 2 L/min. Immediately after the onset of CPB, CO2 was delivered through a biological filter at a flow rate of 3 L/min into the thoracic cavity. After placing the aortic cross-clamp, retrograde cardioplegia was administered and asystole was achieved; a myocardial temperature of 10[degree sign]C was noted. The left atrium was opened, and a cardiac sump was placed in the left atrium and connected to suction and run at 0.9 L/min from the roller pump. The field suction was also placed in the chest cavity and run at 0.5 L/min. Blood flow ranged from 2.5 to 3.3 L/min throughout the hypothermic period, with mixed venous oxygen saturations ranging from 70% to 90%. After cooling the patient to 26.7[degree sign]C, ABG analysis performed at 37[degree sign]C (alpha-stat) were PaO2 276 mm Hg, PaCO2 100 mm Hg, pH 7.06, and BE -4. The sweep rate was increased to 5.5 L/min and the FIO2 was set at 0.5. The repeat ABG analysis, reflecting the changed settings, were PaO2 290 mm Hg, PaCO2 67 mm Hg, pH 7.19, and BE -3. The sweep rate was adjusted to 8 L/min. Subsequent ABG analysis, reflecting the sweep rate of 8 L/min, were PaO2 293 mm Hg, PaCO2 60 mm Hg, pH 7.24, and BE -2. Pancuronium 5 mg and lorazepam 2 mg were administered. A 5 1/4-in., 16-gauge angiocath was inserted into the top of the venous reservoir and connected to a Datex gas analyzer (Datex Instrumentarium, Helsinki, Finland). The CO2 in the reservoir was measured at 118 mm Hg, the maximum that can be recorded on the monitor. At this point, the sump was turned off and field suction was removed from the chest cavity and set at 4 L/min. This maneuver purged the reservoir of all residual CO2, as evidenced on the Datex monitor. ABG values were then PaO2 294 mm Hg, PaCO2 30 mm Hg, pH 7.46, and BE 0. Turning the cardiac sump back on, CO2 levels in the reservoir again increased to 118 mm Hg. High sweep rates were maintained throughout the remainder of CPB. The remainder of the operative and postoperative hospital course was uneventful, with no further episodes of acidosis. The patient was discharged from the hospital on the sixth postoperative day. Discussion We describe a case of severe hypercarbia and respiratory acidosis, associated with minimal metabolic acidosis, occurring during CPB. Differential diagnoses of hypercarbia included laboratory error, increased production of CO2 either endogenously or exogenously, and/or inadequate excretion of CO2. Laboratory error may have been either a measurement error or a reporting error. After the first reported PaCO2 of 100 mm Hg, laboratory error was ruled out by repeat measurements, and confirmation was obtained from the laboratory that the analyzers had been accurately calibrated and that the reported values had not been corrected for temperature, i.e., the values were alpha-stat, not pH-stat. Decreased excretion of CO2 during CPB may be caused by oxygenator failure. The Division of Perfusion Services at our institution has been able to establish a performance curve for each oxygenator currently in use. This performance curve allows prediction of the approximate FIO2 and sweep rate settings required for patients of different weights. The sweep gas flow refers to the rate of ventilatory gas flow through the oxygenator and is directly related to gas exchange. Although increasing sweep rates did reduce the PaCO2, the settings were well outside the usual performance range for the oxygenator, raising the possibility of oxygenator failure. CO2 removal and oxygenation are directly related to the oxygenator membrane surface area, the integrity of the membrane surface, and the integrity of the blood path. However, because oxygenation was adequate as reflected by a PaO2, appropriate for the FIO2, adequate venous oxygen saturation, and minimal metabolic acidosis, oxygenator failure seems unlikely. Excessive endogenous production of CO2 may occur with malignant hyperthermia, thyroid storm, neuroleptic malignant syndrome, and-with insufficient anesthesia-excessive catecholamine release and shivering. Pancuronium and lorazepam were administered to exclude any possibility, however unlikely, of insufficient anesthesia and muscle relaxation. Thyroid storm and neuroleptic malignant syndrome were judged to be unlikely in a patient with no history of thyroid disease or neuroleptic drug use. Furthermore, CPB is usually associated with depression of thyroid hormones [4]. Malignant hyperthermia (MH) is a potentially lethal cause of increased CO2 production. We did use isoflurane, a MH-triggering drug. Hypothermia, use of central nervous system depressants, and a nondepolarizing muscle relaxant may delay or attenuate the manifestations of MH [5], such as in our cardiac surgical patient under large-dose opioid anesthesia during CPB. However, MH is usually associated with marked metabolic acidosis as well as respiratory acidosis, and therefore was considered unlikely in this patient. This left exogenous production of CO2 as the most likely explanation for the persistent hypercarbia. Oxygen and compressed air from hospital supply lines were the ventilatory gases used for the heart-lung machine. As part of the daily prebypass checklist, the ventilatory gases were passed through an oxygen blender over the full range of blender settings (FIO2 of 21%-100%) and correlated with an in-line O2 analyzer. Although this test did not identify the nonoxygen portion of the ventilatory gases, the fact that we were able to decrease PaCO2 by increasing sweep rates or by maneuvers that excluded CO2 suction from the surgical field demonstrated that the nonoxygen portion of the ventilatory gases was not the source of exogenous CO2. Furthermore, no other operating rooms, including another cardiac surgical room using the same wall source of compressed air, reported problems with hypercarbia. We hypothesized that CO2 flooding the surgical field was being aspirated via the cardiac sump in the left atrium, as well as the field suction, and returned to the hard shell venous reservoir. Our hypothesis was confirmed through a series of maneuvers passing a catheter into the reservoir and connected to a gas analyzer. The design of the venous reservoir allows venting of the unit through a circumferential gap at the top of the unit. Because CO2 is heavier than air, it tends to be trapped in the reservoir, and air will be vented. The venous blood and cardiotomy drainage mix to some extent in the defoamer and, because of high solubility and diffusibility of CO2, the gas would be easily dissolved in the blood in the reservoir. In this particular case, a combination of events probably led to the aspiration of a significant volume of CO2 into the oxygenator. Placement of the field suction in proximity to the CO2 source and the location of the left ventricular sump in the lowest point of the surgical field made it easy for CO2 to be aspirated and probably accounted for the severe hypercarbia we observed. The danger of systemic air embolism in open heart surgery has long been recognized [1]. Fatalities from systemic air embolism result from air embolism into the coronary arteries and the ensuing ischemic heart failure and, less commonly, from cerebral air embolism [1]. Because of its high solubility, CO2 embolism may be more easily tolerated than air embolism. Moore and Braselton [6] injected air or CO2 into the pulmonary veins of dogs and cats and found that, whereas a bolus injection of as much as 3 mL/lb of CO2 was well tolerated, as little as 0.6 mL/lb of air was uniformly fatal. Hence, CO2 flooding of open heart surgical fields came to be recommended [2,3]. However, the exact technique and purported benefits of the procedure have not been clearly documented or systematically demonstrated. Even embolism of CO2, when massive, can lead to an adverse outcome, as has been reported during hysteroscopy [7] and laparoscopy [8]. In any case, CO2 flooding would not be expected to affect the incidence or consequences of particulate embolism. van der Linden and Casimir-Ahn [9] examined the occurrences of cerebral air embolization during open heart surgeries using transcranial Doppler monitoring. They demonstrated that there is virtually no embolization during the period of aortic cross-clamping, but that most embolizations occur after unclamping, when the heart fills again and begins to eject. If the procedure is to be used at all, CO2 flooding should be incorporated into the standard de-airing procedures undertaken near the end of CPB, rather than being used continuously while the heart is open. Our surgeons have altered their practice since this case and use CO2 flooding as part of the de-airing procedures. Isolated hypercarbia with respiratory acidosis is usually well tolerated and without sequelae [10]. However, CO2 is a potent cerebral vasodilator [10,11]. Hypercarbia increases cerebral blood flow at any given perfusion pressure, potentially increasing intracranial pressure and compromising cerebral autoregulation [12,13]. Furthermore, because cerebrovascular reactivity to CO2 may be diminished or lost in areas damaged by a vascular insult [14], hypercarbia may potentially divert blood flow away from such areas to those with preserved reactivity and may increase injury. Similarly, hypercarbia may lead to a decrease in perfusion to ischemic myocardium via intramyocardial steal [10]; however, this phenomenon would not be a concern during CPB. Our patient recovered uneventfully from transient hypercarbia, as expected. In summary, we describe a case of profound hypercarbia during CPB as a complication of CO2 flooding used to prevent air embolism related to the open heart procedure. We recommend that the technique of CO2 flooding be limited to part of the de-airing procedures near the end of CPB, rather than being used while the heart is open but not ejecting. The authors thank Gordon Novak, MD, for assistance with preparation of the figure." @default.
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• W2019993149 modified "2023-10-18" @default.
• W2019993149 title "Severe Hypercarbia During Cardiopulmonary Bypass" @default.
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