Sodium bicarbonate use and the risk of hypernatremia in thoracic aortic surgical patients with metabolic acidosis following deep hypothermic circulatory arrest.

OBJECTIVE: Metabolic acidosis after deep hypothermic circulatory arrest (DHCA) for thoracic aortic operations is commonly managed with sodium bicarbonate (NaHCO 3 ). The purpose of this study was to determine the relationships between total NaHCO 3 dose and the severity of metabolic acidosis, duration of mechanical ventilation, duration of vasoactive infusions, and Intensive Care Unit (ICU) or hospital length of stay (LOS). METHODS: In a single center, retrospective study, 87 consecutive elective thoracic aortic operations utilizing DHCA, were studied. Linear regression analysis was used to test for the relationships between the total NaHCO 3 dose administered through postoperative day 2, clinical variables, arterial blood gas values, and short-term clinical outcomes. RESULTS: Seventy-five patients (86%) received NaHCO 3 . Total NaHCO 3 dose averaged 136 ± 112 mEq (range: 0.0-535 mEq) per patient. Total NaHCO 3 dose correlated with minimum pH (r = 0.41, P < 0.0001), minimum serum bicarbonate (r = -0.40, P < 0.001), maximum serum lactate (r = 0.46, P = 0.007), duration of metabolic acidosis (r = 0.33, P = 0.002), and maximum serum sodium concentrations (r = 0.29, P = 0.007). Postoperative hypernatremia was present in 67% of patients and peaked at 12 h following DHCA. Eight percent of patients had a serum sodium ≥ 150 mEq/L. Total NaHCO 3 dose did not correlate with anion gap, serum chloride, not the duration of mechanical ventilator support, vasoactive infusions, ICU or hospital LOS. CONCLUSION: Routine administration of NaHCO 3 was common for the management of metabolic acidosis after DHCA. Total dose of NaHCO 3 was a function of the severity and duration of metabolic acidosis. NaHCO 3 administration contributed to postoperative hypernatremia that was often severe. The total NaHCO 3 dose administered was unrelated to short-term clinical outcomes.

Acousto-Optic Cerebral Blood Flow Monitoring During Induction of Anesthesia in Humans.

BACKGROUND: Past transcranial Doppler (TCD) studies have documented the effects of the sequence of anesthesia induction followed by intubation on cerebral blood flow (CBF) velocity. The purpose of this study was to determine whether acousto-optic CBF monitoring would detect changes in CBF which are known to occur with propofol and subsequent endotracheal intubation. METHODS: Seventy-two patients scheduled for elective non-intracranial surgery were evaluated. A Cerox 3215F (Ornim Medical) acousto-optic CBF monitor was used. The acousto-optic transducers were applied bifrontally prior to induction. Baseline cerebral flow index (CFI) values were obtained for at least 2 min prior to induction, set to a unitless value of 100. Subsequent relative changes in CFI from baseline were determined at the lowest value over 3 min after propofol injection but before laryngoscopy; and the highest value over 5 min after the start of laryngoscopy. CFI data were evaluated using Friedman's test. RESULTS: The median dose of propofol [interquartile range] given was 200 mg [160-250]. CFI decreased to 84 % of baseline after propofol and increased to 147 % of baseline after endotracheal intubation (both p < 0.001); MAP decreased after intravenous induction of anesthesia from 103 ± 15 to 86 ± 15 mmHg (p < 0.001) and then returned following endotracheal intubation to 104 ± 20 mmHg. CONCLUSIONS: Our data are congruent with previous observations made with TCD under similar experimental conditions. Such observations support the notion that acousto-optic monitoring yields valid real-time measures of changes in CBF in humans. Further validation against other quantitative measures of CBF would be appropriate.

Severity and Duration of Metabolic Acidosis After Deep Hypothermic Circulatory Arrest for Thoracic Aortic Surgery.

OBJECTIVE: To determine the severity, duration, and contributing factors for metabolic acidosis after deep hypothermic circulatory arrest (DHCA). DESIGN: Retrospective observational study. SETTING: University hospital. PATIENTS: Eighty-seven consecutive patients undergoing elective thoracic aortic surgery with DHCA. INTERVENTIONS: Regression analysis was used to test for relationships between the severity of metabolic acidosis and clinical and laboratory variables. MEASUREMENTS AND MAIN RESULTS: Minimum pH averaged 7.27±0.06, with 76 (87%) having a pH<7.35; 55 (63%), a pH<7.30; and 7 (8%), a pH<7.20. The mean duration of metabolic acidosis was 7.9±5.0 hours (range: 0.0 - 26.8), and time to minimum pH after DHCA was 4.3±2.0 hours (1.0 - 10.0 hours). Hyperchloremia contributed to metabolic acidosis in 89% of patients. The severity of metabolic acidosis correlated with maximum lactate (p<0.0001) and hospital length of stay (LOS) (r = 0.22, p<0.05), but not with DHCA time, DHCA temperature, duration of vasoactive infusions, or ICU LOS. Patient BMI was the sole preoperative predictor of the severity of postoperative metabolic acidosis. LIMITATIONS: This retrospective analysis involved short-term clinical outcomes related to pH severity and duration, which indirectly may have included the impact of sodium bicarbonate administration. CONCLUSIONS: Metabolic acidosis was common and severe after DHCA and was attributed to both lactic and hyperchloremic acidosis. DHCA duration and temperature had little impact on the severity of metabolic acidosis. The severity of metabolic acidosis was best predicted by the BMI and had minimal effects on short-term outcomes. Preventing hyperchloremic acidosis has the potential to decrease the severity of metabolic acidosis after DHCA.

Examining the relationship between bone mineral density and fracture risk reduction during pharmacologic treatment of osteoporosis.

Osteoporosis is a skeletal disorder characterized by compromised bone strength that predisposes the patient to an increased risk for fracture. Elements of bone strength include bone mineralization, architecture, turnover, size, and bone mineral density (BMD). Measurement of BMD is the most readily available, noninvasive method for assessing osteoporotic fracture risk and is used by the World Health Organization for diagnostic purposes. Because low BMD is predictive of increased fracture risk, it was believed that changes in BMD during pharmacologic therapy for osteoporosis would strongly predict observed fracture risk reductions. We examined the relationship between changes in BMD and reduction in fracture risk during pharmacologic therapy in postmenopausal women with osteoporosis. The correlation between BMD increases and fracture risk reduction during treatment is not consistent; larger increases in BMD do not necessarily correlate with greater reductions in fracture risk. Multiple factors, in addition to BMD, appear to contribute to the increased bone strength and decreased fracture risk achieved with approved drug therapies for osteoporosis. Until the exact relationship of these factors is fully understood, clinicians should continue to evaluate drug efficacy for osteoporosis based on the fracture risk reductions from well-designed clinical trials.