Pulse-contour derived cardiac output measurements in morbid obesity: influence of actual, ideal and adjusted bodyweight

The non-invasive Nexfin cardiac output (CO) monitor shows a low level of agreement with the gold standard thermodilution method in morbidly obese patients. Here we investigate whether this disagreement is related to excessive bodyweight, and can be improved when bodyweight derivatives are used instead. We performed offline analyses of cardiac output recordings of patient data previously used and partly published in an earlier study by our group. In 30 morbidly obese patients (BMI > 35 kg/m2) undergoing laparoscopic gastric bypass, cardiac output was simultaneously determined with PiCCO thermodilution and Nexfin pulse-contour method. We investigated if agreement of Nexfin-derived CO with thermodilution CO improved when ideal and adjusted—instead of actual- bodyweight were used as input to the Nexfin. Bodyweight correlated with the difference between Nexfin-derived and thermodilution-derived CO (r = −0.56; p = 0.001). Bland Altman analysis of agreement between Nexfin and thermodilution-derived CO revealed a bias of 0.4 ± 1.6 with limits of agreement (LOA) from −2.6 to 3.5 L min when actual bodyweight was used. Bias was −0.6 ± 1.4 and LOA ranged from −3.4 to 2.3 L min when ideal bodyweight was used. With adjusted bodyweight, bias improved to 0.04 ± 1.4 with LOA from −2.8 to 2.9 L min. Our study shows that agreement of the Nexfin-derived with invasive CO measurements in morbidly obese patients is influenced by body weight, suggesting that Nexfin CO measurements in patients with a BMI above 35 kg/m2 should be interpreted with caution. Using adjusted body weight in the Nexfin CO-trek algorithm reduced the bias

Comparison of Microcirculatory Perfusion in Obese and Non-Obese Patients Undergoing Cardiac Surgery with Cardiopulmonary Bypass

Obesity is a frequent comorbidity among patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Cardiac surgery with CPB impairs microcirculatory perfusion, which is associated with multiple organ failure. As microvascular function is frequently compromised in obese patients, we studied whether cardiac surgery with CPB has a more detrimental effect on microcirculatory perfusion in obese patients. Sublingual microcirculatory perfusion was measured with sidestream dark field (SDF) imaging in obese patients (body mass index ≥32 kg/m2; n = 14) without type II diabetes mellitus and in lean patients (BMI 20-25 kg/m2; n = 22) undergoing cardiac surgery with CPB. CPB reduced systolic blood pressure and mean arterial pressure more profoundly in lean compared with obese patients (SBP: 38% vs. 18%; MAP: 11% vs. 8%, p < 0.05), and both restored after weaning from CPB. No differences were present in intraoperative glucose, hematocrit, hemoglobin, lactate, and blood gas values between obese and lean patients. Microcirculatory perfusion did not differ between obese and lean patients the day before surgery. CPB decreased microcirculatory perfusion with 9% in both groups, but this was only significant in lean patients (p < 0.05). Three days following surgery, microcirculatory perfusion was restored in both groups. In conclusion, microcirculatory perfusion was equally disturbed during cardiac surgery with CPB in metabolically healthy obese patients compared to lean patients

Myocardial Perfusion and Function Are Distinctly Altered by Sevoflurane Anesthesia in Diet-Induced Prediabetic Rats

Preservation of myocardial perfusion during surgery is particularly important in patients with increased risk for perioperative complications, such as diabetes. Volatile anesthetics, like sevoflurane, have cardiodepressive effects and may aggravate cardiovascular complications. We investigated the effect of sevoflurane on myocardial perfusion and function in prediabetic rats. Rats were fed a western diet (WD; n=18) or control diet (CD; n=18) for 8 weeks and underwent (contrast) echocardiography to determine perfusion and function during baseline and sevoflurane exposure. Myocardial perfusion was estimated based on the product of microvascular filling velocity and blood volume. WD-feeding resulted in a prediabetic phenotype characterized by obesity, hyperinsulinemia, hyperlipidemia, glucose intolerance, and hyperglycemia. At baseline, WD-feeding impaired myocardial perfusion and systolic function compared to CD-feeding. Exposure of healthy rats to sevoflurane increased the microvascular filling velocity without altering myocardial perfusion but impaired systolic function. In prediabetic rats, sevoflurane did also not affect myocardial perfusion; however, it further impaired systolic function. Diet-induced prediabetes is associated with impaired myocardial perfusion and function in rats. While sevoflurane further impaired systolic function, it did not affect myocardial perfusion in prediabetic rats. Our findings suggest that sevoflurane anesthesia leads to uncoupling of myocardial perfusion and function, irrespective of the metabolic state