Performance of popular pulse oximeters compared with simultaneous arterial oxygen saturation or clinical-grade pulse oximetry: a cross-sectional validation study in intensive care patients.

OBJECTIVES: To evaluate the performance of direct-to-consumer pulse oximeters under clinical conditions, with arterial blood gas measurement (SaO2) as reference standard. DESIGN: Cross-sectional, validation study. SETTING: Intensive care. PARTICIPANTS: Adult patients requiring SaO2-monitoring. INTERVENTIONS: The studied oximeters are top-selling in Europe/USA (AFAC FS10D, AGPTEK FS10C, ANAPULSE ANP 100, Cocobear, Contec CMS50D1, HYLOGY MD-H37, Mommed YM101, PRCMISEMED F4PRO, PULOX PO-200 and Zacurate Pro Series 500 DL). Directly after collection of a SaO2 blood sample, we obtained pulse oximeter readings (SpO2). SpO2-readings were performed in rotating order, blinded for SaO2 and completed <10 min after blood sample collection. OUTCOME MEASURES: Bias (SpO2-SaO2) mean, root mean square difference (ARMS), mean absolute error (MAE) and accuracy in identifying hypoxaemia (SaO2 ≤90%). As a clinical index test, we included a hospital-grade SpO2-monitor (Philips). RESULTS: In 35 consecutive patients, we obtained 2258 SpO2-readings and 234 SaO2-samples. Mean bias ranged from -0.6 to -4.8. None of the pulse oximeters met ARMS ≤3%, the requirement set by International Organisation for Standardisation (ISO)-standards and required for Food and Drug Administration (FDA) 501(k)-clearance. The MAE ranged from 2.3 to 5.1, and five out of ten pulse oximeters met the requirement of ≤3%. For hypoxaemia, negative predictive values were 98%-99%. Positive predictive values ranged from 11% to 30%. Highest accuracy (95% CI) was found for Contec CMS50D1; 91% (86-94) and Zacurate Pro Series 500 DL; 90% (85-94). The hospital-grade SpO2-monitor had an ARMS of 3.0% and MAE of 1.9, and an accuracy of 95% (91%-97%). CONCLUSION: Top-selling, direct-to-consumer pulse oximeters can accurately rule out hypoxaemia, but do not meet ISO-standards required for FDA-clearance.

Efficacy of magnesium-amiodarone step-up scheme in critically ill patients with new-onset atrial fibrillation: a prospective observational study.

Amiodarone is considered a first-choice antiarrhythmic drug in critically ill patients with new-onset atrial fibrillation (AF). However, evidence supporting the use of this potentially toxic drug in critically ill patients is scarce. Magnesium sulphate (MgSO4) has shown to be effective for both rate and rhythm control, to act synergistically with antiarrhythmic drugs, and to prevent proarrhythmia. Treatment with MgSO4 may reduce the need for antiarrhythmic drugs such as amiodarone in critically ill patients with new-onset atrial fibrillation. The efficacy of a new institutional protocol was evaluated. Patients were treated with a new institutional protocol for new-onset atrial fibrillation in critically ill patients. An MgSO4 bolus (0.037 g/kg body weight in 15 minutes) was followed by continuous infusion (0.025 g/kg body weight/h). Intravenous amiodarone (loading dose 300 mg, followed by continuous infusion of 1200 mg/24 h) was given to those not responding to MgSO4 within 1 hour. Clinical response was defined as conversion to sinus rhythm or decrease in heart rate <110 beats/min. Sixteen of the 29 patients responded to MgSO4 monotherapy, whereas the addition of amiodarone was needed in 13 patients. Median (range) time until conversion to sinus rhythm after MgSO4 was 2 (1-45) hours. Median (range) conversion time in patients requiring amiodarone was 4 (2-78) hours, and median (range) conversion time in all patients was 3 (1-78) hours. The 24-hour conversion rate was 90%. Relapse atrial fibrillation was seen in 7 patients. The magnesium-amiodarone step-up scheme reduces the need for amiodarone, effectively converts new-onset atrial fibrillation into a sinus rhythm within 24 hours, and seems to be safe in critically ill patients.

Clinical review: treatment of new-onset atrial fibrillation in medical intensive care patients--a clinical framework.

Atrial fibrillation occurs frequently in medical intensive care unit patients. Most intensivists tend to treat this rhythm disorder because they believe it is detrimental. Whether atrial fibrillation contributes to morbidity and/or mortality and whether atrial fibrillation is an epiphenomenon of severe disease, however, are not clear. As a consequence, it is unknown whether treatment of the arrhythmia affects the outcome. Furthermore, if treatment is deemed necessary, it is not known what the best treatment is. We developed a treatment protocol by searching for the best evidence. Because studies in medical intensive care unit patients are scarce, the evidence comes mainly from extrapolation of data derived from other patient groups. We propose a treatment strategy with magnesium infusion followed by amiodarone in case of failure. Although this strategy seems to be effective in both rhythm control and rate control, the mortality remained high. A randomised controlled trial in medical intensive care unit patients with placebo treatment in the control arm is therefore still defendable.