Radical 7

Masimo^® (Masimo Corporation, Irvine, CA, USA) continuous hemoglobin measurement equipment Radical-7 was used with its SpHb^® (Masimo Corpratio registered trademark) sensor. Based on the principles of spectrophotometry and photoplethysmography, the equipment uses a multi-wavelength sensor to distinguish between oxyhemoglobin, deoxyhemoglobin, carboxyhemoglobin, methemoglobin, and plasma. The different wavelengths are expressed in nanometers in Figure 1.

Clinical monitoring was performed by a veterinarian each day, and sedated assessments were performed by the same veterinarian. Animals were sedated with ketamine-HCl (10 mg/kg i.m.) for the clinical assessment. Dexmedetomidine (15 μg/kg i.m.) was administered after clinical assessments to facilitate sampling, and midazolam (0.25 to 0.5 mg/kg i.m.) was added as needed. Radiographs were obtained with a HF100+ Ultralight imaging unit (MinXRay, Northbrook, IL) at 50 kVp, 40 mA, and 0.1 s. Blood pressure was obtained via oscillometry with a Vet25 and an appropriately sized cuff according to the manufacturer’s instructions (SunTech, Morrisville, NC). Oxygen saturation was obtained by pulse oximetry with a Radical 7 (Masimo, Irvine, CA). Radiographs were scored by a veterinary radiologist with experimental group and time point masked. Scoring was performed on a scale of 0 to 3 for each lung lobe or sublobe (18 (link)).
Of the 4 animals that received human plasma, 3 developed signs of a reaction, including vomiting. Both animals receiving normal plasma and one of the animals receiving convalescent plasma developed these reactions. Reactions were controlled with diphenhydramine (4 mg/kg i.m.) and ondansetron (0.2 mg/kg i.m.). On clinical assessment, there was no evidence of aspiration, and oxygen saturation remained good.

Clinical monitoring was performed by a veterinarian each day, and sedated assessments were performed by the same veterinarian. Animals were sedated with ketamine-HCl (10 mg/kg i.m.) for the clinical assessment. Dexmedetomidine (15 μg/kg i.m.) was administered after clinical assessments to facilitate sampling, and midazolam (0.25 to 0.5 mg/kg i.m.) was added as needed. Radiographs were obtained with a HF100+ Ultralight imaging unit (MinXRay, Northbrook, IL) at 50 kVp, 40 mA, and 0.1 s. Blood pressure was obtained via oscillometry with a Vet25 and an appropriately sized cuff according to the manufacturer’s instructions (SunTech, Morrisville, NC). Oxygen saturation was obtained by pulse oximetry with a Radical 7 (Masimo, Irvine, CA). Radiographs were scored by a veterinary radiologist with experimental group and time point masked. Scoring was performed on a scale of 0 to 3 for each lung lobe or sublobe (18 (link)).
Of the 4 animals that received human plasma, 3 developed signs of a reaction, including vomiting. Both animals receiving normal plasma and one of the animals receiving convalescent plasma developed these reactions. Reactions were controlled with diphenhydramine (4 mg/kg i.m.) and ondansetron (0.2 mg/kg i.m.). On clinical assessment, there was no evidence of aspiration, and oxygen saturation remained good.

At our institutes, iNO treatment is optional for symptomatic treatment of hypoxemia. Thus, iNO is administered at the discretion of the intensivist. A number of patients who met the criteria for hypoxemia received low dose iNO (5–10 ppm [ppm]) in addition to routine management. NO gases and equipment were supplied by the Children’s Hospital of Fudan University, as previously described [13 (link)]. Briefly, the NO inhalation device was managed by a flow controller (MFC) (Shanghai Noventek, Shanghai, China). The N₂-based gas mixture flowed into the breathing circuit. The NO/NO₂ electrochemical sensor (NOxBOX Plus®; Bedfont Scientific, Rochester, England) was placed in the breathing circuit near the intubation cannula. Continuous monitoring was instituted to maintain the iNO concentration at 5–10 ppm and NO₂ at less than 3 ppm. Methemoglobin (MetHb) levels were measured once daily using the Radical-7 pulse oximeter (Radical-7® Pulse CO-Oximeter®, Masimo, USA). Side effects included increasing pleural drainage, new-onset bleeding, and thrombocytopenia (platelet count < 500,000/ul). If oxygenation did not improve within 24 h, if any side effects were noted, or if abnormal methemoglobin and NO₂ were observed, iNO therapy was discontinued. When the patient was extubated, iNO was administered via nasal cannula and weaned by decreasing the flow gradually within 24 h.

During the baseline and CWIs, beat‐to‐beat systolic (SAP), diastolic (DAP) and mean (MAP) arterial pressures were measured continuously using a volume‐clamp technique (Finometer, Finapres Medical Systems BV, Amsterdam, the Netherlands), with the pressure cuff placed around the middle phalanx of the left middle finger, and with the reference pressure transducer positioned at the level of the heart. The Finometer‐derived values were verified intermittently by electro‐sphygmomanometry (Omron, M6, Kyoto, Japan). Heart rate (HR) was derived from the arterial pressure curves as the inverse of the inter‐beat interval. Capillary oxyhaemoglobin saturation (SpO2) was monitored at 5 min intervals with an earlobe pulse oximeter (Radical‐7, Masimo, Irvine, CA, USA).