Signal quality assessment of peripheral venous pressure.

Develop a signal quality index (SQI) for the widely available peripheral venous pressure waveform (PVP). We focus on the quality of the cardiac component in PVP. We model PVP by the adaptive non-harmonic model. When the cardiac component in PVP is stronger, the PVP is defined to have a higher quality. This signal quality is quantified by applying the synchrosqueezing transform to decompose the cardiac component out of PVP, and the SQI is defined as a value between 0 and 1. A database collected during the lower body negative pressure experiment is utilized to validate the developed SQI. All signals are labeled into categories of low and high qualities by experts. A support vector machine (SVM) learning model is trained for practical purpose. The developed signal quality index coincide with human experts' labels with the area under the curve 0.95. In a leave-one-subject-out cross validation (LOSOCV), the SQI achieves accuracy 0.89 and F1 0.88, which is consistently higher than other commonly used signal qualities, including entropy, power and mean venous pressure. The trained SVM model trained with SQI, entropy, power and mean venous pressure could achieve an accuracy 0.92 and F1 0.91 under LOSOCV. An exterior validation of SQI achieves accuracy 0.87 and F1 0.92; an exterior validation of the SVM model achieves accuracy 0.95 and F1 0.96. The developed SQI has a convincing potential to help identify high quality PVP segments for further hemodynamic study. This is the first work aiming to quantify the signal quality of the widely applied PVP waveform.

Using the ear photoplethysmographic waveform as an early indicator of central hypovolemia in healthy volunteers utilizing LBNP induced hypovolemia model.

Objective. To study the photoplethysmographic (PPG) waveforms of different locations (ear and finger) during lower body negative pressure (LBNP) induced hypovolemia. Then, to determine whether the PPG waveform can be used to detect hypovolemia during the early stage of LBNP.Approach. 36 healthy volunteers were recruited for progressive LBNP induced hypovolemia, with an endpoint of -60 mmHg or development of hypoperfusion symptoms, whichever comes first. Subjects tolerating the entire protocol without symptoms were designated as high tolerance (HT), while symptomatic subjects were designated as low tolerance (LT). Subjects were monitored with an electrocardiogram, continuous noninvasive blood pressure monitor, and two pulse oximetry probes, one on the ear (Xhale) and one the finger (Nellcor). Stroke volume was measured non-invasively utilizing Non-Invasive Cardiac Output Monitor (NICOM, Cheetah Medical). The waveform morphology was analyzed using novel PPG waveforms indices, including phase hemodynamic index (PHI) and amplitude hemodyamaic index and were evaluated from the ear PPG and finger PPG at different LBNP stages.Main results. The PHI, particularly the phase relationship between the second harmonic and the fundamental component of the ear PPG denoted as∇φ2,during the early stage of LBNP (-15 mmHg) in the HT and LT groups is statistically significantly different (pvalue = 0.0033) with the area under curve 0.81 (CI: 0.616-0.926). The other indices are not significantly different. The 5 fold cross validation shows that∇φ2during the early stage of LBNP (-15 mmHg) as the single index could predict the tolerance of the subject with the sensitivity, specificity, accuracy andF1 as 0.771 ± 0.192, 0.71 ± 0.107, 0.7 ± 0.1 and 0.771 ± 0.192 respectively.Significance. The ear's PPG PHI which compares the phases of the fundamental and second harmonic has the potential to be used as an early predictor of central hypovolemia.

Anesthesia for Obstetric Disasters.

Over the past 30 years, maternal mortality has increased in the United States to 18 deaths per 100,000 live births. Obstetric emergencies, including hemorrhage, hypertensive disorders in pregnancy, HELLP syndrome, and amniotic fluid embolism, and anesthesia complications, including high neuraxial blockade, local anesthetic systemic toxicity, and the difficult obstetric airway, contribute to maternal cardiac arrest and maternal and fetal morbidity and mortality. Expeditious intervention by the obstetric anesthesiologist is critical in these emergent scenarios, and knowledge of best practices is essential to improve maternal and fetal outcomes.

Anesthesia for Obstetric Disasters.

Over the past 30 years, maternal mortality has increased in the United States to 18 deaths per 100,000 live births. Obstetric emergencies, including hemorrhage, hypertensive disorders in pregnancy, HELLP syndrome, and amniotic fluid embolism, and anesthesia complications, including high neuraxial blockade, local anesthetic systemic toxicity, and the difficult obstetric airway, contribute to maternal cardiac arrest and maternal and fetal morbidity and mortality. Expeditious intervention by the obstetric anesthesiologist is critical in these emergent scenarios, and knowledge of best practices is essential to improve maternal and fetal outcomes.