The PhysioNet/Computing in Cardiology Challenge focused on the early detection of sepsis from clinical data. A total of 40,336 patient records from two distinct hospital systems were shared with participants while 22,761 patient records from three distinct hospital systems were sequestered as hidden test sets. Each patient record contained up to 40 measurements of vital sign, laboratory, and demographics data for over 2.5 million hourly time windows and over 15 million data points. We used the Sepsis-3 clinical criteria to define the onset time of sepsis.We challenged participants to design automated, opensource algorithms for predicting sepsis 6 hours before clinical recognition of sepsis. We developed a novel, clinical utility-based evaluation metric to assess each algorithm that rewards early sepsis predictions and penalizes late or missed predictions and false alarms.A total of 104 teams from academia and industry submitted a total of 853 entries during the official phase of the Challenge. We accepted 90 abstracts based on Challenge entries for presentations at Computing in Cardiology. We also compared entries to ensure that approaches from different teams remained independent. This article presents our analysis and discusses the implications of the Challenge for early sepsis predictions and related sequential prediction tasks.

We have examined the effect of remifentanil on the haemodynamic response to orotracheal intubation in a randomized, double-blind study. We studied 40 patients allocated to one of four groups of 10 each, to receive the following immediately before induction of anaesthesia: remifentanil 1 microgram kg-1 bolus over 30 s, followed by an infusion of 0.5 microgram kg-1 min-1; saline placebo only; glycopyrrolate 200 micrograms and remifentanil 1 microgram kg-1 bolus over 30 s, followed by an infusion of 0.5 microgram kg-1 min-1; or glycopyrrolate 200 micrograms only. Anaesthesia was induced with propofol, vecuronium and 1% isoflurane with 66% nitrous oxide in oxygen. The trachea was intubated under direct laryngoscopy 3 min after induction of anaesthesia. Arterial pressure and heart rate were measured non-invasively, immediately before induction of anaesthesia and then at 1-min intervals. Remifentanil was found to effectively attenuate the pressor response to intubation (P < 0.05 for the increase in mean arterial pressure; P < 0.01 for the increase in heart rate). In the absence of a concurrent vagolytic agent, remifentanil was associated with bradycardia or hypotension, or both, in five of 10 patients, compared with one patient who received remifentanil and glycopyrrolate.

Why the myocardial oxygen extraction ratio (ERm) is decreased during septic shock in humans is unknown. Therefore, we calculated ERm in 15 anesthetized pigs by measuring arterial and coronary venous oxygen content. We measured myocardial lactate flux, myocardial contractility, and global myocardial blood flow and its distribution. After baseline measurements, animals received either saline (n = 6) or 50 micrograms/kg of endotoxin (n = 9). Measurements were repeated for 4 h. After endotoxin, ERm decreased from 67 +/- 12% at baseline to 36 +/- 10% (P < 0.01) at 1 h and 54 +/- 10% (P < 0.05) at 4 h, associated with an increased myocardial blood flow that was heterogeneous. Neither myocardial oxygen nor lactate consumption decreased in the endotoxin group, and changes in left ventricular contractility were not correlated with changes in ERm. We conclude that the decrease in ERm after endotoxin infusion is due to both increased blood flow and mismatching between myocardial oxygen delivery and demand. Impaired myocardial oxygen extraction capacity during sepsis did not cause global myocardial tissue hypoxia.

To determine whether receptors stimulated by the injection of capsaicin into the pulmonary circulation cause reflex changes in airway size, six dogs were anesthetized with chloralose, paralyzed with succinylcholine, and mechanically ventilated (2 cm H2O PEEP). Intrapulmonary airways were outlined with tantalum dust, and diameters were determined by taking serial roentgenograms at end expiration. Capsaicin (20 micrograms/kg) injected into the right ventricle significantly decreased airway diameter (20%), heart rate, aortic pressure, and pulmonary artery pressure. In contrast, capsaicin injected into the left ventricle did not alter airway diameter or aortic pressure, although heart rate and pulmonary artery pressure decreased but to a lesser extent than after right ventricular injection. After vagotomy, capsaicin had no effect on airway diameter or heart rate but aortic pressure and pulmonary artery pressure increased slightly. Results suggest that pulmonary receptors sensitive to capsaicin and accessible via the pulmonary circulation produce reflex bronchoconstriction. One possible function of this vagal reflex is to assist fluid movement from microvasculature to peribronchial space by reducing peribronchial pressure.