Inadvertent severe hypercapnia during general anesthesia: drop-in oxygen saturation or electrocardiography changes; which one warns us earlier?

Background During general anesthesia especially when the nurse or anesthesiologist forgets to change manual to controlled mode after successful endotracheal intubation, capnography shows End-tidal Co2 above 20 mmHg after checking the place of the tracheal tube and will remain on the screen permanently. In this scenario, the patient receives a high concentration of oxygen, and Spo2 (oxygen saturation) does not drop for a long time which is too late to intervene. It has been all-time questionable which one of the cardiac dysrhythmias or Spo2 dropping occurs earlier. Results Medical records of seven deceased patients reviewed. All of them had electrocardiogram changes including premature ventricular contraction or bradycardia as a first warning sign. Oxygen saturation remains above 95% even with cardiac dysrhythmia. Conclusions Bradycardia and premature ventricular contraction were the first warning findings for severe hypercapnia during general anesthesia and occurred earlier than dropping oxygen saturation. Furthermore, the normal capnography waveform is more reliable than the End-tidal Co2 number for monitoring.

A point-mutation in the C-domain of CMP-sialic acid synthetase leads to lethality of medaka due to protein insolubility

Vertebrate CMP-sialic acid synthetase (CSS), which catalyzes the synthesis of CMP-sialic acid (CMP-Sia), consists of a 28 kDa-N-domain and a 20 kDa-C-domain. The N-domain is known to be a catalytic domain; however, the significance of the C-domain still remains unknown. To elucidate the function of the C-domain at the organism level, we screened the medaka TILLING library and obtained medaka with non-synonymous mutations (t911a), or single amino acid substitutions of CSS, L304Q, in the C-domain. Prominently, most L304Q medaka was lethal within 19 days post-fertilization (dpf). L304Q young fry displayed free Sia accumulation, and impairment of sialylation, up to 8 dpf. At 8 dpf, a marked abnormality in ventricular contraction and skeletal myogenesis was observed. To gain insight into the mechanism of L304Q-induced abnormalities, L304Q was biochemically characterized. Although bacterially expressed soluble L304Q and WT showed the similar Vmax/Km values, very few soluble L304Q was detected when expressed in CHO cells in sharp contrast to the WT. Additionally, the thermostability of various mutations of L304 greatly decreased, except for WT and L304I. These results suggest that L304 is important for the stability of CSS, and that an appropriate level of expression of soluble CSS is significant for animal survival.

Very Large-Scale Integration for Premature Ventricular Contraction Detection Using a Convolutional Neural Network

We propose a very large-scale integration (VLSI) chip for premature ventricular contraction (PVC) detection. The chip contains a convolutional neural network (CNN) for detecting the abnormal heartbeats associated with PVCs in 12-lead electrocardiogram signals. The proposed CNN comprises two convolutional layers and a fully connected layer; in testing, it achieved a high PVC detection accuracy of [Formula: see text]. Created by using a [Formula: see text]-[Formula: see text]m CMOS process, the developed chip consumes [Formula: see text] mW with a clock frequency of 50 MHz and gate count of [Formula: see text] K. Compared with the previously designed VLSI chips, the proposed CNN chip achieves higher accuracy in abnormal heartbeat detection.

Alpha and beta myosin isoforms and human atrial and ventricular contraction

Human atrial and ventricular contractions have distinct mechanical characteristics including speed of contraction, volume of blood delivered and the range of pressure generated. Notably, the ventricle expresses predominantly β-cardiac myosin while the atrium expresses mostly the α-isoform. In recent years exploration of the properties of pure α- & β-myosin isoforms have been possible in solution, in isolated myocytes and myofibrils. This allows us to consider the extent to which the atrial vs ventricular mechanical characteristics are defined by the myosin isoform expressed, and how the isoform properties are matched to their physiological roles. To do this we Outline the essential feature of atrial and ventricular contraction; Explore the molecular structural and functional characteristics of the two myosin isoforms; Describe the contractile behaviour of myocytes and myofibrils expressing a single myosin isoform; Finally we outline the outstanding problems in defining the differences between the atria and ventricles. This allowed us consider what features of contraction can and cannot be ascribed to the myosin isoforms present in the atria and ventricles.