Components of heart rate variability have attracted considerable attention in psychology and medicine and have become important dependent measures in psychophysiology and behavioral medicine. Quantification and interpretation of heart rate variability, however, remain complex issues and are fraught with pitfalls. The present report (a) examines the physiological origins and mechanisms of heart rate variability, (b) considers quantitative approaches to measurement, and (c) highlights important caveats in the interpretation of heart rate variability. Summary guidelines for research in this area are outlined, and suggestions and prospects for future developments are considered.

https://www.onlinelibrary.wiley.com/doi/epdf/10.1111/j.1469-8986.1997.tb02140.x

Heart rate variability: Origins, methods, and interpretive caveats

2014 ESC Guidelines on the diagnosis and treatment of aortic diseases: Document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The Task Force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC).

结节病易误诊,据王洪武等~([1])收集国内18篇关于此病误诊的文献,误诊率高达63.2%,当然有误诊就会有误治,如孙永昌等~([2])报道26例结节病在影像学检查诊断的第一印象中拟诊结核5例,其中就有2例完成规范的抗结核治疗,为此应引起临床对本病诊治的重视。

Sarcoidosis

Acute myocardial infarction (MI) is a major cause of death and disability worldwide. In patients with MI, the treatment of choice for reducing acute myocardial ischemic injury and limiting MI size is timely and effective myocardial reperfusion using either thombolytic therapy or primary percutaneous coronary intervention (PPCI). However, the process of reperfusion can itself induce cardiomyocyte death, known as myocardial reperfusion injury, for which there is still no effective therapy. A number of new therapeutic strategies currently under investigation for preventing myocardial reperfusion injury have the potential to improve clinical outcomes in patients with acute MI treated with PPCI.

https://dm5migu4zj3pb.cloudfront.net/manuscripts/62000/62874/JCI62874.v1.pdf

Myocardial ischemia-reperfusion injury: a neglected therapeutic target

The recommendations in this 2015 American Heart Association (AHA) Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care are based on an extensive evidence review process that was begun by the International Liaison Committee on Resuscitation (ILCOR) after the publication of the 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations 1,2 and was completed in February 2015.3,4

In this in-depth evidence review process, ILCOR examined topics and then generated a prioritized list of questions for systematic review. Questions were first formulated in PICO (population, intervention, comparator, outcome) format,5 and then search strategies and inclusion and exclusion criteria were defined and a search for relevant articles was performed. The evidence was evaluated by the ILCOR task forces by using the standardized methodological approach proposed by the Grading of Recommendations Assessment, Development and Evaluation (GRADE) Working Group.6

The quality of the evidence was categorized based on the study methodologies and the 5 core GRADE domains of risk of bias, inconsistency, indirectness, imprecision, and other considerations (including publication bias). Then, where possible, consensus-based treatment recommendations were created.

To create this 2015 Guidelines Update, the AHA formed 15 writing groups, with careful attention to manage conflicts of interest, to assess the ILCOR treatment recommendations and to write AHA treatment recommendations by using the AHA Class of Recommendation (COR) and Level of Evidence (LOE) system. The recommendations made in the Guidelines are informed by the ILCOR recommendations and GRADE classification, in the context of the delivery of medical care in North America. The AHA writing group made new recommendations only on topics specifically reviewed by ILCOR in 2015. This chapter delineates instances where the AHA writing group developed recommendations that are significantly stronger or weaker than the ILCOR statements. In the online …

Part 8: Post-cardiac arrest care: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care

ELECTROMANOMETRIC blood pressure measurements are routine in critically ill patients, and many interventions are based on correct measurements. We report a mini-epidemic of erroneous central venous pressure measurements due to faulty pressure transducer manufacturing resulting in wrong therapeutic decisions. Case Report For invasive pressure monitoring in patients undergoing cardiovascular surgery, we use a color-coded multitransducer system with a single pressurized bag of normal saline for line rinsing. On one day three patients undergoing cardiac surgery attracted attention because central venous pressure (CVP) measured via the atrial port of a pulmonary artery catheter (model 680100, 7.5-French, 110-cm; Becton Dickinson Critical Care Systems, Singapore) was much higher than mean pulmonary artery pressure. This persisted after transducer recalibration and assurance of normal gain settings and also when the pressure recording line was connected to an indwelling trilumen CVP catheter (model UE-24703-ND, 7-French, 30-cm; Arrow Deutschland, Erding, Germany). A change of the pressure transducer system and of connecting cables to the monitor did not alter these findings. However, CVP readings were considered implausible because there were no history or clinical signs of venous congestion or of tricuspid valve regurgitation, and transesophageal echocardiography revealed no right ventricular distention. After clamping the transducer’s rinsing line, CVP decreased substantially in all patients (27 mmHg 4t o 10 4, mean SD), and a typical CVP tracing was seen on the monitor’s display. After declamping, measured CVP again increased to abnormal values (fig. 1). Moreover, rinsing solution leaked continuously out off the transducer’s stopcock during transducer zeroing. Accordingly, false pressure readings resulting from excessive flow of rinsing solution were suspected. After withdrawal of the pulmonary artery catheter tip to a right atrial position, CVP measured via its distal lumen showed normal CVP values similar to the measurements obtained with the CVP transducer with its rinsing line clamped (fig. 1). Only one of the system’s three pressure transducers (the CVP transducer) was affected in each patient. Four additional dysfunctional transducers were identified after they had already been connected to patients, and further nine faulty transducers were detected during an implemented check of the systems before connection. Accordingly, we mailed alert warnings to all intensive care units of our hospital, the transducer system’s manufacturer (Smiths Medical Deutschland GmbH, Kirchseeon, Germany), and to regulatory institutions. Chart review of patients treated before problem detection revealed at least one patient treated inappropriately because of erroneously high CVP readings. Treatment by diuretics and fluid restriction had been stopped only in a preshock state, when transesophageal echocardiography had demonstrated cardiac volume depletion rather than suspected volume overload or cardiac tamponade. Subsequent investigations showed that all affected transducer systems derived from the same charge and had been delivered to various German hospitals. Upon activation of a transducer’s trigger flush knob, 60 ml/min of isotonic saline is normally delivered with the rinsing solution’s pressure maintained at 200 mmHg. With the trigger flush knob in its resting position, rinse solution continuously flows through a laser drilled hole only at 3 ml/h and flow does not interfere with correct pressure measurements. Microscopic examination of the dysfunctional transducers’ inside by the manufacturer revealed a roughened surface and additional holes resulting from excess amounts of solvent agent applied manually during production. This was responsible for an increased flow of rinsing solution (up to 120 ml/h) and for subsequently and artifactually increasing CVP measurements, as outlined schematically in figure 2.

Mini-epidemic of Erroneous Central Venous Pressure Measurements Resulting from the Malproduction of a Specific Part of a Pressure Transducer System

Abstract 4707: Remote Ischemic Preconditioning Reduces Myocardial Injury After Coronary Artery Bypass Surgery With Cristalloid Cardioplegic Arrest

We observed suppression of reactivity to stimulation with cytomegalovirus, muromonab-CD3, and pokeweed mitogen in mononuclear blood cells of patients with early sepsis when compared with postoperat...

Early suppression of peripheral mononuclear blood cells in sepsis in response to stimulation with cytomegalovirus, OKT3, and pokeweed mitogen.

Hypercarbic respiratory drive is mainly determined by PCO(2) and pH with activity of the intracellular Na+/H+ exchanger (NHE) playing an important role in maintaining intracellular pH and respiratory drive. Because NHE activity varies with genetically different G-protein beta3 subunits (GNB3) (C/T polymorphism at nucleotide position 825) different genotypes might alter respiratory regulation. To test the hypothesis that short-term ventilatory responses vary with different GNB3 healthy volunteers with different genotypes (CC, TC, TT) were exposed to either hyperoxic hypercarbia (n=33) or to isocapnic hypoxia (n=31), respectively. There was no difference between CC, TC, and TT genotypes in hypercarbic and hypoxic respiratory drive when assessed as the ratio of minute ventilation over endexpiratory PCO(2) changes (DeltaV.E/DeltaPETCO(2)), maximal tolerable PETCO(2), and ratio of changes in ventilation over arterial haemoglobin desaturation (DeltaV.E/DeltaSO(2)), respectively. Thus, short-term hypercarbic and hypoxic ventilatory drive do not differ between individuals with genotypes encoding different GNB3. Whilst respiratory control may still be influenced by G-protein aberration, other mechanisms seem to have a more important role in controlling ventilation.

Jürgen Peters

Papers

Mini-epidemic of Erroneous Central Venous Pressure Measurements Resulting from the Malproduction of a Specific Part of a Pressure Transducer System

Abstract 4707: Remote Ischemic Preconditioning Reduces Myocardial Injury After Coronary Artery Bypass Surgery With Cristalloid Cardioplegic Arrest

Early suppression of peripheral mononuclear blood cells in sepsis in response to stimulation with cytomegalovirus, OKT3, and pokeweed mitogen.

Human G protein β3 subunit variant does not alter hypercarbic or hypoxic ventilatory response

Genetic variations in G-protein signal pathways influence progression of coronary artery calcification: Results from the Heinz Nixdorf Recall study