The prognostic value of end tidal carbon dioxide during cardiac arrest: A systematic review

Introduction

Cardiac arrest is a common presentation to the emergency care system. The decision to terminate CPR is often challenging to heath care providers. An accurate, early predictor of the outcome of resuscitation is needed. The purpose of this systematic review is to evaluate the prognostic value of ETCO₂ during cardiac arrest and to explore whether ETCO₂ values could be utilised as a tool to predict the outcome of resuscitation.

Method

Literature search was performed using Medline and EMBASE databases to identify studies that evaluated the relationship between ETCO₂ during cardiac arrest and outcome. Studies were thoroughly evaluated and appraised. Summary of evidence and conclusions were drawn from this systematic literature review.

Results

23 observational studies were included. The majority of studies showed that ETCO₂ values during CPR were significantly higher in patients who later developed ROSC compared to patients who did not. Several studies suggested that initial ETCO₂ value of more than 1.33 kPa is 100% sensitive for predicting survival making ETCO₂ value below 1.33 kPa a strong predictor of mortality. These studies however had several limitations and the 100% sensitivity for predicting survival was not consistent among all studies.

Conclusion

ETCO₂ values during CPR do correlate with the likelihood of ROSC and survival and therefore have prognostic value. Although certain ETCO₂ cut-off values appears to be a strong predictor of mortality, the utility of ETCO₂ cut-off values during CPR to accurately predict the outcome of resuscitation is not fully established. Therefore, ETCO₂ values cannot be used as a mortality predictor in isolation.     

Durable mechanical circulatory support devices

Individuals afflicted with advanced systolic heart failure who have become unresponsive to standard medical and electrical therapies are categorized as having American Heart Association stage D heart failure. The high mortality rates for medically treated stage D heart failure have not improved in the last 10 years, and patients at this advanced stage require either palliative measures or surgical management of heart failure. In recent years, surgically implanted ventricular assist devices (VADs) have become available for long-term use and are now commonly used as a therapy for advanced heart failure. The data generated from this early experience have clearly shown that VADs improve survival and quality of life in patients with advanced heart failure when implanted as a temporary measure or as long-term support. However, with a growing heart failure population, there is much work to be done to continually improve VAD technology, patient selection criteria, and postimplantation management to define the optimal role for assist devices in the management of systolic heart failure.     

Top-down effects on early visual processing in humans: a predictive coding framework

An increasing number of human electroencephalography (EEG) studies examining the earliest component of the visual evoked potential, the so-called C1, have cast doubts on the previously prevalent notion that this component is impermeable to top-down effects. This article reviews the original studies that (i) described the C1, (ii) linked it to primary visual cortex (V1) activity, and (iii) suggested that its electrophysiological characteristics are exclusively determined by low-level stimulus attributes, particularly the spatial position of the stimulus within the visual field. We then describe conflicting evidence from animal studies and human neuroimaging experiments and provide an overview of recent EEG and magnetoencephalography (MEG) work showing that initial V1 activity in humans may be strongly modulated by higher-level cognitive factors. Finally, we formulate a theoretical framework for understanding top-down effects on early visual processing in terms of predictive coding.     

2019 HRS expert consensus statement on evaluation,risk stratification,and management of arrhythmogenic cardiomyopathy: Executive summary

Arrhythmogenic cardiomyopathy (ACM) is an arrhythmogenic disorder of the myocardium not secondary to ischemic, hypertensive, or valvular heart disease. ACM incorporates a broad spectrum of genetic, systemic, infectious, and inflammatory disorders. This designation includes, but is not limited to, arrhythmogenic right/left ventricular cardiomyopathy, cardiac amyloidosis, sarcoidosis, Chagas disease, and left ventricular noncompaction. The ACM phenotype overlaps with other cardiomyopathies, particularly dilated cardiomyopathy with arrhythmia presentation that may be associated with ventricular dilatation and/or impaired systolic function. This expert consensus statement provides the clinician with guidance on evaluation and management of ACM and includes clinically relevant information on genetics and disease mechanisms. PICO questions were utilized to evaluate contemporary evidence and provide clinical guidance related to exercise in arrhythmogenic right ventricular cardiomyopathy. Recommendations were developed and approved by an expert writing group, after a systematic literature search with evidence tables, and discussion of their own clinical experience, to present the current knowledge in the field. Each recommendation is presented using the Class of Recommendation and Level of Evidence system formulated by the American College of Cardiology and the American Heart Association and is accompanied by references and explanatory text to provide essential context. The ongoing recognition of the genetic basis of ACM provides the opportunity to examine the diverse triggers and potential common pathway for the development of disease and arrhythmia.     

Breathing during cardiac arrest following exercise: A new function of the respiratory system?

We have found in four sheep that, following a muscular exercise, minute ventilation is maintained for 34-131 s during a cardiac arrest (CA), at a magnitude (from 28.2 and 54.7 l min(-1)) similar to the level of ventilation (and thus proportional to the metabolic rate) preceding the period of asystole. Breathing was maintained despite the lack of pulmonary blood flow and the cessation of the muscle contractions, leading to a dramatic reduction in alveolar FCO(2) (1.9 ± 1%). Secondly, swings in arterial blood pressure (ABP) were observed (pulse pressure of 31 ± 3 Torr) in phase with breathing movements in place of the cardiac activity. This "protective" response, deprived from any role in blood gas homeostasis, as circulation is virtually abolished, is not predictable from the traditional respiratory control feedback systems thought to be involved in exercise. We are presenting the view that this response, dissociated from the pulmonary gas exchanges, is the expression of a rudimentary defense mechanism aimed at limiting the consequences of an acute failure of the cardiac pump by the thoraco-abdominal pump.