Short Communication, Icrj Vol: 11 Issue: 1

A Study of Cardiac Arrests in Intensive Care Units

Marlow Barnett^*

Department of Public Health, Experimental and Forensic Medicine, Endocrinology and Nutrition Unit, University of Pavia, Pavia, Italy

*Corresponding Author:

Marlow Barnett
Department of Public Health, Experimental and Forensic Medicine, Endocrinology and Nutrition Unit, University of Pavia, Pavia, Italy
E-mail:marlowbarnett@icloud.com

Received date:  03 January, 2022; Manuscript No. ICRJ-22-56783;
Editor assigned date: 05 January, 2022; PreQC No. ICRJ-22-56783(PQ);
Reviewed date: 17 January, 2022; QC No ICRJ-22-56783;
Revised date: 27 January, 2022; Manuscript No. ICRJ-22-56783(R);
Published date: 03 February, 2022; DOI: 10.4172/2324-8602.1000452.
Citation: Marlow (2022) A Study of Cardiac Arrests in Intensive Care Units. Int J Cardiovasc Res 11:1.

Abstract

Keywords: Cardiovascular

Abstract

Cardiac Arrest (CA) is a leading cause of death in the World and a serious public health concern. Conventional Cardiopulmonary Resuscitation (CPR) is now the sole effective form of resuscitation that improves prognosis. Extracorporeal Membrane Oxygenation (ECMO) is a complicated and expensive procedure that necessitates technical knowledge. It isn't deemed standard of care in every hospital and should only be used in high-volume settings. Extracorporeal Cardiopulmonary Resuscitation (ECPR) is a combination of ECMO and CPR that allows patients with CA who have resisted conventional CPR to achieve hemodynamic and respiratory stability. This method enables for simultaneous treatment of the underlying cause of CA while preserving organ perfusion.
ECPR should not be used routinely in all patients with refractory CA, according to current evidence. As a result, it's crucial to pick the right people who will benefit from this surgery. Increasing access to ECPR and reducing the period of low blood flow by doing high-quality CPR may increase the survival rate of patients with refractory CA. Patients who receive ECPR appear to have superior neurological outcomes. The purpose of this narrative review is to offer the most recent literature on ECPR and to elucidate its potential therapeutic role, as well as to provide an in-depth description of equipment and setup, patient selection, and post-ECPR patient management.

Introduction

An abrupt and sustained loss of consciousness with pulse lessens and apnoea or agonal breathing is classified as cardiac arrest in clinical terms [1]. In terms of underlying disease, beginning rhythm, time in no flow, and concurrent health concerns, it is a heterogeneous disorder. The pathophysiology of cardiac arrest is mostly caused by cardiac, metabolic, or mechanical factors. The most important prognostic factor at the moment of initial presentation is the rhythm, which dictates urgent therapy and is influenced by underlying pathology, time from collapse to rhythm recording, and bystander Cardiopulmonary Resuscitation (CPR).
Primary cardiac pathology is the underlying cause of Out-of-Hospital Cardiac Arrest (OHCA) in the majority of patients, and one-third have a shock able rhythm, which rises to two-thirds when the period from collapse to resuscitation is less than a few minutes. The proportion of patients with original cardiac pathology is lower in patients with In-Hospital Cardiac Arrest (IHCA), and patients are more likely to appear with Pulseless Electrical Activity (PEA) as the initial rhythm, indicating variations in patient characteristics and underlying pathology [2]. A systole is common in both categories when the period between collapse and resuscitation is prolonged.
The pathophysiology of cardiac arrest caused by a primary cardiac cause was described by Weisfeldt and Becker as a time-sensitive three-phase model. The electrical phase lasts 4â??5 minutes, and with early defibrillation, survival chances are more than 50%. Recurrent of shock-resistant ventricular fibrillation, on the other hand, affects 10% to 25% of all OHCA, and when defibrillation fails, anti-arrhythmic medications are routinely utilized [3]. If spontaneous circulation is restored, anti-arrhythmics may reduce the risks of an arrhythmia continuing or repeating. Anti-arrhythmic medications affect the defibrillation threshold in different ways, and most anti-arrhythmics also have pro-arrhythmic effects.
After 4-5 minutes, the circulatory phase begins, during which tissue hypoxia and the accumulation of metabolites lower the chances of effective defibrillation. The importance of restoring Coronary Perfusion Pressure (CPP) cannot be overstated. A CPP of >20â??40 mmHg has been linked to an increased likelihood of conversion to PEA or asystole with defibrillation in animal trials, as well as an increased likelihood of conversion to PEA or asystole with defibrillation if appropriate CPP is not established. During resuscitation, one human study found a positive link between initial and maximal CPP and ROSC, with early CPP being a better predictor of eventual ROSC than no-flow time. The rationale for vasopressor therapy during resuscitation is improved hemodynamics during the circulatory phase [4].
Because of global ischemia and reperfusion injury, survival is poor during the metabolic phase (i.e.>10â??15 minutes), and the favorable benefits of circulatory supportive measures are minimized. Valenzuela discovered that delaying CPR for more than 10 minutes rendered defibrillation ineffective in terms of survival in an OHCA patient survival model. Furthermore, if defibrillation was delayed for more than 10 minutes, the benefit of urgent CPR decreased. It will be difficult to demonstrate advantage if a large number of patients with protracted circulatory arrest are included in cardiac arrest trials, because survival is poor regardless of therapy [5]. Early CPR and defibrillation have been demonstrated to improve cardiac arrest survival and is well established in treatment algorithms. Several pharmacological interventions are interesting from a theoretical standpoint, but supporting clinical data in human research is lacking. We chose to analyze the literature on human studies of drug therapy in cardiac arrest over the last 25 years to synthesize the evidence foundation for drug therapy in cardiac arrest.

Statistical Analysis of Cardiac Arrest

We utilized the Mantelâ??Haenszel test of trend for categorical variables and linear regression for continuous variables to assess changes in baseline characteristics over time. Multivariable regression models employing generalized-estimation equations were built for the total cohort and according to beginning rhythm to see if survival to discharge had increased with time [6]. The clustering of patients within hospitals was taken into account in these models. We used Zou's method to directly estimate rate ratios instead of odds ratios by choosing a Poisson distribution and included a robust variance estimate in our models when survival exceeded 10%. With 2000 as the reference year, our independent variable, calendar year, was included as a categorical variable [7].
To generate yearly risk-adjusted survival rates for the study period, we multiplied the adjusted rate ratio for each year (2001 through 2009) by the observed survival rate for the reference year [8]. These rates show the predicted survival for each year if the patient case mix remained the same as the previous year. We also calculated adjusted rate ratios for year-to-year survival trends using the calendar year as a continuous variable.
Age, sex, race, concomitant disorders, therapeutic measures in situ at the time of cardiac arrest, cardiac arrest characteristics, and select hospital variables were all factored into our models. S2 in the Supplementary Appendix has a complete list of the variables utilized in the multivariable models [9]. We accounted for the amount of years of hospital participation for each arrest to ensure that any survival tendencies were independent of the length of hospital participation in the registry. By introducing an interaction term with calendar year in the model, we were able to see if survival trends differed by age group (65 years vs. 65 years), race, and sex. Finally, we conducted these analyses solely for patients in hospitals with at least 8 years of registry participation to rule out the potential that our findings were related to the recruitment of higher-performing hospitals over time [10].
Except for race (6.6%), CPC score at admission (14.6%), time of cardiac arrest (0.9%), hospital factors (4.5%), and CPC score at discharge (4.6%), all covariates and outcomes had complete data. Multiple imputations were used to impute missing patient-level covariates, which were believed to be missing at random. Because there was no discernible difference between the results with and without imputation, only the former is reported. For the outcome of the CPC score at discharge, no imputation was used.

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