18 research outputs found

    Metabolomics improves the histopathological diagnosis of asphyxial deaths: an animal proof-of-concept model

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    The diagnosis of mechanical asphyxia remains one of the most difficult issues in forensic pathology. Asphyxia ultimately results in cardiac arrest (CA) and, as there are no specific markers, the differential diagnosis of primitive CA and CA secondary to asphyxiation relies on circumstantial details and on the pathologist experience, lacking objective evidence. Histological examination is currently considered the gold standard for CA post-mortem diagnosis. Here we present the comparative results of histopathology versus those previously obtained by 1H nuclear magnetic resonance (NMR) metabolomics in a swine model, originally designed for clinical purposes, exposed to two different CA causes, namely ventricular fibrillation and asphyxia. While heart and brain microscopical analysis could identify the damage induced by CA without providing any additional information on the CA cause, metabolomics allowed the identification of clearly different profiles between the two groups and showed major differences between asphyxiated animals with good and poor outcomes. Minute-by-minute plasma sampling allowed to associate these modifications to the pre-arrest asphyxial phase showing a clear correlation to the cellular effect of mechanical asphyxia reproduced in the experiment. The results suggest that metabolomics provides additional evidence beyond that obtained by histology and immunohistochemistry in the differential diagnosis of CA

    The pathophysiologies of asphyxial vs dysrhythmic cardiac arrest: Implications for resuscitation and post-event management

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    Background Cardiac arrest is not a uniform condition and significant heterogeneity exists within all victims with regard to the cause of cardiac arrest. Primary cardiac (dysrhythmic) and asphyxial causes together are responsible for most cases of cardiac arrest at all age groups. The purpose of this article is to review the pathophysiologic differences between dysrhythmic and asphyxial cardiac arrest in the prearrest period, during the no-flow state, and after successful cardiopulmonary resuscitation. Methods The electronic databases of PubMed/Medline, Scopus, and Cochrane were searched for relevant literature and studies. Results/Discussion Significant differences exist between dysrhythmic and asphyxial cardiac arrest regarding their pathophysiologic pathways and affect consequently the postresuscitation period. Laboratory data indicate that asphyxial cardiac arrest leads to more widespread postresuscitation brain damage compared with dysrhythmic cardiac arrest. Regarding postresuscitation myocardial dysfunction, few studies have addressed a comparison of the 2 conditions with controversial results. Conclusions Asphyxial cardiac arrest differs significantly from dysrhythmic cardiac arrest with regard to pathophysiologic mechanisms, neuropathologic damage, postresuscitation organ dysfunction, and response to therapy. Both conditions should be considered and treated in a different manner. © 2015 Elsevier Inc

    Stress ECHO beyond coronary artery disease. Is it the holy grail of cardiovascular imaging?

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    Stress echocardiography (SE) is a very useful method in clinical practice, because it offers important information of both the patient's functional status and hemodynamic changes during stress. Therefore, SE provides strong diagnostic and prognostic data in a wide spectrum of cardiovascular diseases. This review summarizes the clinical applications of SE in conditions beyond coronary artery disease (CAD) and highlights practical recommendations and key issues for each condition that need further investigation. SE is an established method for the evaluation of symptomatic and asymptomatic patients with valvular heart disease (VHD) and cardiomyopathies, and provides important information regarding prognosis and management of patients with congenital heart disease, pulmonary hypertension or diastolic dysfunction. Moreover, when one or multiple VHD and cardiomyopathy or CAD coexist in one patient, SE is a very useful clinical tool for the evaluation of etiology and symptomatology. © 2018 Wiley Periodicals, Inc

    The role of thyroid hormones in acute coronary syndromes: Prognostic value of alterations in thyroid hormones

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    The prognosis of acute coronary syndromes (ACS) is affected by many factors. Normal thyroid homeostasis is known to alter during various critical illnesses, a condition that has been shown to correlate with the severity of the disease and increased mortality. The purpose of this article is to review literature to emphasize the considerable association of thyroid function with the cardiovascular system and summarize all existing evidence with regard to the role of thyroid hormones alterations during ACS. The electronic databases of PubMed, Medline, Scopus, and Cochrane were searched for relevant literature and studies. Alterations in thyroid hormone plasma concentrations, especially low triiodothyronine (T3) levels, represent a hormonal imbalance that is not uncommon among patients suffering an acute coronary event. Many studies have identified this abnormal thyroid hormonal status to be related to worse prognosis. Although further large-scale clinical trials are needed, the low T3 syndrome manifesting in patients during ACS might be useful in prognostic stratification. © 2017 Wiley Periodicals, Inc

    The pathophysiologies of asphyxial vs dysrhythmic cardiac arrest: Implications for resuscitation and post-event management

    No full text
    Cardiac arrest is not a uniform condition and significant heterogeneity exists within all victims with regard to the cause of cardiac arrest. Primary cardiac (dysrhythmic) and asphyxial causes together are responsible for most cases of cardiac arrest at all age groups. The purpose of this article is to review the pathophysiologic differences between dysrhythmic and asphyxial cardiac arrest in the prearrest period, during the no-flow state, and after successful cardiopulmonary resuscitation

    Intraarrest rhythms and rhythm conversion in asphyxial cardiac arrest

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    Objectives: The objective was to analyze the cardiac arrest rhythms presenting during asphyxial cardiac arrest (ACA). Methods: Asphyxial cardiac arrest was induced in 30 Landrace large white piglets, aged 12 to 15 weeks and with a mean (±SD) weight of 20 (±2) kg. After the onset of cardiac arrest, the animals were left untreated for 4 minutes, after which cardiopulmonary resuscitation was commenced. Heart rhythms were monitored from the onset of asphyxia until return of spontaneous circulation or death. Results: After endotracheal tube clamping and prior to cardiac arrest, normal sinus rhythm was noted in 14 animals, atrial fibrillation in two animals, Mobitz II atrioventricular block in 10 animals, and third-degree atrioventricular block in four animals. At the onset of cardiac arrest, seven animals had ventricular fibrillation (VF), two had asystole, and 21 had pulseless electrical activity (PEA). During the 4-minute period of untreated arrest, however, significant changes in the monitored rhythm were noted; at the end of the fourth minute, 19 animals had VF, two animals had asystole, and nine animals had PEA. Conclusions: The most common rhythm after 4 minutes of untreated ACA was VF, while in 57% of animals, PEA was spontaneously converted to VF during the cardiac arrest interval. © 2015 by the Society for Academic Emergency Medicine

    Determinants of venous return in steady-state physiology and asphyxia-induced circulatory shock and arrest: an experimental study

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    Background: Mean circulatory filling pressure (Pmcf) provides information on stressed volume and is crucial for maintaining venous return. This study investigated the Pmcf and other determinants of venous return in dysrhythmic and asphyxial circulatory shock and arrest. Methods: Twenty Landrace/Large-White piglets were allocated into two groups of 10 animals each. In the dysrhythmic group, ventricular fibrillation was induced with a 9 V cadmium battery, while in the asphyxia group, cardiac arrest was induced by stopping and disconnecting the ventilator and clamping the tracheal tube at the end of exhalation. Mean circulatory filling pressure was calculated using the equilibrium mean right atrial pressure at 5–7.5 s after the onset of cardiac arrest and then every 10 s until 1 min post-arrest. Successful resuscitation was defined as return of spontaneous circulation (ROSC) with a MAP of at least 60 mmHg for a minimum of 5 min. Results: After the onset of asphyxia, a ΔPmca increase of 0.004 mmHg, 0.01 mmHg, and 1.26 mmHg was observed for each mmHg decrease in PaO2, each mmHg increase in PaCO2, and each unit decrease in pH, respectively. Mean Pmcf value in the ventricular fibrillation and asphyxia group was 14.81 ± 0.5 mmHg and 16.04 ± 0.6 mmHg (p < 0.001) and decreased by 0.031 mmHg and 0.013 mmHg (p < 0.001), respectively, for every additional second passing after the onset of cardiac arrest. With the exception of the 5–7.5 s time interval, post-cardiac arrest right atrial pressure was significantly higher in the asphyxia group. Mean circulatory filling pressure at 5 to 7.5 s after cardiac arrest predicted ROSC in both groups, with a cut-off value of 16 mmHg (AUC = 0.905, p < 0.001). Conclusion: Mean circulatory filling pressure was higher in hypoxic hypercapnic conditions and decreased at a lower rate after cardiac arrest compared to normoxemic and normocapnic state. A Pmcf cut-off point of 16 mmHg at 5–7.5 s after cardiac arrest can highly predict ROSC. © 2022, The Author(s)
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