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Point of Care ultrasound (POCUS) of the lungs, also known as lung ultrasound (LUS), has emerged as a technique that allows for the diagnosis of many respiratory pathologies with greater accuracy and speed compared to conventional techniques such as chest x-ray and auscultation. The goal of this narrative review is to provide a simple and practical approach to LUS for critical care, pulmonary, and anesthesia providers, as well as respiratory therapists and other health care providers to be able to implement this technique into their clinical practice. In this review, we will discuss the basic physics of LUS, provide a hands-on scanning technique, describe LUS findings seen in normal and pathological conditions (such as mainstem intubation, pneumothorax, atelectasis, pneumonia, aspiration, COPD exacerbation, cardiogenic pulmonary edema, ARDS, and pleural effusion) and also review the training necessary to achieve competence in LUS. [ABSTRACT FROM AUTHOR]

Objectives: The number and distribution of lung ultrasound (LUS) imaging artifacts termed B‐lines correlate with the presence of acute lung disease such as infection, acute respiratory distress syndrome (ARDS), and pulmonary edema. Detection and interpretation of B‐lines require dedicated training and is machine and operator‐dependent. The goal of this study was to identify radio frequency (RF) signal features associated with B‐lines in a cohort of patients with cardiogenic pulmonary edema. A quantitative signal indicator could then be used in a single‐element, non‐imaging, wearable, automated lung ultrasound sensor (LUSS) for continuous hands‐free monitoring of lung fluid. Methods: In this prospective study a 10‐zone LUS exam was performed in 16 participants, including 12 patients admitted with acute cardiogenic pulmonary edema (mean age 60 ± 12 years) and 4 healthy controls (mean age 44 ± 21). Overall,160 individual LUS video clips were recorded. The LUS exams were performed with a phased array probe driven by an open‐platform ultrasound system with simultaneous RF signal collection. RF data were analyzed offline for candidate B‐line indicators based on signal amplitude, temporal variability, and frequency spectrum; blinded independent review of LUS images for the presence or absence of B‐lines served as ground truth. Predictive performance of the signal indicators was determined with receiving operator characteristic (ROC) analysis with k‐fold cross‐validation. Results: Two RF signal features—temporal variability of signal amplitude at large depths and at the pleural line—were strongly associated with B‐line presence. The sensitivity and specificity of a combinatorial indicator were 93.2 and 58.5%, respectively, with cross‐validated area under the ROC curve (AUC) of 0.91 (95% CI = 0.80–0.94). Conclusion: A combinatorial signal indicator for use with single‐element non‐imaging LUSS was developed to facilitate continuous monitoring of lung fluid in patients with respiratory illness. [ABSTRACT FROM AUTHOR]

Natanim Degefu,1 Abera Jambo,2 Shambel Nigusse,2 Mesay Dechasa,2 Tigist Gashaw,3 Melaku Getachew4 1Department of Pharmaceutics, School of Pharmacy, Haramaya University, Harar, Ethiopia; 2Department of Clinical Pharmacy, School of Pharmacy, Haramaya University, Harar, Ethiopia; 3Department of Pharmacology, School of Pharmacy, Haramaya University, Harar, Ethiopia; 4Department of Emergency and Critical Care Medicine, School of Medicine, College of Health and Medical Sciences, Haramaya University, Harar, EthiopiaCorrespondence: Melaku Getachew, Department of Emergency and critical care medicine, School of Medicine, College of Health and Medical Sciences, Haramaya University, P.O. Box: 138, Harar, Ethiopia, Tel +251953137119, Email melakug02@gmail.comBackground: Despite cardiogenic pulmonary edema is the most common phenotype of acute heart failure (AHF), studies on its burden and associated factors are limited. This study aimed to assess the burden and contributing factors of cardiogenic pulmonary edema in patients with acute heart failure admitted to a tertiary hospital in eastern Ethiopia.Patients and Methods: An institution-based cross-sectional study was conducted on the medical records (n = 276) of patients with AHF between February 01, 2018, and January 31, 2023. A simple random sampling technique was used to select participants from the study population. Bivariable and multivariable logistic regression analyses were used to assess factors associated with the development of cardiogenic pulmonary edema. A P-value ≤ 0.05 was considered as statistically significant.Results: The prevalence of cardiogenic pulmonary edema was 47.8% in AHF patients. Rural residence (adjusted odds ratio (AOR),9.54), smoking (AOR,3.17), comorbidity (AOR,2.1), and underlying cardiovascular disease (ischemic heart disease, chronic rheumatic valvular heart disease, and hypertensive heart disease with AOR: 6.71, 8.47, and 12.07, respectively) were significantly associated with the development of cardiogenic pulmonary edema in patients with AHF.Conclusion: Nearly half of the patients with AHF had cardiogenic pulmonary edema. Being a rural dweller, cigarette smoking, comorbidities, and underlying cardiac illness were significantly associated with the development of cardiogenic pulmonary edema in patients with AHF.Keywords: acute heart failure, cardiogenic pulmonary edema, Ethiopia, tertiary hospital

Cardiogenic pulmonary edema (CPE) is characterized by the development of acute respiratory failure associated with the accumulation of fluid in the lung’s alveolar spaces due to an elevated cardiac filling pressure. All cardiac diseases, characterized by an increasing pressure in the left side of the heart, can cause CPE. High capillary pressure for an extended period can also cause barrier disruption, which implies increased permeability and fluid transfer into the alveoli, leading to edema and atelectasis. The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of procoagulant processes, cell death, and mechanical stretch. Reactive oxygen and nitrogen species (RONS) can modify or damage ion channels, such as epithelial sodium channels, which alters fluid balance. Some studies claim that these patients may have higher levels of surfactant protein B in the bloodstream. The correct approach to patients with CPE should include a detailed medical history and a physical examination to evaluate signs and symptoms of CPE as well as potential causes. Second-level diagnostic tests, such as pulmonary ultrasound, natriuretic peptide level, chest radiograph, and echocardiogram, should occur in the meantime. The identification of the specific CPE phenotype is essential to set the most appropriate therapy for these patients. Non-invasive ventilation (NIV) should be considered early in the treatment of this disease. Diuretics and vasodilators are used for pulmonary congestion. Hypoperfusion requires treatment with inotropes and occasionally vasopressors. Patients with persistent symptoms and diuretic resistance might benefit from additional approaches (i.e., beta-agonists and pentoxifylline). This paper reviews the pathophysiology, clinical presentation, and management of CPE.

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Echocardiographic indices of the inferior vena cava have been associated with elevated right atrial pressures in humans. Describe caudal vena caval (CVC) sonographic dimensions in healthy cats compared to cats with cardiogenic cavitary effusion (CCE), cardiogenic pulmonary edema (CPE), or non-cardiac causes of cavitary effusion (NCE). 30 healthy control cats and 52 client-owned cats with CCE, CPE, or NCE examined at two university hospitals. Sagittal 2-dimensional (2D) and M-mode CVC dimensions were acquired from the subxiphoid view. Caudal vena cava collapsibility index (CVC-CI) was calculated. Variables were compared between study groups using Kruskal–Wallis and Dunn's Bonferroni testing. Receiver operating characteristic curves were used to assess sensitivity and specificity for diagnostic categories. Healthy cats had sagittal 2D and M-mode (median, interquartile range) CVC maximal dimensions of 2.4 mm (1.3–4.0) and 3.4 mm (1.5–4.9) and CVC-CI of 52% (45.2–61.8) and 55% (47.8–61.3), respectively. The CVC maximal dimensions in healthy controls were smaller than in cats with cavitary effusions or pulmonary edema (all P<0.05). CVC-CI was different between CCE and NCE (P<0.0001) with cutoffs of CVC-CI ≤38% (2D) or ≤29% (M-mode) being 90.5% and 85.7% sensitive, and 94.4% and 100% specific for diagnosis of CCE, respectively. Caudal vena cava measurements are larger in cats with cavitary effusions and cats with CPE than healthy cats. In cats with cavitary effusion, decreased CVC-CI, ≤38% (2D) or ≤29% (M-mode), was helpful in distinguishing between cardiogenic and noncardiogenic etiology. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This meta-analysis was performed to evaluate the diagnostic efficacy of lung ultrasound (LUS) in cardiogenic pulmonary edema. MATERIALS AND METHODS: An electronic search of databases, including MEDLINE, Embase, PubMed, and Web of Science, was performed to collect clinical studies on ultrasound diagnosis of cardiogenic pulmonary edema from inception to 23 March 2023. The number of patients with true-positive, true-negative, false-positive, and false-negative cardiogenic pulmonary edema diagnosed by LUS was collected, and the R package was used to analyze the diagnostic efficacy of LUS. RESULTS: Nine pieces of literature were finally included with 2,097 participants, including 1,047 patients with cardiogenic heart failure. Across the nine included papers, the pooled sensitivity of LUS in the included studies was 0.92 (95% CI: 0.84, 0.97) with a maximum sensitivity of 0.99 (95% CI: 0.96 to 1.00) and a minimum of 0.59 (95% CI: 0.50, 0.68). The pooled specificity of the included studies was 0.87 (95% CI: 0. 82, 0.91) with a maximum specificity of 0.93 (95% CI: 0.90-0.95) and a minimum of 0.80 (95% CI: 0.67, 0.89). The pooled AUC was 0.93 (95% CI: 0.84 to 0.97), suggesting a high diagnostic value of LUS in cardiogenic pulmonary edema. CONCLUSIONS: Lung ultrasound offers a good diagnostic efficacy for cardiogenic pulmonary edema. Further standardization of the examination method is required to provide a reference for the clinical use of LUS. [ABSTRACT FROM AUTHOR]

Acute heart failure and arterial thromboembolism are common complications of hypertrophic cardiomyopathy in cats. These conditions have many common links in pathogenesis, so analyzing the differences between them improves the understanding of the impact of vessel occlusion on the body. In the study, 40 clinical cases were analyzed and two groups were formed: the first – cats with arterial thromboembolism and the second – cats with acute heart failure. The data from anamnesis, clinical examination and echocardiographic examination were collected. Age, sex, breed, weight, temperature, frequency of respiratory movements, signs of dyspnea, presence of pulmonary edema, presence of free fluid in the chest and pericardial cavities were analyzed. The following echocardiographic parameters were analyzed: left ventricular wall thickness, left ventricular end-systolic and end-diastolic dimensions, diameters of the aorta and left atrium, heart rate and left ventricular contraction fraction. It was established that the majority of animals from both groups were males. Acute heart failure was registered mainly in young cats (M = 3.7), in contrast to animals with arterial thromboembolism (M = 6.7), (P < 0.01). There was no significant difference in the values of rectal temperature, weight, heart rate, aortic diameter, and left ventricular contraction fraction. Most animals from both groups had signs of dyspnoea. The difference in the frequency of respiratory movements was significant (P < 0.01). In cats with acute heart failure, pulmonary edema was diagnosed in 85%, free fluid in the thoracic and/or pericardial cavities in 55 %. In animals with thromboembolism, edema was found in 45 %, and effusion in the chest and/or pericardial cavities in 30 % of animals. The established differences indicate that arterial thromboembolism develops in animals that have had heart pathology for a longer period of time, whereas acute heart failure occurs more suddenly in cats [ABSTRACT FROM AUTHOR]

Abstract Background Patients with acute respiratory failure caused by cardiogenic pulmonary edema (CPE) may require mechanical ventilation that can cause further lung damage. Our aim was to determine the impact of ventilatory settings on CPE mortality. Methods Patients from the LUNG SAFE cohort, a multicenter prospective cohort study of patients undergoing mechanical ventilation, were studied. Relationships between ventilatory parameters and outcomes (ICU discharge/hospital mortality) were assessed using latent mixture analysis and a marginal structural model. Results From 4499 patients, 391 meeting CPE criteria (median age 70 [interquartile range 59–78], 40% female) were included. ICU and hospital mortality were 34% and 40%, respectively. ICU survivors were younger (67 [57–77] vs 74 [64–80] years, p

Simple Summary: Cardiogenic pulmonary edema (CPE) is the leading cause of cats visiting emergency hospitals with respiratory distress. The association of physical examination and venous blood gas parameters with the survival of cats with CPE was retrospectively investigated. Thirty-six cats were ultimately included, and eight of them died within 12 h after their presentation to our hospital. The Mann–Whitney U test with Bonferroni correction was used to compare the parameters. Cats that died within 12 h had significantly lower rectal temperatures and higher PvCO2 than those that did not die within 12 h. Moreover, vasoconstrictor use was related to death within 12 h of presentation and higher PvCO2. A large number of prospective studies should be performed to validate these results. Cats urgently visit emergency hospitals due to respiratory distress, and the chief cause is cardiogenic pulmonary edema (CPE). Although cats with CPE were frequently encountered in clinics, the prognostic factors were poorly reported. The objective of this retrospective study was to investigate the association of physical examination and venous blood gas parameters with the survival of cats with CPE in an emergency hospital. Thirty-six cats with CPE were ultimately included in the present study, and eight of them died within 12 h after their presentation to our hospital. Statistical analyses of clinical parameters between cats that died within 12 h and those that survived for 12 h were conducted using Mann–Whitney U test with Bonferroni correction. Cats that died within 12 h had significantly lower rectal temperatures and higher PvCO2 than those that did not die within 12 h. Moreover, hypotension and vasoconstrictor use were related to death within 12 h of presentation and higher PvCO2. These findings indicated the prognostic utility of body temperature and PvCO2, and the association between hypercapnia and the severity of CPE or hypotension. A large number of prospective studies should be performed to validate these results. [ABSTRACT FROM AUTHOR]

Background: Patients with acute respiratory failure caused by cardiogenic pulmonary edema (CPE) may require mechanical ventilation that can cause further lung damage. Our aim was to determine the impact of ventilatory settings on CPE mortality. Methods: Patients from the LUNG SAFE cohort, a multicenter prospective cohort study of patients undergoing mechanical ventilation, were studied. Relationships between ventilatory parameters and outcomes (ICU discharge/hospital mortality) were assessed using latent mixture analysis and a marginal structural model. Results: From 4499 patients, 391 meeting CPE criteria (median age 70 [interquartile range 59–78], 40% female) were included. ICU and hospital mortality were 34% and 40%, respectively. ICU survivors were younger (67 [57–77] vs 74 [64–80] years, p < 0.001) and had lower driving (12 [8–16] vs 15 [11–17] cmH2O, p < 0.001), plateau (20 [15–23] vs 22 [19–26] cmH2O, p < 0.001) and peak (21 [17–27] vs 26 [20–32] cmH2O, p < 0.001) pressures. Latent mixture analysis of patients receiving invasive mechanical ventilation on ICU day 1 revealed a subgroup ventilated with high pressures with lower probability of being discharged alive from the ICU (hazard ratio [HR] 0.79 [95% confidence interval 0.60–1.05], p = 0.103) and increased hospital mortality (HR 1.65 [1.16–2.36], p = 0.005). In a marginal structural model, driving pressures in the first week (HR 1.12 [1.06–1.18], p < 0.001) and tidal volume after day 7 (HR 0.69 [0.52–0.93], p = 0.015) were related to survival. Conclusions: Higher airway pressures in invasively ventilated patients with CPE are related to mortality. These patients may be exposed to an increased risk of ventilator-induced lung injury. Trial registration Clinicaltrials.gov NCT02010073 [ABSTRACT FROM AUTHOR]

Abstract Background Small‐breed dogs commonly have concurrent myxomatous mitral valve disease (MMVD) and lower respiratory tract disease (LRTD). Hypothesis Small‐breed dogs with preclinical MMVD and concurrent LRTD have more B‐lines on point‐of‐care lung ultrasound (POC‐LUS) compared to dogs without concurrent LRTD and are prone to misdiagnose as cardiogenic pulmonary edema (CPE). Animals A total of 114 small‐breed dogs with preclinical MMVD. Methods A prospective study was conducted, in which POC‐LUS was obtained and the number of B‐lines was calculated by a single clinician using the Veterinary Bedside Lung Ultrasound Examination protocol. The presence/absence of LRTD was assessed by clinicians blinded to the POC‐LUS results. Results Fifty and 64 dogs were in ACVIM stage B1 and B2, respectively. The presence of LRTD was prevalent in 74.6% (85/114) of small‐breed dogs with preclinical MMVD. When a previously reported criterion for CPE diagnosis (≥2 sites with >3 B‐lines/site) was applied, false‐positive results were observed in 15.8% (18/114) of dogs with preclinical MMVD. The summated number of B‐lines (3 vs. 1, P = .003), as well as the false‐positive rate (20% vs 3%, P = .04), were significantly higher in dogs with LRTD compared with dogs without LRTD. Multivariable logistic regression showed the presence of abnormalities other than B‐line on POC‐LUS (eg, thickened pleura or consolidation) could predict false‐positive results (odds ratio = 3.75, 95% confidence intervals 1.12‐12.54; P = .03) after adjustment for other clinical and echocardiographic factors. Conclusions and Clinical Importance Concurrent LRTD and abnormalities other than B‐lines should be considered in the interpretation of POC‐LUS in MMVD dogs.

This study reports the efficacy of the vasodilator sodium nitroprusside (SNP), for treatment of acute cardiogenic pulmonary edema in dogs. For this study, the patients were divided into the SNP only treatment group, the SNP, furosemide and dobutamine treatment group, and non-SNP treatment group. Seven dogs, 6 dogs and 2 dogs were favorable responders in SNP only group, group with SNP, furosemide and dobutamine and non-SNP treatment group, each. The results of this study suggest that SNP can be an effective alternative therapy for dogs with acute cardiogenic pulmonary edema. [ABSTRACT FROM AUTHOR]

Background Adult respiratory distress syndrome (ARDS) and acute cardiogenic pulmonary edema (CPE) are common clinical issues. Based on clinical data, it is a big challenge to differentiate between both. Secondary to many limitations of computed tomography, chest ultrasound (CUS) provides pleuropulmonary signs that help in differentiation. Objective The current work aimed to assess the accuracy of CUS in differentiating CPE from ARDS. Patients and methods This is a cross-sectional study conducted on patients admitted to different ICUs with pulmonary edema, comprising 25 patients with CPE and 35 patients with ARDS. CUS, ECG, echocardiography, and chest radiograph were done for all patients. Results The mean age of patients with ARDS was 48.90±11.23 years, whereas the mean age of patients with CPE was 49.10±10.10 years. The majority of both groups were males. Systolic dysfunction and pneumonia were the most frequent etiology in CPE and ARDS, respectively. All patients in both groups had alveolar-interstitial syndrome. Pleural line, absence of lung sliding, and the spared area were presented in all cases with ARDS and absent in those with CPE. Moreover, none of those with CPE had lung pulse, but this finding was presented in 18 (51.4%) patients with ARDS. Conclusion CUS can help in differentiating ARDS from CPE in clinical practice. Based on CUS findings, absent or reduced lung sliding, pleural line abnormalities, and spared areas are diagnostic of ARDS. [ABSTRACT FROM AUTHOR]

Myxomatous mitral valve disease (MMVD) is the most common heart disease in small breed dogs. Dogs with MMVD commonly show clinical signs of dyspnea due to cardiogenic pulmonary edema (CPE). Reticulocytosis in the absence of anemia (RAA) is a hematological finding in hypoxic conditions. We aimed to assess the prevalence of RAA in dogs with CPE due to MMVD, and evaluate whether RAA is reversible with amelioration of dyspnea. Twenty-nine client-owned dogs with CPE due to MMVD were included. Dogs who died within 6 weeks of the onset of CPE were included in the non-survival group, while the others comprised the survival group. Of the 21 dogs, RAA was observed in 17 dogs (80.9%). In the RAA group, the absolute reticulocyte count significantly decreased as CPE resolved (p < 0.001). The mean absolute reticulocyte count in the RAA group was 163.90 ± 50.77 on the first measurement and 78.84 ± 25.64 after resolution of CPE. In the RAA group, no significant differences in mean absolute reticulocyte count were observed between the survival and non-survival groups at either the first or second measurement. Our results indicate that RAA occurs in dogs with MMVD-related CPE and can resolve after resolution of CPE. [ABSTRACT FROM AUTHOR]

Background: Despite significant advances in the treatment of heart failure, the prognosis of acute cardiogenic pulmonary edema (ACPE) continues to be a serious problem. The objective of this study is to determine the risk factors affecting in-hospital mortality in patients with ACPE. Methods: We enrolled 305 patients who were hospitalized with cardiogenic pulmonary edema as a diagnosis. Clinical, biochemical and echocardiographic variables were collected and analysed. The patients were divided into two groups according to the presence of mortality. Both groups were evaluated in terms of clinical features during admission to the emergency department (ED) and factors affecting in-hospital mortality. Results: Forty-two patients died and the mortality rate was 13.8%. To determine the factors affecting mortality, multiple logistic regression analysis was performed. In the regression analysis, it was seen that age at admission to the ED (OR:1.75, 95% CI 1.18-3.05, p:0.014), systolic blood pressure (OR:0.95, 95% CI 0.31-0.98, p:0.040), presence of acute myocardial infarction (OR:4.17, 95% CI 1.85-7.13, p:0.001), positive troponin (OR:5.47, 95% Cl 1.07-7.46, p:0.011), atrial fibrillation rhythm (OR;3.16, 95% CI 1.81-8.02, p:0.010), inotropic drug usage (OR;5.61, 95% CI 1.87-9.24, p:0.013) increased in-hospital mortality. Conclusion: Our findings could help clinicians in identifying patients with poor prognosis early in the presence of identified risk factors.

Cats urgently visit emergency hospitals due to respiratory distress, and the chief cause is cardiogenic pulmonary edema (CPE). Although cats with CPE were frequently encountered in clinics, the prognostic factors were poorly reported. The objective of this retrospective study was to investigate the association of physical examination and venous blood gas parameters with the survival of cats with CPE in an emergency hospital. Thirty-six cats with CPE were ultimately included in the present study, and eight of them died within 12 h after their presentation to our hospital. Statistical analyses of clinical parameters between cats that died within 12 h and those that survived for 12 h were conducted using Mann–Whitney U test with Bonferroni correction. Cats that died within 12 h had significantly lower rectal temperatures and higher PvCO2 than those that did not die within 12 h. Moreover, hypotension and vasoconstrictor use were related to death within 12 h of presentation and higher PvCO2. These findings indicated the prognostic utility of body temperature and PvCO2, and the association between hypercapnia and the severity of CPE or hypotension. A large number of prospective studies should be performed to validate these results.

Background: Small‐breed dogs commonly have concurrent myxomatous mitral valve disease (MMVD) and lower respiratory tract disease (LRTD). Hypothesis: Small‐breed dogs with preclinical MMVD and concurrent LRTD have more B‐lines on point‐of‐care lung ultrasound (POC‐LUS) compared to dogs without concurrent LRTD and are prone to misdiagnose as cardiogenic pulmonary edema (CPE). Animals: A total of 114 small‐breed dogs with preclinical MMVD. Methods: A prospective study was conducted, in which POC‐LUS was obtained and the number of B‐lines was calculated by a single clinician using the Veterinary Bedside Lung Ultrasound Examination protocol. The presence/absence of LRTD was assessed by clinicians blinded to the POC‐LUS results. Results: Fifty and 64 dogs were in ACVIM stage B1 and B2, respectively. The presence of LRTD was prevalent in 74.6% (85/114) of small‐breed dogs with preclinical MMVD. When a previously reported criterion for CPE diagnosis (≥2 sites with >3 B‐lines/site) was applied, false‐positive results were observed in 15.8% (18/114) of dogs with preclinical MMVD. The summated number of B‐lines (3 vs. 1, P =.003), as well as the false‐positive rate (20% vs 3%, P =.04), were significantly higher in dogs with LRTD compared with dogs without LRTD. Multivariable logistic regression showed the presence of abnormalities other than B‐line on POC‐LUS (eg, thickened pleura or consolidation) could predict false‐positive results (odds ratio = 3.75, 95% confidence intervals 1.12‐12.54; P =.03) after adjustment for other clinical and echocardiographic factors. Conclusions and Clinical Importance: Concurrent LRTD and abnormalities other than B‐lines should be considered in the interpretation of POC‐LUS in MMVD dogs. [ABSTRACT FROM AUTHOR]

Proficiency in basic lung ultrasound is highly recommended for clinicians in general and internal medicine. This article will review and provide guidance for novice users on how to use lung ultrasound in clinical practice, through a pathology-oriented approach. The authors recommend a 12-zone protocol and describe how to perform and apply it in clinical practice while examining patients with clinical suspicion for the following diseases: pleural effusion, heart failure, pneumonia (bacterial and viral), interstitial lung disease, and pneumothorax., Competing Interests: Disclosure The authors have nothing to disclose., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Due to population aging, we are currently confronted with an increased number of chronic heart failure patients. The primary purpose of this study was to implement a noncontact system that can predict heart failure exacerbation through vocal analysis. We designed the system to evaluate the voice characteristics of every patient, and we used the identified variations as an input for a machine-learning-based approach. We collected data from a total of 16 patients, 9 men and 7 women, aged 65–91 years old, who agreed to take part in the study, with a detailed signed informed consent. We included hospitalized patients admitted with cardiogenic acute pulmonary edema in the study, regardless of the precipitation cause or other known cardiovascular comorbidities. There were no specific exclusion criteria, except age (which had to be over 18 years old) and patients with speech inabilities. We then recorded each patient's voice twice a day, using the same smartphone, Lenovo P780, from day one of hospitalization—when their general status was critical—until the day of discharge, when they were clinically stable. We used the New York Heart Association Functional Classification (NYHA) classification system for heart failure to include the patients in stages based on their clinical evolution. Each voice recording has been accordingly equated and subsequently introduced into the machine-learning algorithm. We used multiple machine-learning techniques for classification in order to detect which one turns out to be more appropriate for the given dataset and the one that can be the starting point for future developments. We used algorithms such as Artificial Neural Networks (ANN), Support Vector Machine (SVM) and K-Nearest Neighbors (KNN). After integrating the information from 15 patients, the algorithm correctly classified the 16th patient into the third NYHA stage at hospitalization and second NYHA stage at discharge, based only on his voice recording. The KNN algorithm proved to have the best classification accuracy, with a value of 0.945. Voice is a cheap and easy way to monitor a patient's health status. The algorithm we have used for analyzing the voice provides highly accurate preliminary results. We aim to obtain larger datasets and compute more complex voice analyzer algorithms to certify the outcomes presented. [ABSTRACT FROM AUTHOR]

One of the most common causes of death in cats with cardiomyopathy is pulmonary edema. Different forms of feline cardiomyopathies can have a diverse clinical signs. The onset of clinical signs is often related to recent stressful situation such as visiting a clinic or transportation. It is unknown how to identify animals which are predisposing to pulmonary edema and death. The evaluation of literary data has confirmed that there are insufficient researches in this area. Also it is reliably unknown, which changes in clinical status or on ECHO could be markers of death in cats at cardiogenic pulmonary edema. This article is highlights the topic of estimation of risk assessment of death in cats in case of cardiogenic pulmonary edema. All types of cardiomyopathies were diagnosed in this study. We included cats whose owners addressed the clinic complaining of dyspnea and worsening of activity. An echocardiographic and radiological examination was performed in the clinic. The authors paid aƩention to the following markers: the degree of radiological changes in pulmonary parenchyma, data of clinical examinations, the degree of changes of left ventricular and the size of left atrium. It was found that main marker of death in cats at cardiogenic pulmonary edema is the left atrium to aorta more then 2,2. Severe changes in lung parenchyma on X-ray and decrease in left ventricular systolic function also increase the risk of cardiac death in acute heart failure. Left ventricular myocardial thickness and the presence of spontaneous contrast do not affect survival during the first days of hospitalization. Most likely, these changes have more impact on overall life expectancy

Myxomatous mitral valve disease (MMVD) is the most common heart disease in small breed dogs. Dogs with MMVD commonly show clinical signs of dyspnea due to cardiogenic pulmonary edema (CPE). Reticulocytosis in the absence of anemia (RAA) is a hematological finding in hypoxic conditions. We aimed to assess the prevalence of RAA in dogs with CPE due to MMVD, and evaluate whether RAA is reversible with amelioration of dyspnea. Twenty-nine client-owned dogs with CPE due to MMVD were included. Dogs who died within 6 weeks of the onset of CPE were included in the non-survival group, while the others comprised the survival group. Of the 21 dogs, RAA was observed in 17 dogs (80.9%). In the RAA group, the absolute reticulocyte count significantly decreased as CPE resolved (p < 0.001). The mean absolute reticulocyte count in the RAA group was 163.90 ± 50.77 on the first measurement and 78.84 ± 25.64 after resolution of CPE. In the RAA group, no significant differences in mean absolute reticulocyte count were observed between the survival and non-survival groups at either the first or second measurement. Our results indicate that RAA occurs in dogs with MMVD-related CPE and can resolve after resolution of CPE.

The recent advances in lung ultrasound for the diagnosis of cardiogenic pulmonary edema are outstanding; however, the mechanism of vertical artifacts known as B-lines used for the diagnosis has not yet been fully elucidated. The theory of “acoustic trap” is useful when considering the generation of vertical artifacts. Basic research in several studies supports the theory. Published studies with pilot experiments indicate that clarification of the relationship between the length and intensity of vertical artifacts and physical or acoustic composition of sources may be useful for differentiating cardiogenic pulmonary edema from lung diseases. There is no international consensus with regard to the optimal settings of ultrasound machines even though their contribution to the configuration of vertical artifacts is evident. In the clinical setting, the configuration is detrimentally affected by the use of spatial compound imaging, the placement of the focal point at a deep level, and the use of multiple focus. Simple educational materials using a glass microscope slide also show the non-negligible impact of the ultrasound machine settings on the morphology of vertical artifacts.

Acute heart failure (AHF) and acute decompensation of chronic heart failure (ADHF) are urgent health problems. The main tasks of the managing the patients with these conditions include the achieving of optimal and stable resolution of edema and dyspnea, the tissue perfusion improving, the severity of clinical symptoms reducing, the exercise tolerance increasing, the progression of heart failure preventing, the preventing of the target organs dysfunction, complications, decompensations and hospitalizations, the increasing of survival and improving the quality of life. The algorithm for diagnosis, clinical patient profiles recognition, pharmacological (including diuretics, vasodilators, inotropes, vasopressors, anticoagulants, etc.) and non-pharmacological (including oxygen therapy, non-invasive and invasive ventilation, etc.) approaches to the management of AHF and ADHF are presented in accordance with contemporary guidelines.

Due to population aging, we are currently confronted with an increased number of chronic heart failure patients. The primary purpose of this study was to implement a noncontact system that can predict heart failure exacerbation through vocal analysis. We designed the system to evaluate the voice characteristics of every patient, and we used the identified variations as an input for a machine-learning-based approach. We collected data from a total of 16 patients, 9 men and 7 women, aged 65–91 years old, who agreed to take part in the study, with a detailed signed informed consent. We included hospitalized patients admitted with cardiogenic acute pulmonary edema in the study, regardless of the precipitation cause or other known cardiovascular comorbidities. There were no specific exclusion criteria, except age (which had to be over 18 years old) and patients with speech inabilities. We then recorded each patient’s voice twice a day, using the same smartphone, Lenovo P780, from day one of hospitalization—when their general status was critical—until the day of discharge, when they were clinically stable. We used the New York Heart Association Functional Classification (NYHA) classification system for heart failure to include the patients in stages based on their clinical evolution. Each voice recording has been accordingly equated and subsequently introduced into the machine-learning algorithm. We used multiple machine-learning techniques for classification in order to detect which one turns out to be more appropriate for the given dataset and the one that can be the starting point for future developments. We used algorithms such as Artificial Neural Networks (ANN), Support Vector Machine (SVM) and K-Nearest Neighbors (KNN). After integrating the information from 15 patients, the algorithm correctly classified the 16th patient into the third NYHA stage at hospitalization and second NYHA stage at discharge, based only on his voice recording. The KNN algorithm proved to have the best classification accuracy, with a value of 0.945. Voice is a cheap and easy way to monitor a patient’s health status. The algorithm we have used for analyzing the voice provides highly accurate preliminary results. We aim to obtain larger datasets and compute more complex voice analyzer algorithms to certify the outcomes presented.

Background: The acute respiratory distress syndrome (ARDS) and cardiogenic pulmonary edema (CPE) are both characterized by an increase in lung edema that can be measured by computed tomography (CT). The aim of this study was to compare possible differences between patients with ARDS and CPE in the morphologic pattern, the aeration, and the amount and distribution of edema within the lung. Methods: Lung CT was performed at a mean positive end-expiratory pressure level of 5 cm H2O in both groups. The morphological evaluation was performed by two radiologists, while the quantitative evaluation was performed by a dedicated software. Results: A total of 60 patients with ARDS (20 mild, 20 moderate, 20 severe) and 20 patients with CPE were enrolled. The ground-glass attenuation regions were similarly present among the groups, 8 (40%), 8 (40%), 14 (70%), and 10 (50%), while the airspace consolidations were significantly more present in ARDS. The lung gas volume was significantly lower in severe ARDS compared to CPE (830 [462] vs 1120 [832] mL). Moving from the nondependent to the dependent lung regions, the not inflated lung tissue significantly increased, while the well inflated tissue decreased (ρ = 0.96-1.00, P <.0001). Significant differences were found between ARDS and CPE mostly in dependent regions. In severe ARDS, the estimated edema was significantly higher, compared to CPE (757 [740] vs 532 [637] g). Conclusions: Both ARDS and CPE are characterized by a similar presence of ground-glass attenuation and different airspace consolidation regions. Acute respiratory distress syndrome has a higher amount of not inflated tissue and lower amount of well inflated tissue. However, the overall regional distribution is similar within the lung. [ABSTRACT FROM AUTHOR]

Pulmonary edema has many causes; differentiating between these conditions is important. The purpose of this review article is to describe the pathophysiology of pulmonary edema, thereby explaining the imaging findings that differentiate between etiologies. Chest computed tomography provides details on the physiological response and the changes in the anatomical structures of pulmonary edema. An understanding of the pathophysiology underlying the imaging findings facilitates the correct identification of the cause of pulmonary edema. [ABSTRACT FROM AUTHOR]

One of the most common causes of death in cats with cardiomyopathy is pulmonary edema. Different forms of feline cardiomyopathies can have a diverse clinical signs. The onset of clinical signs is often related to recent stressful situation such as visiting a clinic or transportation. It is unknown how to identify animals which are predisposing to pulmonary edema and death. The evaluation of literary datahas confirmed that there are insufficient researches in this area. Also it is reliably unknown, which changes in clinical status or on ECHO could be markers of death in cats at cardiogenic pulmonary edema. This article is highlights the topic of estimation of risk assessment of death in cats in case of cardiogenic pulmonary edema. All types of cardiomyopathies were diagnosed in this study. We included cats whose owners addressed the clinic complaining of dyspnoea and worsening of activity. An echocardiographic and radiological examination was performed in the clinic. The authors paid attention to the following markers: the degree of radiological changes in pulmonary parenchyma, data of clinical examinations, the degree of changes of left ventricular and the size of left atrium. It was found that main marker of death in cats at cardiogenic pulmonary edema is the left atrium to aorta more then 2,2. Severe changes in lung parenchyma on X-ray and decrease in left ventricular systolic function also increase the risk of cardiac death in acute heart failure. Left ventricular myocardial thickness and the presence of spontaneous contrast do not affect survival during the first days of hospitalization. Most likely, these changes have more impact on overall life expectancy. [ABSTRACT FROM AUTHOR]

Aims: Evaluation of the efficacy of prehospital non-invasive ventilation (NIV) in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD) and cardiogenic pulmonary edema (CPE).Material and Methods: Consecutive patients who were prehospitally treated by Emergency Physicians using NIV were prospectively included. A step-by-step approach escalating NIV-application from continuous positive airway pressure (CPAP) to continuous positive airway pressure supplemented by pressure support (CPAP-ASB) and finally bilevel inspiratory positive airway pressure (BIPAP) was used. Patients were divided into two groups according to the prehospital NIV-treatment-time (NIV-group 1: ≤15 min, NIV-group 2: >15 min). In addition, a historic control group undergoing standard care was created. Endpoints were heart rate, peripheral oxygen saturation, breathing rate, systolic blood pressure, and a dyspnea score.Results: A total of 99 patients were analyzed (NIV-group 1: n = 41, NIV-group 2: n = 58). The control group consisted of 30 patients. The majority of NIV-patients (90%) received CPAP-ASB, while CPAP without ASB was conducted in 8% and BIPAP-ventilation in 2% of all cases. Technical application of NIV lasted 6.1 ± 3.8 min. NIV-treatment-time was as follows: NIV-group 1: 13.1 ± 3.2 min, NIV-group 2: 22.8 ± 5.9 min. Differences between baseline- and hospital admission values of all endpoints showed significantly better improvement in NIV-groups compared to the control group (p < 0.001). The stabilizing effect of NIV in terms of vital parameters was comparable between both NIV-groups, independent of the duration of treatment (n.s.).Conclusion: Prehospital NIV-treatment should be performed in patients with COPD-exacerbation and CPE, even if the distance between emergency scene and hospital is short. [ABSTRACT FROM AUTHOR]

In contrast to water-soluble respiratory tract irritants in their gas phase, the physicochemical properties of 'hydrophilicity' vs. 'lipophilicity' are the preponderant factors that dictate the site of major retention of the gas at the portal of entry. The lipophilic physical properties of phosgene gas facilitate retention in the alveolar region lined with amphipathic pulmonary surfactant (PS). The relationship between exposure and adverse health outcomes is complex, may vary over time, and is dependent on the biokinetics, biophysics, and pool size of PS relative to the inhaled dose of phosgene. Kinetic PS depletion is hypothesized to occur as inhalation followed by inhaled dose-dependent PS depletion. A kinetic model was developed to better understand the variables characterizing the inhaled dose rates of phosgene vs. PS pool size reconstitution. Modeling and empirical data from published evidence revealed that phosgene gas unequivocally follows a concentration x exposure (C × t) metric, independent of the frequency of exposure. The modeled and empirical data support the hypothesis that the exposure standards of phosgene are described best by a C × t time-averaged metric. Modeled data favorably duplicate expert panel-derived standards. Peak exposures within a reasonable range are of no concern. • Interaction of pulmonary surfactant with phosgene causing a cardiogenic pulmonary edema. • Modeling of the turnover of pulmonary surfactant in rats and humans for risk assessment. • Analysis of adverse interactions of phosgene and anti-ininflammatory glucocorticoids. • Validation of modeled data by comparison of empirical and expert panel derived data. [ABSTRACT FROM AUTHOR]