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Journal of Cardiothoracic and Vascular... Apr 2018Pulmonary edema increasingly is recognized as a perioperative complication affecting outcome. Several risk factors have been identified, including those of cardiogenic... (Review)
Review
Pulmonary edema increasingly is recognized as a perioperative complication affecting outcome. Several risk factors have been identified, including those of cardiogenic origin, such as heart failure or excessive fluid administration, and those related to increased pulmonary capillary permeability secondary to inflammatory mediators. Effective treatment requires prompt diagnosis and early intervention. Consequently, over the past 2 centuries a concentrated effort to develop clinical tools to rapidly diagnose pulmonary edema and track response to treatment has occurred. The ideal properties of such a tool would include high sensitivity and specificity, easy availability, and the ability to diagnose early accumulation of lung water before the development of the full clinical presentation. In addition, clinicians highly value the ability to precisely quantify extravascular lung water accumulation and differentiate hydrostatic from high permeability etiologies of pulmonary edema. In this review, advances in understanding the physiology of extravascular lung water accumulation in health and in disease and the various mechanisms that protect against the development of pulmonary edema under physiologic conditions are discussed. In addition, the various bedside modalities available to diagnose early accumulation of extravascular lung water and pulmonary edema, including chest auscultation, chest roentgenography, lung ultrasonography, and transpulmonary thermodilution, are examined. Furthermore, advantages and limitations of these methods for the operating room and intensive care unit that are critical for proper modality selection in each individual case are explored.
Topics: Extravascular Lung Water; Humans; Lung; Pulmonary Edema; Radiography, Thoracic; Thermodilution
PubMed: 29174750
DOI: 10.1053/j.jvca.2017.08.028 -
The American Journal of the Medical... Dec 2019The initial events in cardiogenic pulmonary edema involve hemodynamic pulmonary congestion with high capillary pressures. This causes increased fluid transfer out of... (Review)
Review
The initial events in cardiogenic pulmonary edema involve hemodynamic pulmonary congestion with high capillary pressures. This causes increased fluid transfer out of capillaries into the interstitium and alveolar spaces. High capillary pressures can also cause barrier disruption which increases permeability and fluid transfer into the interstitium and alveoli. Fluid in alveoli alters surfactant function and increases surface tension. This can lead to more edema formation and to atelectasis with impaired gas exchange. Patients with barrier disruption have increased levels of surfactant protein B in the circulation, and these levels often remain high after the initial clinical improvement. Routine clinical assessment may not identify patients with increased extravascular fluid in the lungs; pulmonary ultrasound can easily detect pulmonary edema in patients with acute decompensation and in patients at risk for decompensation. Studies using serial pulmonary ultrasound could help characterize patients with cardiogenic pulmonary edema and help identify subgroups who need alternative management. The conventional management of cardiogenic pulmonary edema usually involves diuresis, afterload reduction and in some cases noninvasive ventilation to reduce the work of breathing and improve oxygenation. Patients with persistent symptoms, abnormal chest x-rays and diuretic resistance might benefit from alternative approaches to management. These could include beta agonists and pentoxifylline which warrant more study in patients with cardiogenic pulmonary edema.
Topics: Body Fluids; Heart; Humans; Pulmonary Edema; Ultrasonography
PubMed: 31813466
DOI: 10.1016/j.amjms.2019.09.011 -
Journal of Veterinary Emergency and... Mar 2023To review various types of noncardiogenic pulmonary edema (NCPE) in cats and dogs. (Review)
Review
OBJECTIVE
To review various types of noncardiogenic pulmonary edema (NCPE) in cats and dogs.
ETIOLOGY
NCPE is an abnormal fluid accumulation in the lung interstitium or alveoli that is not caused by cardiogenic causes or fluid overload. It can be due to changes in vascular permeability, hydrostatic pressure in the pulmonary vasculature, or a combination thereof. Possible causes include inflammatory states within the lung or in remote tissues (acute respiratory distress syndrome [ARDS]), airway obstruction (post-obstructive pulmonary edema), neurologic disease such as head trauma or seizures (neurogenic pulmonary edema), electrocution, after re-expansion of a collapsed lung or after drowning.
DIAGNOSIS
Diagnosis of NCPE is generally based on history, physical examination, and diagnostic imaging. Radiographic findings suggestive of NCPE are interstitial to alveolar pulmonary opacities in the absence of signs of left-sided congestive heart failure or fluid overload such as cardiomegaly or congested pulmonary veins. Computed tomography and edema fluid analysis may aid in the diagnosis, while some forms of NCPE require additional findings to reach a diagnosis.
THERAPY
The goal of therapy for all types of NCPE is to preserve tissue oxygenation and reduce the work of breathing. This may be achieved by removing the inciting cause (eg, airway obstruction) and cage rest in mild cases and supplemental oxygen in moderate cases and may require mechanical ventilation in severe cases.
PROGNOSIS
Prognosis is generally good for most causes of veterinary NCPE except for ARDS, although data are scarce for some etiologies of NCPE.
Topics: Pulmonary Edema; Animals; Cats; Dogs; Dog Diseases; Cat Diseases; Respiratory Distress Syndrome; Transfusion-Related Acute Lung Injury; Electric Injuries; Airway Obstruction
PubMed: 36815753
DOI: 10.1111/vec.13278 -
Seminars in Respiratory and Critical... Feb 2019Acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure caused by noncardiogenic pulmonary edema. Despite five decades of basic and... (Review)
Review
Acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure caused by noncardiogenic pulmonary edema. Despite five decades of basic and clinical research, there is still no effective pharmacotherapy for this condition and the treatment remains primarily supportive. It is critical to study the molecular and physiologic mechanisms that cause ARDS to improve our understanding of this syndrome and reduce mortality. The goal of this review is to describe our current understanding of the pathogenesis and pathophysiology of ARDS. First, we will describe how pulmonary edema fluid accumulates in ARDS due to lung inflammation and increased alveolar endothelial and epithelial permeabilities. Next, we will review how pulmonary edema fluid is normally cleared in the uninjured lung, and describe how these pathways are disrupted in ARDS. Finally, we will explain how clinical trials and preclinical studies of novel therapeutic agents have further refined our understanding of this condition, highlighting, in particular, the study of mesenchymal stromal cells in the treatment of ARDS.
Topics: Humans; Mesenchymal Stem Cells; Pulmonary Edema; Respiratory Distress Syndrome
PubMed: 31060086
DOI: 10.1055/s-0039-1683996 -
Advances in Respiratory Medicine Oct 2023Cardiogenic pulmonary edema (CPE) is characterized by the development of acute respiratory failure associated with the accumulation of fluid in the lung's alveolar... (Review)
Review
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.
Topics: Humans; Pulmonary Edema; Lung; Heart Failure; Oxygen; Vasodilator Agents; Emergency Medicine
PubMed: 37887077
DOI: 10.3390/arm91050034 -
Revue Medicale de Liege May 2018Acute heart failure is a common cause of admission in emergency department. Management requires rapid support when haemodynamic or respiratory parameters are altered.... (Review)
Review
Acute heart failure is a common cause of admission in emergency department. Management requires rapid support when haemodynamic or respiratory parameters are altered. Identifying enabling factors and their specific treatment is an integral part of management. The most common clinical presentation is volume overload, whose treatment remains the combination of diuretics and vasodilators. In case of impaired perfusion, various inotropic supports may be considered, but also more and more circulatory assistance devices.
Topics: Acute Disease; Algorithms; Diuretics; Heart Failure; Humans; Pulmonary Edema; Vasodilator Agents
PubMed: 29926563
DOI: No ID Found -
Intensive Care Medicine Oct 2022In critically ill patients, fluid infusion is aimed at increasing cardiac output and tissue perfusion. However, it may contribute to fluid overload which may be harmful.... (Review)
Review
In critically ill patients, fluid infusion is aimed at increasing cardiac output and tissue perfusion. However, it may contribute to fluid overload which may be harmful. Thus, volume status, risks and potential efficacy of fluid administration and/or removal should be carefully evaluated, and monitoring techniques help for this purpose. Central venous pressure is a marker of right ventricular preload. Very low values indicate hypovolemia, while extremely high values suggest fluid harmfulness. The pulmonary artery catheter enables a comprehensive assessment of the hemodynamic profile and is particularly useful for indicating the risk of pulmonary oedema through the pulmonary artery occlusion pressure. Besides cardiac output and preload, transpulmonary thermodilution measures extravascular lung water, which reflects the extent of lung flooding and assesses the risk of fluid infusion. Echocardiography estimates the volume status through intravascular volumes and pressures. Finally, lung ultrasound estimates lung edema. Guided by these variables, the decision to infuse fluid should first consider specific triggers, such as signs of tissue hypoperfusion. Second, benefits and risks of fluid infusion should be weighted. Thereafter, fluid responsiveness should be assessed. Monitoring techniques help for this purpose, especially by providing real time and precise measurements of cardiac output. When decided, fluid resuscitation should be performed through fluid challenges, the effects of which should be assessed through critical endpoints including cardiac output. This comprehensive evaluation of the risk, benefits and efficacy of fluid infusion helps to individualize fluid management, which should be preferred over a fixed restrictive or liberal strategy.
Topics: Cardiac Output; Critical Illness; Fluid Therapy; Hemodynamics; Humans; Pulmonary Edema; Thermodilution
PubMed: 35945344
DOI: 10.1007/s00134-022-06808-9 -
Current Opinion in Critical Care Aug 2019This review summarizes current understanding of the pathophysiology of cardiogenic pulmonary edema, its causes and treatment. (Review)
Review
PURPOSE OF REVIEW
This review summarizes current understanding of the pathophysiology of cardiogenic pulmonary edema, its causes and treatment.
RECENT FINDINGS
The pathobiology and classification of pulmonary edema is more complex than the hydrostatic vs. permeability dichotomy of the past. Mechanisms of alveolar fluid clearance and factors that affect the clearance rate are under intensive study to find therapeutic strategies. Patients need early stabilization of oxygenation and ventilation, preferably with high-flow nasal cannula oxygen or noninvasive ventilation whereas the diagnostic cause is quickly sought with echocardiography and other testing.
SUMMARY
Treatments must be initiated early, whereas evaluation still is occurring and requires multimodality intervention. The general treatment of cardiogenic pulmonary edema includes diuretics, possibly morphine and often nitrates. The appropriate use of newer approaches - such as, nesiritide, high-dose vasodilators, milrinone, and vasopressin receptor antagonists - needs larger clinical trials.
Topics: Heart Diseases; Humans; Pulmonary Edema
PubMed: 31116110
DOI: 10.1097/MCC.0000000000000626 -
Hematology. American Society of... Nov 2018Transfusion-related acute lung injury (TRALI) and transfusion-associated circulatory overload (TACO) are the leading causes of transfusion-related morbidity and... (Review)
Review
Transfusion-related acute lung injury (TRALI) and transfusion-associated circulatory overload (TACO) are the leading causes of transfusion-related morbidity and mortality. These adverse events are characterized by acute pulmonary edema within 6 hours of a blood transfusion and have historically been difficult to study due to underrecognition and nonspecific diagnostic criteria. However, in the past decade, in vivo models and clinical studies utilizing active surveillance have advanced our understanding of their epidemiology and pathogenesis. With the adoption of mitigation strategies and patient blood management, the incidence of TRALI and TACO has decreased. Continued research to prevent and treat these severe cardiopulmonary events is focused on both the blood component and the transfusion recipient.
Topics: Blood Transfusion; Female; Humans; Male; Pulmonary Edema; Transfusion-Related Acute Lung Injury
PubMed: 30570487
DOI: 10.1182/asheducation-2018.1.585 -
Chest May 2021
Topics: Humans; Immersion; Pulmonary Edema
PubMed: 33965126
DOI: 10.1016/j.chest.2020.12.017