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Thrombosis Research Jun 2021Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and ultimately necrosis of the lung parenchyma. It is most... (Review)
Review
Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and ultimately necrosis of the lung parenchyma. It is most commonly caused by acute pulmonary embolism (PE), with a reported incidence of around 30%. Following an occlusion of the pulmonary artery, the bronchial arteries are recruited as primary source of perfusion of the pulmonary capillaries. The relatively higher blood pressure in the bronchial circulation causes an increase in the capillary blood flow, leading to extravasation of erythrocytes (i.e. alveolar hemorrhage). If this hemorrhage cannot be resorbed, it results in tissue necrosis and infarction. Different definitions of pulmonary infarction are used in literature (clinical, radiological and histological), although the diagnosis is nowadays mostly based on radiological characteristics. Notably, the infarcted area is only replaced by a fibrotic scar over a period of months. Hence and formally, the diagnosis of pulmonary infarction cannot be confirmed upon diagnosis of acute PE. Little is known of the impact and relevance of pulmonary infarction in acute PE, and whether specific management strategies should be applied to prevent and/or treat complications such as pain, pneumonia or post-PE syndrome. In this review we will summarize current knowledge on the pathophysiology, epidemiology, diagnosis and prognosis of pulmonary infarction in the setting of acute PE. We highlight the need for dedicated studies to overcome the current knowledge gaps.
Topics: Acute Disease; Humans; Lung; Pulmonary Artery; Pulmonary Embolism; Pulmonary Infarction
PubMed: 33862471
DOI: 10.1016/j.thromres.2021.03.022 -
Vascular Health and Risk Management 2021The causes and mechanisms of increased cardiac troponin T and I (cTnT and cTnI) concentrations are numerous and are not limited to acute myocardial infarction (AMI)... (Review)
Review
The Main Causes and Mechanisms of Increase in Cardiac Troponin Concentrations Other Than Acute Myocardial Infarction (Part 1): Physical Exertion, Inflammatory Heart Disease, Pulmonary Embolism, Renal Failure, Sepsis.
The causes and mechanisms of increased cardiac troponin T and I (cTnT and cTnI) concentrations are numerous and are not limited to acute myocardial infarction (AMI) (ischemic necrosis of cardiac myocytes). Any type of reversible or irreversible cardiomyocyte injury can result in elevated serum cTnT and cTnI levels. Researchers and practitioners involved in the diagnosis and treatment of cardiovascular disease, including AMI, should know the key causes and mechanisms of elevated serum cTnT and cTnI levels. This will allow to reduce or completely avoid diagnostic errors and help to choose the most correct tactics for further patient management. The purpose of this article is to discuss the main causes and mechanisms of increase in cardiac troponins concentrations in frequently occurring physiological (physical exertion, psycho-emotional stress) and pathological conditions (inflammatory heart disease, pulmonary embolism, chronic renal failure and sepsis (systemic inflammatory response)) not related to myocardial infarction.
Topics: Acute Disease; Biomarkers; Humans; Myocardial Infarction; Physical Exertion; Pulmonary Embolism; Pulmonary Heart Disease; Renal Insufficiency; Sepsis; Troponin; Troponin I; Troponin T
PubMed: 34584417
DOI: 10.2147/VHRM.S327661 -
CASE (Philadelphia, Pa.) Feb 2024Two-dimensional transthoracic echocardiogram, short axis view of the main pulmonary artery (MPA, ) demonstrates a saddle pulmonary embolism (PE) with the highly...
Two-dimensional transthoracic echocardiogram, short axis view of the main pulmonary artery (MPA, ) demonstrates a saddle pulmonary embolism (PE) with the highly correlative axial display from the contrast-enhanced computed tomography scan (). , aorta; , pulmonary artery (From Graphical Abstract, , Eugene Yuriditsky, MD )Graphical abstractTwo-dimensional transthoracic echocardiogram, short axis view of the main pulmonary artery (MPA, ) demonstrates a saddle pulmonary embolism (PE) with the highly correlative axial display from the contrast-enhanced computed tomography scan (). , aorta; , pulmonary artery (From Graphical Abstract, , Eugene Yuriditsky, MD ).
PubMed: 38425572
DOI: 10.1016/j.case.2023.12.024 -
La Revue de Medecine Interne Oct 2019Oxygen therapy is used to reverse hypoxemia since more than a century. Current usage is broader and includes routine oxygen administration despite normoxemia which may... (Review)
Review
Oxygen therapy is used to reverse hypoxemia since more than a century. Current usage is broader and includes routine oxygen administration despite normoxemia which may result in prolonged periods of hyperoxemia. While systematic oxygen therapy was expected to be of benefit in some ischemic diseases such as stroke or acute myocardial infarction, recent randomised controlled trials (RCTs) have challenged this hypothesis by showing the absence of clinical improvement. Although oxygen is known to be toxic at high inspired oxygen fractions, a recent meta-analysis of RCTs revealed the life-threatening effect of hyperoxemia, with a dose-dependent relationship. Several recommendations have therefore been updated: (i) to monitor peripheral oxygen saturation (SpO) as a surrogate for arterial oxygen saturation (SaO); (ii) to initiate oxygen only when the lower SpO threshold is crossed; (iii) to titrate the delivered oxygen fraction to maintain SpO within a target range; and (iv) to stop supplying oxygen when the upper limit of SpO is surpassed, in order to prevent hyperoxemia. The lower and upper limits of SpO depend on the presence of risk factors for oxygen-induced hypercapnia (Chronic obstructive pulmonary disease, asthma, and obesity-associated hypoventilation). For patients at risk, oxygen therapy should be started when SpO is≤88% and stopped when it is>92%. For patients without risk factors, oxygen therapy should be started when SpO is≤92% and stopped when it is >96%. High-flow oxygen should only be used in a few diseases such as carbon monoxide poisoning, cluster headaches, sickle cell crisis and pneumothorax.
Topics: Acute Disease; Cell Hypoxia; Heart Arrest; Humans; Hypercapnia; Hyperoxia; Hypoxia; Myocardial Infarction; Oxygen; Oxygen Inhalation Therapy; Partial Pressure; Practice Guidelines as Topic; Pulmonary Disease, Chronic Obstructive; Reference Values; Respiratory Insufficiency; Risk Factors; Sepsis; Stroke
PubMed: 31054779
DOI: 10.1016/j.revmed.2019.04.003 -
Open Access Emergency Medicine : OAEM 2019Shock index (SI) is defined as the heart rate (HR) divided by systolic blood pressure (SBP). It has been studied in patients either at risk of or experiencing shock from...
Shock index (SI) is defined as the heart rate (HR) divided by systolic blood pressure (SBP). It has been studied in patients either at risk of or experiencing shock from a variety of causes: trauma, hemorrhage, myocardial infarction, pulmonary embolism, sepsis, and ruptured ectopic pregnancy. While HR and SBP have traditionally been used to characterize shock in these patients, they often appear normal in the compensatory phase of shock and can be confounded by factors such as medications (eg, antihypertensives, beta-agonists). SI >1.0 has been widely found to predict increased risk of mortality and other markers of morbidity, such as need for massive transfusion protocol activation and admission to intensive care units. Recent research has aimed to study the use of SI in patients immediately on arrival to the emergency department (ED). In this review, we summarize the literature pertaining to use of SI across a variety of settings in the management of ED patients, in order to provide context for use of this measure in the triage and management of critically ill patients.
PubMed: 31616192
DOI: 10.2147/OAEM.S178358 -
Thrombosis Research Jul 2020COVID-19 may predispose to both venous and arterial thromboembolism due to excessive inflammation, hypoxia, immobilisation and diffuse intravascular coagulation. Reports...
INTRODUCTION
COVID-19 may predispose to both venous and arterial thromboembolism due to excessive inflammation, hypoxia, immobilisation and diffuse intravascular coagulation. Reports on the incidence of thrombotic complications are however not available.
METHODS
We evaluated the incidence of the composite outcome of symptomatic acute pulmonary embolism (PE), deep-vein thrombosis, ischemic stroke, myocardial infarction or systemic arterial embolism in all COVID-19 patients admitted to the ICU of 2 Dutch university hospitals and 1 Dutch teaching hospital.
RESULTS
We studied 184 ICU patients with proven COVID-19 pneumonia of whom 23 died (13%), 22 were discharged alive (12%) and 139 (76%) were still on the ICU on April 5th 2020. All patients received at least standard doses thromboprophylaxis. The cumulative incidence of the composite outcome was 31% (95%CI 20-41), of which CTPA and/or ultrasonography confirmed VTE in 27% (95%CI 17-37%) and arterial thrombotic events in 3.7% (95%CI 0-8.2%). PE was the most frequent thrombotic complication (n = 25, 81%). Age (adjusted hazard ratio (aHR) 1.05/per year, 95%CI 1.004-1.01) and coagulopathy, defined as spontaneous prolongation of the prothrombin time > 3 s or activated partial thromboplastin time > 5 s (aHR 4.1, 95%CI 1.9-9.1), were independent predictors of thrombotic complications.
CONCLUSION
The 31% incidence of thrombotic complications in ICU patients with COVID-19 infections is remarkably high. Our findings reinforce the recommendation to strictly apply pharmacological thrombosis prophylaxis in all COVID-19 patients admitted to the ICU, and are strongly suggestive of increasing the prophylaxis towards high-prophylactic doses, even in the absence of randomized evidence.
Topics: Acute Disease; Anticoagulants; Arterial Occlusive Diseases; Brain Ischemia; COVID-19; Coronavirus Infections; Critical Illness; Embolism; Female; Hospitals, Teaching; Hospitals, University; Humans; Incidence; Male; Middle Aged; Myocardial Infarction; Netherlands; Pandemics; Pneumonia, Viral; Pulmonary Embolism; Thrombophilia; Venous Thrombosis
PubMed: 32291094
DOI: 10.1016/j.thromres.2020.04.013 -
QJM : Monthly Journal of the... Oct 2019Influenza viruses infect the upper respiratory system, causing usually a self-limited disease with mild respiratory symptoms. Acute lung injury, pulmonary microvascular... (Review)
Review
Influenza viruses infect the upper respiratory system, causing usually a self-limited disease with mild respiratory symptoms. Acute lung injury, pulmonary microvascular leakage and cardiovascular collapse may occur in severe cases, usually in the elderly or in immunocompromised patients. Acute lung injury is a syndrome associated with pulmonary oedema, hypoxaemia and respiratory failure. Influenza virus primarily binds to the epithelium, interfering with the epithelial sodium channel function. However, the main clinical devastating effects are caused by endothelial dysfunction, thought to be the main mechanism leading to pulmonary oedema, respiratory failure and cardiovascular collapse. A significant association was found between influenza infection and acute myocardial infarction (AMI). The incidence of admission due to AMI during an acute viral infection was six times as high during the 7 days after laboratory confirmation of influenza infection as during the control interval (10-fold in influenza B, 5-fold in influenza A, 3.5-fold in respiratory syncytial virus and 2.7-fold for all other viruses). Our review will focus on the mechanisms responsible for endothelial dysfunction during influenza infection leading to cardiovascular collapse and death.
Topics: Acute Lung Injury; Atherosclerosis; Endothelium, Vascular; Humans; Influenza, Human; Myocardial Infarction; Orthomyxoviridae
PubMed: 30605546
DOI: 10.1093/qjmed/hcy305 -
Emergency Medicine Clinics of North... May 2023The physiologic changes in pregnancy predispose the pregnant patient to a variety of potential cardiovascular complications. In this article, we discuss the major... (Review)
Review
The physiologic changes in pregnancy predispose the pregnant patient to a variety of potential cardiovascular complications. In this article, we discuss the major cardiovascular disorders of pregnancy and their management, highlight specific diagnostic challenges, and discuss new developments in the field. Topics covered in this article include venous thromboembolism, acute myocardial infarction, peripartum cardiomyopathy, and aortic dissection.
Topics: Pregnancy; Female; Humans; Myocardial Infarction; Cardiomyopathies; Aortic Dissection; Venous Thromboembolism; Pregnancy Complications, Cardiovascular
PubMed: 37024161
DOI: 10.1016/j.emc.2023.01.005 -
Expert Review of Respiratory Medicine 2023Given the heterogeneity of predisposing factors associated with pulmonary infarction (PI) and the lack of clinically relevant outcomes among patients with acute...
BACKGROUND
Given the heterogeneity of predisposing factors associated with pulmonary infarction (PI) and the lack of clinically relevant outcomes among patients with acute pulmonary embolism (PE) complicated by PI, further investigation is required.
METHODS
Retrospective study of patients with central PE in an 11-year period. Data were stratified according to the diagnosis of PI. Multivariable logistic regression analysis was used to analyze factors associated with PI development and determine if PI was associated with severe hypoxemic respiratory failure and mechanical ventilation use.
RESULTS
Of 645 patients with central PE, 24% ( = 156) had PI. After adjusting for demographics, comorbidities, and clinical features on admission, only age (OR 0.98, CI 0.96-0.99; = 0.008) was independently associated with PI. Regarding outcomes, 35% ( = 55) had severe hypoxemic respiratory failure, and 19% ( = 29) required mechanical ventilation. After adjusting for demographics, PE severity, and right ventricular dysfunction, PI was independently associated with severe hypoxemic respiratory failure (OR 1.78; CI 1.18-2.69, = 0.005) and mechanical ventilation (OR 1.92; CI 1.14-3.22, = 0.013).
CONCLUSIONS
Aging is a protective factor against PI. In acute central PE, subjects with PI had higher odds of developing severe hypoxemic respiratory failure and requiring mechanical ventilation.
Topics: Humans; Retrospective Studies; Pulmonary Infarction; Respiratory Insufficiency; Pulmonary Embolism; Respiration, Artificial; Acute Disease
PubMed: 37750314
DOI: 10.1080/17476348.2023.2263359