Pulmonary Edema I: Cardiogenic Pulmonary Edema

2021 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Pulmonary Edema ◽  
Clinical Characteristics ◽  
Distress Syndrome ◽  
Capillary Permeability ◽  
Treatment Options ◽  
Experimental Models ◽  
Lung Mechanics ◽  
Cardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome). This review focuses on cardiogenic pulmonary edema and describes the general approach to patients with suspected cardiogenic pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of cardiogenic pulmonary edema are reviewed. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with cardiogenic pulmonary edema and treatment options. This review contains 3 figures, 4 tables, and 29 references Keywords: cardiogenic pulmonary edema, congestive heart failure, pulmonary edema, Starling’s law

Pulmonary Edema I: Cardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Pulmonary Edema ◽  
Clinical Characteristics ◽  
Distress Syndrome ◽  
Capillary Permeability ◽  
Treatment Options ◽  
Experimental Models ◽  
Lung Mechanics ◽  
Cardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome). This review focuses on cardiogenic pulmonary edema and describes the general approach to patients with suspected cardiogenic pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of cardiogenic pulmonary edema are reviewed. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with cardiogenic pulmonary edema and treatment options. This review contains 3 figures, 4 tables, and 24 references. Key words: cardiogenic pulmonary edema, congestive heart failure, pulmonary edema, Starling’s law

Pulmonary Edema I: Cardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Pulmonary Edema ◽  
Clinical Characteristics ◽  
Distress Syndrome ◽  
Capillary Permeability ◽  
Treatment Options ◽  
Experimental Models ◽  
Lung Mechanics ◽  
Cardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome). This review focuses on cardiogenic pulmonary edema and describes the general approach to patients with suspected cardiogenic pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of cardiogenic pulmonary edema are reviewed. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with cardiogenic pulmonary edema and treatment options. This review contains 3 figures, 4 tables, and 24 references. Key words: cardiogenic pulmonary edema, congestive heart failure, pulmonary edema, Starling’s law

Neutrophil-activating peptide-2 in patients with pulmonary edema from congestive heart failure or ARDS

1993 ◽  
Vol 264 (5) ◽  
pp. L490-L495 ◽  
Author(s):  
A. B. Cohen ◽  
M. D. Stevens ◽  
E. J. Miller ◽  
M. A. Atkinson ◽  
G. Mullenbach ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
High Performance Liquid Chromatography ◽  
Liquid Chromatography ◽  
Pulmonary Edema ◽  
High Performance ◽  
Distress Syndrome ◽  
Normal Subjects ◽  
Antigen Concentration ◽  
Fluid Formation

We carried out studies to determine whether the neutrophil-activation peptide-2 (NAP-2) plays a role in the recruitment and/or degranulation of neutrophils into the lungs of patients with the adult respiratory distress syndrome (ARDS) or congestive heart failure (CHF). NAP-2 precursors plus NAP-2 (beta-thromboglobulin-like antigen) were measured in lung fluids and plasmas with a radioimmunoassay, and NAP-2 was separated from its precursors by high-performance liquid chromatography. Pulmonary edema fluids (PEFs) from patients with CHF contained higher concentrations of the beta-thromboglobulin-like antigen than PEFs from patients with ARDS, and bronchoalveolar lavage fluids (BALs) from patients with ARDS contained higher concentrations of beta-thromboglobulin-like antigen than BALs from normal subjects. beta-Thromboglobulin-like antigen concentration was 4.1-fold greater in PEFs from patients with CHF than in their plasmas. Chemotactically active NAP-2 was also demonstrated in PEFs but not in plasmas from patients with CHF and ARDS. These data suggest that significant platelet degranulation occurred into the lungs of the patients with CHF and that NAP-2 and other platelet constituents may contribute to fluid formation in patients with CHF.

Pulmonary Edema II: Noncardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Diffuse Alveolar Damage ◽  
Lung Resection ◽  
Upper Airway ◽  
Experimental Models ◽  
Lung Mechanics

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome [ARDS]). This review focuses on noncardiogenic pulmonary edema and describes the general approach to patients with suspected pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of noncardiogenic pulmonary edema are reviewed. Miscellaneous causes of pulmonary edema are discussed, including neurologic insults, exposure to high altitude, reexpansion of a collapsed lung, lung transplantation, upper airway obstruction, drugs, and lung resection. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with noncardiogenic pulmonary edema, the definition of ARDS, causes of ARDS, and treatments for ARDS that do not involve ventilation. This review contains 3 figures, 9 tables, and 55 references. Key words: acute respiratory distress syndrome, diffuse alveolar damage, noncardiogenic pulmonary edema, pulmonary edema

Pulmonary Edema II: Noncardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Diffuse Alveolar Damage ◽  
Lung Resection ◽  
Upper Airway ◽  
Experimental Models ◽  
Lung Mechanics

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome [ARDS]). This review focuses on noncardiogenic pulmonary edema and describes the general approach to patients with suspected pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of noncardiogenic pulmonary edema are reviewed. Miscellaneous causes of pulmonary edema are discussed, including neurologic insults, exposure to high altitude, reexpansion of a collapsed lung, lung transplantation, upper airway obstruction, drugs, and lung resection. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with noncardiogenic pulmonary edema, the definition of ARDS, causes of ARDS, and treatments for ARDS that do not involve ventilation. This review contains 3 figures, 9 tables, and 55 references. Key words: acute respiratory distress syndrome, diffuse alveolar damage, noncardiogenic pulmonary edema, pulmonary edema

Peripheral chemoreceptors in health and disease

2004 ◽  
Vol 96 (1) ◽  
pp. 359-366 ◽  
Author(s):  
Nanduri R. Prabhakar ◽  
Ying-Jie Peng
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Defense Mechanism ◽  
Experimental Models ◽  
Cellular Mechanisms ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Oxygen Homeostasis ◽  
Arterial Blood ◽  
Carotid Bodies

Peripheral chemoreceptors (carotid and aortic bodies) detect changes in arterial blood oxygen and initiate reflexes that are important for maintaining homeostasis during hypoxemia. This mini-review summarizes the importance of peripheral chemoreceptor reflexes in various physiological and pathophysiological conditions. Carotid bodies are important for eliciting hypoxic ventilatory stimulation in humans and in experimental animals. In the absence of carotid bodies, compensatory upregulation of aortic bodies as well as other chemoreceptors contributes to the hypoxic ventilatory response. Peripheral chemoreceptors are critical for ventilatory acclimatization at high altitude. They also contribute in part to the exercise-induced hyperventilation, especially with submaximal and heavy exercise. During pregnancy, hypoxic ventilatory sensitivity increases, perhaps due to the actions of estrogen and progesterone on chemoreceptors. Augmented peripheral chemoreceptors have been implicated in early stages of recurrent apneas, congestive heart failure, and certain forms of hypertension. It is likely that chemoreceptors tend to maintain oxygen homeostasis and act as a defense mechanism to prevent the progression of the morbidity associated with these diseases. Experimental models of recurrent apneas, congestive heart failure, and hypertension offer excellent opportunities to unravel the cellular mechanisms associated with altered chemoreceptor function.

Acute Pulmonary Edema Complicating Tonsillectomy and Adenoidectomy

PEDIATRICS ◽  
1985 ◽  
Vol 75 (1) ◽  
pp. 112-114
Author(s):  
ARTHUR N. FEINBERG ◽  
CHARLES L. SHABINO
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Continuous Positive Airway Pressure ◽  
Pulmonary Edema ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Medical Personnel ◽  
Acute Onset ◽  
Respiratory Support ◽  
Acute Pulmonary Edema

In summary, we have presented two cases to illustrate the problem of postoperative pulmonary edema following tonsillectomy and adenoidectomy. Furthermore, we have discussed the difficulty in predicting those patients who will develop this complication. Because of the potential seriousness and unpredictability of acute pulmonary edema following tonsillectomy for chronic obstruction, it is important that medical personnel, including pediatricians caring for patients after tonsillectomy, be able to readily recognize this phenomenon of acute onset of congestive heart failure and treat it rapidly with diuretics, continuous positive airway pressure, and respiratory support as needed.

Management of Hepatic Hemangioendotheliomas of Infancy by Transarterial Embolization: A Report of Two Cases

PEDIATRICS ◽  
1984 ◽  
Vol 73 (4) ◽  
pp. 546-549
Author(s):  
D. H. JOHNSON ◽  
A. M. VINSON ◽  
F. H. WIRTH ◽  
H. J. PRESBERG ◽  
G. HARKINS ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Vascular Malformations ◽  
Transarterial Embolization ◽  
Treatment Options ◽  
Surgical Excision ◽  
Vascular Tumors ◽  
Artery Ligation ◽  
Abdominal Ultrasonography ◽  
Abdominal Masses

Hepatic hemangioendotheliomas are uncommon vascular tumors which present as abdominal masses, unexplained jaundice, bleeding disorders, or congestive heart failure.1-3 Death often results from congestive heart failure despite appropriate treatment with digoxin and diuretics.4 Verification of hepatic vascular malformations rests on selective angiography,5 hepatic scintigraphy,6 computed tomography,7 and abdominal ultrasonography.8 Successful treatment of heart failure depends on elimination of the malformation's left-to-right shunt and its adverse cardiac effects. Present theapeutic recommendations for symptomatic patients remain divided. Treatment options include surgical excision of localized lesions,9 hepatic artery ligation,10 radiation,11 and glucocorticoid therapy12,13, often combinations of these programs are used.

CONGESTIVE HEART FAILURE AND PULMONARY EDEMA

1984 ◽  
pp. 516-552
Author(s):  
GERALD C. TIMMIS ◽  
Douglas C. Westveer ◽  
Timothy A. Nelson ◽  
Andrew M. Hauser ◽  
James R. Stewart ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Pulmonary Edema
Sign in / Sign up

Export Citation Format

Share Document