Edema In Congestive Heart Failure Research Articles

123 Deep-Learning Generated B-Line Score Mirrors Clinical Progression of Disease for Patients Admitted With Shortness of Breath or Hypoxia

Thoracic ultrasound can evaluate the lungs for fluid in the alveolar and interstitial spaces of the lung, based on the presence of artifacts known as B-lines. Degree of B-lines may provide an independent measure of severity of pulmonary edema in congestive heart failure. Artificial intelligence can be used to provide objective data, improve interpretations by novice users, and allow processing of large amount of data for research. The aim of this study is to determine the association between a B-line score using a deep learning algorithm with the degree of pulmonary congestion based on clinical assessment and its variation with response to treatment. This single-center, prospective, observational study enrolled adult patients presenting with dyspnea or hypoxia and suspected to have congestive heart failure at an urban academic ED from July 2018 to May 2019. Subjects found to have any B-lines on initial lung ultrasound were followed through their hospital course and included in this analysis. Admitted patients underwent daily ultrasonography. Clips of 8 lung zones (right and left anterior/lateral and superior/inferior) were obtained using the Philips LumifyTM ultrasound system with sector probe. Demographics, vital signs, lab values, and imaging results were also collected. A previously published deep learning algorithm was refined to rate the severity of B-lines on a scale of 0-4 in 0.5 increments. Average severity for all 8 zones at each time-point for each patient was calculated. A clinical congestion score (0-18 scale), based on presence of dyspnea, orthopnea, fatigue, JVD, rales and pedal edema was calculated. Mixed effects modeling was used to investigate the association between B-line score as independent variable and clinical congestion score as dependent variable, accounting for variation on the person level and longitudinal data. Missing data was excluded from analysis. Covariates tested included patient and exam level data (sex, age, presence of selected comorbidities, baseline sodium and hemoglobin, creatinine, vital signs, oxygen delivery amount and delivery method, diuretic dose). There were 242 unique subjects with 722 complete sets of 8-zone clips included in the analysis. For the mixed effects model, chosen covariates were: sex, baseline sodium, baseline hemoglobin, respiratory rate, CHF, chronic obstructive pulmonary disease, fraction of inspired oxygen, oxygen delivery method (eg, nasal cannula, non-rebreather, ventilator), total loop diuretic dose on day of exam, and the 8-zone DL obtained B-line score. There was no collinearity. The 8-zone B-line score was significantly associated with clinical congestions core, with coefficient of 0.73 (p<0.001). A deep learning generated B-line score mirrors clinical course for subjects admitted patients with shortness of breath or hypoxia, independent of other patient and clinical factors. B-line quantification using AI can provide an objective and independent measure of pulmonary congestion in patients with congestive heart failure and can be used to help monitor clinical progress.

Nova uloga spironolaktona u terapijskom pristupu rezistentnoj hipertenziji - spironolakton u terapiji rezistentne hipertenzije

Spironolactone is a competitive nonselective mineralocorticoid receptor blocker with high affinity for aldosterone; therefore, it is widely used as a diuretic and antihypertensive. Because of these properties it is used in the treatment of edema in congestive heart failure, liver cirrhosis with ascites and edema, nephrotic syndrome, malignant ascites, severe heart failure and primary hyperaldosteronism. Spironolactone is recommended for the treatment of resistant hypertension. Narrative review aims to present the pharmacodynamic and pharmacokinetic profile of spironolactone, and describe its position in the treatment of resistant hypertension.

Congestive Heart Failure versus Inflammatory Carcinoma in Breast.

Inflammatory breast cancer is a rare highly malignant form of breast cancer. Clinical signs and symptoms with histologic examination usually confirm the diagnosis. There are rare reports of breast edema of congestive heart failure which were difficult to differentiate from inflammatory carcinoma. The differential becomes more difficult when congestive heart failure is associated with unilateral breast edema. We present a case of a 70-year-old woman with congestive heart failure associated with unilateral breast edema and skin thickening simulating inflammatory breast carcinoma on mammography.

Impaired Ca 2+ ‐signaling protects lungs from development of severe hydrostatic lung edema in congestive heart failure (CHF)

Impaired Ca ²⁺ ‐signaling protects lungs from development of severe hydrostatic lung edema in congestive heart failure (CHF)

Historical Perspectives

When pharmacologic closure of patent ductus arteriosus (PDA) in the preterm infant using indomethacin was introduced in 1976, there was a paucity of knowledge about the factors controlling the caliber of the ductus arteriosus both before and after birth. Additionally, mortality and morbidity of prematurity (associated with what was then usually referred to as hyaline membrane disease) was remarkably high in the early 1970s. As early as the 1950s, some neonatologists recognized PDA as a complication of what later became designated as “respiratory distress syndrome” (RDS), although it was not until the advent of intermittent mandatory ventilation (IMV) and continuous positive airway pressure (CPAP) that the concept gained prominence. Patency of the ductus appeared to be a major complication, especially in the smallest of preterm babies (at that time, < 1,350 g]) and usually carried a terminal prognosis. The advent of IMV and CPAP kept these small babies alive for a sufficient period of time for the patent ductus to become recognized progressively as a distinct clinical entity and an important early complication of preterm birth. Observant neonatologists noted that babies who had RDS often improved up to a point, beyond which they worsened. The usual story was that the baby experienced ventilatory failure, was treated with mechanical ventilation, and began to improve, with lower inspired oxygen requirements. After a few days, when discussions ensued about taking the baby off the ventilator, the infant’s improvement would cease. The radiographic picture changed from a clearing of the initial ground glass appearance coupled with a relatively small heart to an enlarging heart and the pulmonary edema of congestive heart failure due to a left-to-right shunt across the PDA. Beginning in the mid-1960s, aggressive surgeons advocated operative closure of the PDA in these small preterm infants, but multiple centers consistently reported unacceptably high …

Effects of supplemental oxygen on forearm vasodilation in humans.

Supplemental O2 reduces cardiac output and raises systemic vascular resistance in congestive heart failure. In this study, 100% O2 was given to normal subjects and peak forearm flow was measured. In experiment 1, 100% O2 reduced blood flow and increased resistance after 10 min of forearm ischemia (flow 56.7 +/- 7.9 vs. 47.8 +/- 6.7 ml.min-1.100 ml-1; P < 0.02; vascular resistance 1.7 +/- 0.2 vs. 2.4 +/- 0.4 mmHg.min.100 ml.ml-1; P < 0.03). In experiment 2, lower body negative pressure (LBNP; -30 mmHg) and venous congestion (VC) simulated the high sympathetic tone and edema of congestive heart failure. Postischemic forearm flow and resistance were measured under four conditions: room air breathing (RA); LBNP+RA; RA+LBNP+VC; and 100% O2+LBNP+VC. LBNP and VC did not lower peak flow. However, O2 raised minimal resistance (2.3 +/- 0.4 RA; 2.8 +/- 0.5 O2+LBNP+VC, P < 0.04). When O2 alone (experiment 1) was compared with O2+LBNP+VC (experiment 2), no effect of LBNP+VC on peak flow or minimum resistance was noted, although the return rate of flow and resistance toward baseline was increased. O2 reduces peak forearm flow even in the presence of LBNP and VC.

Mammographic and Sonographic Findings of Unilateral Breast Edema in Congestive Heart Failure: A Case Report

Unilateral breast edema has many causes, though among these, congestive heart failure is rare. We report mamographic and sonographic findings of unilateral breast edema due to congestive heart failure. Mammography showed diffuse increase density and skin thickening but no evidence of mass or calcification. Ultrasonography showed skin thickening and increased echogenicity in the subcutaneous fat layer, while in the dermal layer, with tubular and reticular anechoic structures sugestive of dilated lymphatics were seen . After treatment of the heart failure, resolution of the abnormalities seen on mammogram established that these were secondary findings.

Diuretic Treatment for the Sodium Retention of Congestive Heart Failure

The use of diuretics for the treatment of sodium retention in congestive heart failure was evaluated. Particular focus was given to the altered renal response to diuretics in patients with heart failure and adverse responses to diuretic therapy. Highlighted information included historical aspects of the development of diuretics, mechanisms of sodium retention, the physiologic and clinical response to diuretics, and the altered pharmacokinetics and pharmacodynamics of diuretics in congestive heart failure. Despite more than 60 years of empiric diuretic use in heart failure, the actual database regarding the long-term efficacy, adverse effects, and altered mortality outcome in heart failure is relatively small. Existent pharmacokinetic and pharmacodynamic data are typically not collected within the context of heart failure efficacy trials. In addition to altered electrolyte transport and total-body electrolyte depletion, diuretics may be associated with adverse neurohormonal activation. Thus, guidelines for acute and long-term therapy with diuretics in heart failure remain somewhat empiric. Diuretics will remain a mainstay for the treatment of edema in congestive heart failure but must be accompanied by moderate sodium restriction. However, large clinical trials of diuretics would be necessary to demonstrate that improved clinical efficacy with edema reduction is not offset by adverse effects, which include electrolyte depletion, ventricular arrhythmias, and subsequent increased mortality.

Unilateral Breast Edema in Congestive Heart Failure - A Mimic of Diffuse Carcinoma

Mammography in a patient with congestive heart failure showed unilateral skin thickening and a reticular pattern mimicking diffuse carcinoma. Resolution after treatment of the heart failure established the abnormality as secondary to dependent edema.

Transcapillary Oncotic Pressure in the Edema of Congestive Heart Failure

Tissue fluid and plasma oncotic pressure levels were measured in an unselected group of 13 patients presenting with congestive heart failure. Patients had a mean serum albumin of 3.6 g/dl +/- (SD) 0.35; serum oncotic pressure was 22.23 +/- 1.8 mm Hg; tissue fluid (lower leg) oncotic pressure was 0.985 +/- 0.34 mm Hg. The oncotic pressure gradient between plasma and tissue fluid was 21.25 Hg +/- 1.7. This is about 10 mm Hg greater than delta pi in normal man. The high value in congestive heart failure is a mechanism to protect against the formation of edema. The possible mechanisms responsible for the formation of edema in congestive heart failure are discussed.

Endocrine factors in congestive heart failure

HERE IS impressive evidence that patients with congestive heart failure fail to excrete sodium and lack ability to maintain sodium balance. The evidence is both clinical and experimental. First, it is a basic clinical fact that a diet severely restricted in sodium will improve the condition of patients with congestive heart failure and that salt loads will aggravate it. Braunwald et al. l have recently devised a sodium tolerance test that clearly demonstrates the inability of patients with congestive heart failure to excrete a salt load. Similar findings were observed by Barge? in dogs with congestive heart failure induced experimentally by pulmonary stenosis and tricuspid insufficiency. Tricuspid insufficiency alone in dogs produced a rise in right atria1 pressure with definite al.terations in sodium excretion but without signs of congestive heart failure. However, the combination of tricuspid insufficiency and pulmonary artery stenosis in dogs results in a state of congestive heart failure similar to that seen in man with failure to excrete salt loads. In such an animal preparation, an infusion of 3.5 per cent sodium chloride solution directly into one renal artery produces no rise in sodium excretion, in contrast to the findings in similar experiments, performed in a normal dog. This failure of sodium excretion occurs without any change in the rate of glomerular filtration. These findings are convincing evidence of the increased tubular rea.bsorption of sodium in dogs with congestive heart failure. Second, a normal rate of glomerular filtration has been found in a number of patients with frank congestive heart failure.3s4 Bradley and Blake4 emphasized the absence of any significant change in this rate in many patients during or after recovery from congestive heart failure. They pointed out that in some patients the rate of glomerular filtration even fell during recovery without in any way preventing the diuretic response to therapy. It should also be recalled that in many cases of parenchymatous renal diseases, such as nephrosclerosis, pyelonephritis or glomerulonephritis, the rate of glomerular filtration may be extremely low without any evidence of edema formation. These observations again indicate the importance of increased tubular reabsorption of sodium in the pathogenesis of edema in congestive heart failure. Third, many investigators have emphasized the low concentration of sodium in the urine, sweat and saliva of patients with congestive heart failure, thereby indicating the presence of increased mineralocorticoid activity in the blood. Fourth, detailed studies of renal hemodynamics

The role of aldosterone in the pathogenesis of congestive heart failure.

The effect of aldosterone on electrolytes and water diuresis was examined on 3 groups of human and dog, i.e. normal, mild heart disease and congestive failure.In control group, the administration of d-aldosterone prior to mannitol or saline infusion led to a large amount of potassium diuresis but did not decrease sodium excretion in urine. This phenomenon is regarded as the initial effect of aldosterone for electrolytes and water diuresis.In patients and dogs with heart disease without edema, however, aldosterone showed differential effects between mannitol and saline infusion. By mannitol, potassium excretion was unchanged despite reduced sodium excretion, but by saline the former was increased and the latter was unchanged.In patients and dogs with congestive heart failure, whether on mannitol or on saline, the pre-treatment of aldosterone minimized the sodium excretion in urine, but the potassium excretion was almost as same as that in normal cases and in mild heart disease.These observations lead to the following conclusions.(1) The increased aldosterone secretion itself is not the only necessary cause of edema.(2) The sodium in renal tubules is reabsorbed by 2 ways; one is through Na-K exchange and the other is effected by the sodium reabsorption independent of Na-K exchange, and aldosterone can act on both processes differently according to the condition of patient or animal.(3) The second way will act in initial effect and escape phenomenon in normal human and dog, but it will show the strong sodium retaining effect in human and dog with congestive heart failure.(4) Aldosterone may probably aggravate the edema in congestive heart failure, but it might not be the primary cause of edema and its primary cause is rather the altered tubular responsiveness to aldosterone.

ALDOSTERONE AND THE EDEMA OF CONGESTIVE HEART FAILURE.

The role of the adrenal in the pathogenesis of the edema of congestive heart failure has been debated for many years. Deming and Luetscher 1 in 1950 showed that the urine of patients with congestive failure contained a substance promoting sodium retention. This substance was subsequently identified by Simpson, Tait, Luetscher, and others to be aldosterone, and has been found in elevated amounts in the urine of patients with congestive heart failure by many investigators. 2-5 It has been postulated that the reduced renal blood flow secondary to lowered cardiac output in congestive failure leads to release of renin and enzymatic conversion of plasma factors to angiotensin II and stimulation of aldosterone secretion. 6 Another possible mechanism of the hyperaldosteronuria begins with elevated venous pressure and transudation of fluid and electrolytes from the vascular system. This is postulated to stimulate the production of aldosterone by way of as yet unelucidated

Effect of chlorothiazide on electrolyte transport in man; its use in the treatment of edema of congestive heart failure, nephrosis, and cirrhosis.

Thirty-two hospital patients in advanced states of fluid retention from heart failure, cirrhosis, and nephrosis were given a new sulfonamide compound, chlorothiazide, to induce diuresis. Chlorothiazide, given orally in a dosage of 2.0 Gm. per day, was found to be at least as potent as an organic mercurial agent in promoting diuresis. The compound was effective in all types of edema studied, a finding which perhaps supports the hypothesis that similar mechanisms operate in the abnormal renal retention of sodium in heart failure, hepatic cirrhosis, and nephrosis. Chlorothiazide promises to be useful whenever reduction in stores of body sodium is desirable, and therefore may also be of value in hypertension and in steroid edema. In addition, the compound may contribute to a further understanding of renal tubular mechanisms involved in edema formation, since the study suggests a site of action different from other known diuretics.

The triad of tachycardia, digitalis toxicity and mercurial-fast edema in congestive heart failure complicated by pulmonary embolism

ULMONARY embolism is of frequent occurrence,1-.3 particularly in patients with congestive heart failure. 4-6 The clinical features of thromboembolic phenomena have been well defined in non-cardiac disease,‘,” but the manner in which pulmonary embolism may disturb congestive heart failure has not been clear. Attention was called to this problem by the development, in a number of patients with pulmonary emboli, of the triad of intractable edema, disproportionate tachycardia and digitalis toxicity. This investigation was undertaken to evaluate the occurrence of this triad in patients who died of chronic congestive heart failure complicated by pulmonary embolism and to compare them with another group of patients with fatal heart failure whose course was not thus complicated.

Autopsy incidence of pulmonary embolism in coronary heart disease.

Article1 May 1950AUTOPSY INCIDENCE OF PULMONARY EMBOLISM IN CORONARY HEART DISEASETHOMAS J. MORAN, M.D.THOMAS J. MORAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-32-5-949 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe incidence of pulmonary embolism in coronary heart disease has received increasing attention in the past few years, following the introduction of anti-coagulant therapy in thrombo-embolic disease. Adequate statistics are not yet available as to the efficacy of such therapy, due partly to the fact that relatively few reports on the autopsy incidence of pulmonary embolism in coronary heart disease have been published. Several such reports1, 2, 3dealing with the incidence of thrombo-embolic phenomena in myocardial infarction have been quoted rather frequently as providing a logical basis for Dicumarol therapy. Other reports have dealt with the causes of death...Bibliography1. HellersteinMartin HKJW: Incidence of thrombo-embolic lesions accompanying myocardial infarction, Am. Heart J. 33: 443-452, 1947. CrossrefMedlineGoogle Scholar2. NayBarnes RMAR: Incidence of embolic or thrombotic processes during immediate convalescence from acute infarction, Am. Heart J. 30: 65-76, 1945. CrossrefGoogle Scholar3. Blumer G: The importance of embolism as a complication of cardiac infarction, Ann. Int. Med. 11: 499-504, 1937. LinkGoogle Scholar4. EppingerKennedy ECJA: The cause of death in coronary thrombosis with special reference to pulmonary embolism, Am. J. M. Sc. 195: 104-106, 1938. CrossrefGoogle Scholar5. WoodsBarnes RMAR: Factors influencing immediate mortality rate following acute coronary occlusion, Proc. Staff Meet., Mayo Clin. 16: 341-345, 1941. Google Scholar6. Moran TJ: Pulmonary embolism in nonsurgical patients with prostatic thrombosis, Am. J. Clin. Path. 17: 205-208, 1947. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Danville, Virginia*Received for publication July 17, 1948.From the Department of Pathology, Pittsburgh City Home and Hospitals, Mayview, Pennsylvania, and the Department of Pathology, Memorial Hospital, Danville, Virginia. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPulmonary EmbolismCongestive heart failureCardiovascular collapse and pulseless idioventricular rhythmPathogenesis of pulmonary infarctionCurrent status of antithrombotic therapy in cardiovascular diseaseAnesthetic Management of Patients with Cardiac DiseaseEffect of coronary shock on tolerance to pulmonary embolusRECURRENT PULMONARY EMBOLISM-INCIDENCE, PREDISPOSING FACTORS AND PROGNOSISThe pathologic basis of sudden deathThe angiographic diagnosis of acute pulmonary embolism: Evaluation of criteriaCorrelation of lung photoscans with pulmonary angiography in pulmonary embolismPULMONARY EMBOLISM IN PSYCHIATRIC PATIENTSFrequency of Pulmonary Thromboembolism in ManPulmonary Embolism: A Commonly Missed Clinical EntityPulmonary EmbolismMyocardial Infarction—A Ten-year Experience in a Midwestern General HospitalC. T. ANASTASSIADIS, M.D., S. E. SIVERTSON, M.D.Case 21-1961Pulmonary EmbolismDie LungenembolieDie Coronarerkrankungen. Coronarinsuffizienz, Angina pectoris und HerzinfarktPulmonary embolism and infarctionAnticoagulation Therapy for Congestive Heart FailureThe triad of tachycardia, digitalis toxicity and mercurial-fast edema in congestive heart failure complicated by pulmonary embolismClinical Differentiation of Pulmonary Infarction: (Correlation of Clinical and Pathologic Findings) 1 May 1950Volume 32, Issue 5Page: 949-953KeywordsAnticoagulant therapyAutopsyCoronary heart diseaseMyocardial infarctionPulmonary diseasesPulmonary embolism ePublished: 1 December 2008 Issue Published: 1 May 1950 PDF downloadLoading ...

FATAL MERCURIALISM DUE TO PROLONGED INTRAVENOUS ADMINISTRATION OF A MERCURIAL DIURETIC

Excerpt The clinical use of organic mercurials to control the edema of congestive heart failure has had widespread clinical application since their introduction a generation ago.1, 2, 3These diuret...

URINE VOLUME AND TOTAL RENAL SODIUM EXCRETION DURING WATER DIURESIS

Excerpt The value of drastically reducing sodium intake in treating the edema of congestive heart failure is generally accepted. Concerning the optimal water intake during such sodium restriction r...

Studies on congestive heart failure: I. The importance of restriction of salt as compared to water

1. 1. Twenty-three patients who were suffering from congestive heart failure were studied with a view to learning the relative importance of sodium chloride and water with respect to the accumulation and disappearance of edema. 2. 2. The restriction of salt to a level below the output in the urine always resulted in a decrease in the amount of edema. Usually, a diet containing as little as 1.0 Gm. of salt in twenty-four hours was sufficient to cause diuresis or a cessation in the accumulation of edema, but the salt content of the ordinary “salt-free” diet was not low enough. 3. 3. When the intake of salt was sufficiently restricted, the amount of fluid taken did not usually affect the edema. 4. 4. Occasionally diuresis was observed to increase when the patient was taking plenty of fluids, and to decrease when fluids were rigidly restricted. 5. 5. When renal insufficiency accompanied heart failure, a high intake of fluids resulted in symptoms similar to those of “water intoxication”. 6. 6. These studies suggest that restriction of salt is important in the control of the edema of congestive heart failure, but that the restriction of fluids is of little value.

Observations on the causes of edema in congestive heart failure: Smirk, F. H.: Clin. Sc. 2: 317, 1936

Observations on the causes of edema in congestive heart failure: Smirk, F. H.: Clin. Sc. 2: 317, 1936