Transient Mediastinal Enlargement: An Unusual Computed Tomographic Manifestation of Pulmonary Venous Hypertension and Congestive Heart Failure

Respiration ◽  
2000 ◽  
Vol 67 (2) ◽  
pp. 216-218 ◽  
Author(s):  
Jeffrey A. Miller ◽  
Sohail Contractor ◽  
Pierre Maldjian ◽  
Leo Wolansky
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Venous Hypertension ◽  
Computed Tomographic

scholarly journals Protein-Losing Enteropathy and Plastic Bronchitis After the Fontan Operation

2018 ◽  
Vol 38 (6) ◽  
pp. e5-e12 ◽  
Author(s):  
Christine Peyton
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Complex Disease ◽  
Fontan Procedure ◽  
Fontan Operation ◽  
Venous Pressure ◽  
Venous Hypertension ◽  
Plastic Bronchitis ◽  
Protein Losing Enteropathy ◽  
Fontan Physiology

Protein-losing enteropathy and plastic bronchitis remain challenging to treat despite recent treatment advances. Protein-losing enteropathy and plastic bronchitis have been diagnosed in patients with cardiomyopathy, constrictive pericarditis, and congestive heart failure. This article focuses on patients with protein-losing enteropathy or plastic bronchitis following the Fontan procedure. Patients with single-ventricle physiology who have undergone the Fontan procedure are at risk for these conditions. Fontan physiology predisposes patients to chronically low cardiac output, increased central venous pressure, and congestive heart failure. These altered hemodynamics lead to increased mesenteric vascular resistance, resulting in venous hypertension and congestion in protein-losing enteropathy. Plastic bronchitis is a complex disease in which chronic high lymphatic pressures from Fontan physiology cause acellular bronchial casts to develop. These entities may also occur in patients with normal Fontan hemodynamics. This article also covers medical and surgical interventions for protein-losing enteropathy and plastic bronchitis. (Critical Care Nurse. 2018;38[6]:e5–e12)

Detection of intra-cardiac thrombi and congestive heart failure in cats using computed tomographic angiography

2018 ◽  
Vol 59 (4) ◽  
pp. 412-422 ◽  
Author(s):  
Kyle P. Vititoe ◽  
Ryan C. Fries ◽  
Stephen Joslyn ◽  
Laura E. Selmic ◽  
Mark Howes ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Computed Tomographic Angiography ◽  
Computed Tomographic ◽  
Tomographic Angiography

Inhalation of the Phosphodiesterase-3 Inhibitor Milrinone Attenuates Pulmonary Hypertension in a Rat Model of Congestive Heart Failure

2007 ◽  
Vol 106 (1) ◽  
pp. 124-131 ◽  
Author(s):  
Thomas Hentschel ◽  
Ning Yin ◽  
Alexander Riad ◽  
Helmut Habbazettl ◽  
Jörg Weimann ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Vascular Resistance ◽  
Rat Model ◽  
Intravenous Infusion ◽  
Left Ventricular ◽  
Venous Hypertension ◽  
Systemic Hemodynamics ◽  
Phosphodiesterase 3 ◽  
Arterial Blood

Background Most patients with congestive heart failure (CHF) develop pulmonary venous hypertension, but right ventricular afterload is frequently further elevated by increased pulmonary vascular resistance. To investigate whether inhalation of a vasodilatory phosphodiesterase-3 inhibitor may reverse this potentially detrimental process, the authors studied the effects of inhaled or intravenous milrinone on pulmonary and systemic hemodynamics in a rat model of CHF. Methods In male Sprague-Dawley rats, CHF was induced by supracoronary aortic banding, whereas sham-operated rats served as controls. Milrinone was administered as an intravenous infusion (0.2-1 microg.kg body weight.min) or by inhalation (0.2-5 mg/ml), and effects on pulmonary and systemic hemodynamics and lung water content were measured. Results In CHF rats, intravenous infusion of milrinone reduced both pulmonary and systemic arterial blood pressure. In contrast, inhalation of milrinone predominantly dilated pulmonary blood vessels, resulting in a reduced pulmonary-to-systemic vascular resistance ratio. Repeated milrinone inhalations in 20-min intervals caused a stable reduction of pulmonary artery pressure. No hemodynamic effects were detected when 0.9% NaCl was administered instead of milrinone or when milrinone was inhaled in sham-operated rats. No indications of potentially adverse effects of milrinone inhalation in CHF, such as left ventricular volume overload, were detected. Moreover, lung edema was significantly reduced by repeated milrinone inhalation. Conclusion If these results can be confirmed in humans, inhalation of nebulized milrinone may present a novel, effective, safe, and pulmonary selective strategy for the treatment of pulmonary venous hypertension in CHF.

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