Pulmonary artery hypertension chronic

AHF acute heart failure, CHF chronic heart failure, CRF chronic renal failure, NEP neutral endopeptidase, ECE endothelin converting enzyme, PAH pulmonary arterial hypertension. 

Fruehauf S, Steiger S, Topaly J, Ho AD. Pulmonary artery hypertension during interferon-alpha therapy for chronic myelogenous leukemia. Ann Hematol 2001 80(5) 308-10. 

Girard, G., Lehot, J.-J., Pannetier, J.-C., Filley, S., Ffrench, P., and Estanove, S. (1992). Inhaled nitric oxide after mitral valve replacement in patients with chronic pulmonary artery hypertension. Anesthesiology 77, 880-883. 

Another compound which has received much attention recently is Ciba 31531-Ba. This product (IV) was reported to have a vasodilator effect on the pvilmonary circulation in the open chest, right heart-bypass cat with fixed cardiac output. It was suggested that the compound caused pulmonary vasodilatation by exerting a direct effect on the vasculature. Moreover, Ciba 31531-Ba was found to reduce experimental pulmonary arterial hypertension in dogs when administered intravenously in doses of 1-2 mg/kg. In the same article it was reported that, when a dose of 400 mg q. i. d. was administered orally to 16 patients with chronic cor... 

Ng CS, Wells AU, Padley SP. A CT sign of chronic pulmonary arterial hypertension the ratio of main pulmonary artery to aortic diameter. J Thorac Imaging 1999 14(4) 270-278. 

On lung examination, tachypnea and bibasUar dry crackles can be found in any clinical presentation of HP. Wheezing, provoked by small airway obstruction, is uncommon but when present, may lead to an erroneous diagnosis, i.e., asthma. Patients with chronic HP may develop digital clubbing, pulmonary arterial hypertension, and even cor pulmonale (1,38). 

Figure 1 (A) Anteroposterior chest radiograph of a 33-year-old patient with subacute HP showing diffuse ground-glass attenuation. (B) Bird-related chronic HP. Chest radiograph shows shortening of the lung fields, diffuse reticulonodular opacities, and signs of pulmonary arterial hypertension. Abbreviation HP, hypersensitivity pneumonitis.

Many disorders benefit from exercise (Pederson Saltin, 2005). These include asthma, cancer, chronic heart failure, coronary artery disease, chronic obstructive pulmonary disease (COPD), depression, type 1 diabetes melUtus, type 2 diabetes melUtus, hypertension, intermittent claudication, osteoarthritis, osteoporosis, rheumatoid arthritis and obesity. 

The vascular changes of COPD include a thickening of pulmonary vessels and often are present early in the disease. These changes can be attributed to chronic inflammation and may lead to endothelial dysfunction of the pulmonary arteries. Later, structural changes lead to an increase in pulmonary pressures, especially during exercise. In severe COPD, secondary pulmonary hypertension leads to the development of right-sided heart failure. 

Surprisingly, pulmonary edema does not occur in patients with severe pulmonary hypertension (primary pulmonary hypertension), even though their pulmonary artery pressure may be chronically elevated as high as 45 mm Hg above the normal value of 13 mm Hg. The reason for this is that the arterial bed is severely narrowed in pulmonary hypertension thus the alveolar capillaries are not exposed to the increased pressures and there is no engorgement of blood in the pulmonary vasculature (Ingram and Braunwald, 1980). 

Pulmonary hypertension is characterized by a chronically elevated pulmonary artery pressure. As described in previous sections of this chapter, under normal conditions, the pulmonary artery pressure has a systolic value of 18 to 25 mm Hg, a diastolic value of 6 to 10 mm Hg, and a mean value ranging from 12 to 16 mm Hg. Pulmonary hypertension exists when the pulmonary artery systolic and mean pressures exceed 30 and 20 mm Hg, respectively. In the disease state, the pressure in the pulmonary artery may fluctuate widely and is often so high that it equals the blood pressure in the systemic arterial bed. As would be expected, pulmonary vascular resistance is also extremely high in patients with pulmonary hypertension. In addition, patients with this disease exhibit an enlarged right ventricle and an enlargement of the main pulmonary artery and its branches. Systemic hemodynamic parameters, however, such as cardiac output, cardiac index, systemic artery pressure, and pulmonary artery wedge pressure are usually not elevated. 

Hypoxia. Hypoxia is undoubtedly a cause of pulmonary hypertension in patients with chronic bronchitis and emphysema or in people residing at high altitudes (Grossman and Braunwald, 1980). However, the role for hypoxia as a determinant of primary pulmonary hypertension is less clear. Support for a hypoxia-linked mechanism in primary pulmonary hypertension is the fact that this stimulus is the most effective and consistent inducer of pulmonary hypertension in all species. Hypoxia exerts its greatest effect by constricting the arterioles and precapillaries through a mechanism independent of autonomic innervation. In addition, hypoxia can cause hypertrophy and hyperplasia of the pulmonary arterial smooth muscle (Naeye, 1965). 

Diazoxide is a potent vasodilator chemically resembling the thiazides, but it is not a diuretic. Diazoxide can be administered both parenterally and orally. Caution has been stressed when diazoxide is administered as an intravenous bolus into the pulmonary artery because the solution is highly alkaline (pH 11.6) and irritating to vascular tissue (Cotter and Honey, 1980). In one study with chronic oral diazoxide administration (300-600 mg/day), five of seven patients had important side effects including diabetes mellitus, fluid retention, nausea, vomiting, and postural hypertension that required discontinuation of the drug (Wise, 1983). 

Fig. 10.1. Chest radiograph in a patient with advanced chronic beryllium disease shows abnormality predominating in the upper lobes, consisting of coarse well-defined nodules, which appear to coalesce in areas. Some of the nodules appear calcified. There is moderate upper lobe volume loss with superior hilar retraction and some anatomic distortion. Hilar enlargement is likely due to a combination of adenopathy and pulmonary arterial enlargement due to pulmonary hypertension...

First- and second-trimester abortion Cervical reopening Induction of labor Augmentation of labor Postpartum hemorrhage Ectopic pregnancy Lactation suppression In gastrointestinal disease Peptic ulceration Liver transplantation Chemotherapy-induced mucosal lesions In cardiovascular disease Congenital cardiac malformations Raynaud s syndrome Chronic obstructive pulmonary disease Adult respiratory distress syndrome Pulmonary hypertension Arterial occlusive disease Extracorporeal circulation In urology Erectile dysfunction... 

Felodipine is a dihydropyridine derivative with diuretic properties (1). Its diuretic properties are not unique but are shared by other dihydropyridines. Its vasodilator-related adverse effects include flushing, headache, and tachycardia (2,3). Reduced arterial oxygen saturation has been seen in patients given intravenous felodipine for pulmonary hypertension (4,5). Along with amlodipine, but unlike other calcium channel blockers, felodipine may be safer in severe chronic heart failure accompanied by angina or hypertension. 

In cardiovascular disease Congenital cardiac malformations Raynaud s syndrome Chronic obstructive pulmonary disease Adult respiratory distress syndrome Pulmonary hypertension Arterial occlusive disease Extracorporeal circulation... 

Key M male F female DM diabetes mellltus HTN hypertension CAD coronary artery disease COPD chronic obstructive pulmonary disease CHF congestive heart failure ESRD end stage renal disease OSPS oral sodium phosphate solution PEG polyethylene glycol AKI acute kidney Injury na not available HD hemodialysis. 

Nonselective 8-blockers should be avoided in hypertensive patients with asthma, chronic obstructive pulmonary disease (COPD), and peripheral vascular disease. //3-Blockers (carvedilol and labetalol) will not result in unopposed a constriction like pure -blockers can and may be used in peripheral arterial disease. However, similar to nonselective 8-blockers, they should be avoided in patients with asthma and COPD. If a hypertensive patient with mild to moderate asthma or COPD requires a 8-blocker to treat a compelling indication, a 8i-selective agent should be selected, and the lowest effective dose should be used. ... 

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