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CONSULTA

Hipertensión pulmonar

 

 

1: Mayo Clin Health Lett 2002 Jan;20(1):1-3

Pulmonary hypertension. High blood pressure in the lungs.

Publication Types:

Review

 

 

2: Crit Care Nurse 2000 Dec;20(6):31-40

Intravenous epoprostenol: a new therapy for primary pulmonary hypertension.

Sabo J A, Nord C P.

Fairview-University Medical Center, St Paul, Minn, USA.

Publication Types:

Review

 

 

3: Crit Care Nurse 2000 Apr;20(2):22-8; quiz 29-30

Managing pulmonary hypertension in heart transplantation: meeting the challenge.

Coe P F.

Medical University of South Carolina, Charleston, USA.

The most common measurements of pulmonary hypertension include systolic and mean pulmonary artery pressures, PVR, and transpulmonary gradient. Pulmonary artery pressures greater than 50 mm Hg, PVR greater than 6 Woods units, and transpulmonary gradient greater than 15 mm Hg that are unresponsive to optimal vasodilators are contraindications to orthotopic heart transplantation. Therapies used to reduce PVR in the cardiac catheterization laboratory include high-flow oxygen; sublingual nitroglycerin; and intravenous inotropic agents, vasodilators, and selective pulmonary vasodilators. Systemic hypotension may be an undesirable side effect of vasodilators. Inhaled agents such as nitric oxide and prostacyclin are specific to the pulmonary vasculature and reduce PVR without causing systemic hypotension. All pharmacological therapies used to optimize pulmonary hemodynamics before transplantation can be used during transplantation in patients who are at high risk for acute right ventricular failure and death after orthotopic heart transplantation because of elevated pulmonary hemodynamic values. Use of larger donor hearts for patients with elevated PVR and referral for heart-lung transplantation are potential treatment options. A heterotopic heart transplantation might also be attempted. However, because of the poor success with heterotopic transplantation, other options such as treatment with inhaled pulmonary vasodilators show much more promise and are associated with long-term survival after transplantation. Finally, nursing knowledge and implementation of transplantation protocols are essential for continued assessment and management of candidates for heart transplantation who are cared for in the intensive care or coronary care unit.

Publication Types:

Review

 

 

4: N Engl J Med 2001 Nov 15;345(20):1465-72

Chronic thromboembolic pulmonary hypertension.

Fedullo PF, Auger WR, Kerr KM, Rubin LJ.

Department of Medicine, University of California, San Diego, Medical Center, La Jolla 92037-1300, USA.

Publication Types:

Review

 

 

5: N Engl J Med 2001 Aug 2;345(5):319-24

Mutation in the gene for bone morphogenetic protein receptor II as a cause of primary pulmonary hypertension in a large kindred.

Newman JH, Wheeler L, Lane KB, Loyd E, Gaddipati R, Phillips JA 3rd, Loyd JE.

Center for Lung Research, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA. john.newman@med.va.gov

BACKGROUND: Most patients with primary pulmonary hypertension are thought to have sporadic, not inherited, disease. Because clinical disease develops in only 10 to 20 percent of persons carrying the gene for familial primary pulmonary hypertension, we hypothesized that many patients with apparently sporadic primary pulmonary hypertension may actually have familial primary pulmonary hypertension. METHODS: In a study conducted over 20 years, we developed a registry of 67 families affected by familial primary pulmonary hypertension. Through patient referrals, extensive family histories, and correlation of family pedigrees, we discovered shared ancestry among five subfamilies. We established the diagnosis of primary pulmonary hypertension by direct evaluation of patients and review of autopsy material and medical records. We assessed some family members for mutations in the gene encoding bone morphogenetic protein receptor II (BMPR2), which has recently been found to cause familial primary pulmonary hypertension. RESULTS: We linked five separately identified subfamilies that included 394 known members spanning seven generations, which were traced back to a founding couple in the mid-1800s. Familial primary pulmonary hypertension has been diagnosed in 18 family members, 12 of whom were first thought to have sporadic disease. The conditions of 7 of the 18 were initially misdiagnosed as other cardiopulmonary diseases. Six members affected with familial primary pulmonary hypertension and 6 of 10 at risk for carriage have been undergone genotype analysis, and they have the same mutation in BMPR2, a transversion of thymine to guanine at position 354 in exon 3. CONCLUSIONS: Many cases of apparently sporadic primary pulmonary hypertension may be familial. Failure to detect familial primary pulmonary hypertension results from incomplete expression within families, skipped generations, and incomplete family pedigrees. The recent discovery of mutations in BMPR2 should make it possible to identify those with susceptibility to disease.

 

 

6: Crit Care Clin 2001 Apr;17(2):453-67

Severe pulmonary hypertension: critical care clinics.

McLaughlin VV, Rich S.

Center for Pulmonary Heart Disease, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA.

Pulmonary hypertension has many causes and therapies. A meticulous evaluation is critical. Substantial advances in medical therapy have occurred over the past decade, and the future treatment of this syndrome is promising, with many new medications on the horizon.

Publication Types:

Review

 

 

7: South Med J 2001 Jun;94(6):635-9 [Texto completo]

Pulmonary hypertension associated with HIV infection.

Seoane L, Shellito J, Welsh D, de Boisblanc BP.

Section of Pulmonary/Critical Care Medicine, Louisiana State University Health Sciences Center, New Orleans, USA.

Pulmonary hypertension occurs with increased frequency among patients with human immunodeficiency virus (HIV) infection. Although the pathogenesis of HIV-associated pulmonary hypertension remains unknown, it appears to occur independently of other risk factors associated with pulmonary vasculopathy, such as chronic hepatitis C infection and intravenous drug use. Signs and symptoms are typical of those immunocompetent patients with primary pulmonary hypertension, but because many HIV-infected patients are receiving intensive medical supervision, the diagnosis of pulmonary hypertension is often made at an earlier stage. Acute responses to epoprostenol are similar to those among non-HIV-infected individuals, but the benefits of long-term, intravenous treatment with epoprostenol in HIV-infected patients is unknown. Future investigations should define the true incidence of pulmonary hypertension and the long-term effects of epoprostenol on survival among HIV-infected individuals. Physicians should be alert to possible pulmonary hypertension in persons infected with HIV.

Publication Types:

Review

 

 

8: Am Fam Physician 2001 May 1;63(9):1789-98 [Texto completo]

Diagnosis and treatment of pulmonary hypertension.

Nauser TD, Stites SW.

Division of Pulmonary and Critical Care Medicine, University of Kansas Medical Center, Kansas City, MO 66160-7381, USA.

Primary pulmonary hypertension is a rare disease of unknown etiology, whereas secondary pulmonary hypertension is a complication of many pulmonary, cardiac and extrathoracic conditions. Chronic obstructive pulmonary disease, left ventricular dysfunction and disorders associated with hypoxemia frequently result in pulmonary hypertension. Regardless of the etiology, unrelieved pulmonary hypertension can lead to right-sided heart failure. Signs and symptoms of pulmonary hypertension are often subtle and nonspecific. The diagnosis should be suspected in patients with increasing dyspnea on exertion and a known cause of pulmonary hypertension. Two-dimensional echocardiography with Doppler flow studies is the most useful imaging modality in patients with suspected pulmonary hypertension. If pulmonary hypertension is present, further evaluation may include assessment of oxygenation, pulmonary function testing, high-resolution computed tomography of the chest, ventilation-perfusion lung scanning and cardiac catheterization. Treatment with a continuous intravenous infusion of prostacyclin improves exercise capacity, quality of life, hemodynamics and long-term survival in patients with primary pulmonary hypertension. Management of secondary pulmonary hypertension includes correction of the underlying cause and reversal of hypoxemia. Lung transplantation remains an option for selected patients with pulmonary hypertension that does not respond to medical management.

Publication Types:

Review

 

 

9: Hosp Pract (Off Ed) 2001 Mar 15;36(3):29-32, 37-40 [Texto completo]

New approaches to pulmonary hypertension.

Russo-Magno PM, Hill NS.

Brown University School of Medicine, Providence, RI, USA.

Careful evaluation will often reveal secondary--and perhaps reversible--factors contributing to pulmonary hypertension. For primary disease, there are now a variety of treatments, ranging from calcium channel blockers to lung

transplantation.

Publication Types:

Review

 

 

10: Heart 2001 Apr;85(4):475-80

Pulmonary arterial hypertension: new ideas and perspectives.

Galie N, Torbicki A.

Institute of Cardiology, University of Bologna, Italy. n.galie@bo.nettuno.it

Publication Types:

Review

 

 

11: Chest 2001 Mar;119(3):970-3

One-year continuous inhaled nitric oxide for primary pulmonary hypertension.

Perez-Penate G, Julia-Serda G, Pulido-Duque JM, Gorriz-Gomez E, Cabrera-Navarro P.

Service of Pneumology, Hospital General de Gran Canaria Dr. Negrin, Las Palmas de Gran Canaria, Spain. gperez@correo.hpino.rcanaria.es

We describe a case of long-term administration of nitric oxide (NO) in a 32-year-old man who was admitted with exertional dyspnea and anasarca. A diagnosis of primary pulmonary hypertension was made. An acute vasodilator trial with inhaled NO showed a 5% reduction of the mean pulmonary artery pressure. Long-term NO inhalation therapy was initiated. Twenty days later, the dyspnea improved, the anasarca resolved, and the PaO(2) level increased. After 12 months of NO therapy, the patient remained stable and no signs of toxicity or tachyphylaxis were observed. To our knowledge, this is the first report of 1 year of continuously inhaled NO in an adult patient with primary pulmonary hypertension. These findings suggest that prolonged NO therapy might be an effective alternative, at a lower cost, to the continuous IV infusion of epoprostenol.

Publication Types:

Review

 

 

12: Chest 2000 Oct;118(4):1133-41

HIV-Related pulmonary hypertension: analytic review of 131 cases.

Mehta NJ, Khan IA, Mehta RN, Sepkowitz DA.

Department of Medicine, Long Island College Hospital, Brooklyn, NY, USA.

OBJECTIVE: To report two new cases of HIV-related pulmonary hypertension and to review and analyze the existing reports on the subject. METHOD: Two new cases of HIV-related pulmonary hypertension are described, and the cases, case series, and related articles on the subject in all languages were identified through a comprehensive MEDLINE search. RESULTS: Among the 131 reviewed cases, 54% were male, and the age range was 2 to 56 years (mean, 33 years). The interval between the diagnosis of HIV disease and the diagnosis of pulmonary hypertension was 33 months. In 82% of cases, pulmonary hypertension was related solely to HIV infection. Presenting symptoms were progressive shortness of breath (85%), pedal edema (30%), nonproductive cough (19%), fatigue (13%), syncope or near-syncope (12%), and chest pain (7%). The mean (+/- SD) pulmonary arterial systolic BP was 67 +/- 18 mm Hg (n = 116), and diastolic BP was 40+/-11 mm Hg (n = 39). Pulmonary vascular resistance was 983+/-420 dyne. s. cm(-5) (n = 29). Chest radiographs demonstrated cardiomegaly (72%) and pulmonary artery prominence (71%). Right ventricular hypertrophy was the most common electrocardiographic finding (67%). Dilatation of the right heart chambers was the most common echocardiographic finding (98%). Plexogenic pulmonary arteriopathy was the most common histopathology (78%). Pulmonary function tests demonstrated mild restrictive patterns with variably reduced diffusing capacities. The responses to vasodilator agents and antiretroviral therapy was variable. Sixty-six patients died during a median follow-up period of 8 months. The median length of time from diagnosis to death was 6 months. CONCLUSION: HIV infection is an independent risk factor for the development of pulmonary hypertension. The appearance of unexplained cardiopulmonary symptoms in HIV-infected individuals should suggest pulmonary hypertension.

Publication Types:

Review

 

 

13: Mayo Clin Proc 2000 Jun;75(6):625-30

Pulmonary hypertension: diagnostics and therapeutics.

Krowka MJ.

Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minn 55905, USA.

Pulmonary hypertension (PH) may develop because of a spectrum of insults to the lungs; in some patients, there seems to be no cause. Noninvasive tests, such as standard chest radiography, electrocardiography, and transthoracic Doppler echocardiography, provide effective screening if PH is suspected. This synopsis focuses on these screening studies and the more common clinical problems, including primary cardiac abnormalities, obstructive sleep apnea, chronic pulmonary embolism, pulmonary parenchymal problems, connective tissue disorders, cirrhosis with portal hypertension, and use of appetite suppressants, that should be considered when PH exists. Treatment options for PH, including intravenous prostacyclin (epoprostenol), and investigational agents such as subcutaneous or oral prostacyclin analogues and oral endothelin receptor antagonists are described.

Publication Types:

Review

 

 

 

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