Pulmonary HTN or Pulmonary Hypertension is a kind of a high blood pressure which affects the arteries in the lungs as well as the right side of human heart. Pulmonary htn begins when the tiny arteries in the lungs, which is called as pulmonary arteries, and capillaries become so narrowed or destroyed.
Thursday, November 6, 2008
Pulmonary HTN Treatment
Pulmonary HTN or Pulmonary Hypertension is a kind of a high blood pressure which affects the arteries in the lungs as well as the right side of human heart.
Pulmonary htn begins when the tiny arteries in the lungs, which is called as pulmonary arteries, and capillaries become so narrowed or destroyed. This will makes it harder for blood to flow through the lungs, which then raises the pressure within arteries in the lungs. As the pressure builds, the heart's right ventricle has to work harder to pump the blood through the lungs, eventually it will causing the heart muscle to weaken and then eventually fail completely.
Pulmonary htn is one of the serious illness which becomes progressively worse and it is sometimes become very fatal. Pulmonary htn isn't curable. However, many treatments are available that can help lessen the symptoms and it will improve the quality of life.
Pulmonary htn treatment is determined by whether the PH is venous, arterial, hypoxic, miscellaneous or thromboembolic. Since the pulmonary venous htn is synonymous with congestive heart failure, so the treatment's main goal is to optimize the left ventricular function by the use of beta blockers, diuretics, ACE inhibitors, etc., or to replace/repair the aortic valve or the mitral valve.
In Pulmonary Arterial Htn, the lifestyle changes, diuretics, digoxin, oxygen therapy and oral anticoagulants are considered conventional therapy, merely it have never been proven to be beneficial in randomized manner.
High dose of the calcium channel blockers are very useful in only 5 percent of IPAH patients who are vasoreactive by the Swan-Ganz catheter. Unfortunately, they have been largely misused, they are being prescribed to a lot of patients with non-vasoreactive Pulmonary Arterial Htn, leading to excess mortality and morbidity. The criteria for vasoreactivity have changed. Only those patients whose mean pulmonary artery pressure falls by more than 10 mm Hg to less than 40 mm Hg with an unchanged or increased cardiac output when challenged with adenosine, epoprostenol, or nitric oxide are considered vasoreactive.[8] Of these, only half of the patients are responsive to calcium channel blockers in the long term.[9]
A number of agents has recently been introduced for primary and secondary PAH. The trials supporting the use of these agents have been relatively small, and the only measure consistently used to compare their effectivity is the "6 minute walking test". Many have no data on mortality benefit or time to progression.
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