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A pulmonary artery wedge pressure being less than 15 mmHg (also measured by right heart catheterization) excludes post-capillary bed (in the veins distal to the capillary bed) pulmonary hypertension. Pulmonary arterial hypertension is a subgroup of pulmonary hypertension and is categorized as World Health Organization as group 1. [3]
Treatment of pulmonary hypertension is determined by whether the PH is arterial, venous, hypoxic, thromboembolic, or miscellaneous. If it is caused by left heart disease, the treatment is to optimize left ventricular function by the use of medication or to repair/replace the mitral valve or aortic valve. [68]
Several classes of medications, collectively referred to as antihypertensive medications, are available for treating hypertension. Use should take into account the person's cardiovascular risk (including risk of myocardial infarction and stroke), as well as blood pressure readings, in order to gain a more accurate picture of the person's risks.
Diffusing capacity of the lung (D L) (also known as transfer factor) measures the transfer of gas from air in the lung, to the red blood cells in lung blood vessels. It is part of a comprehensive series of pulmonary function tests to determine the overall ability of the lung to transport gas into and out of the blood.
[42] [43] Hydralazine and its derivatives are also used in the treatment of severe hypertension, although they should be avoided in emergencies. [43] They are no longer indicated as first-line therapy for high blood pressure due to side effects and safety concerns, but hydralazine remains a drug of choice in gestational hypertension. [42]
Increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction. [9] [11] Increased capillary pressure (hydrostatic pressure) with over-distention of the capillary beds and increased permeability of the vascular endothelium, also known as "stress failure."
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It may allow other indications for the drug to be identified. Discovery that sildenafil inhibits phosphodiesterase-5 (PDE-5) proteins, for example, enabled this drug to be repurposed for pulmonary arterial hypertension treatment, since PDE-5 is expressed in pulmonary hypertensive lungs. [11] [12]
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