Pulmonary Hypertension: A Clinical Case Study

Abstract

The pathophysiology of pulmonary hypertension can vary, depending on the cause. It can be classified as idiopathic/ primary, or it can be secondary to a variety of conditions, such as congenital heart defects, collagen vascular diseases, liver cirrhosis, infections, drugs and radiation therapy, and it can occur postoperatively for several reasons. It can be a result of increased pulmonary vascular resistance due to lung conditions such as COPD, or after lung resection surgeries [1]. Secondary pulmonary arterial hypertension due to cardiac or respiratory diseases can be caused by volume or pressure overload leading to proliferation of pulmonary vasculature and therefore obstruction. Lung parenchymal diseases lead to vascular changes causing vasoconstriction. This increased vascular resistance causes increased right ventricular after load, and eventually hypertrophy and failure [4]. When lung parenchyma is destroyed (as in COPD), there is a destruction of vasculature as well. Hyperinflation of the lungs compresses vascular beds, thus resulting in an increase in PVR. Polycythemia, which can result from chronic hypoxemia, increases the viscosity of the blood and contributes to hypertension as well, and alveolar hypoxia also causes pulmonary vasoconstriction. Over time, this leads to hypertrophy of the tunica media of the pulmonary vessels, fibrosis of the tunica intima, and an overall narrower lumen. This increase in vascular resistance and pressures leads to an increased right ventricular afterload, leading to dilation and hypertrophy of cardiac muscle mass in order to maintain cardiac output [1].