Genetic factors may account for mutations in the blood vessels which may manifest in the increased prevalence of smooth muscle cells and fibroblasts in the walls of the blood vessels (Ali, Summer, and Levitzky, 2005).
Pulmonary hypertension may also be caused by congenital heart defects like atrial septal defect, ventricular septal defect, patent ductus arteriosus, and congenital heart problems which have left to right shunts (Ali, Summer & Levitzky, 2005).
In instances when the pulmonary hypertension would worsen, the right-side pressure may overwhelm systemic pressure and “poorly oxygenated mixed venous blood bypasses the lungs and enters the systemic circulation, causing severe shunt-related hypoxemia” (Ali, Summer & Levitzky, p.129, 2005).
Non-specific symptoms like dyspnea on exertion, fatigue, angina pectoris, and syncope (Ali, Summer & Levitzky, 2005). These are however symptoms which also apply to other cardiopulmonary disorders like ischemic and valvular heart disorder.
Hoarseness is a symptom more specific to pulmonary hypertension because it is caused by compression of the recurrent laryngeal nerve due to the enlarged main pulmonary artery (Ali, Summer & Levitzky, 2005).
In cases of cardiac overload, sodium and water retention increases under the influence of the aldosterone hormone. Sodium and water retention consequently manifests as volume overload causing distended neck veins (jugular vein distention), ascites, and leg edema.
Other symptoms may include tachypnea, dizziness, apprehension, fear, persistent hypoxemia, excessive fatigue, and cyanosis (Canobbio, 2006). Dizziness, fatigue and syncope are largely due to insufficient cardiac output (Newman, 2008).
Initial diagnostic tests may include chest x-ray, spirometry, ECG, and echocardiography, and CBC following a complaint of significant exertional dyspnea in patients who seem relatively