When high blood pressure is present within the arteries supplying blood to lungs, pulmonary hypertension (PH) is evident. Among individuals who are healthy, the pressure within these arteries is much lower compared to the rest of the body. Nonetheless, individuals presenting with pulmonary hypertension symptoms often experience a pulmonary arterial pressure of roughly 40/20 milliliters of mercury (mm Hg), which translates to an average of 25 mm Hg. Normally, individuals experience a pulmonary arterial pressure of about 25/10 mm Hg and an overall pressure of about 120/80 mm Hg. As such, having higher-pressure indications within these arteries translates to pulmonary hypertension.
Moreover, the persistence of pulmonary hypertension leads to the ineffectiveness of the right ventricle, which pumps blood to the pulmonary arteries. On the other hand, pulmonary arterial hypertension (PAH) is an autonomous clinical subgroup with the characterization of having pre-capillary PH and increased pulmonary vascular resistance (PVR) in the absence of other chronic rare diseases such as chronic thromboembolic PH and lung disease (Neema & Kumar, 2017). The initiation and exacerbation of PH causes increased pressure within the blood vessels of the lungs resulting in the overworking of the heart, which leads to other morbid and possibly mortal symptoms.
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Etiology and Risk Factors
While the cause of PH is ultimately unclear, fundamentally, an individual’s genes and/or other medical conditions can cause pulmonary hypertension. Particular medical conditions often lead to the damaging and alteration of blood vessels in terms of blockages, which eventually causes PH. The past two decades have seen the rise in research and clinical advances attuned to pulmonary arterial hypertension, which has, in turn, resulted in clearer comprehension of the condition. For example, in 2000, a genetic cause materialized in two subsets of a study, leading to an in-depth understanding of its genetic cause ( Pulmonary Hypertension , n.d.). Essentially, within these subsets, receptor mutations unusually named bone morphogenetic protein receptor type 2 (BMPR2) were the cause of heritable PAH in more than 85 percent of families affected. Moreover, in over 10 to 20 percent, the BMPR2 mutation is observable.
In terms of diseases leading to the condition of PH, various associations have been brought forth. Among these include connective tissue diseases, predominantly scleroderma; congenital heart diseases; human immunodeficiency virus (HIV) infection, the ingestion of stimulant drugs; and congenital heart disease. Nonetheless, most common pulmonary hypertension are innately idiopathic. Concerning environmental or microbial causes, little is known. However, inflammation mediators considered molecular in nature affect or interact with molecules that essentially alter pulmonary blood vessels. Moreover, the ingestion of stimulant drugs such as amphetamines and cocaine causes or increases pulmonary hypertension. Regarding the impact of age and prevalence of gender, PAH, a specific type of PH affects young individuals and women predominantly than men ( Pulmonary Hypertension , n.d.). On average, individuals with PAH receive a diagnosis by age 36, with a three-year post-diagnosis survival attained by less than 50 percent of those affected.
Pathophysiological Processes
Essentially, in the development of PH, an increase in pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) results in higher-pressure loads to the right ventricle (RV), which in turn leads to the development of hypertrophy (Neema & Kumar, 2017). In normal cases, the regulation of the perfusion to the myocardium of the RV is intact throughout systole and diastole, due to intraventricular pressures that are low. Nonetheless, the occurrence of PH alters the perfusion, thereby, mimicking the left ventricle (LV) resulting in a dependence on diastolic durations and diastolic arterial pressure, which is the heart rate. Hypertrophied RV requires time to recuperate adequately through reloading and timed rhythm, which is its nature.
As such, changes to these determinants lead to significant decreases in RV functioning and overall cardiac output (CO) (Zong, Tune & Downey, 2005). Medically, in terms of systolic functioning, the effect of afterload increases on RV is more significant than that of the performance of the LV. Therefore, this leads to the flattening of the interventricular septum (IVS) and in more severe cases, the IVS bulges and intrudes the LV causing a distortion in the diastolic filling, increasing pressure to the diastolic process, and eventually leading to a decrease in CO. In normal conditions, the IVS is decidedly important when it comes to LV and RV functioning; contributing one-third of the RV stroke, this distortion of IVS results in PH.
Clinical Manifestations and Complications
Essentially, the signs and symptoms of PH are hard to identify due to their similarity with other medical conditions. In some cases, individuals may have symptoms for years prior to their PH diagnosis. Eventually, such symptoms become worse and can eventually lead to serious complications such as severe right heart failure. Based on data from the national registry of America, the most frequent symptoms include dyspnea, which occurs in more than 60 percent of patients; fatigue, occurring in 19 percent of patients; pre-syncope or syncope, occurring in 13 percent of patients (Shin & Semigran, 2010). Other clinical manifestations include chest pain, dry cough, light-headedness, abdomen, leg, or feet swelling, wheezing, and hoarseness. Complications that abound from PH include anemia, arrhythmias, lung bleeds, heart failure, liver damage, and pericardial effusion (Shin & Semigran, 2010). In women who are pregnant, such complications can be life-threatening for both the mother and the baby.
Diagnostics
Diagnosis often entails a two-step process that entails the examination of clinical features as well as other noninvasive investigations (Hambly, Alawfi & Mehta, 2016). Clinical features examinations take place through the following steps:
Symptoms: fatigue, unexplained dyspnea, exertion intolerance, edema
Physical findings: peripheral edema, elevated jugular venous pressure among others
Medical history and risk factors: liver cirrhosis, HIV infection, connective tissue disease among others
Noninvasive findings include:
Electrocardiography
Chest radiography
Echocardiography
Tests of the pulmonary function
References
Hambly, N., Alawfi, F., & Mehta, S. (2016). Pulmonary hypertension: diagnostic approach and optimal management. Canadian Medical Association Journal , 188 (11), 804-812. doi: 10.1503/cmaj.151075
Neema, P., & Kumar, A. (2017). Severe pulmonary hypertension and right ventricular failure. Indian Journal Of Anaesthesia , 61 (9), 753. doi: 10.4103/ija.ija_420_17
American Thoracic Society. Pulmonary Hypertension [Ebook]. Retrieved from https://www.thoracic.org/patients/patient-resources/breathing-in-america/resources/chapter-17-pulmonary-hypertension.pdf
Shin, J., & Semigran, M. (2010). Heart Failure and Pulmonary Hypertension. Heart Failure Clinics , 6 (2), 215-222. doi: 10.1016/j.hfc.2009.11.007
Zong, P., Tune, J., & Downey, H. (2005). Mechanisms of Oxygen Demand/Supply Balance in the Right Ventricle. Experimental Biology And Medicine , 230 (8), 507-519. doi: 10.1177/153537020523000801
