Hypertension is asymptomatic in nature and one of the most common cardiovascular diseases. Approximately 74.5 million people are affected by hypertension in the United States alone. Another name for hypertension is also known as high blood pressure. The condition is caused due to force of blood against the wall of the arteries. High blood pressure leads to increase in strokes, risk of heart attacks and heart diseases.


Developmental Etiology, Physiology and Clinical Manifestations of HTN

Much uncertainty still surrounds pathophysiology of HTN. Between 2 and 5 percent of the patients often, have an underlying adrenal or renal diseases as the main reason for their raised blood pressure. In the maintenance of normal blood pressure, a number of physiological mechanisms are often involved and their derangement contributes to the development of essential hypertension.

Many interrelated factors contribute to the raised blood pressure in hypertensive patients and it is probable that their relative roles may defer between individuals. Among the intensively studied factors that have been researched are obesity, salt intake, insulin, sympathetic nervous system, resistance and the renin-angiotensin system. Other factors also evaluated, include endothelial dysfunction manifested by changes in nitric oxide and endothelin, intrauterine nutrition and low birth weight, genetics and neurovascular anomalies (Bakris, 2007).

Primary hypertension may also develop due to genetic or environmental factors, or secondary causes that have vascular, etiologies and endocrine factors in their progression. A small percentage of patients between 2 to 10 percent have a secondary cause and essential or primary hypertension accounts for the remaining 90 to 95 percent of adult cases. Often Hypertensive emergencies are characterized by poor compliance or inadequate medication. Symptoms such as dizziness, nosebleeds, and headache, and chest pain, shortness of breath and palpitation of the heart are caused by hypertension (Beevers, Lip & O'Brien, 2001).

Age in Relation to HTN

Age and hypertension are related aspects. With aging, the risk of acquiring hypertension increases. Adult physiologic changes in hypertension can be understood better by reviewing it from the aspect of age and the changes that occur during HTN progression. In that, it is common knowledge that HTN is a serious disease that affects one-third of American adults, and two-thirds of people over age 65. Age increases the risk to hypertension because people become less active, their arteries harden, kidney function decreases, and body becomes sensitive to salt, as it cannot process salt effectively. However, the risk of hypertension increases in phases, for example after 30 years and after 50 years.

Age-related changes occur even among the healthiest. The body's systems of older people often become affected. This is explained by the changes in the mitigation of calcium which migrates from teeth and bones into the blood vessels due to the declined heart output. Malfunction of kidneys, liver, lings as well as acquiring cataracts are often commonly related to HTN progression in patients. However, disabilities should not be automatically linked with these changes. Regular exercise, intellectual and social stimulation, and healthy diet can help delay or prevent rapid HTN progression (Wild Iris Medical Education, 1998).

Hypertension development is not mainly due to the aging process, even though the elderly exhibit a high incidence of hypertension. With the understanding that aging has an affects all major organ systems inclusive of the kidney, central nervous system and peripheral vasculature they still age differently according to the extent of the HNT progression in the system. The impact age has on cardiovascular functions and HTN progression should be handled from the aspect of the variable used to measure and define cardiac functions and the population studied, Probably the most constant findings in the studies of age influence on HTN patients is the large difference in the older population for nearly every cardiovascular variable (Skopfkuchen, 1995).

Regulatory and Compensatory Mechanisms Relating to HTN

Systematic blood flow and oxygen distribution to peripheral organs and tissues is always under neuroendocrine control. Compensatory mechanism occur fast to correct any dysfunction or incorrect blood flow or blood pressure in the body. The compensatory mechanisms ensure that there is a short-term advantage to active cells. However, it provides a long-term destruction to the cardiovascular organ and the body system when they are chronically activated. In terms of thermoregularity, adrenoceptor blockade reduces the reactivity that occurs in the cooling process and vessel reaction to cold is the same as the intact normotensive rats. To regulate blood pressure, the body uses several compensatory mechanisms. They involve changing the diameter of volume of blood in the blood vessels, small arteries and the amount of blood pumped from the heart. These mechanisms return to normal blood pressure after it decreases or increases during normal activities like sleep or exercise.

The veins narrow and widen so that to effectively contain the normal capacity of the blood. During their constriction, they reduce their ability to hold large amounts of blood this is to allow more blood to be pumped into the arteries since a large amount returns to the heart. As a result, there is increase in the blood pressure. This system works opposite, if the veins dilate there will be an increase in blood pressure due to the increased capacity of blood and less blood is let into the heart. The body can change the amount of blood pumped during each heartbeat as long as resistance to blood flow in the arteries remains constant it achieves this by making each contraction stronger or weaker as a regulatory mechanism to achieve balance in the system.

Specialized cells, known as baroreceptors, act as sensors that activate the compensatory mechanisms in the body system. The sensors that are located within arteries constantly monitor blood pressure. Those in the large arteries of the chest and neck are particularly important. Any change in the blood pressure triggers compensatory mechanisms sensors that act to effectively maintain and steady the anomaly in blood pressure (Bakris, 2007).

Pathophysiological Principles to Management HTN in PPHN Patients

Despite the fact that pathophysiologic mechanisms that characterize persistent pulmonary hypertension of the newborn (PPHN) requires strict and specific therapeutic concepts, it is focused on the treatment of symptoms of cardiovascular abnormalities and respiratory failure. However, for those who have severe PPHN and do not respond to optimized conventional ventilator support, they should be provided with extracorporeal membrane oxygenation and high frequency oscillatory ventilation. Principals of pathophysiological management in HTN patients in this article are explained from the aspect of PPHN infant patients; that is, persistent pulmonary hypertension of the newborn (PPHN) necessitate rather specific therapeutic concepts though various pathophysiological mechanisms in the majority of infants with PPHN management focus on the treatment of cardiovascular abnormalities and the symptoms of respiratory failure. Optimized conventional ventilatory support and high-frequency oscillatory ventilation are available for the few neonates with severe PPHN who fail to respond to extracorporeal membrane oxygenation (Bakris, 2007).

Cardiovascular abnormalities treatment should be based on the systematic and pulmonary circulation and the pathophysiological events in the heart of the newborn with PPHN condition. The main aim for applying the PPHN therapy on the pathophysiological principles is for the support of myocardial function and reduce right ventricular afterload. With this understanding, the application of inhalational nitric oxide therapy as a new therapy to effectively reduce resistance in the pulmonary vascular system can help in addressing the HNT condition, which targets the vascular organs (Skopfkuchen, 1995).

Physiologic Responses to Treatment of Resistant HTN

Resistant hypertension (RH) is one of the factors that increase cardiovascular mortality and morbidity. The most known characteristics shown by patients who experience resistant hypertension include obstructive sleep apnea, obesity and aldosterone covering the mosaic of phenotype in excess. These patients also experience increased sympathetic nervous system activity. Some other effects include insulin resistance, endothelial dysfunction and aldosterone effects.

Successful HTN physiologic responses treatment requires reversal of lifestyle and identification of the factors that contribute to appropriate treatment and diagnosis, use of effective multidrug regimens and treatment resistance of secondary hypertension causes. In particular, there has not been a study on the subgroup of patients with resistance to hypertension, however observational assessments have allowed for identification of lifestyles and demographic characteristics that are linked with resistant hypertension strand of HTN. The secondary cause of the role of hypertension in promoting treatment resistance is well documented. In addition broader mechanisms identification for the treatment resistance is still lacking. Attempts to elucidate potential genetic causes of resistant hypertension have been limited (Wild Iris Medical Education, 1998).

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Hypertension is recognized as one of the most important preventable causes of premature mortality and morbidity. However, despite the fact that there are available antihypertensive drugs that are effective, many patients still leave its effects uncontrolled. The causes of the distinction between uncontrolled hypertension, true resistant hypertension and pseudo resistance need a systematic approach to the patient. Uncontrolled BP pathophysiology if understood will help in future efforts of improving the outcome of hypertension in a high-risk population.

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