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  • Hypertension refers to an abnormal elevation of systemic arterial pressure. Although hypertension is largely asymptomatic, chronic hypertensive burden on the vasculature significantly increases the risk of a variety of cardiac and vascular pathologies. Before delving into the following discussion it may be helpful to review mechanisms of Systemic Arterial Pressure Regulation.
  • Overview
    • Systemic Arterial Pressures display a wide range within the population and defining the threshold at which pressure is considered pathological is on some level arbitrary. Epidemiological studies have shown that there is a graded increase in risk for future cardiovascular events as the values for either systolic and diastolic pressures increases. In most clinics today the following schema is utilized to stratify the systemic arterial pressures of patients.
  • Clinical Categories
    • Normal: (Diastolic less than 80 mm Hg) AND (Systolic less than 120 mm Hg)
    • Pre-Hypertension: (Diastolic between 80 - 90 mm Hg) OR (Systolic between 120-139 mm Hg)
    • Stage I Hypertension: (Diastolic between 90 - 99 mm Hg) OR (Systolic between 140 - 159 mm Hg)
    • Stage II Hypertension: (Diastolic greater than 100 mm Hg) OR (Systolic greater than 160 mm Hg)
  • Overview
    • For nearly 90% of hypertensive patients there exists no identifiable source of their elevated arterial pressure and this is termed Idiopathic or "Essential Hypertension". In roughly 10% of hypertensive patients, their elevated blood pressure can be attributed to a definable cause and is thus termed "Secondary Hypertension". Overall, hypertension is extremely common and incidence of essential hypertension increases progressively with age and the majority of individuals developing clinical hypertension by their sixth decade. Below we discuss some of the current theories as to what may cause Essential Hypertension and identify major causes of Secondary Hypertension.
  • Essential Hypertension
    • Essential Hypertension is a diagnosis of exclusion and likely reflects a complex, multi-factorial disease process which involves multiple, subtle derangements in normal systemic arterial pressure regulation initiated by both genetic and environmental sources. Several studies have shown a familial component to Essential Hypertension; however, simple genetic linkages to particular genes have not clearly identified
    • Essential Hypertension is also frequently co-morbid with hyperlipidemia, obesity, and Type II DM and is a component of metabolic syndrome. Whatever the cause, patients with essential hypertension may have subtle hyper-activation of their cardiovascular SNS tone and thus derangements in autonomic control of systemic arterial pressure. Additionally, subtle defects in renal salt and water handling may lead to excess fluid retention due to derangements in the RAAS System.
  • Secondary Hypertension
    • Renal Parenchymal Disease: Any disease process which damages nephrons will reduce the capacity of the kidneys to filter blood and result in elevations in extracellular fluid volume that ultimately translate to elevations in arterial pressure. Renal parenchymal diseases represent the most common cause of secondary hypertension and include any etiology of nephritic syndrome along with chronic renal failure, among others.
    • Renal Vascular Disease: Any cause of renal artery stenosis will reduce the arterial pressure encountered by the kidneys, resulting in compensatory renal elevation of salt and water resorption, ultimately leading to systemic hypertension
    • Coarctation of Aorta: Aortic coarctation also reduces the arterial pressure encountered by the kidneys, resulting in compensatory renal elevation in salt and water resorption
    • Hyperaldosteronism: Inappropriate elevation of plasma aldosterone levels leads to excessive salt resorption by kidneys and thus increased extracellular fluid volume and in turn arterial pressures
    • Cushing Syndrome: At high levels, plasma glucocorticoid can mimic the action of aldosterone
    • Pheochromocytoma: These catecholamine-secreting tumors result in widespread inappropriate activation of SNS tone on the cardiovascular system.
Clinical Consequences
  • Overview
    • Hypertension itself is relatively asymptomatic; however, the long-term presence of elevated systemic arterial pressures can cause significant pathological changes in a number of organ systems and increase the risk of notable complications.
  • Hypertensive Heart Disease
    • Elevated systemic arterial pressures increase the left ventricular afterload and thus require greater tension within the left ventricular myocardium to successfully eject blood. The heart generally compensates for this increased tension demand by undergoing concentric ventricular hypertrophy which increases ventricular wall thickness and thus reduces the tension required for ejection courtesy of the Law of Laplace. Although concentric ventricular hypertrophy can compensate for the increased hypertensive afterload, physical thickening of the ventricular wall renders the left ventricle less compliant. Consequently, sufficient filling of the thickened left ventricle during diastole can only be achieved with elevations of the left atrial pressure which can be transmitted retrogradely into the pulmonary circulation causing pulmonary edema and thus dyspnea. Eventually however, chronically elevated afterload results in progressive deterioration of cardiac function and signs and symptomology of left heart failure may emerge which in turn can induce right heart failure.
  • Hypertensive Vascular Disease
    • Chronic hypertension produces the characteristic morphological changes of arteriosclerosis. In addition, hypertension significantly increases the progression of atherosclerosis throughout the body. Increased atherosclerotic burden in coronary arteries explains the increased risk of ischemic heart disease and myocardial infarctions in hypertensive individuals. Increased atherosclerotic burden in the carotid arteries and cerebral arteries explains the increased risk of strokes in hypertensive individuals. Chronic hypertension can also weaken large arteries such as the aorta, explaining the increased risk of aortic dissection in hypertensive individuals.
  • Hypertensive Renal Disease