Hypertension is not just one illness but a syndrome with multiple brings about. In most situations, the trigger remains unfamiliar, and also the instances are lumped collectively under the term essential hypertension. However, mechanisms are continuously becoming found out that explain hypertension in new subsets of the formerly monolithic category of important hypertension, and the percentage of instances within the important class continues to decline.
Present suggestions from the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of Higher Blood Stress define typical blood tension as systolic stress less than 120 mm Hg and diastolic stress less than 80 mm Hg. Hypertension is defined as an arterial stress greater than 140/90 mm Hg in adults on at least three consecutive visits towards the doctor’s office.
People whose blood pressure is between typical and 140/90 mm Hg are considered to have pre-hypertension and people whose blood stress falls in this category should appropriately modify their lifestyle to lower their blood pressure to below 120/80 mm Hg. As noted, systolic pressure normally rises throughout life, and diastolic pressure rises until age 50-60 years but then falls, so that pulse stress continues to increase. Within the past, emphasis has been on treating individuals with elevated diastolic stress.
Nevertheless, it now seems that, particularly in elderly individuals, treating systolic high blood pressure is equally essential or even more so in reducing the cardiovascular issues of high blood pressure.
The most common cause of hypertension is increased peripheral vascular resistance. However, because blood pressure equals total peripheral resistance times cardiac output, prolonged increases in cardiac output can also cause hypertension.
These are seen, for example, in hyperthyroidism and beriberi. In addition, increased blood volume causes high blood pressure, especially in individuals with mineralocorticoid excess or renal failure (see later discussion); and increased blood viscosity, if it is marked, can increase arterial pressure.
High blood pressure by itself does not cause symptoms. Headaches, fatigue, and dizziness are sometimes ascribed to hypertension, but nonspecific symptoms such as these are no more common in hypertensives than they are in normotensive controls.
Instead, the condition is found out during routine screening or when patients seek medical advice for its issues. These issues are serious and potentially fatal. They include myocardial infarction, congestive heart failure, thrombotic and hemorrhagic strokes, hypertensive encephalopathy, and renal failure. This really is why higher blood pressure is generally known as “the silent killer”.
Physical findings are also absent in early high blood pressure, and observable alterations are generally discovered only in advanced severe cases. These may include hypertensive retinopathy (ie, narrowed arterioles seen on funduscopic examination) and, in more severe instances, retinal hemorrhages and exudates along with swelling from the optic nerve head (papilledema).
Prolonged pumping against an elevated peripheral resistance causes left ventricular hypertrophy, which can be detected by echocardiography, and cardiac enlargement, which can be detected on physical examination. It is essential to listen with the stethoscope over the kidneys because in renal hypertension (see later discussion) narrowing from the renal arteries may trigger bruits.
These bruits are usually continuous throughout the cardiac cycle. It has been recommended that the blood pressure response to rising in the sitting to the standing position be determined. A blood stress rise on standing sometimes occurs in essential high blood pressure presumably because of a hyperactive sympathetic response towards the erect posture.
This rise is usually absent in other forms of hypertension. Most individuals with essential high blood pressure (60%) have normal plasma renin activity, and 10% have high plasma renin activity. However, 30% have low plasma renin activity. Renin secretion may be reduced by an expanded blood volume in some of these patients, but in others the cause is unsettled, and low-renin important high blood pressure has not yet been separated in the rest of essential high blood pressure as a distinct entity.
In many individuals with hypertension, the condition is benign and progresses slowly; in others, it progresses rapidly. Actuarial data indicate that on average untreated hypertension reduces life expectancy by 10-20 years.
Atherosclerosis is accelerated, and this in turn leads to ischemic heart disease with angina pectoris and myocardial infarctions, thrombotic strokes and cerebral hemorrhages, and renal failure. Another complication of severe high blood pressure is hypertensive encephalopathy, in which there is confusion, disordered consciousness, and seizures. This condition, which requires vigorous treatment, is probably due to arteriolar spasm and cerebral edema.
In all forms of hypertension regardless of trigger, the condition can suddenly accelerate and enter the malignant phase. In malignant hypertension, there is widespread fibrinoid necrosis of the media with intimal fibrosis in arterioles, narrowing them and leading to progressive severe retinopathy, congestive heart failure, and renal failure. If untreated, malignant high blood pressure is usually fatal in 1 year.
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