Monday, January 18, 2010



Hypertension


Hypertension means high blood pressure. This generally means:
  • Systolic blood pressure is consistently over 140 (systolic is the "top" number of your blood pressure measurement, which represents the pressure generated when the heart beats)
  • Diastolic blood pressure is consistently over 90 (diastolic is the "bottom" number of your blood pressure measurement, which represents the pressure in the vessels when the heart is at rest
Either or both of these numbers may be too high.


Classifying Blood Pressure in Adults
Blood pressure is classified by its severity because treatment is based, in part, on severity. When a person's systolic and diastolic pressures fall into different categories, the higher category is used to classify blood pressure. For instance, 160/92 is classified as stage 2 hypertension, and 150/115 is classified as stage 3 hypertension.
The optimal blood pressure for minimizing the risk of cardiovascular problems (such as heart attack and heart failure) and stroke is below 120/80 mm Hg.







Pre-hypertension is when your systolic blood pressure is between 120 and 139 or your diastolic blood pressure is between 80 and 89 on multiple readings. If you have pre-hypertension, you are likely to develop high blood pressure at some point. Therefore, your doctor will recommend lifestyle changes to bring your blood pressure down to normal range.

Etiology and Pathogenesis

Primary hypertension: Primary (essential) hypertension is of unknown etiology; its diverse hemodynamic and pathophysiologic derangements are unlikely to result from a single cause. Heredity is a predisposing factor, but the exact mechanism is unclear. Environmental factors (eg, dietary Na, obesity, stress) seem to act only in genetically susceptible persons. Isolated, perfused kidneys from Dahl salt-sensitive rats (which are genetically prone to hypertension when fed a high-salt diet) do not excrete water or Na as rapidly as those from Dahl salt-resistant rats, even before hypertension develops.
The pathogenic mechanisms must lead to increased total peripheral vascular resistance (TPR) by inducing vasoconstriction, to increased cardiac output (CO), or to both because BP equals CO (flow) times resistance. Although expansion of intravascular and extravascular fluid volume is widely claimed to be important, such expansion can only raise BP by increasing CO (by increasing venous return to the heart), by increasing TPR (by causing vasoconstriction), or by both; it frequently does neither.
Abnormal Na transport across the cell wall due to a defect in or inhibition of the Na-K pump (Na+,K+-ATPase) or due to increased permeability to Na+ has been described in some cases of hypertension. The net result is increased intracellular Na, which makes the cell more sensitive to sympathetic stimulation. Because Ca follows Na, it is postulated that the accumulation of intracellular Ca (and not Na per se) is responsible for the increased sensitivity. Na+,K+-ATPase may also be responsible for pumping norepinephrine back into the sympathetic neurons to inactivate this neurotransmitter. Thus, inhibition of this mechanism could conceivably enhance the effect of norepinephrine. Defects in Na transport have been described in normotensive children of hypertensive parents.
Stimulation of the sympathetic nervous system raises BP, usually more in hypertensive or prehypertensive patients than in normotensive patients. Whether this hyperresponsiveness resides in the sympathetic nervous system itself or in the myocardium and vascular smooth muscle that it innervates is unknown, but it can often be detected before sustained hypertension develops. A high resting pulse rate, which can be a manifestation of increased sympathetic nervous activity, is a well-known predictor of subsequent hypertension. Some hypertensive patients have a higher-than-normal circulating plasma catecholamine level at rest, especially early in clinical development.
Drugs that depress sympathetic nervous activity frequently reduce BP in patients with primary hypertension. However, this observation cannot be considered evidence for implicating the sympathetic nervous system as the causative factor in primary hypertension. In hypertensive patients, the baroreflexes tend to sustain rather than counteract hypertension, a phenomenon known as "resetting the barostats," which may be a result rather than a cause of hypertension. Some hypertensive patients have defective storage of norepinephrine, thus permitting more to circulate.
In the renin-angiotensin-aldosterone system, the juxtaglomerular apparatus helps regulate volume and pressure. Renin, a proteolytic enzyme formed in the granules of the juxtaglomerular apparatus cells, catalyzes conversion of the protein angiotensinogen to angiotensin I, a decapeptide. This inactive product is cleaved by a converting enzyme, mainly in the lung but also in the kidney and brain, to an octapeptide, angiotensin II, which is a potent vasoconstrictor that also stimulates release of aldosterone. Also found in the circulation, the des-ASP heptapeptide (angiotensin III) is as active as angiotensin II in stimulating aldosterone release but has much less pressor activity.
Renin secretion is controlled by at least four mechanisms that are not mutually exclusive: A renal vascular receptor responds to changes in tension in the afferent arteriolar wall; a macula densa receptor detects changes in the delivery rate or concentration of NaCl in the distal tubule; circulating angiotensin has a negative feedback effect on renin secretion; and the sympathetic nervous system stimulates renin secretion via the renal nerve mediated by betareceptors.
Plasma renin activity (PRA) is usually normal in patients with primary hypertension but is suppressed in about 25% and elevated in about 15%. Hypertension is more likely to be accompanied by low renin levels in blacks and the elderly. The accelerated (malignant) phase of hypertension is usually accompanied by elevated PRA. Although angiotensin is generally acknowledged to be responsible for renovascular hypertension, at least in the early phase, there is no consensus regarding the role of the renin-angiotensin-aldosterone system in patients with primary hypertension, even in those with high PRA.
The mosaic theory states that multiple factors sustain elevated BP even though an aberration of only one was initially responsible; eg, the interaction between the sympathetic nervous system and the renin-angiotensin-aldosterone system. Sympathetic innervation of the juxtaglomerular apparatus in the kidney releases renin; angiotensin stimulates autonomic centers in the brain to increase sympathetic discharge. Angiotensin also stimulates production of aldosterone, which leads to Na retention; excessive intracellular Na enhances the reactivity of vascular smooth muscle to sympathetic stimulation.
Hypertension leads to more hypertension. Other mechanisms become involved when hypertension due to an identifiable cause (eg, catecholamine release from a pheochromocytoma, renin and angiotensin from renal artery stenosis, aldosterone from an adrenal cortical adenoma) has existed for some time. Smooth muscle cell hypertrophy and hyperplasia in the arterioles resulting from prolonged hypertension reduce the caliber of the lumen, thus increasing TPR. In addition, trivial shortening of hypertrophied smooth muscle in the thickened wall of an arteriole will reduce the radius of an already narrowed lumen to a much greater extent than if the muscle and lumen were normal. This may be why the longer hypertension has existed, the less likely surgery for secondary causes will restore BP to normal.
Deficiency of a vasodilator substance rather than excess of a vasoconstrictor (eg, angiotensin, norepinephrine) may cause hypertension. The kallikrein system, which produces the potent vasodilator bradykinin, is beginning to be studied. Extracts of renal medulla contain vasodilators, including a neutral lipid and a prostaglandin; absence of these vasodilators due to renal parenchymal disease or bilateral nephrectomy would permit BP to rise. Modest hypertension sensitive to Na and water balance is characteristic in anephric persons (renoprival hypertension).
Endothelial cells produce potent vasodilators (nitric oxide, prostacyclin) and the most potent vasoconstrictor, endothelin. Therefore, dysfunction of the endothelium could have a profound effect on BP. The endothelium's role in hypertension is being investigated. Evidence that hypertensive persons have decreased activity of nitric oxide is preliminary.
Secondary hypertension: Secondary hypertension is associated with renal parenchymal disease (eg, chronic glomerulonephritis or pyelonephritis, polycystic renal disease, collagen disease of the kidney, obstructive uropathy) or pheochromocytoma, Cushing's syndrome, primary aldosteronism, hyperthyroidism, myxedema, coarctation of the aorta, or renovascular disease. It may also be associated with the use of excessive alcohol, oral contraceptives, sympathomimetics, corticosteroids, cocaine, or licorice.
Hypertension associated with chronic renal parenchymal disease results from combination of a renin-dependent mechanism and a volume-dependent mechanism. In most cases, increased renin activity cannot be demonstrated in peripheral blood, and meticulous attention to fluid balance usually controls BP.

Pathology

No early pathologic changes occur in primary hypertension. Ultimately, generalized arteriolar sclerosis develops; it is particularly apparent in the kidney (nephrosclerosis) and is characterized by medial hypertrophy and hyalinization. Nephrosclerosis is the hallmark of primary hypertension. Left ventricular hypertrophy and, eventually, dilation develop gradually. Coronary, cerebral, aortic, renal, and peripheral atherosclerosis are more common and more severe in hypertensives because hypertension accelerates atherogenesis. Hypertension is a more important risk factor for stroke than for atherosclerotic heart disease. Tiny Charcot-Bouchard aneurysms, frequently found in perforating arteries (especially in the basal ganglia) of hypertensives, may be the source of intracerebral hemorrhage.

Hemodynamics

Not all patients with primary hypertension have normal CO and increased TPR. CO is increased, and TPR is inappropriately normal for the level of CO in the early labile phase of primary hypertension. TPR increases and CO later returns to normal, probably because of autoregulation. Patients with high, fixed diastolic pressures often have decreased CO. The role of the large veins in the pathophysiology of primary hypertension has largely been ignored, but venoconstriction early in the disease may contribute to the increased CO.
Plasma volume tends to decrease as BP increases, although some patients have expanded plasma volumes. Hemodynamic, plasma volume, and PRA variations are evidence that primary hypertension is more than a single entity or that different mechanisms are involved in different stages of the disorder.
Renal blood flow gradually decreases as the diastolic BP increases and arteriolar sclerosis begins. GFR remains normal until late in the disease, and, as a result, the filtration fraction is increased. Coronary, cerebral, and muscle blood flow are maintained unless concomitant severe atherosclerosis is present in these vascular beds.
In the absence of heart failure, CO is normal or increased, and peripheral resistance is usually high in hypertension due to pheochromocytoma, primary aldosteronism, renal artery disease, and renal parenchymal disease. Plasma volume tends to be high in hypertension due to primary aldosteronism or renal parenchymal disease and may be subnormal in pheochromocytoma.
Systolic hypertension (with normal diastolic pressure) is not a discrete entity. It often results from increased CO or stroke volume (eg, labile phase of primary hypertension, thyrotoxicosis, arteriovenous fistula, aortic regurgitation); in elderly persons with normal or low CO, it usually reflects inelasticity of the aorta and its major branches (arteriosclerotic hypertension).
Symptoms   
Usually, no symptoms are present. Occasionally, you may experience a mild headache. If your headache is severe, or if you experience any of the symptoms below, you must be seen by a doctor right away. These may be a sign of dangerously high blood pressure (called malignant hypertension) or a complication from high blood pressure.
  • tiredness
  • confusion
  • vision changes
  • angina-like chest pain (crushing chest pain)
  • heart failure
  • blood in urine
  • nosebleed
  • irregular heartbeat
  • ear noise or buzzing

Signs and tests   
Hypertension may be suspected when the blood pressure is high at any single measurement. It is confirmed through blood pressure measurements that are repeated over time. Blood pressure consistently elevated over 140 systolic or 90 diastolic is called hypertension. Your doctor will look for signs of complications to your heart, kidneys, eyes, and other organs in your body.

Systolic blood pressure consistently between 130 and 139 or diastolic blood pressure consistently between 80 and 89 is called pre-hypertension. Your doctor will recommend and encourage lifestyle changes including weight loss, exercise, and nutritional changes.

Tests for suspected causes and complications may be performed. These are guided by the symptoms presented, history, and results of examination.

Treatment   

The goal of treatment is to reduce blood pressure to a level where there is decreased risk of complications. Treatment may occur at home with close supervision by the health care provider, or may occur in the hospital.

Medications may include diuretics, beta-blockers, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), or alpha blockers. Medications such as hydralazine, minoxidil, diazoxide, or nitroprusside may be required if the blood pressure is very high.
Have your blood pressure checked at regular intervals (as often as recommended by your doctor.)
Lifestyle modifications: Extra rest, prolonged vacations, moderate weight reduction, and dietary Na restriction are not as effective as antihypertensive drug therapy. Patients with uncomplicated hypertension need not restrict their activities as long as their BP is controlled. Dietary restrictions can help control diabetes mellitus, obesity, and blood lipid abnormalities. In stage 1 hypertension, weight reduction to ideal levels, modest dietary Na restriction to < 2 g/day, and alcohol consumption to < 1 oz/day may make drug therapy unnecessary. Prudent exercise should be encouraged. Smoking should be unambiguously discouraged.

Dietary Approach to Stop Hypertension 1

Expectations (prognosis)
An untreated hypertensive patient is at great risk of disabling or fatal left ventricular failure, MI, cerebral hemorrhage or infarction, or renal failure at an early age. Hypertension is the most important risk factor predisposing to stroke. It is one of three risk factors (along with cigarette smoking and hypercholesterolemia) predisposing to coronary atherosclerosis. The higher the BP and the more severe the changes in the retina, the worse the prognosis. Fewer than 5% of patients with group 4 or malignant hypertension characterized by papilledema and < 10% of patients with group 3 changes in the fundus survive 1 yr without treatment. Effective medical control of hypertension will prevent or forestall most complications and will prolong life in patients with ISH or diastolic hypertension. Coronary artery disease is the most common cause of death among treated hypertensive patients. Systolic BP is a more important predictor of fatal and nonfatal cardiovascular events than diastolic BP. In a follow-up of men screened for the Multiple Risk Factor Intervention Trial, overall mortality was related to systolic BP, regardless of diastolic BP.

Complications   
  • hypertensive heart disease
  • heart attacks
  • congestive heart failure
  • blood vessel damage (arteriosclerosis)
  • aortic dissection
  • kidney damage
  • kidney failure
  • stroke
  • brain damage
  • loss of vision 

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