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HIGH BLOOD PRESSURE

Hypertension
ICD-10 I10-I15
ICD-9 401
For other forms of hypertension see hypertension (disambiguation).

Hypertension or high blood pressure is a medical condition wherein the blood pressure is chronically elevated. While it is formally called arterial hypertension, the word "hypertension" without a qualifier usually refers to arterial hypertension.

Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure.

Contents

Definition

Blood pressure is a continuously distributed variable and the risk of associated cardiovascular disease likewise rises continuously. The point at which blood pressure is defined as hypertension is therefore somewhat arbitrary. Presently finding sustained blood pressure of 140/90 mmHg or above, measured on both arms is generally regarded as diagnostic. Because blood pressure readings in many individuals are highly variable — especially in the office setting — the diagnosis of hypertension should be made only after noting a mean elevation on two or more readings on two or more office visits, unless the elevations are severe or associated with compelling indications such as diabetes mellitus, chronic kidney disease, heart failure, post-myocardial infarction, stroke, and high coronary disease risk.

Recently, the JNC 7 (The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure)[1] has defined blood pressure 120/80 mmHg to 139/89 mmHg as "prehypertension." Prehypertension is not a disease category; rather, it is a designation chosen to identify individuals at high risk of developing hypertension.

In patients with diabetes mellitus or kidney disease studies have shown that blood pressure over 130/80 mmHg should be considered a risk factor and may warrant treatment. Even lower numbers are considered diagnostic using home blood pressure monitoring devices.

Etiology of Essential Hypertension

Environment

A number of environmental factors have been implicated in the development of hypertension, including salt intake, obesity, occupation, alcohol intake, family size, excessive noise exposure.[2], and crowding.


Salt Sensitivity

Sodium is the environmental factor that has received the greatest attention. It is to be noted that aproximately 60% of the essential hypertension population is responsive to sodium intake.

Role of Renin

Renin is an enzyme secreted by the juxtaglomerular cells of the kidney and linked with aldosterone in a negative feedback loop.The range of plasma renin activities observed in hypertensive subjects is broader than in normotensive individuals. In consequence, some hypertensive patients have been defined as having low-renin and others as having high-renin essential hypertension.

Insulin Resistance

Insulin is a [hormone] secreted by the pancreas.It main purpose is to regualte the levels of glucose in the body, it also has some other efects. Insulin resistance and/or hyperinsulinemia have been suggested as being responsible for the increased arterial pressure in some patients with hypertension. This feature is now widely recognized as part of syndrome X, or the metabolic syndrome.


Genetics Hypertension is one of the most common complex genetic disorders, with genetic heritability averaging 30%. Data supporting this view emerge from animal studies as well as in population studies in humans. Most of these studies support the concept that the inheritance is probably multifactorial or that a number of different genetic defects each have an elevated blood pressure as one of their phenotypic expressions.

More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing.

Other Etiologies

There are some anecdotal or transient causes of high blood pressure. These are not to be confused with the disease called hypertension in which there is an intrinsic physiopathological mechanism as described above.

Etiology of Secondary Hypertension

Only in a small minority of patients with elevated arterial pressure can a specific cause be identified. These individuals will probably have an endocrine or renal defect that if corrected would bring blood pressure back to normal values.

Renal Hypertension

Hypertension produced by renal disease.A simple explanation for renal vascular hypertension is that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin-angiotensin system.

Adrenal Hypertension

Hypertension is a feature of a variety of adrenal cortical abnormalities. In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension.
In patients with pheochromocytoma increased secretion of epinephrine and norepinephrine by a tumor (most often located in the adrenal medulla) causes excessive stimulation of [adrenergic receptors], which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid).

Hypercalcemia

Coarctation of the Aorta


  • Age. Over time, the number of collagen fibers in artery and arteriole walls increases, making blood vessels stiffer. With the reduced elasticity comes a smaller cross-sectional area in systole, and so a raised mean arterial blood pressure.

Pathophysiology

Most of the secondary mechanisms associated with essential hypertension are generally fully understood, and are outlined at secondary hypertension. However, those associated with essential (primary) hypertension are far less understood. What is known is that cardiac output is raised early in the disease course, with total peripheral resistance (TPR) normal; over time cardiac output drops to normal levels but TPR is increased. Three theories have been proposed to explain this:

  • Inability of the kidneys to excrete sodium, resulting in natriuretic factor (note: the existence of this substance is theoretical) being secreted to promote salt excretion with the side-effect of raising total peripheral resistance.
  • An overactive renin / angiotension system leads to vasoconstriction and retention of sodium and water. The increase in blood volume leads to hypertension.
  • An overactive sympathetic nervous system, leading to increased stress responses.

Is is also known that hypertension is highly hereditable and polymorphic (more than one gene) and a few candidate genes have been postulated as particiapting in the etiology of this condition.]].[3] [4] [5]

Signs and symptoms

Hypertension is usually found incidentally - "case finding" - by healthcare professionals. It normally produces no symptoms.

Malignant hypertension (or accelerated hypertension) is distinct as a late phase in the condition, and may present with headaches, blurred vision and end-organ damage.

It is recognised that stressful situations can increase the blood pressure; if a normally normotensive patient has a high blood pressure only when being reviewed by a healthcare professional, this is colloquially termed white coat effect. Since most of what we know of hypertension and its outcome with or without modification is based on large series of readings in doctors' offices and clinics (e.g., Framingham), it is difficult to be sure that white-coat hypertension is not significant. Ambulatory monitoring may help determine whether traffic and ticket inspectors produce similar sustained rises.

Hypertension is often confused with mental tension, stress and anxiety. While chronic anxiety is associated with poor outcomes in people with hypertension, it alone does not cause it.

Hypertensive urgencies and emergencies

Hypertension is rarely severe enough to cause symptoms. These typically only surface with a systolic blood pressure over 240 mmHg and/or a diastolic blood pressure over 120 mmHg. These pressures without signs of end-organ damage (such as renal failure) are termed "accelerated" hypertension. When end-organ damage is possible or already ongoing, but in absence of raised intracranial pressure, it is called hypertensive emergency. Hypertension under this circumstance needs to be controlled, but prolonged hospitalization is not necessarily required. When hypertension causes increased intracranial pressure, it is called malignant hypertension. Increased intracranial pressure causes papilledema, which is visible on ophthalmoscopic examination of the retina.

Complications

While elevated blood pressure alone is not an illness, it often requires treatment due to its short- and long-term effects on many organs. The risk is increased for:

Pregnancy

Main article: Hypertension of pregnancy

Although few women of childbearing age have high blood pressure, up to 10% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome and eclampsia. Follow-up and control with medication is therefore often necessary.

Diagnosis

Measuring blood pressure

Diagnosis of hypertension is generally on the basis of a persistently high blood pressure. Usually this requires three separate measurements at least one week apart. Exceptionally, if the elevation is extreme, or end-organ damage is present then the diagnosis may be applied and treatment commenced immediately.

Obtaining reliable blood pressure measurements relies on following several rules and understanding the many factors that influence blood pressure reading.

For instance, measurements in control of hypertension should be at least 1 hour after caffeine, 30 minutes after smoking and without any stress. Cuff size is also important. The bladder should encircle and cover two-thirds of the length of the arm. The patient should be sitting for a minimum of five minutes. The patient should not be on any adrenergic stimulants, such as those found in many cold medications.

When taking manual measurements, the person taking the measurement should be careful to inflate the cuff suitably above anticipated systolic pressure. A stethoscope should be placed lightly over the brachial artery. The cuff should be at the level of the heart and the cuff should be deflated at a rate of 2 to 3 mmHg/s. Systolic pressure is the pressure reading at the onset of the sounds described by Korotkoff (Phase one). Diastolic pressure is then recorded as the pressure at which the sounds disappear (K5) or sometimes the K4 point, where the sound is abruptly muffled. Two measurements should be made at least 5 minutes apart, and, if there is a discrepancy of more than 5 mmHg, a third reading should be done. The readings should then be averaged. An initial measurement should include both arms. In elderly patients who particularly when treated may show orthostatic hypotension, measuring lying sitting and standing BP may be useful. The BP should at some time have been measured in each arm, and the higher pressure arm preferred for subsequent measurements.

BP varies with time of day, as may the effectiveness of treatment, and archetypes used to record the data should include the time taken. Analysis of this is rare at present.

Distinguishing primary vs. secondary hypertension

Once the diagnosis of hypertension has been made it is important to attempt to exclude or identify reversible (secondary) causes.

Blood tests commonly performed in a newly diagnosed hypertension patient

Epidemiology

The level of blood pressure regarded as deleterious has been revised down during years of epidemiological studies. A widely-quoted and important series of such studies is the Framingham Heart Study carried out in an American town: Framingham, Massachusetts. The results from Framingham and of similar work in Busselton, Western Australia have been widely applied. To the extent that people are similar this seems reasonable, but there are known to be genetic variations in the most effective drugs for particular sub-populations. Recently (2004), the Framingham figures have been found to overestimate risks for the UK population considerably. The reasons are unclear. Nevertheless the Framingham work has been an important element of UK health policy.

Treatment

Lifestyle modification

Doctors recommend weight loss and regular exercise as the first steps in treating mild to moderate hypertension. These steps are highly effective in reducing blood pressure, but easier to suggest than to achieve, and most patients with moderate or severe hypertension end up requiring indefinite drug therapy to bring their blood pressure down to a safe level. Discontinuing smoking does not directly reduce blood pressure, but is very important for people with hypertension because it reduces the risk of many dangerous outcomes of hypertension, such as stroke and heart attack.

Mild hypertension is usually treated by diet, exercise and improved physical fitness. A diet rich in fruits and vegetables and fat-free dairy foods and low in fat and sodium lowers blood pressure in people with hypertension. Dietary sodium (salt) causes hypertension in some people and reducing salt intake decreases blood pressure in a third of people. Regular mild exercise improves blood flow, and helps to lower blood pressure.

Reduction of environmental stressors such as high sound levels and over-illumination can be an additional method of ameliorating hypertension.

Medications

See main article: Antihypertensives

There are many classes of medications for treating hypertension, together called antihypertensives, which — by varying means — act by lowering blood pressure. Evidence suggests that reduction of the blood pressure by 5-6 mmHg can decrease the risk of stroke by 40%, of coronary heart disease by 15-20%, and reduces the likelihood of dementia, heart failure, and mortality from vascular disease.

Which type of medication to use initially for hypertension has been the subject of several large studies. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) recommends starting with a thiazide diuretic if single therapy is being initiated and another medication is not indicated.[1] This is based on a slightly better outcome for chlortalidone in the ALLHAT study versus other anti-hypertensives and because thiazide diuretics are relatively cheap.[6] A subsequent smaller study (ANBP2) published after the JNC7 did not show this small difference in outcome and actually showed a slightly better outcome for ACE-inhibitors in older male patients.[7]

Despite thiazides being cheap, effective, and recommended as the best first-line drug for hypertension by many experts, they are not prescribed as often as some newer drugs. Arguably, this is because they are off-patent and thus rarely promoted by the drug industry.[8]

Physicians may start with non-thiazide antihypertensive medications if there is a compelling reason to do so. An example is the use of ACE-inhibitors in diabetic patients who have evidence of kidney disease, as they have been shown to both reduce blood pressure and slow the progression of diabetic nephropathy.[9] In patients with coronary artery disease or a history of a heart attack, beta blockers and ACE-inhibitors both lower blood pressure and protect heart muscle over a lifetime, leading to reduced mortality.

Commonly used drugs include:

The aim of treatment should be blood pressure control (<140/90 mmHg for most patients, and lower in certain contexts such as diabetes or kidney disease). Each added drug may reduce the systolic blood pressure by 5-10 mmHg, so often multiple drugs are necessary to achieve blood pressure control.

References

  1. ^ a b Chobanian AV et al (2003). "The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report.". JAMA 289: 2560-72. PMID 12748199.
  2. ^ van Kempen EMM, Kruize H, Boshuizen HC et al (March 2002). "The Association between Noise Exposure and Blood Pressure and Ischemic Heart Disease: A Meta-analysis". Environmental Health Perspectives 110 (3): 307-17. PMID 11882483.
  3. ^ Sagnella GA, Swift PA (June 2006). "The Renal Epithelial Sodium Channel: Genetic Heterogeneity and Implications for the Treatment of High Blood Pressure". Current Pharmaceutical Design 12 (14): 2221-2234. PMID 16787251.
  4. ^ Johnson JA, Turner ST (June 2005). "Hypertension pharmacogenomics: current status and future directions.". Curruent Opinion in Molecular Therapy 7 (3): 218-225. PMID 15977418.
  5. ^ Hideo Izawa; Yoshiji Yamada et al (May 2003). "Prediction of Genetic Risk for Hypertension". Hypertension 41 (5): 1035-1040. PMID 12654703.
  6. ^ ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group (Dec 18 2002). "Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)". JAMA 288 (23): 2981-97. PMID 12479763.
  7. ^ Wing LM, Reid CM, Ryan P et al (Feb 13 2003). "A comparison of outcomes with angiotensin-converting--enzyme inhibitors and diuretics for hypertension in the elderly". NEJM 348 (7): 583-92. PMID 12584366.
  8. ^ Wang TJ, Ausiello JC, Stafford RS (1999). "Trends in Antihypertensive Drug Advertising, 1985–1996". Circulation 99: 2055-2057. PMID 10209012.
  9. ^ Ruggenenti P, Perna A, Gherardi G, Gaspari F, Benini R, Remuzzi G. (1998). "Renal function and requirement for dialysis in chronic nephropathy patients on long-term ramipril: REIN follow-up trial. Gruppo Italiano di Studi Epidemiologici in Nefrologia (GISEN). Ramipril Efficacy in Nephropathy.". Lancet 352: 1252-6. PMID 9788454.

Treatment guidelines need to be updated in accordance with the latest NICE guidelines.

See also

External links