Chronic hypertension: Difference between revisions

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'''Associate Editor in Chief''': Firas Ghanem, M.D. and Atif Mohammad, M.D.
'''Associate Editor in Chief''': Firas Ghanem, M.D. and Atif Mohammad, M.D.


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==[[Hypertension overview|Overview]]==


==Overview==
==[[Hyptertension classification|Classification]]==
'''Hypertension''', commonly referred to as "'''high blood pressure'''" or '''HTN''', is a medical condition in which the [[blood pressure]] is chronically elevated.<ref>{{KMLEref|hypertension|07-04-17}}</ref> While it is formally called '''arterial hypertension''', the word "hypertension" without a qualifier usually refers to [[artery|arterial]] hypertension. Hypertension can be classified as either '''essential''' (primary) or '''secondary'''. Essential hypertension indicates that no specific medical cause can be found to explain a patient's condition. [[Secondary hypertension]] indicates that the high blood pressure is a result of (i.e. secondary to) another condition, such as [[kidney disease]] or certain [[tumor]]s (especially of the [[adrenal gland]]). Persistent hypertension is one of the risk factors for [[stroke]]s, [[myocardial infarction|heart attacks]], [[heart failure]] and arterial [[aneurysm]], and is a leading cause of [[chronic renal failure]].  Even moderate elevation of arterial blood pressure leads to shortened life expectancy.  At severely high pressures, mean arterial pressures 50% or more above average, a person can expect to live no more than just a few years unless appropriately treated.<ref>Textbook of Medical Physiology, 7th Ed., Guyton & Hall, Elsevier-Saunders, ISBN 0-7216-0240-1, page 220.</ref>


Hypertension is considered to be present when a person's [[systole (medicine)|systolic]] blood pressure is consistently 140 mmHg or greater, and/or their [[diastole|diastolic]] blood pressure is consistently 90&nbsp;mmHg or greater.<ref>http://www.nlm.nih.gov/cgi/mesh/2007/MB_cgi?mode=&index=6693</ref> Recently, as of 2003, the ''Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure''<ref name="jnc7">{{
==[[Hypertension pathophysiology|Pathophysiology]]==
cite journal
|url=http://jama.ama-assn.org/cgi/content/full/289.19.2560v1
|author=Chobanian AV et al
|journal=[[Journal of the American Medical Association|JAMA]]
|title=The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report.
|year = 2003
|volume = 289
|pages = 2560-72
|pmid = 12748199
}}</ref> 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. The [http://www.mayoclinic.com/health/high-blood-pressure/DS00100/DSECTION=6 Mayo Clinic website] specifies blood pressure is "normal if it's below 120/80" but that "some data indicate that 115/75 mm Hg should be the gold standard." In patients with [[diabetes mellitus]] or [[Nephropathy|kidney disease]] studies have shown that blood pressure over 130/80 mmHg should be considered high and warrants further treatment. Even lower numbers are considered diagnostic using home blood pressure monitoring devices.
{|
|-style="background:silver; color:black"
| '''''Blood Pressure''''' || '''''Systolic''''' (mm Hg) || '''''Diastolic''''' (mm Hg)
|-style="background:silver; color:black"
| '''Optimal''' || '''< 120''' || '''< 80'''
|- style="background:silver; color:black"
| '''Normal''' || '''< 130''' || '''< 85'''
|-style="background:silver; color:black"
| '''High Normal''' || '''130-139''' || '''85-89'''
|-style="background:silver; color:black"
| '''Mild Hypertension''' || '''140-159''' || '''90-99'''
|-style="background:silver; color:black"
| '''Moderate Hypertension''' || '''160-179''' || '''100-109'''
|-style="background:silver; color:black"
| '''Severe Hypertension''' || '''180-209''' || '''110-119'''
|-style="background:silver; color:black"
| '''Very Severe Hypertension''' || '''> 210''' || '''> 120'''
|}


=== Salt sensitivity ===
==[[Hypertension epidemiology and demographics|Epidemiology & Demographics]]==
[[Salt#Health effects|Sodium]] is the environmental factor that has received the greatest attention. Approximately 60% of the essential hypertension population is responsive to sodium intake. This is due to the fact that increasing amounts of salt in a person's bloodstream causes the body to draw more water, increasing the pressure on the blood vessel walls.In addition to sodium,choride plays an important role as it causes volume expansion increasing blood pressure as sodium with combined iwth other anions does not increase blood pressure.<ref>{{cite journal |author=Kurtz TW, Al-Bander HA, Morris RC |title="Salt-sensitive" essential hypertension in men. Is the sodium ion alone important? |journal=[[N. Engl. J. Med.]] |volume=317 |issue=17 |pages=1043–8 |year=1987 |month=October |pmid=3309653 |doi= |url=}}</ref>
Also salt sensitivity is known to be increased in increasing age,obesity,African americans and metabolic syndrome.<ref>{{cite journal |author=Obarzanek E, Proschan MA, Vollmer WM, ''et al.'' |title=Individual blood pressure responses to changes in salt intake: results from the DASH-Sodium trial |journal=[[Hypertension]] |volume=42 |issue=4 |pages=459–67 |year=2003 |month=October |pmid=12953018 |doi=10.1161/01.HYP.0000091267.39066.72 |url=http://hyper.ahajournals.org/cgi/pmidlookup?view=long&pmid=12953018}}</ref>
====Mechanisms====
The known mechanisms for salt-sensitvity is incraesed salt intake over a long period of time leads to impaired excretion of salt which causes hypertension.But there are several other pathways involved in the pathophysiology of salt-sensitivity leading to hypertension.A recent study showed that salt-sensitive patients are known to have a dysregulated Renin-Angiotensin pathway and patients show an abnormal vascular response to Angiotensin II.<ref>{{cite journal |author=Chamarthi B, Williams JS, Williams GH |title=A mechanism for salt-sensitive hypertension: abnormal dietary sodium-mediated vascular response to angiotensin-II |journal=[[J. Hypertens.]] |volume=28 |issue=5 |pages=1020–6 |year=2010 |month=May |pmid=20216091 |doi=10.1097/HJH.0b013e3283375974 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0263-6352&volume=28&issue=5&spage=1020}}</ref>
Increased sodium re absorption, though not well understood is mostly related abnormalities across Na-H proximal tubule channels,Na-K-Cl co-transporter across the thick ascending limb,Na-Cl distal tubule co-transporter and epithelial Na channels.Dietary deficiency in potassium is also known to trigger increased sodium sensitivity in patients in particular African-Americans, but the mechanism is still not clearly determined.


==[[Hypertension natural history|Complications]]==


=== Role of renin ===
==[[Hypertension causes|Causes of Hypertension]]==
[[Renin]] is a [[hormone]] secreted by the [[juxtaglomerular cell]]s of the kidney and linked with [[aldosterone]] in a negative feedback loop. The range of renin activity observed in hypertensive subjects tends to be broader than in normotensive individuals. In consequence, some hypertensive patients have been defined as having low-renin and others as having essential hypertension. Low-renin hypertension is more common in African Americans than Caucasians and may explain why they tend to respond better to diuretic therapy than drugs that interfere with the renin-angiotensin system.


High Renin levels predispose to Hypertension:
==[[Hypertension differential diagnosis|Complete List of Differential Diagnoses]]==
Increased Renin --> Increased Angiotensin II --> Increased Vasoconstriction, Thirst/ADH and Aldosterone --> Increased Sodium Reabsorption in the Kidneys (DCT and CD) --> Increased Blood Pressure.
 
=== Insulin resistance ===
[[Insulin]] is a polypeptide [[hormone]] secreted by the [[pancreas]]. Its main purpose is to regulate the levels of [[glucose]] in the body antagonistically with [[glucagon]] through negative feedback loops. Insulin also exhibits vasodilatory properties. In normotensive individuals, insulin may stimulate sympathetic activity without elevating mean arterial pressure. However, in more extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity may over-ride the vasodilatory effects of insulin. 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 [[metabolic syndrome|syndrome X]], or the [[metabolic syndrome]].
 
=== Sleep apnea ===
[[Sleep apnea]] is a common, under-recognized cause of hypertension.<ref name="Sleep Apnea">{{
cite journal
|url=http://www.aafp.org/afp/20020115/229.html
|author=Silverberg DS, Iaina A and Oksenberg A
|journal=American Family Physicians
|title=Treating Obstructive Sleep Apnea Improves Essential Hypertension and Quality of Life
|year = 2002
|month = January
|volume = 65
|issue = 2
|pages = 229-36
|pmid = 11820487
}}</ref> It is best treated with [[UPPP]], [[tonsilectomy]], [[adenoidectomy]], [[sinus surgery]], or weight loss, nocturnal nasal [[CPAP|positive airway pressure]], or the [[Mandibular advancement splint]] (MAS).
 
=== Genetics ===
Hypertension is one of the most common complex 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 below.
 
== 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, could bring blood pressure back to normal values.
 
;Renal hypertension
:Hypertension produced by diseases of the [[kidney]]. This includes diseases such as [[polycystic kidney disease]] or chronic [[glomerulonephritis]]. Hypertension can also be produced by diseases of the [[renal artery|renal arteries]] supplying the kidney. This is known as [[renovascular hypertension]]; it is thought 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 [[catecholamines]] such as [[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]]).
 
;[[Coarctation of the aorta]]
 
;Diet
:The North American diet that is high in fat and salt has been proven to exacerbate hypertension. A study in the U.S. found that patients placed on a strict [[vegetarian]] diet showed a significant benefit to their condition over the one year. Certain medications, especially NSAIDS (Motrin/ibuprofen) and steroids can cause hypertension.  Imported licorice (''Glycyrrhiza glabra'') inhibits the 11-hydroxysteroid hydrogenase enzyme (catalyzes the reaction of cortisol to cortison) which allows cortisol to stimulate the Mineralocorticoid Receptor (MR) which will lead to effects similar to hyperaldosteronism, which itself is a cause of hypertension. [Reference: Harrisons Internal Medicine, online edition (2007-04-14)]
 
;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.
 
;[[Acromegaly]]
 
== Pathophysiology ==
Most of the secondary mechanisms associated with 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]] factors such as [[Atrial Natriuretic Factor]] 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.
It is also known that hypertension is highly heritable and [[polygenic]] (caused by more than one gene) and a few candidate [[genes]] have been postulated in the etiology of this condition.<ref name="polymorphism">{{cite journal |author= Sagnella GA, Swift PA |journal=Current Pharmaceutical Design |title=The Renal Epithelial Sodium Channel: Genetic Heterogeneity and Implications for the Treatment of High Blood Pressure |year = 2006 |month = June |volume = 12 |issue = 14 |pages = 2221-2234 |id = PMID 16787251}}</ref><ref name="polymorphism2">{{cite journal |author= Johnson JA, Turner ST |journal=Current Opinion in Molecular Therapy |title=Hypertension pharmacogenomics: current status and future directions. |year = 2005 |month = June |volume = 7 |issue = 3 |pages = 218-225 |id = PMID 15977418}}</ref><ref name="polymorphism3">{{cite journal|author= Hideo Izawa; Yoshiji Yamada et al |journal=Hypertension |title=Prediction of Genetic Risk for Hypertension |year = 2003 |month = May |volume = 41 |issue = 5 |pages = 1035-1040 |id = PMID 12654703 | url=http://hyper.ahajournals.org/cgi/content/short/01.HYP.0000065618.56368.24v1}}</ref>
 
== Signs and symptoms ==
Hypertension is usually found incidentally - "case finding" - by healthcare professionals during a routine checkup. The only test for hypertension is a blood pressure measurement. Hypertension in isolation usually produces no symptoms although some people report headaches, fatigue, dizziness, blurred vision, facial flushing or [[tinnitus]]. <ref>{{cite web|url=http://www.treatment-for.com/high-blood-pressure-symptoms.htm|title=Symptoms of High Blood Pressure}}</ref>
 
[[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.
 
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. Accelerated hypertension is associated with somnolence, confusion, visual disturbances, and nausea and vomiting (hypertensive encephalopathy). <ref name=health.am>{{cite web | H. Michael MacMay, MD, MPH; Michael Sutters, MD | title =Hypertension symptoms and signs | publisher=Armenian Medical Network | work =Systemic Hypertension - Hypertension Health Center | url=http://www.health.am/hypertension/hypertension-symptoms-and-signs/ | year = 2006}}</ref>
 
=== 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 [[ophthalmoscopy|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:
* [[Cerebrovascular accident]] (CVAs or strokes)
* [[Myocardial infarction]] (heart attack)
* [[Hypertensive cardiomyopathy]] ([[heart failure]] due to chronically high blood pressure)
* [[Hypertensive retinopathy]] - damage to the [[retina]]
* [[Hypertensive nephropathy]] - [[chronic renal failure]] due to chronically high blood pressure
 
=== Pregnancy ===
{{main|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.
 
===Children and adolescents ===
As with adults, blood pressure is a variable parameter in children. It varies between individuals and within individuals from day to day and at various times of the day. The epidemic of childhood obesity, the risk of developing left ventricular hypertrophy, and evidence of the early development of atherosclerosis in children would make the detection of and intervention in childhood hypertension important to reduce long-term health risks; however, supporting data are lacking.
 
Most childhood hypertension, particularly in preadolescents, is secondary to an underlying disorder. Renal parenchymal disease is the most common (60 to 70 percent) cause of hypertension. Adolescents usually have primary or essential hypertension, making up 85 to 95 percent of cases. <ref name=aafp>{{cite web | GREGORY B. LUMA, M.D., and ROSEANN T. SPIOTTA, M.D., Jamaica Hospital Medical Center | title =Hypertension in Children and Adolescents | publisher=American Academy of Family Physicians | work =Hypertension in Children and Adolescents | url=http://www.aafp.org/afp/20060501/1558.html | year = 2006}}</ref>
==Complete List of Differential Diagnoses<ref>isbn=140510368X Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:85</ref><ref>isbn=1591032016 Sailer, Christian, Wasner, Susanne.  Differential Diagnosis Pocket.  Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:194-195</ref>==
* [[Acromegaly]]
* [[Acute Renal Failure]]
* After [[kidney transplantation]]
* [[Alcohol]] withdrawal
* Analgesic [[nephritis]]
* [[Aneurysm]]
* [[Anxiety]]
* [[Aortic isthmus stenosis]]
* [[Aortic Regurgitation]]
* [[Arteriosclerosis]]
* [[Arteriovenous fistula]]
* [[Arteritis]]
* [[Burns]]
* [[Bartter's Syndrome]]
* [[Carcinoid Syndrome]]
* [[Chronic Renal Disease]]
* [[Coarctation of aorta]]
* [[Cocaine]] use
* Compression [[tumor]]
* [[Congenital adrenal hyperplasia]]
* [[Conn's Syndrome]]
* [[Cushing's Syndrome]]
* [[Diabetic nephropathy]]
* Dialysis
* [[Dissection of the aorta]]
* Dissection of the [[renal arteries]]
* [[Drugs]]
* [[Eclampsia]]
* [[Elevated intracranial pressure]]
* Embolism or thrombosis of the [[renal artery]]
* [[Endothelin]] producing tumor
* Fibromuscular hyperplasia
* Gestational hypertension
* [[Guillain-Barre Syndrome]]
* [[Gitelman's Syndrome]]
* [[Hydronephrosis]]
* [[Hyperthyroidism]]
* [[Hyperventilation]]
* [[Hypoglycemia]]
* Interstitial [[nephritis]]
* Kidney involvement in systemic diseases
* [[Liddle's Syndrome]]
* [[Meningitis]]
* [[Obesity]]
* [[Pain]]
* [[Pancreatitis]]
* [[Patent ductus arteriosus]]
* Perioperative
* Perirenal hematoma
* [[Pheochromocytoma]]
* [[Polycystic kidney disease]]
* [[Polycythemia]]
* [[Polyradiculitis]]
* [[Porphyria]]
* Post-exercise
* [[Preeclampsia]]
* [[Pregnancy]]-induced hypertension
* [[Primary hyperaldosteronism]]
* [[Primary hyperparathyroidism]]
* [[Quadriplegia]]
* Reflux nephropathy
* [[Renal Artery Stenosis]]
* [[Renin]] producing tumors
* [[Retroperitoneal Fibrosis]]
* [[Sleep Apnea]]
* [[Stress]]
* [[Third degree AV block]]
* [[Thrombosis]]
* [[Transfusion]] of large blood volumes
* Trauma to the [[renal artery]]
* [[Traumatic brain injury]]
* "White coat" hypertension


== Diagnosis ==
== Diagnosis ==
===Measuring blood pressure===
: [[Hypertension history & symptoms|Signs and symptoms]] | [[Hypertension blood pressure|Measuring blood pressure]] | [[Hypertension physical examination|Physical Examination]] | [[Hypertension laboratory tests|Laboratory Tests]] | [[Hypertension additional tests#Electrocardiogram|Electrocardiogram]] | [[Hypertension additional tests#Chest X-ray|Chest X-ray]] | [[Hypertension additional tests#MRI or CT|MRI or CT]] | [[Hypertension additional tests#Echocardiography or Ultrasound|Echocardiography or Ultrasound]]  
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<ref name="pmid7707630">{{cite journal| author=Reeves RA| title=The rational clinical examination. Does this patient have hypertension? How to measure blood pressure. | journal=JAMA | year= 1995 | volume= 273 | issue= 15 | pages= 1211-8 | pmid=7707630 | doi=10.1001/jama.1995.03520390071036|}} </ref>.
 
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. The person should inflate the cuff to 200 mmHg and then slowly release the air while palpating the radial pulse. After one minute, the cuff should be reinflated to 30 mmHg higher than the pressure at which the radial pulse was no longer palpable. 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 [[Korotkoff sound|sounds]] described by [[Nikolai Korotkoff|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 [[Medical informatics|archetypes]] used to record the data should include the time taken.  Analysis of this is rare at present.
 
Automated machines are commonly used and reduce the variability in manually collected readings <ref name="pmid2294682">{{cite journal | author = White W, Lund-Johansen P, Omvik P | title = Assessment of four ambulatory blood pressure monitors and measurements by clinicians versus intraarterial blood pressure at rest and during exercise. | journal = Am J Cardiol | volume = 65 | issue = 1 | pages = 60-6 | year = 1990 | id = PMID 2294682}}</ref>. Routine measurements done in medical offices of patients with known hypertension may incorrectly diagnose 20% of patients with uncontrolled hypertension <ref name="pmid16050862">{{cite journal | author = Kim J, Bosworth H, Voils C, Olsen M, Dudley T, Gribbin M, Adams M, Oddone E | title = How well do clinic-based blood pressure measurements agree with the mercury standard? | journal = J Gen Intern Med | volume = 20 | issue = 7 | pages = 647-9 | year = 2005 | id = PMID 16050862}}</ref>
 
===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. 
* Over 90% of adult hypertension has no clear cause and is therefore called '''essential/primary hypertension'''. Often, it is part of the [[metabolic syndrome|metabolic "syndrome X"]] in patients with [[insulin resistance]]: it occurs in combination with [[diabetes mellitus]] (type 2), [[combined hyperlipidemia]] and [[central obesity]]. 
* [[Secondary hypertension]] is more common in preadolescent children, with most cases caused by [[renal disease]]. Primary or [[essential hypertension]] is more common in adolescents and has multiple risk factors, including obesity and a family history of hypertension. <ref name="pmid16719248">{{cite journal | author = Luma GB, Spiotta RT | title = Hypertension in children and adolescents. | journal = Am Fam Physician | volume = 73 | issue = 9 | pages = 1558-68 | month = may | year = 2006 | id = PMID 16719248}}</ref>
 
===Investigations commonly performed in newly diagnosed hypertension===
Tests are undertaken to identify possible causes of secondary hypertension, and seek evidence for end-organ damage to the heart itself or the eyes (retina) and kidneys. Diabetes and raised cholesterol levels being additional risk factors for the development of cardiovascular disease are also tested for as they will also require management.
 
[[Blood test]]s commonly performed include:
* [[Creatinine]] ([[renal function]]) - to identify both underlying renal disease as a cause of hypertension and conversely hypertension causing onset of kidney damage. Also a baseline for later monitoring the possible side-effects of certain antihypertensive drugs.
* [[Electrolyte]]s ([[sodium]], [[potassium]])
* [[Glucose]] - to identify [[diabetes mellitus]]
* [[Cholesterol]]
 
Additional tests often include:
* Testing of urine samples for [[proteinuria]] - again to pick up underlying kidney disease or evidence of hypertensive renal damage.
* [[Electrocardiogram]] (EKG/ECG) - for evidence of the heart being under strain from working against a high blood pressure. Also may show resulting thickening of the heart muscle ([[left ventricular hypertrophy]]) or of the occurrence of previous silent cardiac disease (either subtle electrical conduction disruption or even a myocardial infarction).
* [[Chest X-ray]] - again for signs of cardiac enlargement or evidence of [[Congestive heart failure|cardiac failure]].
 
== Physical Examination ==
* Look for end organ disease:
*:* [[Coronary Artery Disease]] (CAD) symptoms
*:* Retinal hemorrhage
*:* Retinalvenous crossing changes
*:* Vascular disease
* Heart exam
* Lung exam
* Neurological Examination
* Possible symptoms:
*:* [[Osteoporosis]]
*:* [[Obesity]]
*:* Muscle weakness
*:* Moon facies
*:* [[Hirsutism]]
*:* Elevated lipids
*:* Elevated sugar
*:* Low [[potassium]]
*:* Elevated [[creatinine]]
*:* [[Ddx:Headache|Headaches]]
*:* [[Palpitation]]s
*:* Diaphoresis
*:* Labile blood pressure
 
== Laboratory Findings ==
* [[Urinalysis]]
* [[Glucose]]
* [[Blood urea nitrogen]] ([[BUN]]) / [[creatinine]]
* Basic metabolic panel
* [[Calcium]]
* [[Lipid]]s
* Urinary [[albumin]]
* [[Glomerular filtration rate]]
=== Electrolyte and Biomarker Studies ===
* [[Electrolyte]]s
=== [[Electrocardiogram]] ===
* ECG to make accurate diagnosis
=== Echocardiography or Ultrasound ===
* [[Echocardiogram]] for diagnosis
===MRI or CT===
* see [[Cardiac MRI]] in [[Hypertension]]
 
== 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 ==
== Treatment ==
<!---need to be updated in accordance with the latest NICE guidelines (28th June 2006) --->
<!---need to be updated in accordance with the latest NICE guidelines (28th June 2006) --->
===Lifestyle modification (nonpharmacologic treatment)===
: [[Hypertension lifestyle modification|Lifestyle modification]] (nonpharmacologic treatment) | [[Hypertension medical treatment|Medical Treatment]]
* [[weight loss|Weight reduction]] and regular aerobic exercise (e.g. jogging) are recommended as the first steps in treating mild to moderate hypertension. Regular mild exercise improves blood flow and helps to reduce resting heart rate and blood pressure. These steps are highly effective in reducing blood pressure, although drug therapy is still necessary for many patients with moderate or severe hypertension to bring their blood pressure down to a safe level.
 
* Reducing [[sodium chloride|sodium (salt)]] [[Dieting|diet]] is proven very effective: it decreases blood pressure in about 60% of people (see above). Many people choose to use a [[salt substitute]] to reduce their salt intake.
 
* Additional dietary changes beneficial to reducing blood pressure includes the [[DASH diet]] (Dietary Approaches to Stop Hypertension), which is rich in fruits and vegetables and low fat or fat-free dairy foods. This diet is shown effective based on National Institutes of Health sponsored research. In addition, an increase in daily calcium intake has also been shown to be highly effective in reducing blood pressure. Fruits, vegetables, and nuts have the added benefit of increasing dietary [[potassium]], which theoretically can offset the effect of sodium and act on the kidney to decrease blood pressure.
 
* Discontinuing [[tobacco smoking]] and alcohol drinking has been shown to lower blood pressure. The exact mechanisms are not fully understood, but blood pressure (especially systolic) always transiently increases following alcohol and/or nicotine consumption. Besides, abstention from cigarette smoking is important for people with hypertension because it reduces the risk of many dangerous outcomes of hypertension, such as stroke and heart attack. Note that coffee drinking (caffeine ingestion) also increases blood pressure transiently, but does ''not'' produce chronic hypertension.
 
* Relaxation therapy, such as meditation, that reduces environmental stress, [[Noise health effects|high sound levels]] and [[over-illumination]] can be an additional method of ameliorating hypertension. [[Biofeedback]] is also used [http://www.mayoclinic.org/news2006-rst/3334.html] particularly device guided paced breathing [http://www.emaxhealth.com/106/5912.html] [http://www.medscape.com/viewarticle/539099]. Obviously, the effectiveness of relaxation therapy relies on the patient's attitude and compliance.
 
===Impact of race===
{{seealso|Race and health}}
In a summary of recent research Jules P. Harrell, Sadiki Hall, and James Taliaferro  describe how a growing body of research has explored the impact of encounters with racism or discrimination on physiological activity. "Several of the studies suggest that higher blood pressure levels are associated with the tendency not to recall or report occurrences identified as racist and discriminatory."<ref>[http://www.ajph.org/cgi/content/abstract/93/2/243 Physiological Responses to Racism and Discrimination: An Assessment of the Evidence]</ref> In other words, failing to recognize instances of racism has a direct impact on the blood pressure of the person experiencing the racist event. Investigators have reported that physiological arousal is associated with laboratory analogues of ethnic discrimination and mistreatment.
 
The interaction between high blood pressure and racism has also been documented in studies by [[Claude Steele]], Joshua Aronson, and Steven Spencer on what they term "stereotype threat".<ref>African Americans and high blood pressure: the role of stereotype threat. Blascovich J, Spencer SJ, Quinn D and Steele C. Department of Psychology, University of California, Santa Barbara 93106, USA.</ref>
 
===Medications===
{{main|Antihypertensive}}
There are many classes of medications for treating hypertension, together called [[antihypertensive]]s, which &mdash; by varying means &mdash; 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.
 
The aim of treatment should be blood pressure control to <140/90 mmHg for most patients, and lower in certain contexts such as diabetes or kidney disease (some medical professionals recommend keeping levels below 120/80 mmHg).[http://www.webmd.com/content/article/73/88927.htm] Each added drug may reduce the systolic blood pressure by 5-10 mmHg, so often multiple drugs are necessary to achieve blood pressure control.
 
Commonly used drugs include:
*[[ACE inhibitor]]s such as [[captopril]], [[enalapril]], [[fosinopril]] (Monopril), [[lisinopril]] (Zestril), [[quinapril]], [[ramipril]] (Altace)
*[[Angiotensin II receptor antagonist]]s: eg, [[telmisartan]] (Micardis, Pritor), [[irbesartan]] (Avapro), [[losartan]] (Cozaar), [[valsartan]] (Diovan), [[candesartan]] (Atacand)
*[[Alpha blocker]]s such as [[doxazosin]], [[prazosin]], or [[terazosin]]
*[[Beta blocker]]s such as [[atenolol]], [[labetalol]], [[metoprolol]] (Lopressor, Toprol-XL), [[propranolol]].
*[[Calcium channel blocker]]s such as nifedipine (Adalat®)<ref>[http://www.adalat.com/professionals-home/research/publications/ Kragten JA, Dunselman PHJM. Nifedipine gastrointestinal therapeutic system (GITS) in the treatment of coronary heart disease and hypertension. Expert Rev Cardiovasc Ther 5 (2007):643-653. FULL TEXT!] </ref> [[amlodipine]] (Norvasc), [[diltiazem]], [[verapamil]]
*Direct renin inhibitors such as [[aliskiren]] (Tekturna)
*[[Diuretic]]s: eg, [[bendroflumethiazide]], [[chlortalidone]], [[hydrochlorothiazide]] (also called HCTZ)
*Combination products (which usually contain HCTZ and one other drug)
 
====Influence of age and race on medication efficacy====
A [[randomized controlled trial]] by the Veterans Affairs Cooperative Study Group on Antihypertensive Agents reported the influence of patient age and race on the proportion of patients whose blood pressure was controlled by different agents.<ref name="pmid8446138">{{cite journal |author=Materson BJ, Reda DJ, Cushman WC, ''et al'' |title=Single-drug therapy for hypertension in men. A comparison of six antihypertensive agents with placebo. The Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents |journal=N. Engl. J. Med. |volume=328 |issue=13 |pages=914-21 |year=1993 |pmid=8446138 |doi=|url=http://content.nejm.org/cgi/content/full/328/13/914}}</ref><ref name="pmid8177286">{{cite journal |author=Materson BJ, Reda DJ |title=Correction: single-drug therapy for hypertension in men |journal=N. Engl. J. Med. |volume=330 |issue=23 |pages=1689 |year=1994 |pmid=8177286 |doi=|url=http://content.nejm.org/cgi/content/full/330/23/1689}} [http://content.nejm.org/cgi/content/full/330/23/1689/T1 Summary]</ref> For example:
* Less than 7% of young white patients responded to a [[diuretic]] ([[hydrochlorothiazide]])
* Only 6% of older black patients responded to an [[ACE inhibitor]] ([[captopril]])
The effect of age and race are in part due to differences in plasma [[renin]] activity.<ref name="pmid1538559">{{cite journal |author=Blaufox MD, Lee HB, Davis B, Oberman A, Wassertheil-Smoller S, Langford H |title=Renin predicts diastolic blood pressure response to nonpharmacologic and pharmacologic therapy |journal=JAMA |volume=267 |issue=9 |pages=1221-5 |year=1992 |pmid=1538559 |doi=}}</ref><ref name="pmid9777817">{{cite journal |author=Preston RA, Materson BJ, Reda DJ, ''et al'' |title=Age-race subgroup compared with renin profile as predictors of blood pressure response to antihypertensive therapy. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents |journal=JAMA |volume=280 |issue=13 |pages=1168-72 |year=1998 |pmid=9777817 |doi=}}</ref>
 
====Choice of initial medication====
Which type of many medications should be used initially for hypertension has been the subject of several large studies and various national guidelines.
 
Regarding cardiovascular outcomes, the ALLHAT study showed a slightly better outcome and cost-effectiveness for the [[thiazide]] diuretic [[chlortalidone]] compared to other anti-hypertensives in an ethnically mixed population.<ref name="allhat">{{cite journal
|url=http://jama.ama-assn.org/cgi/content/full/288/23/2981
|author=ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group
|journal=[[Journal of the American Medical Association|JAMA]]
|title=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)
|year = 2002
|month = Dec 18
|volume = 288
|issue = 23
|pages = 2981-97
|id = PMID 12479763
}}</ref>
Whilst a subsequent smaller study (ANBP2) did not show this small difference in outcome and actually showed a slightly better outcome for ACE-inhibitors in older white male patients.<ref name="anbp2">{{
cite journal
|url=http://content.nejm.org/cgi/content/abstract/348/7/583
|author=Wing LM, Reid CM, Ryan P et al
|journal=[[N Engl J Med|NEJM]]
|title=A comparison of outcomes with angiotensin-converting--enzyme inhibitors and diuretics for hypertension in the elderly
|year = 2003
|month = Feb 13
|volume =  348
|issue = 7
|pages = 583-92
|id = PMID 12584366
}}</ref>
 
Whilst thiazides are 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.<ref name="promotion">{{cite journal
|url=http://circ.ahajournals.org/cgi/content/full/99/15/2055
|author=Wang TJ, Ausiello JC, Stafford RS
|journal=Circulation
|title=Trends in Antihypertensive Drug Advertising, 1985–1996
|year = 1999
|volume = 99
|pages = 2055-2057
|id = PMID 10209012
}}</ref> 
<br /><br />
Due to their metabolic impact (hypercholesterinemia, impairment of glucose tolerance, increased risk of developing [[Diabetes mellitus type 2]]), the use of thiazides as first line treatment for essential hypertension has been repeatedly questioned and strongly disencouraged.<ref>{{cite journal | author = Lewis PJ, Kohner EM, Petrie A, Dollery CT | title = Deterioration of glucose tolerance in hypertensive patients on prolonged diuretic treatment | journal = Lancet | volume  = 307 | issue = 7959 | pages = 564 - 566 | year = 1976 | id = PMID 55840 }} </ref>  <ref>{{cite journal | author = Murphy MB, Lewis PJ, Kohner E, Schumer B, Dollery CT | title = Glucose intolerance in hypertensive patients treated with diuretics; a fourteen-year follow-up | journal = Lancet | volume = 320 | issue = 8311 | pages = 1293 - 1295 | year = 1982 | id = PMID 6128594 }}</ref>  <ref>{{cite journal | author =Messerli FH, Williams B,Ritz E | title = Essential hypertension | journal = Lancet | volume = 370 | issue = 9587 | pages = 591-603| year = 2007 | id = PMID }}</ref> 
<br /><br />
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]].<ref name=ruggenenti>{{cite journal
|url=http://linkinghub.elsevier.com/retrieve/pii/S014067369804433X
|author=Ruggenenti P, Perna A, Gherardi G, Gaspari F, Benini R, Remuzzi G.
|journal=Lancet
|title=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.
|year = 1998
|volume = 352
|pages = 1252-6
|id = PMID 9788454
}}</ref> 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.
 
===Advice in the United Kingdom===
The risk of [[beta-blocker]]s provoking [[type 2 diabetes]] led to their downgrading to fourth-line therapy in the United Kingdom in June 2006<ref>{{cite web | author= Sheetal Ladva | title=NICE and BHS launch updated hypertension guideline | url=http://www.nelm.nhs.uk/Record%20Viewing/viewRecord.aspx?id=567178 | date=28/06/2006 | publisher=[[National Institute for Health and Clinical Excellence]]}}</ref>, in the revised national guidelines.<ref>{{cite web | title=Hypertension: management of hypertension in adults in primary care | url=http://www.nice.org.uk/download.aspx?o=CG034quickrefguide | format=PDF | publisher=[[National Institute for Health and Clinical Excellence]]}}</ref>
 
===Advice in the United States===
The ''Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure'' (JNC 7) in the United States recommends starting with a [[thiazide diuretic]] if single therapy is being initiated and another medication is not indicated.<ref name="jnc7" />


===Systolic hypertension===
===Systolic hypertension===
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{{Circulatory system pathology}}
{{Circulatory system pathology}}
{{SIB}}
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[[zh-min-nan:Ko-hoeh-ap]]
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[[bg:Хипертония]]

Revision as of 14:46, 29 June 2011

Hypertension
ICD-10 I10,I11,I12,
I13,I15
ICD-9 401.x
OMIM 145500
DiseasesDB 6330
MedlinePlus 000468
eMedicine med/1106  ped/1097 emerg/267

Hypertension Main page

Overview

Causes

Classification

Primary Hypertension
Secondary Hypertension
Hypertensive Emergency
Hypertensive Urgency

Screening

For patient information click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor in Chief: Firas Ghanem, M.D. and Atif Mohammad, M.D.

Overview

Classification

Pathophysiology

Epidemiology & Demographics

Complications

Causes of Hypertension

Complete List of Differential Diagnoses

Diagnosis

Signs and symptoms | Measuring blood pressure | Physical Examination | Laboratory Tests | Electrocardiogram | Chest X-ray | MRI or CT | Echocardiography or Ultrasound

Treatment

Lifestyle modification (nonpharmacologic treatment) | Medical Treatment

Systolic hypertension

Further information: Systolic hypertension

See also

References

External links

Major studies

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