Basic life support (BLS) is the level of medical care which is used for patients with life-threatening illnesses or injuries until the patient can be given full medical care at a hospital. It can be provided by trained medical personnel, including emergency medical technicians, paramedics, and by laypersons who have received BLS training. BLS is generally used in the pre-hospital setting, and can be provided without medical equipment.

Many countries have guidelines on how to provide basic life support (BLS) which are formulated by professional medical bodies in those countries. The guidelines outline algorithms for the management of a number of conditions, such as cardiac arrest, choking and drowning. BLS generally does not include the use of drugs or invasive skills, and can be contrasted with the provision of Advanced Life Support (ALS). Most laypersons can master BLS skills after attending a short course. Firefighter, lifeguards, and police officers are often required to be BLS certified. BLS is also immensely useful for many other professions, such as daycare providers, teachers and security personnel and social workers especially working in the hospitals and ambulance drivers.

CPR provided in the field increases the time available for higher medical responders to arrive and provide ALS care. An important advance in providing BLS is the availability of the automated external defibrillator or AED. This improves survival outcomes in cardiac arrest cases.

Basic life support consists of a number of life-saving techniques focused on the medicine "CAB"s (previously known as ABC. was recently changed by the American Heart Association) of pre-hospital emergency care:

• Circulation : providing an adequate blood supply to tissue, especially critical organs, so as to deliver oxygen to all cells and remove metabolic waste, via the perfusion of blood throughout the body.

• Airway : the protection and maintenance of a clear passageway for gases (principally oxygen and carbon dioxide) to pass between the lungs and the atmosphere.

• Breathing : inflation and deflation of the lungs (respiration) via the airway

Healthy people maintain the CABs by themselves. In an emergency situation, due to illness (medical emergency) or trauma, BLS helps the patient ensure his or her own CABs, or assists in maintaining for the patient who is unable to do so. For airways, this will include manually opening the patients airway (Head tilt/Chin lift or jaw thrust) or possible insertion of oral (Oropharyngeal airway) or nasal (Nasopharyngeal airway) adjuncts, to keep the airway unblocked (patent). For breathing, this may include artificial respiration, often assisted by emergency oxygen. For circulation, this may include bleeding control or Cardiopulmonary Resuscitation (CPR) techniques to manually stimulate the heart and assist its pumping action.

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BLS in the United States

BLS in the United States is generally identified with Emergency Medical Technicians-Basic (EMT-B). However, the American Heart Association's BLS protocol is designed for use by laypeople, as well as students and others certified first responder, and to some extent, higher medical function personnel. It includes cardiac arrest, respiratory arrest, drowning, and foreign body airway obstruction (FBAO, or choking). EMT-B is the highest level of healthcare provider that is limited to the BLS protocol; higher medical functions use some or all of the Advanced Cardiac Life Support (ACLS) protocols, in addition to BLS protocols.

The algorithm for providing basic life support to adults in the USA was published in 2005 in the journal Circulation by the American Heart Association (AHA).[1]

The AHA uses four-link "Chain of Survival" to illustrate the steps needed to resuscitate a collapsed victim:

• Early recognition of the emergency and activation of emergency medical services

• Early bystander CPR, so as not to delay treatment until arrival of EMS

• Early use of a defibrillator

• Early advanced life support and post-resuscitation care

Bystanders with training in BLS can perform the first 3 of the 4 steps.

Basic Life Support 2011 Guideline

Steps in resuscitation are now DRS C-A-B in this sequence

- Check for Danger

- Check for Response

- ‘S’ has been added for Send for help

- ‘A’ directs rescuers to open the Airway

- ‘B’ directs rescuers to check Breathing but no need to deliver rescue breaths

- ‘C’ directs rescuers to perform 30 Compressions to patients who are unresponsive and not breathing normally, followed by 2 rescue breaths

- ‘D’ directs rescuers to attach an AED as soon as it is available and follow prompts

The major change is that in the patient who is unresponsive and not breathing CPR commences with chest compressions rather than rescue breaths. If unwilling / unable to perform rescue breathing, then perform compression-only CPR, as any attempt at resuscitation is better than no attempt; and should be encouraged.

Adult BLS sequence

• C-A-B is recommended in the new AHA EU guidelines.Keeping these facts as such follow the sequence introduced by AHA guidelines 2010 recommendations C-A-B should be followed in learning and teaching BLS.

• Ensure that the scene is safe.

• Assess the victim's level of consciousness by asking loudly and shaking at the shoulders "Are you okay?" and scan chest for breathing movement visually.If no response call for help by shouting for ambulance or EMS and ask for an AED( which is available in offices and building floors).

Assess:* If the patient is breathing normally, and pulse is present then the patient should be placed in the recovery position and monitored. Transport if required, or wait for the EMS to arrive and take over.

• If patient is not breathing assess pulse at the carotid on your side for an adult, at the brachial for a child and infant for 5 seconds and not more than 10 seconds; begin immediately with chest compressions at a rate of 30 chest compressions in 18 seconds followed by two rescue breaths in 5 seconds each lasting for 1 second.

If the victim has no suspected cervical spine trauma, open the airway using the head-tilt/chin-lift maneuver; if the victim has suspected neck trauma, the airway should be opened with the jaw-thrust technique. If the jaw-thrust is ineffective at opening/maintaining the airway, a very careful head-tilt/chin-lift should be performed.

• Blind finger-sweeps should never be performed, as they may push foreign objects deeper into the airway.This procedure has been discarded as this may push the foreign body down the airway and increase chances of an obstruction.

Continue chest compression at a rate of 100 compressions per minute for all age groups, allowing chest to recoil in between. For adults push up to 5 cm and for child up to 4cm. For infants up to 3cm or 1/3 of the chest diameter antero-posteriorly.Keep counting aloud. Press hard and fast maintaining the rate of at about 100/minute.Allow recoil of chest fully between each compression.After every 30 chest compressions give two rescue breaths in adult and child victim, Continue for five cycles or two minutes before re-assessing pulse.

• Look, listen, and feel for breathing for at least 5 seconds and no more than 10 seconds.This is another step that has been discarded and considered loss of valuable time.

• Attempt to administer two artificial ventilations using the mouth-to-mouth technique, or a bag-valve-mask (BVM). The mouth-to-mouth technique is no longer recommended, unless a face shield is present. Verify that the chest rises and falls; if it does not, reposition (i.e. re-open) the airway using the appropriate technique and try again. If ventilation is still unsuccessful, and the victim is unconscious, it is possible that they have a foreign body in their airway. Begin chest compressions, stopping every 30 compressions, re-checking the airway for obstructions, removing any found, and re-attempting ventilation.

• If the ventilations are successful, assess for the presence of a pulse at the carotid artery. If a pulse is detected, then the patient should continue to receive artificial ventilation's at an appropriate rate and transported immediately. Otherwise, begin CPR at a ratio of 30:2 compressions to ventilation's at 100 compressions/minute for 5 cycles.

• After 5 cycles of CPR, the BLS protocol should be repeated from the beginning, assessing the patient's airway, checking for spontaneous breathing, and checking for a spontaneous pulse as per new protocol sequence C-A-B. Laypersons are commonly instructed not to perform re-assessment, but this step is always performed by healthcare professionals (HCPs).

If an AED is available it should be activated immediately and its directives followed and (if indicated), call for clearance before defibrillation/shock should be performed. If defibrillation is performed,begin chest compression immediately after shock.

• BLS protocols continue until (1) the patient regains a pulse, (2) the rescuer is relieved by another rescuer of equivalent or higher training (See Abandonment), (3) the rescuer is too physically tired to continue CPR, or (4) the patient is pronounced dead by a medical doctor.[1]

• At the end of five cycles of CPR, always perform assessment via the AED for a shockable rhythm, and if indicated, defibrillate, and repeat assessment before doing another five cycles.

• The CPR cycle is often abbreviated as 30:2 (30 compressions, 2 ventilation's or breaths).

Note CPR for infants and children uses a 15:2 cycle when two rescuers are performing CPR (but still uses a 30:2 if there is only one rescuer). Two person CPR for an infant also requires the "two hands encircling thumbs" technique for the rescuer performing compressions.

Drowning

Rescuers should provide CPR as soon as an unresponsive victim is removed from the water. In particular, rescue breathing is important in this situation.

A lone rescuer is typically advised to give CPR for a short time before leaving the victim to call emergency medical services.

Since the primary cause of cardiac arrest and death in drowning and choking victims is hypoxia, it is more important to provide rescue breathing as quickly as possible in these situations, whereas for victims of VF cardiac arrest chest compressions and defibrillation are more important.

Hypothermia

• In unresponsive victims with hypothermia, the breathing and pulse should be checked for 30 to 45 seconds as both breathing and heart rate can be very slow in this condition.

• If cardiac arrest is confirmed, CPR should be started immediately. Wet clothes should be removed, and the victim should be insulated from wind. CPR should be continued until the victim is assessed by advanced care providers.

Foreign body airway obstruction (choking)

• Rescuers should intervene in victims who show signs of severe airway obstruction, such as a silent cough, cyanosis, or inability to speak or breathe.

• If a victim is coughing forcefully, rescuers should not interfere with this process.

• If a victim shows signs of severe airway obstruction, abdominal thrusts should be applied in rapid sequence until the obstruction is relieved. If this is not effective, chest thrusts can also be used. Chest thrusts can also

be used in obese victims or victims in late pregnancy. Abdominal thrusts should not be used in infants under 1 year of age due to risk of causing injury.

• If a victim becomes unresponsive he should be lowered to the ground, and the rescuer should call emergency medical services and initiate CPR. When the airway is opened during CPR, the rescuer should look into the mouth for an object causing obstruction, and remove it if it is evident.

Adult BLS guidelines in the United Kingdom were also published in 2005 by the Resuscitation Council (UK),[2] based on the 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations (CoSTR) published in November 2005.[3]

Adult BLS sequence

• Ensure the safety of the victim, the rescuer, and any bystanders.

• Check the victim for a response by gently shaking the victim's shoulders and asking loudly "Are you all right?"

• If the victim responds, leave him in the position in which he was found provided there is no further danger, try to find out what is wrong with him and get help if needed, and reassess him regularly.

• If the victim does not respond, turn him on to his back and open the airway using the head-tilt/chin-lift. Shout for help.

• Look, listen and feel for normal breathing for no more than 10 seconds. If the victim is breathing normally, turn him into the recovery position and get help. Continue to check for breathing.

• If the victim is not breathing normally, call for an ambulance.

These guidelines differ from previous versions in a number of ways:

• They allow the rescuer to diagnose cardiac arrest if the victim is unresponsive and not breathing normally.

• Rescuers are taught to give chest compressions in the center of the chest, rather than measuring from the lower border of the sternum.

• Rescue breaths should be given over 1 second rather than 2 seconds.

• For an adult victim, the initial 2 rescue breaths should be omitted, so that 30 chest compressions are given immediately after a cardiac arrest has been diagnosed.

These changes were introduced to simplify the algorithm, to allow for faster decision making and to maximize the time spent giving chest compressions; this is because interruptions in chest compressions have been shown to reduce the chance of survival.[4] It is also acknowledged that rescuers may either be unable, or unwilling, to give effective rescue breaths; in this situation, continuing chest compressions alone is advised, although this is only effective for about 5 minutes.[5]

Adult choking sequence

• Assess the severity of airway obstruction. If the victim is able to speak and cough effectively, the obstruction is mild. If the victim is unable to speak or cough effectively, or is unable to breathe or is breathing with a wheezy sound, the airway obstruction is severe.

• If the victim has signs of mild airway obstruction, encourage him to continue coughing; do nothing else.

• If the victim has signs of severe airway obstruction, and is conscious, give up to 5 back blows (sharp blows between the shoulder blades with the victim leaning well forwards). Check to see if the obstruction has cleared after each blow. If 5 back blows fail to relieve the obstruction, give up to 5 abdominal thrusts, again checking if each attempt has relieved the obstruction.

• If the obstruction is still present, and the victim still conscious, continue alternating 5 back blows and 5 abdominal thrusts.

• If the victim becomes unconscious, lower him to the ground, call an ambulance, and begin CPR.

What Is an Arrhythmia?

An arrhythmia (ah-RITH-me-ah) is a problem with the rate or rhythm of the heartbeat. During an arrhythmia, the heart can beat too fast, too slow, or with an irregular rhythm.

A heartbeat that is too fast is called tachycardia (TAK-ih-KAR-de-ah). A heartbeat that is too slow is called bradycardia (bray-de-KAR-de-ah).

Most arrhythmias are harmless, but some can be serious or even life threatening. During an arrhythmia, the heart may not be able to pump enough blood to the body. Lack of blood flow can damage the brain, heart, and other organs.

Understanding the Heart's Electrical System

To understand arrhythmias, it helps to understand the heart's internal electrical system. The heart's electrical system controls the rate and rhythm of the heartbeat.

With each heartbeat, an electrical signal spreads from the top of the heart to the bottom. As the signal travels, it causes the heart to contract and pump blood.

Each electrical signal begins in a group of cells called the sinus node or sinoatrial (SA) node. The SA node is located in the heart's upper right chamber, the right atrium (AY-tree-um). In a healthy adult heart at rest, the SA node fires off an electrical signal to begin a new heartbeat 60 to 100 times a minute.

From the SA node, the electrical signal travels through special pathways in the right and left atria. This causes the atria to contract and pump blood into the heart's two lower chambers, the ventricles (VEN-trih-kuls).

The electrical signal then moves down to a group of cells called the atrioventricular (AV) node, located between the atria and the ventricles. Here, the signal slows down just a little, allowing the ventricles time to finish filling with blood.

The electrical signal then leaves the AV node and travels along a pathway called the bundle of His. This pathway divides into a right bundle branch and a left bundle branch. The signal goes down these branches to the ventricles, causing them to contract and pump blood to the lungs and the rest of the body.

The ventricles then relax, and the heartbeat process starts all over again in the SA node. (For more information about the heart's electrical system, including detailed animations, go to the Health Topics How the Heart Works article.)

A problem with any part of this process can cause an arrhythmia. For example, in atrial fibrillation (A-tre-al fi-bri-LA-shun), a common type of arrhythmia, electrical signals travel through the atria in a fast and disorganized way. This causes the atria to quiver instead of contract.

Outlook

There are many types of arrhythmia. Most arrhythmias are harmless, but some are not. The outlook for a person who has an arrhythmia depends on the type and severity of the arrhythmia.

Even serious arrhythmias often can be successfully treated. Most people who have arrhythmias are able to live normal, healthy lives.

IBW & ABW calculatorFormula. IBW Estimated ideal body weight in (kg) Males: IBW = 50 kg + 2.3 kg for each inch over 5 feet. Females: IBW = 45.5 kg + 2.3 kg for each inch over 5 feet.www.manuelsweb.com/IBW.htm

Asphyxia or asphyxiation (from Greek α- "without" and σφύξις sphyxis, "heartbeat") is a condition of severely deficient supply of oxygen to the body that arises from being unable to breathe normally. An example of asphyxia is choking. Asphyxia causes generalized hypoxia, which primarily affects the tissues and organs. It can be caused by improper ventilation and charcoal burning in a closed room. Many incidents have been reported (death and comaHypertension

Hypertension (HTN) or high blood pressure, sometimes arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated. This requires the heart to work harder than normal to circulate blood through the blood vessels. Blood pressure involves two measurements, systolic and diastolic, which depend on whether the heart muscle is contracting (systole) or relaxed (diastole) between beats. Normal blood pressure is at or below 120/80 mmHg. High blood pressure is said to be present if it is persistently at or above 140/90 mmHg.

Hypertension is classified as either primary (essential) hypertension or secondary hypertension; about 90–95% of cases are categorized as "primary hypertension" which means high blood pressure with no obvious underlying medical cause.[1] The remaining 5–10% of cases (secondary hypertension) are caused by other conditions that affect the kidneys, arteries, heart or endocrine system.

Hypertension is a major risk factor for stroke, myocardial infarction (heart attacks), heart failure, aneurysms of the arteries (e.g. aortic aneurysm), peripheral arterial disease and is a cause of chronic kidney disease. Even moderate elevation of arterial blood pressure is associated with a shortened life expectancy. Dietary and lifestyle changes can improve blood pressure control and decrease the risk of associated health complications, although drug treatment is often necessary in patients for whom lifestyle changes prove ineffective or insufficient.

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Classification

Classification (JNC7)[2]

Systolic pressure

Diastolic pressure

mmHg kPammH

gkPa

Normal 90–119 12–15.960–79

8.0–10.5

Prehypertension120–139

16.0–18.5

80–89

10.7–11.9

Stage 1 hypertension

140–159

18.7–21.2

90–99

12.0–13.2

Stage 2 hypertension

≥160 ≥21.3 ≥100 ≥13.3

Isolated systolichypertension

≥140 ≥18.7 <90 <12.0

Adults

In people aged 18 years or older hypertension is defined as a systolic and/or a diastolic blood pressure measurement consistently higher than an accepted normal value (currently 139 mmHg systolic, 89 mmHg diastolic: see table — Classification (JNC7)). Lower thresholds are used (135 mmHg systolic or 85 mmHg diastolic) if measurements are derived from 24-hour ambulatory or home monitoring.[3] The presence of other cardiovascular risk factors is taken into account when decisions are made regarding drug treatment. Recent international hypertension guidelines have also created categories below the hypertensive range to indicate a continuum of risk with higher blood pressures in the normal range. JNC7 (2003)[2]

uses the term prehypertension for blood pressure in the range 120-139 mmHg systolic and/or 80-89 mmHg diastolic, while ESH-ESC Guidelines (2007)[4] and BHS IV (2004)[5] use optimal, normal and high normal categories to subdivide pressures below 140 mmHg systolic and 90 mmHg diastolic. Hypertension is also sub-classified: JNC7 distinguishes hypertension stage I, hypertension stage II, and isolated systolic hypertension. Isolated systolic hypertension refers to elevated systolic pressure with normal diastolic pressure and is common in the elderly.[2] The ESH-ESC Guidelines (2007)[4] and BHS IV (2004),[5] additionally define a third stage (stage III hypertension) for people with systolic blood pressure exceeding 179 mmHg or a diastolic pressure over 109 mmHg. Hypertension is classified as "resistant" if medications do not reduce blood pressure to normal levels.[2]

Neonates and infants

Hypertension in neonates is rare, occurring in around 0.2 to 3% of neonates, and blood pressure is not measured routinely in the healthy newborn.[6]

Hypertension can be more common in high risk newborns. A variety of factors, such as gestational age, postconceptional age and birth weight needs to be taken into account when deciding if a blood pressure is normal in a neonate.[6]

Children and adolescents

Hypertension occurs quite commonly in children and adolescents (2-9% depending on age, sex and ethnicity)[7] and is associated with long term risks of ill-heath.[8] It is now recommended that children over the age of 3 have their blood pressure checked whenever they attend for routine medical care or checks, but high blood pressure must be confirmed on repeated visits before characterizing a child as having hypertension.[8] Blood pressure rises with age in childhood and, in children, hypertension is defined as an average systolic or diastolic blood pressure on three or more occasions equal or higher than the 95th percentile appropriate for the sex, age and height of the child. Prehypertension in children is defined as average systolic or diastolic blood pressure that are greater than or equal to the 90th percentile, but less than the 95th percentile.[8] In adolescents, it has been proposed that hypertension and pre-hypertension are diagnosed and classified using the same criteria as in adults.[8]

Signs and symptoms

Hypertension is rarely accompanied by any symptoms, and its identification is usually through screening, or when seeking healthcare for an unrelated problem. A proportion of people with high blood pressure reports headaches (particularly at the back of the head and in the morning), as well as lightheadedness, vertigo, tinnitus (buzzing or hissing in the ears), altered vision or fainting episodes.[9]

On physical examination, hypertension may be suspected on the basis of the presence of hypertensive retinopathy detected by examination of the optic fundi using ophthalmoscopy [10] Classically, the severity of the hypertensive retinopathy changes is graded from grade I–IV, although the milder types may be difficult to distinguish from each other.[10] Ophthalmoscopy findings may also indicate how long a person has been hypertensive.[9]

Secondary hypertension

Main article: Secondary hypertension

Some additional signs and symptoms may suggest secondary hypertension, i.e. hypertension due to some identifiable cause such as kidney diseases or endocrine diseases. For example, truncal obesity, glucose intolerance, moon facies , a "buffalo hump" and purple striae suggest Cushing's syndrome.[11] Thyroid disease and acromegaly can also cause hypertension and have characteristic symptoms and signs.[11] An abdominal bruit may be an indicator of renal artery stenosis , while decreased blood pressure in the lower extremities and/or delayed or absent femoral arterial pulses may indicate aortic coarctation . Labile or paroxysmal hypertension accompanied by headache, palpitations, pallor, and perspiration should prompt suspicions of pheochromocytoma.[11]

Hypertensive crises

Main article: hypertensive emergency

Severely elevated blood pressure (systolic over 180 or diastolic over 110 — sometime termed malignant or accelerated hypertension) is referred to as a "hypertensive crisis", as blood pressures above these levels are known to confer a high risk of complications. People with blood pressures in this range may have no symptoms, but are more likely to report headaches and dizziness.[9] Other symptoms accompanying a hypertensive crisis may include visual deterioration or breathlessness due to heart failure or a general feeling of malaise due to renal failure.[11] Most people with a hypertensive crisis are known to have elevated blood pressure, but additional triggers may have led to a sudden rise.[12]

A "hypertensive emergency", previously "malignant hypertension", is diagnosed when there is evidence of direct damage to one or more organs as a result of the severely elevated blood presure. This may include hypertensive encephalopathy, caused by brain swelling and dysfunction, and characterised by headaches and an altered level of consciousness (confusion or drowsiness). Retinal papilloedema and/or fundal hemorrhages and exudates are another sign of target organ damage. Chest pain may indicate heart muscle damage (which may progress to myocardial infarction) or sometimes aortic dissection, the tearing of the inner wall of the aorta. Breathlessness, cough, and the expectoration of blood-stained sputum are characteristic signs of pulmonary edema, the swelling of lung tissue due to left ventricular failure an inability of the left ventricle of the heart to adequately pump blood from the lungs into the arterial system.[12] Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur.[12] In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage.[12] In contrast there is no evidence that blood pressure needs to be lowered rapidly in hypertensive urgencies where there is no evidence of target organ damage and over aggressive reduction of blood pressure is not without risks [11] Use of oral medications to lower the BP gradually over 24 to 48 h is advocated in hypertensive urgencies.[12]

In pregnancy

Hypertension occurs in approximately 8-10% of pregnancies.[11] Most women with hypertension in pregnancy have pre-existing primary hypertension, but high blood pressure in pregnancy may be the first sign of pre- eclampsia , a serious condition of the second half of pregnancy and puerperium.[11] Pre-eclampsia is characterised by increased blood pressure and the presence of protein in the urine.[11] It occurs in about 5% of pregnancies and is responsible for approximately 16% of all maternal deaths.[11] Pre-eclampsia also doubles the risk of perinatal mortality .[11] Usually there are no symptoms in pre-eclampsia and it is detected by routine screening. When symptoms of pre-eclampsia occur the most common are headache, visual disturbance (often "flashing lights"), vomiting, epigastric pain, and edema. Pre-eclampsia can occasionally progress to a life-threatening condition called eclampsia, which is a hypertensive emergency and has several serious complications including vision loss, cerebral edema,seizures or convulsions, renal failure, pulmonary edema, and disseminated intravascular coagulation [11] [13]

In neonates, infants and children

Failure to thrive, seizures, irritability, lack of energy, and difficulty breathing [14] can be associated with hypertension in neonates and young infants. In older infants and children, hypertension can cause headache, unexplained irritability, fatigue, failure to thrive, blurred vision, nosebleeds, and facial paralysis,[6][14]

Diagram illustrating the main complications of persistent high blood pressure.

Hypertension is the most important preventable risk factor for premature death worldwide.[15] It increases the risk of ischemic heart disease [16] strokes,[11] peripheral vascular disease,[17] and other cardiovascular diseases, including heart failure, aortic aneurysm, diffuse atherosclerosis, and pulmonary embolism.[11][11] Hypertension is also a risk factor for cognitive impairment and dementia, and chronic kidney disease.[11] Other complications include:

• Hypertensive retinopathy

• Hypertensive nephropathy [18]

• Silent stroke is a type of stroke (infarct) that does not have any outward symptoms (asymptomatic), and the patient is typically unaware they have suffered a stroke. Despite not causing identifiable symptoms a silent stroke still causes damage to the brain, and places the patient at increased risk for a major stroke in the future. Hypertension is the major treatable risk factor associated with silent strokes.[19]

Cause

Primary hypertension

Main article: Essential hypertension

Primary (essential) hypertension is the most common form of hypertension, accounting for 90–95% of all cases of hypertension.[1] In almost all contemporary societies, blood pressure rises with aging and the risk of becoming hypertensive in later life is considerable.[20] Hypertension results from a complex interaction of genes and environmental factors. Numerous common genes with small effects on blood pressure have been identified [21] as well as some rare genes with large effects on blood pressure [22] but the genetic basis of hypertension is still poorly understood. Several environmental factors influence blood pressure. Lifestyle factors that lower blood pressure, include reduced dietary salt intake,[23] increased

consumption of fruits and low fat products (Dietary Approaches to Stop Hypertension (DASH diet)), exercise,[24] weight loss [25] reduced alcohol intake,.[26] The possible role of other factors such as stress,[24] caffeine consumption,[27] and vitamin D deficiency [28] are less clear cut. Insulin resistance, which is common in obesity and is a component of syndrome X (or the metabolic syndrome), is also thought to contribute to hypertension.[29] Recent studies have also implicated events in early life (for example low birth weight, maternal smoking and lack of breast feeding) as risk factors for adult essential hypertension,[30] although the mechanisms linking these exposures to adult hypertension remain obscure.

Secondary hypertension

Main article: Secondary hypertension

Secondary hypertension results from an identifiable cause. Renal disease is the most common secondary cause of hypertension.[11] Hypertension can also be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's syndrome or hyperaldosteronism, hyperparathyroidism and pheochromocytoma.[11][31] Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta , excessive liquorice consumption and certain prescription medicines, herbal remedies and illegal drugs.[11][32]

Pathophysiology

Main article: Pathophysiology of hypertension

A diagram explaining factors affecting arterial pressure

In most people with established essential (primary) hypertension, increased resistance to blood flow (total peripheral resistance) accounts for the high pressure and cardiac output is normal.[33] There is evidence that some younger people with prehypertension or 'borderline hypertension' have high cardiac output, an elevated heart rate and normal peripheral resistance, termed hyperkinetic borderline hypertension.[34] These individuals develop the typical features of established essential hypertension in later life as their cardiac output falls and peripheral resistance rises with age.[34] Whether this pattern is typical of all people who ultimately develop hypertension is disputed.[35] The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles,[36] although a reduction in the number or density of capillaries may also contribute.[37] Hypertension is also associated with decreased peripheral venous compliance[38] which may increase venous return, increase cardiac preload and, ultimately, cause diastolic dysfunction. Whether increased active vasoconstriction plays a role in established essential hypertension is unclear.[39]

Pulse pressure - the difference between systolic and diastolic blood pressure is frequently increased in older people with hypertension. This can mean that systolic pressure is abnormally high, but diastolic pressure may be normal or low — a condition termed isolated systolic hypertension.[40] The high pulse pressure in elderly people with hypertension or isolated systolic hypertension is explained by increased arterial stiffness, which typically accompanies aging and may be exacerbated by high blood pressure.[41]

Many mechanisms have been proposed to account for the rise in peripheral resistance in hypertension. Most evidence implicates either:

• Disturbances in renal salt and water handling, particularly abnormalities in the intrarenal renin-angiotensin system [42]

and/or

• Abnormalities of the sympathetic nervous system [43]

These mechanisms are not mutually exclusive and it is likely that both contribute to some extent in most cases of essential hypertension. It has also been suggested that endothelial dysfunction [44] and vascular inflammation [45] may also contribute to increased peripheral resistance and vascular damage in hypertension.

Diagnosis

System Tests

RenalMicroscopic urinalysis, proteinuria, serum BUN (blood urea nitrogen)

and/or creatinine

Endocrine

Serum sodium, potassium, calcium, TSH (thyroid-stimulating hormone).

Metabolic

Fasting blood glucose, total cholesterol, HDL and LDL cholesterol, triglycerides

Other Hematocrit, electrocardiogram, and chest radiograph

Sources: Harrison's principles of internal medicine[46] others[47][48][49][50][51]

Hypertension is diagnosed on the basis of a persistently high blood pressure. Traditionally,[3] this requires three separate sphygmomanometer measurements at one monthly intervals.[52] Initial assessment of the hypertensive patient should include a complete history and physical examination. With the availability of 24-hour ambulatory blood pressure monitors and home blood pressure machines, the importance of not wrongly diagnosing those who have white coat hypertension has led to a change in protocol advice in the United Kingdom, with best practice of now following up a single raised clinic reading with ambulatory measurement, or less ideally with home blood pressure monitoring over the course of 7 days.[3]

Once the diagnosis of hypertension has been made, physicians will attempt to identify the underlying cause based on risk factors and other symptoms, if present. 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.[53]

Laboratory tests can also be performed to identify possible causes of secondary hypertension, and to determine whether hypertension has caused damage to the heart, eyes, and kidneys. Additional tests for diabetes and high cholesterol levels are usually performed because these conditions are additional risk factors for the development of heart disease and require treatment.[1] Typical tests are listed in the table.

Serum creatinine is measured as a test of renal function, to assess the presence of kidney disease, which can be either the cause or the result of hypertension. Serum creatinine alone may overestimate glomerular filtration rate and recent guidelines advocate the use of predictive equations such as the Modification of Diet in Renal Disease (MDRD) formula to estimate glomerular filtration rate (eGFR).[54] eGFR can also provides a baseline measurement of kidney function that can be used to monitor for side effects of certain antihypertensive drugs on kidney function. Additionally, testing of urine samples for protein is used as a secondary indicator of kidney disease. Glucose testing is done to determine if diabetes mellitus is present. Electrocardiogram (EKG/ECG) testing is done to check for evidence that the heart is under strain from high blood pressure. It may also show whether there is thickening of the heart muscle (left ventricular hypertrophy) or whether the heart has experienced a prior minor disturbance such as a silent heart attack. A chest X-ray may be performed to look for signs of heart enlargement or damage to heart tissue.

Prevention

Much of the disease burden of high blood pressure is experienced by people who are not hypertensive.[55] Consequently, population strategies are required to reduce the consequences of high blood pressure and reduce the need for antihypertensive drug therapy. Lifestyle changes are recommended to lower blood pressure, before starting drug therapy. The 2004 British Hypertension Society guidelines[55] proposed the following lifestyle changes consistent with those outlined by the US National High BP Education Program in 2002[56] for the primary prevention of hypertension:

• maintain normal body weight for adults (e.g. body mass index 20–25 kg/m2)

• reduce dietary sodium intake to <100 mmol/ day (<6 g of sodium chloride or <2.4 g of sodium per day)

• engage in regular aerobic physical activity such as brisk walking (≥30 min per day, most days of the week)

• limit alcohol consumption to no more than 3 units/day in men and no more than 2 units/day in women

• consume a diet rich in fruit and vegetables (e.g. at least five portions per day);

• consume a diet with reduced content of saturated and total fat.

Effective lifestyle modification may lower blood pressure as much an individual antihypertensive drug. Combinations of two or more lifestyle modifications can achieve even better results.[55]

Treatment

Lifestyle modifications

The first line of treatment for hypertension is identical to the recommended preventive lifestyle changes [57] and includes: dietary changes[58] physical exercise, and weight loss. These have all been shown to significantly reduce blood pressure in people with hypertension.[59] If hypertension is high enough to justify immediate use of medications, lifestyle changes are still recommended in conjunction with medication. Different programs aimed to reduce psychological stress such as biofeedback, relaxation or meditation are advertised to reduce hypertension. However, in general claims of efficacy are not supported by scientific studies, which have been in general of low quality.[60][61][62]

Regarding dietary changes, a low sodium diet is beneficial. A long term (more than 4 weeks) low sodium diet in Caucasians is effective in reducing blood pressure, both in people with hypertension and in people with normal blood pressure.[63] Also, the DASH diet (Dietary Approaches to Stop Hypertension) is a diet promoted by the National Heart, Lung, and Blood Institute (part of the NIH, a United States government organization) to control hypertension. A major feature of the plan is limiting intake of sodium,[64] and it also generally encourages the consumption of nuts, whole grains, fish, poultry, fruits and vegetables while lowering the consumption of red meats, sweets, and sugar. It is also "rich in potassium, magnesium, and calcium, as well as protein".

Medications

Several classes of medications, collectively referred to as antihypertensive drugs, are currently available for treating hypertension. Drug prescription should take into account the patient's absolute cardiovascular risk (including risk of myocardial infarction and stroke) as well as blood pressure readings, in order to gain a more accurate picture of the patient's cardiovascular profile.[65] If drug treatment is inititated the National Heart, Lung, and Blood Institute's Seventh Joint National Committee on High Blood Pressure (JNC-7)[54] recommends that the physician not only monitor for response to treament but should also assess for any adverse or untoward reaction resulting from the medication(s). Reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by 34%, of ischaemic heart disease by 21%, and reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease.[66] The aim of treatment should be to reduce blood pressure to <140/90 mmHg for most individuals, and lower for individuals with diabetes or kidney disease (some medical professionals recommend keeping levels below 120/80 mmHg).[67] If the blood pressure goal is not met, a change in treatment should be made as therapeutic inertia is a clear impediment to blood pressure control.[68] Comorbidity also plays a role in determining target blood pressure, with lower BP targets applying to patients with end-organ damage or proteinuria.[65]

Often multiple medications are needed to be combined to achieve the goal blood pressure. Guidelines on the choice of first line agent and how to best to step up treatment with multiple agents for various subgroups of patients have changed over time and differ between countries.

In the UK low dose thiazide -based diuretic were previously thought the best first line agent,[69] but latest guidelines emphasise calcium channel blockers (CCB) in preference for patients over the age of 55 years or if of African or Caribbean family origin, with angiotensin converting enzyme inhibitors (ACE-I) used first line for younger patients.[70] Preferred dual therapy is generally CCB with an ACE-I, and triple therapy with addition of a thiazide -like diuretic . If a fourth agent is needed then additional diuretics of spironolactone or a higher-dose of a thiazide-like diuretics. Additional agents that may be considered are alpha blockers or beta blockers.[70] Angiotensin II receptor antagonists are suggested as preferable to ACE-I for black people of African or Caribbean family origin, and are an alternative for patients who are unable to tolerate ACE-I. Beta-blockers may be also be considered in younger people, particularly those with an intolerance or contraindication to ACE-I and angiotensin II receptor antagonists, or women of child-bearing potential, or people with evidence of increased sympathetic drive.[70]

Drug combinations

The majority of patients require more than one drug to control their hypertension. JNC7 [54] and ESH-ESC guidelines[4] advocate starting treatment with two drugs when blood pressure is >20 mmHg above systolic or >10 mmHg above diastolic targets. Preferred combinations are renin–angiotensin system inhibitors and calcium channel blockers, or renin–angiotensin system inhibitors and diuretics.[71] Acceptable combinations include calcium channel blockers and diuretics, beta-blockers and diuretics, dihydropyridine calcium channel blockers and beta-blockers, or dihydropyridine calcium channel blockers with either verapamil or diltiazem. Unacceptable combinations are non-dihydropyridine calcium blockers (such as verapamil or diltiazem) and beta-blockers, dual renin–angiotensin system blockade (e.g. angiotensin converting enzyme inhibitor + angiotensin receptor blocker), renin–angiotensin system blockers and beta-blockers, beta-blockers and anti-adrenergic drugs.[71] Combinations of an ACE-inhibitor or angiotensin II–receptor antagonist, a diuretic and an NSAID (including selective COX-2 inhibitors and non-prescribed drugs such as ibuprofen) should be avoided whenever possible due to a high documented risk of acute renal failure. The combination is known colloquially as a "triple whammy" in the Australian health industry.[57]

Fixed dose combinations

Tablets containing fixed combinations of two classes of drugs are available and whilst convenient for the patient, may be best reserved for patients who have been established on the individual components.[72]

In the elderly and very elderly

Treating moderate to severe hypertension decreases death rates and cardiovascular morbidity and mortality in people aged 60 and older.[73] There are limited studies of people over 80 years old but a recent meta-analysis that pooled results from several clinical trials concluded that antihypertensive treatment reduced cardiovascular deaths and disease, but did not significantly reduce total death rates.[73] The recommended BP goal is advised as <140/90 mm Hg with thiazide diuretics being the first line medication in America,[74] but in the revised UK guidelines calcium-channel blockers are advocated as first line with targets of clinic readings <150/90, or <145/85 on ambulatory or home blood pressure monitoring.[70]

Resistant

Guidelines for treating resistant hypertension have been published in the UK[75] and US.[76]

Epidemiology

In the year 2000 it is estimated that nearly one billion people or ~26% of the adult population had hypertension worldwide.[77] It was common in both developed (333 million ) and undeveloped (639 million) countries.[77] However rates vary markedly in different regions with rates as low as 3.4% (men) and 6.8% (women) in rural India and as high as 68.9% (men) and 72.5% (women) in Poland.[78]

In 1995 it is estimated that 43 million people in the United States had hypertension or were taking antihypertensive medication, almost 24% of the adult population.[79] The prevalence of hypertension in the United States is increasing and reached 29% in 2004.[80][81] It is more common in blacks and native Americans and less in whites and Mexican Americans, rates increase with age, and is greater in the southeastern United States. Hypertension is more prevalent in men (though menopause tends to decrease this difference) and those of low socioeconomic status.[1]

In children

The prevalence of high blood pressure in the young is increasing.[82] Most childhood hypertension, particularly in preadolescents, is secondary to an underlying disorder. Aside from obesity, kidney disease is the most common (60–70%) cause of hypertension in children. Adolescents usually have primary or essential hypertension, which accounts for 85–95% of cases.[83]

History

Image of veins from Harvey's Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus

Modern understanding of the cardiovascular system began with the work of physician William Harvey (1578–1657), who described the circulation of blood in his book "De motu cordis". The English clergyman Stephen Hales made the first measurement of blood pressure in 1733,[84] in horses.[85]

Descriptions of hypertension as a disease came among others from Thomas Young in 1808 and especially Richard Bright in 1836.[84] The first report of elevated blood pressure in a patient without evidence of kidney disease was made by Frederick Akbar Mahomed (1849–1884).[86] However hypertension as a clinical entity came into being in 1896 with the invention of the cuff-based sphygmomanometer by Scipione Riva- Rocci in 1896.[87]

This allowed blood pressure to be measured in the clinic. In 1905, Nikolai Korotkoff improved the technique by describing the Korotkoff sounds that are heard when the artery is ausculated with a stethoscope while the sphygmomanometer cuff is deflated.[85]

The concept of essential hypertension ('hypertonie essential') was introduced in 1925 by the physiologist Otto Frank to describe elevated blood pressure for which no cause could be found. In 1928, the term malignant hypertension was coined by physicians from the Mayo Clinic to describe a syndrome of very high blood pressure, severe retinopathy and adequate kidney function which usually resulted in death within a year from strokes, heart failure or kidney failure.[88] A prominent sufferer of severe hypertension was Franklin D. Roosevelt.[89] However, while the menace of severe or malignant hypertension was well recognised, the risks of more moderate elevations of blood pressure were uncertain and the benefits of treatment doubtful. Consequently, hypertension was often classified into "malignant" and "benign". In 1931, John Hay, Professor of Medicine at Liverpool University, wrote that "there is some truth in the saying that the greatest danger to a man with a high blood pressure lies in its discovery, because then some fool is certain to try and reduce it".[90][91] This view was echoed by the eminent US cardiologist Paul Dudley White in 1937, who suggested that "hypertension may be an important compensatory mechanism which should not be tampered with, even were it certain that we could control it".[92]

Charles Friedberg's 1949 classic textbook "Diseases of the Heart",[93] stated that "people with 'mild benign' hypertension ... [defined as blood pressures up to levels of 210/100 mm Hg] ... need not be treated".[91] However the tide of medical opinion was turning: it was increasingly recognised in the 1950s that "benign" hypertension was not harmless.[94] Over the next decade increasing evidence accumulated from actuarial reports[85][95] and longitudinal studies, such as the Framingham Heart Study,[96] that "benign" hypertension increased death and cardiovascular disease, and that these risks increased in a graded manner with increasing blood pressure across the whole spectrum of population blood pressures. Subsequently the National Institutes of Health also sponsored other population studies, which additionally showed that African Americans had a higher burden of hypertension and its complications.[97]

Historically the treatment for what was called the "hard pulse disease" consisted in reducing the quantity of blood by blood letting or the application of leeches.[84] This was advocated by The Yellow Emperor of China, Cornelius Celsus , Galen, and Hipocrates.[84]

In the 19th and 20th centuries, before effective pharmacological treatment for hypertension became possible, three treatment modalities were used, all with numerous side-effects: strict sodium restriction (for example the rice diet [84]), sympathectomy (surgical ablation of parts of the sympathetic nervous system), and pyrogen therapy (injection of substances that caused a fever, indirectly reducing blood pressure).[84][97] The first chemical for hypertension, sodium thiocyanate , was used in 1900 but had many side effects and was unpopular.[84] Several other agents were developed after the Second World War, the most popular and reasonably effective of which were tetramethylammonium chloride and its derivative hexamethonium, hydralazine and reserpine (derived from the medicinal plant Rauwolfia serpentina ). A major breakthrough was achieved with the discovery of the first well-tolerated orally available agents. The first was chlorothiazide, the first thiazide diuretic and developed from the antibiotic sulfanilamide, which became available in 1958;[84][98] it increased salt excretion while preventing fluid accumulation. A randomized controlled trial sponsored by the Veterans Administration comparing hydrochlorothiazide plus reserpine plus hydralazine versus placebo had to be stopped early in a high blood pressure group because those not receiving treatment developed many more complications and it was deemed unethical to withhold treatment from them. The study continued in people with lower blood pressures and showed that treatment even in people with mild hypertension more than halved the risk of cardiovascular death.[99] In 1975, the Lasker Special Public Health Award was awarded to the team that developed chlorothiazide.[97] The results of these studies prompted public health campaigns to increase public awareness of hypertension and promoted the measurement and treatment of high blood pressure. These measures appear to have contributed at least in part to the observed 50% fall in stroke and ischemic heart disease between 1972 and 1994.[97]

Soon more drugs became available to treat hypertension. The British physician James W. Black developed beta blockers in the early 1960s;[100] these were initially used for angina, but turned out to lower blood pressure. Black received the 1976 Lasker Award and in 1988 the Nobel Prize in Physiology or Medicine for his discovery.[97] The next class of antihypertensives to be discovered were calcium channel blockers. The first member was verapamil, a derivative of papaverine that was initially thought to be a beta blocker and used for angina, but then turned out to have a different mode of action and was shown to lower blood pressure.[97] The renin-angiotensin system was known to play an important role in blood pressure regulation, and angiotensin converting enzyme (ACE) inhibitors were developed through rational drug design. In 1977 captopril, an orally active agent, was described;[101] this led to the development of a number of other ACE inhibitors.[97] More recently angiotensin receptor blockers and renin inhibitors have also been introduced as antihypertensive agents.

Society and culture

Economics

High blood pressure is the most common chronic medical problem prompting visits to primary health care providers in USA. The American Heart Association estimated the direct and indirect costs of high blood pressure in 2010 as $76.6 billion.[102] Hypertension affects ≈76,400,000 US adults (≈34% of the US population) and African American adults have among the highest rates of hypertension in the world (44%).[102] In the US 80% of people with hypertension are aware of their condition, 71% take some antihypertensive medication, but only 48% of people aware that they have hypertension are adequately controlled.[102] Adequate management of hypertension can be hampered by inadequacies in the diagnosis, treatment, and/or control of high blood pressure.[103] Health care providers face many obstacles to achieving blood pressure control from their patients, including resistance to taking multiple medications to reach blood pressure goals. Patients also face the challenges of adhering to medicine schedules and making lifestyle changes. Nonetheless, the achievement of blood pressure goals is possible, and most importantly, lowering blood pressure significantly reduces the risk of death due to heart disease and stroke, the development of other debilitating conditions, and the cost associated with advanced medical care.,[104][105]

Awareness

Graph showing, prevalence of awareness, treatment and control of hypertension compared between the four studies of NHANES [80]

The World Health Organization has identified hypertension, or high blood pressure, as the leading cause of cardiovascular mortality. The World Hypertension League (WHL), an umbrella organization of 85 national hypertension societies and leagues, recognized that more than 50% of the hypertensive population worldwide are unaware of their condition.[106] To address this problem, the WHL initiated a global awareness campaign on hypertension in 2005 and dedicated May 17 of each year as World Hypertension Day (WHD). Over the past three years, more national societies have been engaging in WHD and have been innovative in their activities to get the message to the public. In 2007, there was record participation from 47 member countries of the WHL. During the week of WHD, all these countries – in partnership with their local governments, professional societies, nongovernmental organizations and private industries – promoted hypertension awareness among the public through several media and public rallies. Using mass media such as Internet and television, the message reached more than 250 million people. As the momentum picks up year after year, the WHL is confident that almost all the estimated 1.5 billion people affected by elevated blood pressure can be reached.[107]

Hypotension

In physiology and medicine, hypotension is abnormally low blood pressure, especially in the arteries of the systemic circulation.[1] It is best understood as a physiologic state, rather than a disease. It is often associated with shock, though not necessarily indicative of it. Hypotension is the opposite of hypertension, which is high blood pressure. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood. If it is lower than normal then it is called low blood pressure or hypotension. Hypotension is generally considered as systolic blood pressure less than 90 millimeters of mercury (mm Hg) or diastolic less than 60 mm Hg.[2][3] However in practice, blood pressure is considered too low only if noticeable symptoms are present.[4]

For some people who exercise and are in top physical condition, low blood pressure is a sign of good health and fitness.[citation needed]

For many people, low blood pressure can cause dizziness and fainting or indicate serious heart, endocrine or neurological disorders. Severely low blood pressure can deprive the brain and other vital organs of oxygen and nutrients, leading to a life threatening condition called shock.

•

Signs and symptoms

The cardinal symptom of hypotension is lightheadedness or dizziness. If the blood pressure is sufficiently low, fainting and often seizures will occur.

Low blood pressure is sometimes associated with certain symptoms, many of which are related to causes rather than effects of hypotension:

• Chest pain

• Shortness of breath

• Irregular heartbeat

• Fever higher than 38.3 °C (101 °F)

• Headache

• Stiff neck

• Severe upper back pain

• Cough with phlegm

• Prolonged diarrhea or vomiting

• Dyspepsia

• Dysuria

• Foul-smelling urine

• Adverse effect of medications

• Acute, life-threatening allergic reaction

• Seizures

• Loss of consciousness

• Profound fatigue

• Temporary blurring or loss of vision

• In some cases loss of hair

• Connective tissue disorder Ehlers- Danlos Syndrome

Causes

Low blood pressure[5] causes can be due to low blood volume, hormonal changes, widening of blood vessels, medicine side effects, anemia, heart & endocrine problems.

Reduced blood volume, called hypovolemia, is the most common mechanism producing hypotension. This can result from hemorrhage, or blood loss; insufficient fluid intake, as in starvation; or excessive fluid losses from diarrhea or vomiting. Hypovolemia is often induced by excessive use of diuretics. Other medications can produce hypotension by different mechanisms.

Decreased cardiac output despite normal blood volume, due to severe congestive heart failure, large myocardial infarction, heart valve problems, heart attack, heart failure, or extremely low heart rate bradycardia, often produces hypotension and can rapidly progress to cardiogenic shock . Arrhythmias often result in hypotension by this mechanism. Beta blockers can cause hypotension both by slowing the heart rate and by decreasing the pumping ability of the heart muscle. Varieties of meditation and/or other mental-physiological disciplines can create temporary hypotension effects, as well, and should not be considered unusual.

Some heart conditions that can lead to low blood pressure include extremely low heart rate (bradycardia), heart valve problems, heart attack and heart failure. These conditions may cause low blood pressure because they prevent the body from being able to circulate enough blood.

Excessive vasodilation, or insufficient constriction of the resistance blood vessels (mostly arterioles), causes hypotension. This can be due to decreased sympathetic nervous system output or to increased parasympathetic activity occurring as a consequence of injury to the brain or spinal cord or of dysautonomia, an intrinsic abnormality in autonomic system functioning. Excessive vasodilation can also result from sepsis, acidosis, or medications, such as nitrate preparations, calcium channel blockers, angiotensin II receptor blockers ACE inhibitors. Many anesthetic agents and techniques, including spinal anesthesia and most inhalational agents, produce significant vasodilation.

Lower blood pressure is a side effect of certain botanicals, which can also interact with hypotensive medications. An example is theobromine, which lowers blood pressure[6] through its actions as both a vasodilator and a diuretic,[7] and has been used to treat high blood pressure.[8][9]

Pathophysiology

Blood pressure is continuously regulated by the autonomic nervous system, using an elaborate network of receptors, nerves, and hormones to balance the effects of the sympathetic nervous system, which tends to raise blood pressure, and the parasympathetic nervous system, which lowers it. The vast and rapid compensation abilities of the autonomic nervous system allow normal individuals to maintain an acceptable blood pressure over a wide range of activities and in many disease states.

Syndromes

Orthostatic hypotension, also called "postural hypotension", is a common form of low blood pressure. It occurs after a change in body position, typically when a person stands up from either a seated or lying position. It is usually transient and represents a delay in the normal compensatory ability of the autonomic nervous system. It is commonly seen in hypovolemia and as a result of various medications. In addition to blood pressure-lowering medications, many psychiatric medications, in particular antidepressants, can have this side effect. Simple blood pressure and heart rate measurements while lying, seated, and standing (with a two-minute delay in between each position change) can confirm the presence of orthostatic

hypotension. Orthostatic hypotension is indicated if there is a drop in 20 mmHg of systolic pressure (and a 10 mmHg drop in diastolic pressure in some facilities) and a 20 bpm increase in heart rate.

Neurocardiogenic syncope is a form of dysautonomia characterized by an inappropriate drop in blood pressure while in the upright position. Neurocardiogenic syncope is related to vasovagal syncope in that both occur as a result of increased activity of the vagus nerve , the mainstay of the parasympathetic nervous system.

Another, but rarer form, is postprandial hypotension, a drastic decline in blood pressure which occurs 30–75 minutes after eating substantial meals.[10]

When a great deal of blood is diverted to the intestines (a kind of "splanchnic blood pooling") to facilitate digestion and absorption, the body must increase cardiac output and peripheral vasoconstriction in order to maintain enough blood pressure to perfuse vital organs, such as the brain. It is believed that postprandial hypotension is caused by the autonomic nervous system not compensating appropriately, because of aging or a specific disorder.

Diagnosis

For most adults, the healthiest blood pressure is at or below 115/75 mmHg. A small drop in blood pressure, even as little as 20 mmHg, can result in transient hypotension.[11]

Evaluation of neurocardiogenic syncope is done with a tilt table test.

Treatment

The treatment for hypotension depends on its cause. Chronic hypotension rarely exists as more than a symptom. Asymptomatic hypotension in healthy people usually does not require treatment. Adding electrolytes to a diet can relieve symptoms of mild hypotension. In mild cases, where the patient is still responsive, laying the person in dorsal decubitus (lying on the back) position and lifting the legs will increase venous return, thus making more blood available to critical organs at the chest and head. The Trendelenburg position , though used historically, is no longer recommended.[12]

The treatment of hypotensive shock always follows the first four following steps. Outcomes, in terms of mortality, are directly linked to the speed in which hypotension is corrected. In parentheses are the still debated methods for achieving, and benchmarks for evaluating, progress in correcting hypotension. A study[13] on septic shock provided the delineation of these general principles. However, since it focuses on hypotension due to infection, it is not applicable to all forms of severe hypotension.

1. Volume resuscitation (usually with crystalloid)

2. Blood pressure support with a vasopressor (all seem to be equivalent)[14]

3. Ensure adequate tissue perfusion (maintain SvO2 >70 with use of blood or dobutamine)

4. Address the underlying problem (i.e. antibiotic for infection, stent or CABG (coronary artery bypass graft surgery) for infarction, steroids for adrenal insufficiency, etc...)

Medium-term (and less well-demonstrated) treatments of hypotension include:

• Blood sugar control (80-150 by one study)

• Early nutrition (by mouth or by tube to prevent ileus)

• Steroid support