Synonym: high blood pressure
German: arterielle Hypertonie
According to WHO criteria, arterial hypertension is defined as a permanent increase of systolic blood pressure over 140 mmHg, and a diastolic increase to more than 90 mmHg, independent of the situation.
A systolic blood pressure of more than 120 mmHg, or a diastolic blood pressure of more than 80 mmHg is judged as marginal.
The prevalence of arterial hypertension in Western industry nations is relatively high. The findings in different epidemiological studies however partly vary significantly between each other. A study from 2003, which was conducted in 6 European countries, Canada, and the USA, states prevalence of arterial hypertension in Europe at 44% of the population over 35 years of age. For the USA, a prevalence of 28% is stated. As rough approximation, one can say that
of the population in Europe suffer from arterial hypertension.
Arterial hypertension can be classified according to many different aspects, which partly are more based on pathophysiology, partly on clinical findings.
Primary hypertension: Hypertension which develops without visible cause. It is also called essential hypertension. It represents the largest proportion of cases of hypertension in adults (app. 85%). In children, itís exactly the opposite.
Secondary hypertension: This is defined as hypertension that occurs due to another underlying disease, or is caused by detectable factors. Secondary hypertension represents the smaller proportion of cases in adults (app. 15%). In children, itís exactly the opposite. Possible causes include:
Increased blood pressure that is caused by one of the following points is not counted among chronic arterial hypertension:
ESH ("European Society of Hypertension") classifies hypertension according to the measurement value of blood pressure:
|grade||systolic pressure||diastolic pressure|
|Grade 1 (mild)||140-159 mmHg||90-99 mmHg|
|Grade 2 (moderate)||160-179 mmHg||100-109 mmHg|
|Grade 3 (severe)||≥180 mmHg||>110 mmHg|
|Grade I||Hypertension without end organ damage|
|Grade II||Hypertension with end organ damage (z.B. hypertensive retinopathy (grade I and II), plaque formation in larger vessels)|
|Grade III||Hypertension with manifest cardiovascular secondary diseases (eg. angina pectoris, myocardial infarction, stroke, PAD)|
The definitions and classification of the blood pressure values in the guidelines for the treatment of arterial hypertension of the AWMF (German Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften e.V., Association of the Scientific Medical Societies in Germany) follows the definitions of the WHO.
|Category||systolic (mmHg)||diastolic (mmHg)|
|Ideal blood pressure||< 120||< 80|
|Normal blood pressure||120–129||80–84|
|High-normal blood pressure||130–139||85–89|
|Mild hypertension (grade 1)||140–159||90–99|
|Medium hypertension (grade 2)||160–179||100–109|
|Severe hypertension (grade 3)||≥ 180||≥ 110|
|Isolated systolic hypertension||> 140||< 90|
The pathogenesis of primary hypertension is so complex that it could not be fully explained up to now. A reason for that is that blood pressure is affected by many different factors. These included among others the circulating blood volume, blood viscosity, cardiac output, vascular elasticity, vessel cross section and hormonal (renin) as well as neuronal stimulation of the vaso-tonus.
You can differentiate between the following pathogenetic forms:
Here, cardiac output is not increased by influences from the heart. Cardiac output hypertension is prominent in hyperthyroidism. Here, the thyroid hormones stimulate the increased expression of beta-receptors, which (significantly) eases the katecholamine attack on the corresponding receptors of the heart.
This form of hypertension is based on a decrease of elasticity in the arterial system ñ with normal peripheral resistance. The volume elasticity coefficient of the arterial vascular system is increased its pressure reservoir function decreases. This reduces the blood volume storage capability of the vascular system. Clinically, this shows in a greater blood pressure amplitude: Systolic pressure increases, while diastolic pressure remains rather low. Elasticity hypertension is eg. caused by arteriosclerosis of the aorta and the larger arteries.
In case of volume hypertension, blood pressure rises subsequent to an increase of the volume of blood within the vascular system. This needs to be seen separately from edemas, where fluids gather in extravasal tissue. In renal failure, volume hypertension develops due to the increasing inability to further transport the fluids (filter function of the kidneys).
Hypertension usually develops asymptomatically and often causes only uncharacteristic complaints in moderately increased blood pressure values:
In strongly increased blood pressure, the following symptoms can add:
When hypertension is not detected by blood pressure control, it often is only recognized due to its late consequences (silent death).
The diagnosis "hypertension" is firstly made due to the repeated blood pressure measurement on both arms. As thresholds, according to a definition of the WHO, a value of over 140 mmHg is determined for the systolic blood pressure, and a value of 90 mmHg for the diastolic pressure. However, a singular measurement over these standard values doesnít justify a diagnosis of hypertension. It is only confirmed, when at three measurements at different times of day on 3 different days, increased values over the above stated standard are observed. Each measurement of the blood pressure should be carried out at rest, i.e. after 3-5 minutes of the patient being seated. Moreover, you need to make sure that both arms are positioned at the height of the heart.
The basic program of hypertension diagnostics additionally comprises:
The following table shows differential drug therapies of arterial hypertension.
|Middle-aged hypertensive patients without concomitant diseases||Beta blockers, ACE-inhibitors, AT1-antagonists|
|Elderly hypertensive patients without concomitant diseases||Thiazide diuretics, calcium channel blockers of the dihydropyridin type|
|A) Proven additional effects/indications|
|Diabetes mellitus with proteinuria||ACE-inhibitors, AT1-antagonists|
|Heart failure||ACE-inhibitors, diuretics, beta blockers (gradually increasing dosage!)|
|Isolated systolic hypertension||Diuretics (preferred), calcium antagonists (with longterm effect)|
|Myocardial infarction||Beta blockers (without ISA), ACE-inhibitors and AT1-antagonists (in systolic dysfunction and left ventricular hypertrophy. ACE-inhibitors and AT1-antagonists also prevent remodelling and fibrosis in addition to ischemic myocardial areas).|
|B) Favorable effects possible:|
|Angina pectoris||Beta blockers without ISA, calcium antagonists (attention: dihydropyridines are contra-indicated in unstable Angina pectoris)|
|Atrial tachycardia, atrial fibrillation||Beta blockers, clonidin, calcium antagonists (type verapamil and diltiazem)|
|Diabetes mellitus||ACE-inhibitors, AT1-antagonists, cardio-selective beta blockers (low dose), alpha-recceptor blockers|
|Migraine||Beta blockers (without ISA), calcium channel blockers|
|Renal failure||ACE-inhibitors (attention: renosvascular hypertension and serum creatinine ≥ 3mg/dl)|
|B) Adverse effects possible:|
|Obstructive ventilation disorders||Beta blockers|
|Diabetes mellitus||(non-selective) beta blockers, high-dosage diuretics, calcium antagonists|
|Heart failure||Calcium antagonists|
|AV conduction defects||Beta blockers, verapamil type calcium antagonists|
|PAD||(non-selective) beta blockers|
|Renal failure||Potassium-saving drugs, thiazids (not when serum creatinine is >2 mg/dl)|
|Renal artery stenosis||ACE-inhibitors, AT1-antagonists|
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