Arterial hypertension. Definition. Ethioliogy. Pathogenesis. Classification. Clinical pattern. Treatment.
Symptomatic arterial hypertensions. Ethioliogy. Pathogenesis. Classification. Clinical pattern. Treatment.
Hypertonic crisis. Clinical pattern.Classification. Emergency care. Prophylaxis of complications.
Physiology of blood circulation
Common characteristic of blood flow
The direct effect of heart contraction is creation of certain level of blood pressure, which is allows blood circulation.
Blood flow is continuous, although heart pumps the blood by separate portions. It caused by functioning of all components of cardio-vascular system: heart, arteries, arterioles, capillaries, venuls and veins. Besides that continuous blood flow is caused by extracardial factors as skeletal muscle contraction and pressure gradient between abdominal and thoracic cavities. Cardiac output depends on high, mass and area of human body surface. Cardiac output is regulated by contractive activity of cardiac muscle; valve function of full value; blood volume, vascular tonus, blood flow in capillaries; value of blood returning to the heart. In general distribution of cardiac output between different organs corresponds to its functional activity. Part of common blood supply, which every organ gets, depends on necessity in O2 and substrates of energy exchange. Average time of blood circulation measures 20-23 s.
Powers, which causes blood flow
Blood flows in vessels from high pressure to low. Heart pumping causes initial pressure. The highest pressure is large arteries ascending from the heart. Pressure in aorta at the end of systole is 110-
Functional importance of blood circulation system.
Both pulmonary and systemic circulation, compose entire system of blood circulation and function in correlation. The right ventricle is responsible for blood pumping into pulmonary circulation. Here blood is oxygenated and CO2 is taken out. The left ventricle pumps blood into systemic circulation. Blood flow in this part of vascular system provides performing of all other blood functions as regulatory, protective, excretory and others. Both right and left parts of heart pump equal portions of blood into corresponding vessels and function in interconnection to each other. The minute blood volume in pulmonary and systemic circulation is the same.
Circulating blood volume
Blood flowing in vessels is similar to stream of fluid in the pipe, but has a lot of specificities. Fluid stream in the pipe is described by formula:
Q= (P1-P2)/R, where
Q – fluid volume,
P1 – pressure in the beginning of the pipe,
P2 – pressure in the end of the pipe,
R – peripheral resistance of the pipe.
So fluid volume, which flows through the pipe is directly proportional to pressure difference from the end to beginning of pipe; and inversely proportional to peripheral resistance of pipe. As vessels have elastic walls, the blood flow in it, is differ from the same in pipe. Vessel cross-section may change due to neural and endocrine influences according to necessity.
Blood volume flowing through every part of vascular system per time unit is the same. It means that through aorta or cross-section of all arteries, capillaries or veins flows equal volume of blood. This volume per minute is called minute blood volume and measures in adults in rest 4.0 – 6.5 l/min.
Peripheral resistance of vessels
Peripheral resistance in vessels according to Poiseuille’s formula depends on length of vessels (l), viscosity of blood (η) and cross-section of vessel (r):
R= 8lŋ/πr.
In accordance to this formula the highest peripheral resistance might be in the smallest vessels. In reality the highest resistance is observed in arterioles. Average blood flow resistance in adults is equal to 900-2500 din·s/sm5
Paradoxes of blood flow.
In capillaries blood flow resistance is a bit lower because of such mechanism. In capillaries blood cells move one after another, dividing only by plasma, which decreases friction between blood cells and capillary wall. On other side, capillaries are shorter, than arterioles, which caused lower blood flow resistance too.
Viscosity of blood is also important for resistance of vessels. It depends on quantity of blood cells, protein rate in plasma, especially globulins and fibrinogen. Considerable increase of blood viscosity may cause lower blood returning to the heart and than disorders of blood circulation.
In large arteries centralization of blood flow is observed. Blood cells moves in the central part of blood stream, and plasma is peripheral. Instead increase of blood viscosity in arterioles is caused by higher friction between cells and vessels wall.
Linear velocity of blood flow
Blood flow also is characterized by linear velocity of blood circulation:
V=Q/πr2, where
V – linear velocity,
Q – blood volume,
r – radius of vessel.
So it is clear the wider cross-section of vessel the slower linear velocity of blood stream. In large arteries linear velocity is highest (0.1-0.2 m/s). In arterioles it measures 0.002 – 0.003 m/s, in capillaries – near 0.0003 m/s. In veins cross-section decreases and linear velocity increases to 0.001 – 0.05 m/s in large veins and to 0.1 –
Blood pressure
Transversal pressure – is difference between pressure inside the vessel and squeeze of it from the tissues. When increasing the tissue pressure to vessel wall, it closes. Hydrostatic pressure is corresponding to weight of all blood in vessel when it has vertical position. For vessels of head and neck this pressure decreases towards the heart. For vessels of limbs it has outward direction. That is why hydrodynamic pressure in vessels over heart is decreased due to hydrostatical pressure. Below heart hydrodynamic pressure is increased, because it is summarized with hydrodynamic pressure.
Role of changing body position
In horizontal position of the body hydrostatical pressure is equal in every part of the body and hydrodynamic pressure doesn’t depend on it. In vertical position transversal pressure in vessels of limbs creates tension of vessels walls (Laplas low):
Pt=F/r, where
Pt – transversal pressure,
F – vessel tension,
r – radius of vessel.
So it is shown the smaller radius of vessel, the lower tension in vessels walls. Due to this capillaries with thinnest wall don’t crush because of its smallest diameter. Existence of precapillary sphincters permits proper direction of blood pressure so that capillaries may close (plasmatic capillaries).
Index |
Level of arterial pressure |
|
Systolic, mm Hg |
Diastolic, mm Hg |
|
Optimal AP |
< 120 |
< 80 |
Normal AP |
< 130 |
<85 |
Higher–normal АP |
130-139 |
85-89 |
Hypertension І degree Measure hypertension |
140-159 |
90-99 |
140-149 |
90-94 |
|
Hypertension ІI degree |
160-179 |
100-109 |
Hypertension of IIІ degree |
>180 |
>110 |
Isolated systolic hypertension Measure hypertension |
>140 |
<90 |
140-149 |
<90 |
Classification of hypertension (NHLBI, 2003).
Index |
Level of arterial pressure |
|
Systolic, mm Hg |
Diastolic, mm Hg |
|
Normal AP |
< 120 |
< 80 |
Prehypertension |
120-139 |
or 80-89 |
Hypertension І degree |
140-159 |
or 90-99 |
Hypertension ІІ degree |
>160 |
or >100 |
e) Reactions of cardiovascular system on physical load (On dynamic physical load children and teenagers reacted by increase of heart beat, systolic arterial pressure. When the children and teenagers train to physical load they increase the reserve possibility of organism and as adaptive reaction increase rate of heartbeat (not increase the diastolic arterial pressure, decrease systolic arterial pressure). On static physical load children and teenagers reacted by increase arterial pressure. Increase of physical load is preventing development of hypertension.)
Condition of blood circulation in aged and old persons (Common properties of aged organism is decrease intensity of blood circulation in different tissues, organs and systems. It presents redistribution of volume of circulated blood to brain and heart. Elasticity of vessels’ wall decrease, that is why increasing peripheral vessel resistance. In these persons decrease speed of blood stream (may be it connect with decrease of cardiac output), decrease speed of capillary blood stream; change character of blood stream regulatory processes.)
Measuring arterial pressure by Korotkov’s method
Examinee sits at the table, putting right hand on the level of heart. Give cuff on the middle 1/3 of right shoulder and fix. Cuff is fixed well if you can put under it only one finger. Find the pulsation of brachial artery. Give ear to cuff
Auscultatory method
Processing of arterial pressure data
Pulsation pressure may be calculated using the formula:
PP=SP-DP, where
PP – pulsation pressure, SP – systolic pressure, DP – diastolic pressure.
Middle dynamical pressure is equal to:
PP/3+DP
Peripheral vessels resistance is calculated as
PVR=MDP·60·1,333/MBV, where
MBV – minute blood volume
MBV=PR·PP·100/MDP
Note in the conclusion, do results normal or not?
Essential and secondary hypertension
Essential hypertension (morbus hypertonicus) is the condition in which elevated arterial pressure is the leading symptom. Essential hypertension (also called primary hypertension or idiopathic hypertension) is the form of hypertension that by definition, has no identifiable cause. It is the most common type of hypertension, affecting 95% of hypertensive patients, it tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors. Prevalence of essential hypertension increases with age, and individuals with relatively high blood pressure at younger ages are at increased risk for the subsequent development of hypertension. Hypertension can increase the risk of cerebral, cardiac, and renal events. The disease is provoked by nervous and functional disorders in the regulation of the vascular tone. Men and women, mostly over 40, are equally attacked by the disease.
Step 1
First the patient must be made to lie down. Measuring blood pressure while standing is not advisable, as the correct blood pressure is only recorded when a patient is in a supine position. This is the position in which the person’s heart is not under any kind of stress and the heartbeat is normal.
Step 2
The brachial artery is palpable on the medial side of the brachialis tendon which can be found on the inside of the arm. In simple words, flex your arm slightly and you will be able to palpate a tendon and on the inner side of this tendon (towards the body) you will find the brachial artery. So, once the brachial artery is identified, wrap the cuff tightly, around the area, just above the brachial artery. Take care of placing the diaphragm part of the chest-piece of the stethoscope on the brachial artery.
Step 3
After the cuff is secured into place, close the valve and slowly start pumping the air bulb, which will make the mercury column rise. Be sure to do this slowly, so that the person does not feel sudden pain due to ischemia. Also, do not raise the pressure to more than 150mm of Hg to be on the safe side, unless it is known that the person is suffering from high blood pressure. Ideally, raise the pressure till the heart sounds are not heard anymore through the stethoscope.
Step 4
Now, slowly release the pressure and wait till you hear heart sounds. These sounds are known as Korotkoff sounds. They are heard, because the normal streamline flow of blood is suddenly hindered and again, when the pressure is released, the blood flows turbulently and gushes through, causing these sounds. Thus, the level of pressure at which the first sound is heard marks the systolic blood pressure. Then, when the sound slowly starts to fade away and just before, it completely disappears, that reading will mark the diastolic blood pressure.
Step 5
If you perform the procedure but are not sure of the readings you got while measuring blood pressure, you can repeat the procedure immediately, provided the person is not complaining of pain in the arm. During the procedure, if the persons arm suddenly turns white and spasmodic and the person complains of pain, then it is best to immediately release the pressure by opening the valve completely.
The normal blood pressure range is around 120/80 mm of Hg, with 120 signifying the systolic pressure and 80 the diastolic pressure; anything above 140/90 mm of Hg, is normally considered to be a high blood pressure.
Classification
A recent classification recommends blood pressure criteria for defining normal blood pressure, prehypertension, hypertension (stages I and II), and isolated systolic hypertension, which is a common occurrence among the elderly. These readings are based on the average of seated blood pressure readings that were properly measured during 2 or more office visits. In individuals older than 50 years, hypertension is considered to be present when a person’s blood pressure is consistently at least 140 mmHg systolic or 90 mmHg diastolic. Patients with blood pressures over 130/80 mmHg along with Type 1 or Type 2 diabetes, or kidney disease require further treatment.
Prehypertension is an American classification for cases where a person’s blood pressure is elevated above normal but not to the level considered to be hypertension (high blood pressure). The seventh report of the Joint National Committee (JNC 7) proposed a new definition of blood pressure values below 140/90 mm Hg. Prehypertension is considered to be blood pressure readings with a systolic pressure from 120 to
Systolic hypertension. Systolic hypertension is defined as an elevated systolic blood pressure (SBP). If the systolic blood pressure is elevated (>140) with a normal (<90) diastolic blood pressure (DBP), it is called “isolated systolic hypertension”. Systolic hypertension may be due to reduced compliance physiology of the aorta with increasing age. This increases the load on the ventricle and compromises coronary blood flow, eventually resulting in left ventricular hypertrophy, coronary ischemia, and heart failure.
Classification: according to Obrastsov and Strazesko three stages of the disease are classified:
– hypertrophy of the left ventricle;
– proteinuria (or elevation of creatinine level till 0,177 mmol/l;
– narrowing of retinal vessels;
– ultrasonic or X-ray data of atherosclerosis (plaques);
In the 3rd stage complication develops:
– the heart: left ventricular heart failure or myocardial infarction;
– the brain: brain insult, transient hemodynamic disorders, hypertensive encephalopathy;
– eyes: retinal hemorrhage or papiloedema;
– kidneys: creatitine level more than 0,177 mmol/l, renal failure;
– vessels: dissecting aneurism of the aorta, occlusions of arteries.
Classification of blood pressure for adults |
||
Category |
diastolic, mmHg |
|
Normal |
≤ 120 |
≤ 80 |
120 – 139 |
or 80 – 89 |
|
Stage 1 Hypertension |
140 – 159 |
or 90 – 99 |
Stage 2 Hypertension |
160 – 179 |
or 100 – 109 |
≥ 180 |
or ≥ 110 |
Arterial hypertension is defined as rising of arterial blood pressure excess of
Essential hypertension should accurately be differentiated from symptomatic hypertension in which arterial pressure rises as a symptom of some other disease, this symptom being far from the leading one. Symptomatic hypertension occurs in aortic coarctation, atherosclerosis of the aorta and its large branches, in endocrine dysfunction (e.g. Itsenko-Cushing disease, phaeochromocytoma, primary aldosteronism, or the Conn syndrome), affection of the renal parenchyma, occlusive affection of the main renal arteries, and in some other diseases.
Evaluation of Secondary Hypertension
The possibility that an underlying condition is causing hypertension must also be considered; secondary hypertension is often unmanageable until the underlying cause is treated. Among 4000 patients with resistant hypertension who were evaluated during an 18-year period at one tertiary center, secondary causes were found in 10 percent of patients overall and in 17 percent of patients over the age of 60 years.
Chronic renal parenchymal disease, usually resulting from diabetic nephropathy or hypertensive nephrosclerosis, may be the most common cause of secondary hypertension. High blood pressure caused by acute renal parenchymal damages is mainly due to water and sodium retention, therefore timely diuretic treatment often can lower the blood pressure.
While the pathogenesis of hypertension caused by chronic renal parenchymal disease is more complex and it can be caused by many factors. Activation of RAAS (rennin-angiotensin aldosterone system). Renal parenchymal diseases can cause ischemia and hypoxia in the kidneys which will activate the RAAS. Angiotensin II has direct stimulation to vasoconstriction and aldosterone can worsen water and sodium retention so as to further increase high blood pressure.
Other factors that can cause sodium retention and blood volume increase can all cause blood pressure to increase such as decreased GFR, activation of RAAS and sympathetic nervous system, insulin resistance and reduced nitric oxide, etc. What is more, the above mentioned factors can increase vascular resistance and worsen high blood pressure.
Renal parenchymal diseases can affect one or both kidneys. The common unilateral renal parenchymal diseases include reflux nephropathy, chronic pyelonephritis, hydronephrosis and renal gland carcinoma, etc. Early removal of the diseased kidney can cure or greatly improve hypertension.
Common bilateral renal parenchymal diseases include primary and secondary glomerulonephritis, chronic interstitial nephritis and adult polycystic kidney disease.
Whatever the underlying disease of renal parenchymal impairments, the incidence of hypertension will increase along with the severity of renal function damages. It has been reported that more than 90% end stage renal disease patients will have elevated blood pressure. Therefore patients should receive early treatments so as to protect kidney functions and slow down illness progression.
Atherosclerotic renovascular disease, which is particularly prevalent among elderly smokers, is another possible cause. The presence of an abdominal bruit or hypokalemia or a recent increase in the severity of hypertension may suggest the diagnosis of atherosclerotic renovascular disease.
Screening for renovascular disease may be warranted if other causes of resistant hypertension are not identified, since angioplasty and stenting may improve blood pressure. However, in cases of renovascular hypertension caused by atherosclerotic disease, blood pressure often remains high even after intervention, in contrast to hypertension caused by the much less common fibromuscular dysplasia.
Renal artery stenosis (RAS) is the major cause of renovascular hypertension and it accounts for about 1-10% of the 50 million people in the United States who have hypertension. The incidence is less than 1% of cases of mild to moderate HTN. However, it rises to 10 to 45 % in patients with acute (or superimposed upon a preexisting elevation in blood pressure), severe, or refractory hypertension.
Renovascular hypertension (RVHT) denotes nonessential hypertension in which a causal relationship exists between anatomically evident arterial occlusive disease and elevated blood pressure. RVHT is the clinical consequence of renin-angiotensin-aldosterone activation as a result of renal ischemia.
RAS is also being increasingly recognized as an important cause of chronic renal insufficiency and end-stage renal disease. Studies suggest that ischemic nephropathy from RAS may be responsible for 5-22% of advanced renal disease in all patients older than 50 years in US.
Major causes of the renal arterial lesions are:
Atherosclerosis —It is the cause of RAS in >2/3rd of the cases. This primarily affects men over the age of 45 and usually involves the aortic orifice or the proximal main renal artery. This disorder is particularly common in patients with diffuse atherosclerosis, but can occur as a relatively isolated renal lesion.
Fibromuscular dysplasia — are uncommon angiopathies associated with heterogeneous histologic changes that may affect the carotid circulation as well as the visceral and peripheral arteries. In comparison to atherosclerosis, fibromuscular dysplasia most often affects younger women and typically involves the distal main renal artery or the intrarenal branches.
Other less common causes of RAS include:
§ Vasculitis (Takayasu’s arteritis)
§ Dissection of the renal artery.
§ Thromboembolic disease
§ Renal artery aneurysm
§ Renal artery coarctation
§ Extrinsic compression
§ Radiation injury
Summarizes features of and screening tests for these and other causes of secondary hypertension, such as primary aldosteronism (considered to be more common than previously recognized), pheochromocytoma, and sleep apnea (recently recognized to be associated with refractory hypertension). Generally, the decision to screen a patient for such disorders should depend on suggestive findings on history taking, physical examination, or basic laboratory testing. Interventions that are directed at these disorders (e.g., surgery or aldosterone-antagonist therapy for hyperaldosteronism, surgery for pheochromocytoma etc.
Primary aldosteronism (PA; synonym: Conn’s syndrome) is characterized by autonomous aldosterone excess with subsequent suppression of renin levels. The main causes of primary aldosteronism accounting for >95% of cases are aldosterone producing adenoma (APA) and idiopathic primary aldosteronism (IHA). The distinction between these 2 entities is clinically crucial. APA is a curable form of hypertension, and unilateral adrenalectomy results in correction of hypokalemia and blood pressure normalisation in the majority of patients.
Pheochromocytoma hypertensive crisis may manifest with impressively dramatic clinical features. The BP is markedly elevated during the paroxysm and the patient may have profound sweating, marked tachycardia, pallor, numbness, tingling, and coldness of the feet and hands. A single attack may last from a few minutes to hours and may occur as often as several times a day to once a month, or less.
Aetiology and pathogenesis.
Hypertension is one of the most common complex disorders. The etiology of hypertension differs widely amongst individuals within a large population. And by definition, essential hypertension has no identifiable cause. However, several risk factors have been identified.
Hypertension may be secondary to other diseases but over 95% of patients have essential hypertension which is of unknown origin. It is observed though that:
Having a personal family history of hypertension increases the likelihood that an individual develops HPT.
Essential hypertension is four times more common in black than white people, accelerates more rapidly and is often more severe with higher mortality in black patients.
More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing. One of these genes is the angiotensinogen (AGT) gene, studied extensively by Kim et al. They showed that increasing the number of AGT increases the blood pressure and hence this may cause hypertension. Twins have been included in studies measuring ambulatory blood pressure; from these studies it has been suggested that essential hypertension contains a large genetic influence. Supporting data has emerged from animal studies as well as clinical studies in human populations. The majority of these studies support the concept that the inheritance is probably multifactorial or that a number of different genetic defects each has an elevated blood pressure as one of its phenotypic expressions. However, the genetic influence upon hypertension is not fully understood at the moment. It is believed that linking hypertension-related phenotypes with specific variations of the genome may yield definitive evidence of heritability. Another view is that hypertension can be caused by mutations in single genes, inherited on a Mendelian basis.
Hypertension can also be age related, and if this is the case, it is likely to be multifactorial. One possible mechanism involves a reduction in vascular compliance due to the stiffening of the arteries. This can build up due to isolated systolic hypertension with a widened pulse pressure. A decrease in glomerular filtration rate is related to aging and this results in decreasing efficiency of sodium excretion. The developing of certain diseases such as renal microvascular disease and capillary rarefaction may relate to this decrease in efficiency of sodium excretion. There is experimental evidence that suggests that renal microvascular disease is an important mechanism for inducing salt-sensitive hypertension.
Obesity can increase the risk of hypertension to fivefold as compared with normal weight, and up to two-thirds of hypertension cases can be attributed to excess weight. More than 85% of cases occur in those with a Body mass index greater than
Another risk factor is salt (sodium) sensitivity which is an environmental factor that has received the greatest attention. Approximately one third of the essential hypertensive population is responsive to sodium intake. When sodium intake exceeds the capacity of the body to excrete it through the kidneys, vascular volume expands secondary to movement of fluids into the intra-vascular compartment. This causes the arterial pressure to rise as the cardiac output increases. Local autoregulatory mechanisms counteract this by increasing vascular resistance to maintain normotension in local vascular beds. As arterial pressure increases in response to high sodium chloride intake, urinary sodium excretion increases and the excretion of salt is maintained at expense of increased vascular pressures. The increased sodium ion concentration stimulates ADH and thirst mechanisms, leading to increased reabsorption of water in the kidneys, concentrated urine, and thirst with higher intake of water. Also, the water movement between cells and the interstitium plays a minor role compared to this. The relationship between sodium intake and blood pressure is controversial. Reducing sodium intake does reduce blood pressure, but the magnitude of the effect is insufficient to recommend a general reduction in salt intake.
Renin elevation is another risk factor. Renin is an enzyme secreted by the juxtaglomerular apparatus of the kidney and linked with aldosterone in a negative feedback loop. 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 white Americans, and may explain why African Americans tend to respond better to diuretic therapy than drugs that interfere with the Renin-angiotensin system. High renin levels predispose to hypertension by causing sodium retention through the following mechanism: Increased renin → Increased angiotensin II → Increased vasoconstriction, thirst/ADH and aldosterone → Increased sodium reabsorption in the kidneys (DCT and CD) → Increased blood pressure.
Hypertension can also be caused by Insulin resistance and/or hyperinsulinemia, which are components of syndrome X, or the metabolic syndrome. Insulin is a polypeptide hormone secreted by cells in the islets of Langerhans, which are contained throughout 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. Iormotensive 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.
It has been suggested that vitamin D deficiency is associated with cardiovascular risk factors. It has been observed that individuals with a vitamin D deficiency have higher systolic and diastolic blood pressures than average. Vitamin D inhibits renin secretion and its activity, it therefore acts as a “negative endocrine regulator of the renin-angiotensin system”. Hence a deficiency in vitamin D leads to an increase in renin secretion. This is one possible mechanism of explaining the observed link between hypertension and vitamin D levels in the blood plasma.
Also, some authorities claim that potassium might both prevent and treat hypertension.
Recent studies claims that obesity is a risk factor for hypertension because of activation of the renin-angiotensin system (RAS) in adipose tissue, and also linked renin-angiotensin system with insulin resistance, and claims that anyone can cause
the other.
Cigarette smoking, a known risk factor for other cardiovascular disease, may also be a risk factor for the development of hypertension.
It has long been identified as an independent risk factor for cardiovascular disease. Traditionally, emphasis has been placed on elevated DBP as a risk factor for the development of target organ damage. However, as early as 1971, the Framingham study showed that, although DBP was a major determinant of cardiovascular risk in men under 45 years of age, SBP was the stronger risk factor in older men and in women of all ages. Since then, several observational studies have suggested that the pulse pressure (PP) may be a better predictor of cardiovascular complications than SBP or mean arterial pressure.
Overstrain of the central nervous system, caused by prolonged and strong emotional stress and also mental overstrain, are believed to be the main cause of the disease. In some cases essential hypertension develops after brain concussion (concussion-commotion form).
Development of the disease greatly depends on occupation: it occurs mostly in subjects whose occupation is associated with nervous and mental overstrain, e.g. in scientific workers, engineers, physicians, drivers, etc. Familial predispostion is another important factor. The early stage of essential hypertension is characterized by nervous-functional disorder in regulation of the vascular tone. Vegetative-endocrine disorders and changes in the renal regulation of the vascular tone are later steps of the pathological process. Overstrain of the higher nervous activity causes vasopressor adrenal reaction by whivh arterioles of internal organs are narrowed. Next steps are production of rennin, stimulation of rennin-angiotensin system and systemicf vasodilatation; activation of aldosterone secretion.
Pathophysiology
Cardiac output and peripheral resistance are the two determinants of arterial pressure and so blood pressure is normally dependent on the balance between cardiac output and peripheral resistance. Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles. The pathophysiology of essential hypertension is an area of research, and until now remains not well understood, but many theories have been proposed to explain this.
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:
An overactive Renin-angiotensin 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.
Clinical pattern. During the early stage of the disease the patient would usually complain of neurotic disorders: general weakness, impaired work capacity, inability to concentrate during work, deranged sleep, trancient headache, e feeling of heaviness in the heart, vertigo, noise in the ears, and sometimes palpitation. Exertional dyspnoea develops later.
The main objective sign of the disease is elevated arterial pressure (over 140/90 mm Hg) . Blood pressure is liable in early stage of the disease but later stabilizes. Examination of the heart reveals hypertrophy of the left ventricle: expanding apex beat, displacement of the cardiac dullness leftward. The second heart sound is accentuated over the aorta. The pulse becomes firm and tense.
Patients should be asked routinely about the use of medications or other substances that can elevate blood pressure or antagonize the effects of antihypertensive drugs. These substances include sympathomimetic drugs (e.g., ephedra, phenylephrine, cocaine, and amphetamines), herbal supplements (e.g., ginseng and yohimbine), anabolic steroids, appetite suppressants, and erythropoietin, although all these drugs probably account for less than 2 percent of cases of resistant hypertension. Nonsteroidal antiinflammatory drugs and cyclooxygenase-2 inhibitors may raise both systolic and diastolic blood pressure by several mm Hg.
These agents impair the excretion of sodium, which causes volume retention; they also inhibit the production of local renal vasodilative prostaglandins; the therapeutic action of angiotensin-converting–enzyme (ACE) inhibitors and loop diuretics (but not calcium-channel blockers) depends on the availability of these prostaglandins. Efforts should be made to discontinue such agents, although if they are needed for another condition, antihypertensive therapy may need to be modified.
An assessment of dietary and lifestyle factors is also important. Excessive alcohol use (more than three or four drinks per day) and a high sodium intake (typically defined by a urinary sodium excretion of more than 150 mmol per day) may contribute to resistant hypertension; the frequency of salt sensitivity is increased among patients who are at least 60 years of age, patients who are black or obese, and patients with renal impairment. Studies indicate that more than 40 per cent of patients with resistant hypertension are obese, and obese patients may require higher doses of antihypertensive medications than do nonobese patients.
Clonidine withdrawal syndrome can result from abrupt discontinuation of a high-dosage regimen of clonidine, causing a hyperadrenergic state that mimics pheochromocytoma. When clonidine is abruptly discontinued (especially at high dosages) or rapidly tapered, a syndrome consisting of nausea, palpitation, anxiety, sweating, nervousness, and headache, along with marked elevation of the BP has beeoted. Symptoms of clonidine withdrawal can be relieved by reinstituting the clonidine regimen. If there is marked elevation of BP and the patient is experiencing symptoms such as palpitations, chest discomfort, and epigastric discomfort, the IV administration of phentolamine or labetalol is recommended.
Monoamine oxidase inhibitors (MAOIs) can increase the risk of hypertensive crisis in patients who also take drugs such as ephedrine and amphetamines or consume foods containing large quantities of tyramine.
Cocaine-induced hypertensive crisis can cause an abrupt, sudden increase in the systemic BP, resulting in a hypertensive emergency. Neurohumoral factors triggered by cocaine likely cause intense vasoconstriction and thus increase the vascular resistance and the BP. Sudden rise of BP in a previously normotensive individual may result in a serious cardiovascular complication. The BP should be lowered to safe limits without much delay.
The physical examination should begin with an assessment of BP, with an appropriate-size cuff in both upper extremities and in a lower extremity if peripheral pulses are markedly reduced. Brachial, femoral, and carotid pulses should be assessed. A careful cardiovascular examination as well as a thorough neurologic examination, including mental status, should be conducted. This assessment will aid in establishing the degree of involvement of affected target organs and should provide clues to the possible existence of a secondary form of hypertension, such as renovascular hypertension.
Accurate measurement of blood pressure and verification of elevated pressure on multiple occasions over time are important. Ambulatory or home blood-pressure monitoring can identify “white-coat hypertension” (blood pressure that is elevated when measured during an office visit but that is otherwise normal) and prevent unnecessary treatment. White-coat hypertension, present in 20 percent of patients with elevated blood pressure, is associated with a lower cardiovascular risk than is sustained hypertension, but it may be a precursor of sustained hypertension and therefore warrants monitoring.
The diagnosis is based on the findings of at least two or three elevated blood-pressure measurements (in the physician’s office or at home), despite adherence to regimens containing three medications. However, if the blood pressure is above 160/100 mm Hg, additional readings are not necessary for diagnosis. Evaluation (including physical examination and laboratory testing) is routinely warranted to look for evidence of end-organ damage related to hypertension and for other cardiovascular risk factors. Volume overload and elevated sympathetic tone, which are common in patients with uncontrolled blood pressure, may occasionally be suggested by the presence of a rapid pulse rate. Renin levels have not been found to be useful in the prediction of excess volume, though they may be useful in the evaluation of possible secondary causes of hypertension.
Blood pressure should be measured after a patient has been seated quietly for five minutes, with his or her arm supported at heart level and with the use of a properly calibrated and sized cuff. If the cuff is too narrow or too short, readings may be erroneously high (typically by 5 to
Ambulatory blood pressure monitoring (ABPM) is a method of taking regular blood pressure readings, usually over a 24-hour period, as patients conduct their normal activities. A special, automatic blood pressure monitor is used, and patients are asked to keep a diary or log of their activities during the day.
X-rays reveal “aortic” heart configuration. The aorta is elongared, consolidated and dilated.
ECG: left type with displacement of S-T segment, low, negative, or two-phase T wave in the Ist and 2nd standart leads and chest leads V5-V6.
ECG in hypertension (hypertrophy of the left ventricle)
Diagram of normal heart on left compared to a diagram of a hypertrophic .
Elevated BP, as well as the presence of left ventricular hypertrophy
Aortic heart configuration in hypertension
Hypertrophy of the left ventricle as a result of hypertension
farteries.com/hypertension.php
Hypertension
In addition to the history taking and physical examination, several tests are routinely indicated in patients with hypertension: urinalysis, complete blood count, blood chemical tests (measurements of potassium, sodium, creatinine, fasting glucose, total cholesterol, and high-density lipoprotein), and 12-lead electrocardiography. The evaluation should identify signs of cardiovascular, cerebrovascular, or peripheral vascular disease and other cardiovascular risk factors that are frequently present in patients with hypertension. Severe or resistant hypertension or clinical or laboratory findings suggesting the presence of renal disease, adrenal hypertension (due to abnormal mineralocorticoid secretion or pheochromocytoma), or renovascular hypertension should be further investigated. Essential, or primary, hypertension, the focus of this article, is the diagnosis in over 90 percent of cases.
If a secondary cause of hypertension is suspected, appropriate blood and urine samples should be obtained before aggressive therapy is initiated. A careful funduscopic examination should be performed to detect the presence of hemorrhages, exudates, and/or papilledema
Some patients who have what appears to be resistant hypertension have a normal blood pressure at home. This phenomenon has been attributed to transitory, or “white-coat,” resistant hypertension in the physician’s office. Repeated home measurements or 24-hour ambulatory monitoring may differentiate this type of hypertension from truly resistant hypertension. Such measures are warranted in patients undergoing treatment who have consistently high blood-pressure levels in the physician’s office yet have no evidence of target-organ damage. In one study, as many as a third of patients with apparently resistant hypertension had average blood-pressure levels of less than 130/85 mm Hg on 24-hour or home measurement. Some data suggest that blood-pressure values obtained at home or during 24-hour ambulatory procedures correlate better with target-organ involvement, especially left ventricular hypertrophy, than do values obtained in the physician’s office. However, office, or white-coat, hypertension is not benign and should not be ignored.
Rarely, in older patients, what appears to be refractory hypertension may represent inaccurate measurement owing to severely sclerotic arteries (i.e., pseudohypertension). The condition is suggested if the radial pulse remains palpable despite occlusion of the brachial artery by the cuff (the Osler maneuver),16 although this sign is not specific. The presence of this condition can be confirmed by intra-arterial blood-pressure measurement.
Complications
Hypertension is a risk factor for stroke, myocardial infarction, renal failure, congestive heart failure, progressive atherosclerosis. There is a continuous, graded relation between blood pressure and the risk of cardiovascular disease; the level and duration of hypertension and the presence or absence of coexisting cardiovascular risk factors determine the outcome. Treatment of hypertension reduces the risk of stroke, coronary artery disease, and congestive heart failure, as well as overall cardiovascular morbidity and mortality from cardiovascular causes. However, only 54 percent of patients with hypertension receive treatment and only 28 percent have adequately controlled blood pressure
In hypertension heart, eye fundus, kidney and the brain are affected thet is why they are called “target organs”.
Cardiovascular or other target-organ disease denotes left ventricular hypertrophy, angina or prior myocardial infarction, prior coronary revascularization, heart failure, stroke or transient ischemic attack, nephropathy, peripheral arterial disease, and retinopathy.
In the later period of the disease heart failure may develop due to fatigue of the heart muscle as a result of increased arterial pressure. Heart failure is often manifested by acute attaks of cardiac asthma or oedema of the lungs; or chronic circulatory insufficiency may develop.
High arterial pressure in the affected cerebral vessels can derange cerebral circulation. This can cause paralysis, disorders in sensitivity. Cerebral circulation is deranged due to spasms of the vessels, their thrombotic obstruction, hemorrhage due to rupture of the vessel, or diapedetic discharge of erythrocytes.
The affected kidneys become unable to concentrate urine (nicturia or isohyposthenuria develops). Metabolites (otherwise excreted with urine) are retained to provoke uraemia.
Vision may be deteriorated in grave cases. Examination of the fundus occuli reveals its general pallidness; the arteries are narrow and tortuous, the veins are mildly dilated; haemorrhage into the retina (angiospastic retinitis) sometimes observed.
Hypertensive retinopathy is a condition characterized by a spectrum of retinal vascular signs in people with elevated blood pressure. The detection of hypertensive retinopathy with the use of an ophthalmoscope has long been regarded as part of the standard evaluation of persons with hypertension. This clinical practice is supported by both previous and current reports of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC), which list retinopathy as one of several markers of target-organ damage in hypertension. On the basis of the JNC criteria, the presence of retinopathy may be an indication for initiating antihypertensive treatment, even in people with stage 1 hypertension (blood pressure, 140 to 159/90 to
Hypertensive retinopathy
Malignant Hypertensive Retinopathy. Multiple cotton-wool spots (white arrows), retinal hemorrhages (black arrows), and swelling of the optic disk are visible.
Hypertensive retinopathy
Malignant Hypertensive Retinopathy. Multiple cotton-wool spots (white arrows), retinal hemorrhages (black arrows), and swelling of the optic disk are visible.
Hypertensive encephalopathy is a deadly complication of severe hypertension that should be recognized as an emergency and quickly treated. Although encephalopathy occurs mainly in patients with chronic or malignant hypertension, it can also complicate sudden hypertension of brief duration. The clinical manifestations are generated not only by the severity of BP elevation but also by the abrupt rise of BP in a previously normotensive individual. This condition occurs more frequently when the hypertension is complicated by renal insufficiency than when the renal function is normal. The full-blown clinical syndrome of hypertensive encephalopathy may take anywhere from 12 to 48 hours to develop.
A 41-year-old woman with hypertensive encephalopathy. Hypertensive crisis with pheochromcytoma. (A) Coronal FLAIR image shows multiple hyperintense lesions in the subcortical white matter (arrows) and cortex (arrowheads) in both parieto-occipital areas. (B) T2-weighted image shows hyperintense lesions in the cortical and subcortical white matter in the right frontal (arrow) and parieto-occipital areas (arrowheads). (C) DWI shows the left parieto-occipital cortical lesion as hyperintense (arrowheads) and the right frontal subcortical lesion as iso– or slightly hyperintense (arrow). (D) ADC map reveals decreased ADC of the left cortical lesion representing cytotoxic edema (arrowheads). A subcortical lesion in the right frontal lobe shows increased ADC representing vasogenic edema (arrow).
Severe generalized, sudden headache is a prominent clinical manifestation. Neurogenic symptoms consisting of confusion, somnolence, and stupor may appear simultaneous with or following the onset of headache. If untreated, progressive worsening of neurological damage occurs, culminating in coma and death. The patient may be restless and uncooperative during the initial stages of the syndrome. Other clinical features may include projectile vomiting, visual disturbances ranging from blurring to frank blindness, and transient focal neurologic deficits. Sometimes (especially in children) generalized or focal seizures may be the only clinical feature.
On physical examination of the patient, the BP is markedly elevated but there is no certain level of BP above which encephalopathy is likely to develop. The fundi reveal generalized arteriolar spasm with exudates or hemorrhages. Although papilledema is present in most patients with this complication, its absence does not exclude the diagnosis of hypertensive encephalopathy.
Once the diagnosis of hypertensive encephalopathy is likely, the BP should be lowered rapidly to near-normal levels; yet the diastolic BP should probably remain at or slightly above
With the current state of our knowledge, no reliable guidelines can be given for the management of hypertensive crises occurring in patients with cerebrovascular accidents. Based on the pathogenesis of these conditions, especially intracerebral hemorrhage, it is advisable to reduce the BP to near-normal levels or to a degree that will not clinically compromise cerebral function. If there is evidence of progression of the disease or worsening of the neurologic manifestations during treatment, then the therapeutic approach must be reassessed. Precautions should be taken to avoid hypotension in these patients, and it is advisable, therefore, not to lower the diastolic BP to less than
Acute left ventricular failure may be caused by severe and uncontrolled hypertension; the higher the BP, the harder the left ventricle must work. Decreasing the workload of the failing myocardium may improve the heart function. In acute left ventricular failure, myocardial oxygen requirements increase due to increased end-diastolic fiber length and left ventricular volume. This could be particularly unfavorable in patients with concomitant coronary artery disease (CAD).
Left ventricular failure with alveolar edema. This is a posteroanterior chest film in a 48-year-old man. Severe interstitial and alveolar edema exists. Left ventricular enlargement indicates pulmonary venous hypertension secondary to left ventricular failure. The cause of the failure is not apparent. Note the normal azygos vein (arrowheads) and right atrium.
The chest x-ray of a patient with heart failure showing fluid and an enlarged heart shadow.
A raised JVP in a patient with heart failure (used with permission from Wikpedia).
A heart failure patient with peripheral oedema being checked at an annual review.
A . Severe edema in a young primigravida with antepartum eclampsia and
Eclampsia is a potentially serious cardiovascular complication in a pregnant patient. Although the definitive therapy is delivery of the fetus, the BP should be reduced to prevent neurologic, cardiac, and renal damage.
Although other antihypertensive drugs may be effective in reducing the BP, the agent of choice is hydralazine, which has a long record of safety. Animal studies have shown that nitroprusside can cause problems in the fetus; therefore, its use should be reserved for hypertension refractory to hydralazine or methyldopa. The ganglion-blocking drug trimethaphan should be avoided because of the risk of meconium ileus. In pregnancy-induced hypertension, volume depletion may be present and diuretics should be avoided. IV labetalol and hydralazine have been used to treat severe hypertension in pregnancy. ACE inhibitors and angiotensin-receptor blockers should be avoided due to possible fetal/placental toxicity. Magnesium sulfate is also used as adjunctive therapy to control the convulsions.
Hypertensive crisis
Essential hypertension is characterized by periodically recurring trancient elevations of arterial pressure (hypertensive crisis). Development of such crises is preceded by psychic traumas, nervous overstrain, variations in atmospheric pressure, etc.
Hypertensive crisis develops with a sudden elevation of the arterial pressure that can persist from a few hours to several days. The crisis is manifested by sharp headache, feeling of heat, perspiration, palpitation, giddiness, piercing pain in the heart, sometimes by deranged vision, nausea, aid vomiting. In severe crisis, the patient may lose consciousness. The patient is excited, haunted by fears, or is indifferent, somnolent, and inhibited. Auscultation of the heart reveals accentuated second sound over the aorta, and also tachycardia. The pulse is accelerated but can remain unchanged or even decelerated; its tension increases. Arterial pressure increases significantly. ECG shows decreased S-T interval and flattening of the T wave. In the late stages of the disease, with organic changes in the vessels, cerebral circulation may be deranged during crisis; myocardial infarction and acute left-ventricular failure may also develop.
Definitions and probable causes of hypertensive crisis
Hypertensive urgencies can be defined as severe elevations in BP that do not exhibit evidence of target-organ (cardiovascular, renal, CNS) dysfunction or damage. Urgencies can be managed by the administration of oral medications, most often in the emergency department (ED), and follow-up on an outpatient basis. Hypertensive emergencies are severe elevations in systolic and diastolic BP associated with acute target-organ damage that require immediate management in a hospital setting.
Hypertensive crises encompass a spectrum of clinical situations that have in common blood pressure (BP) that is elevated, and progressive or impending target organ damage. Most hypertensive urgencies or emergencies are preventable and are the result of inadequate treatment of mild-to-moderate hypertension or nonadherence to antihypertensive therapy.
Some of examples of hypertensive crises
Traditionally, hypertensive crises have been divided into emergencies and urgencies. Hypertensive emergencies are severe elevations in blood pressure (BP) that are complicated by evidence of progressive target organ dysfunction, and will require immediate BP reduction (not necessarily to normal ranges) to prevent or limit target organ damage. Examples include: hypertensive encephalopathy, intracranial hemorrhage, unstable angina pectoris, or acute myocardial infarction, acute left ventricular failure with pulmonary edema, dissecting aneurysm, or eclampsia. While the level of BP at the time of presentation is usually very high (greater than 180/120 mm Hg), keep in mind that it is not the degree of BP elevation, but rather the clinical status of the patient that defines a hypertensive emergency. For example, a BP of 160/100 mm Hg in a 60-year-old patient who presents with acute pulmonary oedema represents a true hypertensive emergency.
Hypertensive urgencies are severe elevations of BP but without evidence of progressive target organ dysfunction and would be better defined as severe elevations in BP without acute, progressive target organ damage. A traditional term “urgency” has led to aggressive and often excessive treatment of the majority of patients who present to Emergency Departments (ED) with severe hypertension. While these patients may present with levels of BP similar to the hypertensive emergency, and may have evidence of target organ involvement, they do not display evidence of ongoing progressive target organ damage. Most of these patients are, in fact, nonadherent to drug therapy or are inadequately treated hypertensive patients and often present to the ED for other reasons. Patients with severe elevations of BP can be managed in the ED with oral agents and appropriate follow-up within 24 hours to several days depending upon the individual characteristics of the patient. It is the correct differentiation of these two forms of hypertensive crises, however, that presents the greatest challenge to the physician.
Initial Assessment A brief but thorough history should address the duration as well as the severity of hypertension, all current medications including prescription and nonprescription drugs and, of particular importance, the use of recreational drugs. A history of other comorbid conditions and prior cardiovascular or renal disease is essential to the initial evaluation. Direct questioning regarding the level of compliance with current antihypertensive medications may establish inadequacy of treatment or frank noncompliance.
Frequent or continuous monitoring of BP should be established. Look for historical information suggestive of neurologic, cardiovascular, and/or renal symptoms. Check for specific manifestations such as headache, seizures, chest pain, dyspnea, and edema. The level of BP alone does not determine a hypertensive emergency; rather, it is the degree of target organ involvement that will determine the rapidity with which BP should be reduced to a safer level to prevent or limit target organ damage.
Treatment.
· Risk factor modification and lifestyle changes
· If you are overweight or obese, you should lose weight
· Quit smoking
· Be more physically active and less sedentary
· Eat less salt
Here are some of the side effects of commonly used blood pressure lowering medications:
Data from the National Health and Nutrition Examination Survey has demonstrated that if a blood pressure (BP) of 140/90 mm Hg is considered to be normal, only 27% of hypertensive patients are adequately controlled in the United States. For diabetic patients, therefore, it is recommended that BP be reduced below 130/85 mm Hg and for those with renal impairment, evidenced by proteinuria, pressures should be reduced below 125/75 mm Hg. In patients with underlying coronary artery disease, the BP should be reduced below 120/80 mm Hg.
The primary goal of the treatment of hypertension is to prevent cardiovascular disease and death. Coexisting cardiovascular risk factors increase the risks associated with hypertension and warrant more aggressive treatment. The five-year risk of a major cardiovascular event in a 50-year-old man with a blood pressure of 160/110 mm Hg is 2.5 to 5.0 percent; the risk doubles if the man has a high cholesterol level and triples if he is also a smoker.
Trials involving patients with stage 1 or 2 hypertension showed that lowering systolic pressure by 10 to
Determination of the need for drug therapy is based on a combined assessment of the blood-pressure level and the absolute risk of cardiovascular disease. Patients with stage 1 hypertension can be treated with lifestyle modifications alone for up to one year, if they have no other risk factors, or for up to six months, if they have other risk factors. Drug treatment should be provided if blood pressure remains elevated after a trial of lifestyle modifications alone. Lifestyle modifications and antihypertensive therapy are indicated for patients with cardiovascular or other target-organ disease (renal, cardiac, cerebrovascular, or retinal disease) and for those with stage 2 or 3 hypertension. Patients with diabetes are at high risk, and drug therapy is indicated in such patients even if blood pressure is at the high end of the normal range.
Two or more blood-pressure readings separated by two minutes should be averaged. If the pressure is at the high end of the normal range, it should be rechecked yearly. Stage 1 hypertension should be confirmed within two months. Patients with stage 2 hypertension should be evaluated and referred for care within one month; those with stage 3 hypertension should be evaluated immediately or within one week. If systolic and diastolic values are in different categories, the recommendations for the higher reading should be followed.
For patients with multiple risk factors, clinicians should consider drugs as initial therapy along with lifestyle modifications. Clinically important risk factors include smoking, dyslipidemia, diabetes mellitus, an age of more than 60 years, male sex, postmenopausal status in women, and a family history of cardiovascular disease for women under the age of 65 years and men under the age of 55 years.
The Dietary Approaches to Stop Hypertension (DASH) study showed that eight weeks of a diet of fruits, vegetables, low-fat dairy products, whole grains, poultry, fish, and nuts, with limited fats, red meat, and sweets, reduced systolic pressure by
Restriction of sodium intake to
Most clinical trials of lifestyle modifications have been underpowered or of insufficient duration to evaluate the effect of these interventions on major cardiovascular outcomes. However, lifestyle modifications should be encouraged, since they are safe and inexpensive and, when combined with drug therapy, may result in better blood pressure control and an improved quality of life.
Patients should routinely be encouraged to reduce their intake of sodium, lose weight (if appropriate), engage in moderate exercise, and reduce their intake of alcohol (to no more than two to three drinks per day). The degree of blood-pressure lowering expected with each of these approaches is often modest but clinically important — for example, 2 to
Adherence to therapy may be increased by the initiation of a system of follow-up reminders or telephone contacts. The involvement of nurses or nurse practitioners, who may have more time than a physician to discuss potential side effects of medications, has been shown to improve patients’ control of their blood pressure. The use of combination therapy (two medications in one pill) may also improve adherence and, in some cases, may reduce the cost of care.
Complex therapy is required. Reasonable work should be alternated with rest, sufficient sleep, and remedial exercises.
In early stage sedatives should be given to improve sleep and to normalize excitation and inhibition processes. Hypotensive preparations are prescribed to inhibit the increased activity of the vasomotor centers and the synthesis of noradrenaline.
Pharmacological agents. Most antihypertensive drugs reduce blood pressure by 10 to 15 percent. Monotherapy is effective in about 50 percent of unselected patients, and those with stage 2 or 3. hypertension ofteeed more than one drug.
Diuretics, beta-blockers, ACE inhibitors or angiotensin-receptor antagonists and calcium channel blockers are recommended for patients with hypertension.
Diuretics have a limited role in the management of hypertensive emergencies. Diuretics (saluretics) are given to decrease intracellular sodium; aldosterone blocking agents (spironolactone) and other preparations are also given. Diuretics are often the first choice if diet and exercise changes aren’t enough. Also called “water pills,” they help the body shed excess sodium and water to lower blood pressure. That means you’ll urinate more often. Some diuretics may deplete your body’s potassium, causing muscle weakness, leg cramps, and fatigue. Some can increase blood sugar levels in diabetics. Erectile dysfunction is a less common side effect
Beta-blockers work by slowing the heart rate, which means that the heart doesn’t have to work as hard. They are also used to treat other heart conditions, such as an abnormal heart rate called arrhythmia. They may be prescribed along with other medications. Side effects can include insomnia, dizziness, fatigue, cold hands and feet, and erectile dysfunction.
ACE inhibitors reduce your body’s supply of angiotensin II — a substance that makes blood vessels contract and narrow. The result is more relaxed, open (dilated) arteries, as well as lower blood pressure and less effort for your heart. Side effects can include a dry cough, skin rash, or dizziness, and high levels of potassium. Women should not become pregnant while taking an ACE inhibitor.
Combination therapy may improve compliance and achieve the target blood pressure more rapidly.
Clinical experience has shown that antihypertensive drugs given orally as either single or multiple doses can lower the BP immediately in patients with severe hypertension. Obviously, this therapeutic opportunity is most suitable for patients with hypertensive urgencies, not emergencies.
Few data from randomized trials are available to guide the choice of regimen for patients whose blood pressure remains high even though they take several medications; recommendations are based largely on physiological principles and clinical experience. Because volume overload is common among such patients, the most important therapeutic maneuver is generally to add or increase diuretic therapy; more than 60 percent of patients with resistant hypertension may have a response to this approach. Thiazide diuretics are effective in doses of 12.5 to 25.0 mg daily if renal function is normal.
A generally useful strategy is to combine agents from various classes, each of which has one or more of the following effects: a reduction in volume overload (diuretics and aldosterone antagonists), a reduction in sympathetic overactivity (beta-blockers), a decrease in vascular resistance (through the inhibition of the renin–angiotensin system with the use of ACE inhibitors or angiotensin-receptor blockers), the promotion of smooth-muscle relaxation (dihydropyridine calcium-channel blockers and alpha-blockers), and direct vasodilation (hydralazine and minoxidil), although the latter are less well tolerated. An additional medication with a different mechanism of action from others the patient is receiving may further lower the blood pressure or overcome compensatory changes in blood-pressure elevation caused by the first medication without increasing adverse effects.
The most critical decision in the management of hypertensive emergencies is to assess the patient’s clinical state and to ascertain whether the patient’s condition dictates emergency management. The absolute indications for treatment and optimal management depend on the underlying and concomitant conditions. A patient with a true hypertensive crisis should be treated in an ICU.
The choice of oral versus parenteral drug therapy depends on the urgency of the situation, as well as on the patient’s general condition. The level to which the BP should be lowered varies with the type of hypertensive crisis and should be individualized. The choice of parenteral drug is governed by the clinical manifestations and concomitant medical problems associated with hypertensive crisis. There is no predetermined level for the goal of therapy.
Once the hypertensive crisis is resolved and the patient’s clinical condition is stable, the physician should look into factors that might have contributed to the dangerous elevation of BP (nonadherence to prescribed therapy or the presence and/or progression of a secondary form of hypertension such as a renal artery stenosis or renal failure, for example). The physician should discuss long-range and periodic outpatient follow-up plans with the patient, as close follow-up is extremely important.