HYPERTENSION & ITS’S MANAGEMENT IN GENERAL PRACTICE
INTRODUCTION
Hypertension is controllable non-curable cardiovascular disease of human being. The clinical entity of the hypertension is of immense public health importance due to its attribution to considerable morbidity & mortality. It is prevalent in both develop & developing countries. In Bangladesh prevalence of the hypertension was shown to be low in some studies but further studies shown prevalence of hypertension ranged from 12% to 19.6% in different selected population. In some industrialized countries up to 25% of adult is suffering from hypertension. Prevalence in the developing countries seems to be similar to that in European or other technically developed societies ranging from 10% to as much as 20% among adult. High blood pressure is a major risk factor to stroke, coronary heart disease & chronic renal failure. Prevention of essential hypertension is possible by undertaking modification of life style. Though genetic factors plays a great role in causation of hypertension.
ANATOMY OF THE HEART
Heart is a conical hollow muscular pump which circulates blood throughout the whole body. The position of the heart in the mediastinum in such that two thirds of its mass extends to the left of mediastinum with long axix oriented toward the apex of the two ventricles.
The base of the triangle is formed by the plane of the atrioventricul groove. Heart weight approximately 250 to 300 gm in the females & 300 to 350 gm in males. It has four chambers, right & left atrium, right & left ventricles.
Heart has three borders, right borders, left borders & inferor borders. It has four surfaces. Anterior sternocostal surface, inferior diaphragmatic surface, Posterior surface & left surface. Heart is the developed from the vascular tube in pericardial cavity in the transverse septum.
The only significant structure situated anterior to the heart in the upper mediastinum is the thymus gland, posteriorly, the esophagus lies behind the left atrium with the descending aorta nearly in he posterior mediastinium.
GREAT VESSELS OF THE HEART
1. Pulmonary Trunk
2. Aorta with coronary arteries
3. Inferior venacava
4. Superior venacava
5. Pulmonary veins of the left atrium: 04 veins
6. Main branches of aorta: 03 arteries
Brachiocephalic trunk, left common carotid & left subclavian arteries.
BLOOD SUPPLY OF HEART
Heart is supplied by the right and left coronary arteries. Right coronary arises from the anterior sinus of the aorta & passes downwards through atrioventricular groove & pass vertically. Then it turns back at the inferior border of the heart & runs posteriorly on the way it gives nodal conus marginal & posterior interventricular branches.
Main artery anastomosis with the circumflex branch on the left coronary artery, giving another branch as A-V nodal branch. Posterior descending branch pass towards the apex.
Left coronary artery arises from the left posterior aortic sinus and passes downwards and divides into two, anterior descending and circumflex branch, anterior descending branch descends interiorly and anastomosis there with the right descending branch at the apex.
VENOUS DRAINAGE OF THE HEART
1. Venacordisminimae
2. Ant. Cardiac vein
3. Coronary sinus with its five tributaries. They are great middle & small cardiac vein, posterior vein of the left ventricle & oblique vein of the left atrium.
THE CARDIAC CYCLE
The first event in the cardiac cycle is atrial depolarization (a P wave on surface ECG) followed by right atrial and then left atrial contraction. Ventricular activation (the QRS complex of the ECG) follows after a short interval (the PR interval). Left ventricular contraction starts & shortly thereafter right ventricular contraction begins. The increased ventricular pressures exceed the atrial pressure & lose mitral & than the tricuspid valves. Until the aortic & pulmonary valves open the ventricles contract with no change of volume.
When the ventricular pressures rise above the aortic & pulmonary artery pressures, the pulmonary valve & than aortic valve open & ventricular artial pressures, the tricuspid & the mitral valves open.
PHYSIOLOGY OF BLOOD PRESSURE
Blood pressure is the pressure exerted by the blood on the vessel wall at right angles to direction of flow while flowing over it. It is a resultant of cardiac output x total peripheral resistance, i.e. B.P = CO × TPR.
It is obvious from the formula that any condition which alters either cardiac output or total peripheral resistance will alter blood pressure. So the following factors may modify the blood pressure.
a. Cardiac output
b. Pumping action of heart
c. Peripheral resistance
d. Elasticity of atrial wall
e. Blood volume
f. Viscosity of blood
a. CARDIAC OUTPUT:
Alternation in cardiac output will alter the blood pressure. Cardiac output depends upon the venous return, force & frequently of heartbeat. Blood volume affects the blood pressure directly by mainly modifying the cardiac output.
b. PUMPING ACTION OF THE HEART:
Effectual contraction of the heart is the main factor controlling the cardiac output, blood pressure & within the blood vessels.
c. PERIPHERAL RESISTANT:
It is the resistance which blood has to overcome while passing through the periphery. The chief of peripheral resistance is arteriole & a smaller extent the capillaries. Peripheral resistance depends on the followings: i) Viscosity of blood, ii) Elasticity of arterial wall, iii) Lumen of blood vessels.
d. ELASTICITY OF ARTERIAL WALL:
In normal diastolic pressure arterial walls are stressed but due to presence of elastic tissues in their wall < they tend to recoil. Due to elasticity of arterial walls the blood flow is pulsatile in their arteries. On old age the expansion of arterial wall becomes limited due to sclerotic change & the blood pressure rises.
e. BLOOD VOLUME:
Increase in blood volume will raise both the systolic & diastolic pressure due to increased quantity of blood in the arterial system & greater stressing of the arterial walls.
f. VISCOSITY OF THE BLOOD:
Alternation in blood viscosity will alter the peripheral resistance, so alter the blood pressure.
CLASSIFICATION OF BLOOD PRESSURE
Blood pressure is of two types:
1. Systolic blood pressure
2. Diastolic blood pressure
1. Systolic blood pressure: The resultant pressure during the event of cardiac systole is called systolic blood pressure.
2. Diastolic blood pressure: The resultant pressure during the event of cardiac diastole called diastolic blood pressure.
The joint national committee on detection evaluation & treatment of high blood pressure recommends a scheme for the diagnosis of hypertension in patient 18 yrs or older shown below:
| RANGE (mm of Hg) | Category | |
| Diastolic blood pressure: | ||
| 60 to 85 mm of Hg | Normal blood pressure | |
| 85 to 89 mm of Hg | High normal blood pressure | |
| 90 to 104 mm of Hg | Mild Hypertension | |
| 105 to 114 mm of Hg | Moderate Hypertension | |
| 115 and above | Severe Hypertension | |
| Systolic blood pressure: | ||
| (When diastolic B.P. is mm of Hg) | ||
| 140 to 159 mm of Hg | Borderline isolated | |
| Systolic blood pressure | ||
| 160 to above | Isolated systolic hypertension |
REGULATION OF BLOOD PRESSURE
Two major types of arterial pressure control system in the body:
1. Nervous mechanism
2. Hormonal mechanism
NERVOUS MECHANISM:
1. SHORT TERMS REGULATION: Occurs within second to minutes.
Mechanism occurs within seconds:
a. Baroreceptor feed back mechanism.
b. Chemoreceptor feed back mechanism.
c. Central nervous system ischemic mechanism.
Mechanism occurs within minutes:
a. Renin angiotensin vasoconstrictor mechanism.
b. Capillary fluid shift mechanism
c. Stress relaxation changes in vasculature
2. LONG TERMS REGULATION:
d. Renal body fluid mechanism
e. Renin angiotensin mechanism
HORMONAL MECHANISM:
a. Epinephrin-norepinephrin mechanism
b. Vasopressin vaso constrictor mechanism
c. Renin angiotensin vasoconstrictor mechanism
1. THE BARO-RECEPTOR MECHANISM:
By far the best known of the mechanism for arterial pressure control is the baro-receptor reflex. This reflex is initiated by stretch receptors called baroreceptors or pressoreceptors. These receptors are located in the walls of the large systemic arteries. A rise in the arterial pressure stretch the baroreceptors & cause thus to transmit signal into central nervous system & feedback signals are then send back through the autonomic nervous system the circulation to reduce the arterial pressure downward toward normal level. The baro-receptors extremely rapidly change arterial pressure. A decrease in arterial pressure at the baro-receptors elicits an immediate reflex, resulting in strong sympathetic pressure in the head & upper body. Because the baro recepetors system opposes increase or decrease in arterial pressure, it is called a pressure buffer system.
2. CHEMO-RECEPTORS MECHANISM:
It is no a powerful pressure controller in the normal arterial pressure range because it does not respond strongly until arterial pressure falls bellow 80 mm Hg. When arterial pressure falls bellow about 80 mm Hg, the chemo-receptor located in the carotid & aortic bodies become stimulated because of poor delivery of oxygen & poor removal of carbon dioxide from these receptors. Signals from the stimulated chemo-receptors are transmitted to vasomotor center to excite the vasomotor center & then it elevates the arterial pressure towards normal.
3. THE CENTRAL NERVOUS SYSTEM ISCHEMIC RESPONSE:
When the arterial pressure falls extremely low (usually below 40mm Hg) ischemia of the vasomotor center in the medulla oblongata causes powerful signals to spread through out sympathetic nervous system. These constrict the peripheral vessels enhance heart activity & there by elevating arterial pressure back towards normal.
4. THERENIN ANGIOTENSIN VASOCONSTRICTORS MECHANISM:
When the blood flow through the kidneys is decreased, the juxtaglumerular cells secrete rennin into blood. Rennin, itself is an enzyme that splits the end off. One of the plasma proteins called angiotensinogen to release angiotensin (1). The angiotensin (1) is then converted into angiotensin (2). By converting enzyme present in the vessel wall. Angiotensin (2) is a potent vasoconstrictor. So increases the peripheral resistance & thereby rises the arterial blood pressure back toward the normal, other effects of angiotensin are mainly related to the body fluid volumes.
Angiotensin (2) has a direct effects on the kidneys to cause decrease excretion of both salts & water and it also stimulates the secretion of aldesterone by the adrenal cortex, which in turn acts on the kidneys to cause decrease excretion of both salt & water. Both these effects increase the blood volume & regulates the blood pressure:
5. STRESS RELAXATION MECHANISM:
When arterial pressure falls, the pressure usually also falls in most blood storage areas. Conversely a rise in arterial pressure is often associated with a rise in pressure in this same storage area. Therefore a pressure changes cause, vessels gradually to adapt to a new size, thereby accommodating the amount of blood that is available. The phenomenon so called stress relaxation mechanism, which has very limited role in arterial blood pressure control mechanism.
6. CAPILLARY FLUID SHIFT MECHANISM:
Often when the arterial pressure is elevated; the capillary pressure is also elevated. This result in rapid transudation of fluid out the circulation in to the tissue space. The resulting decrease in blood volume initiates a sequence of events that returns the arterial blood pressure back toward normal.
HYPERTENSION
Systemic hypertension is defined as elevated arterial blood pressure at level above generally accepted normal, for example, 140/90 at the age of 20, 160/95 at the age of 50. According to this criteria about 15% of the population can be regarded a hyp0ertnesive. However the morbidity and mortality risk associated with increase blood pressure rise continuously across the range of pressure, although more steeply at higher pressure.
CLASSIFICATION
1. Primary of Essential hypertension: –
It is arterial hypertension of unknown cause & this is diagnosed by exclusion of causes of secondary hypertension. Diagnosis of essential hypertension is made in 95% hypertensive subjects.
2. Secondary hypertension: –
It is the arterial hypertension of known cause. Fewer than 5% of all causes of systolic hypertension are in this category. It is amenable or cured by surgery can easily be specific medical treatment.
Factors influencing the development of essential hypertension: –
1. Genetic & familiar
2. Socio-economic related to social deprivation
3. Dietary factors-Obesity, High salt intake, high alcohol intake, caffeine etc.
4. Hormonal factors: -High rennin, reduced nitric oxide.
5. Neurotransmitter: -acetylcholine, Nor adrenalin etc.
CONCEPT OF ESSENTIAL HYPERTENSION
Concept & causes of essential hypertension had not been clearly established. However since 1890s the term ‘essential hypertension has been widely used as the diagnostic name of hypertension. Essential hypertension is commonly defined, as hypertension in which no recognize cause in found.
Essential hypertension is occasionally called primary hypertension to indicate that hypertension appears first, following the cardiovascular structural changes. The disease is characterized by the elevation of arterial blood pressure accompanying cardiovascular hyper tropic changes. Essential hypertension is a genetically inherited arterial, intrinsic hypertension.
Dictionaries define “essential” as a cause to develop anything by inherent, self existing abnormal, intrinsic factors with no external effective condition, furthermore ‘intrinsic “is defined as a cause belonging to internal, not depending on external circumstances and not being acted upon from the outside. From the historical meaning of “essential” the cause of essential hypertension originates in the intrinsic organ which controls the arterial blood pressure is arterial vessels. From the philosophy, it can be concluded that the cause of essential hypertension is located in the arterial smooth muscle itself.
BORDERLINE HYPERTENSION:
| Range mm Hg | Category |
| Diastolic<85 | Normal Blood Pressure |
| 85-89 | High normal |
| 90-104 | Mild Hypertension |
| 105-114 | Moderate Hypertension |
| 115 & above | Serve Hypertension |
| Systolic “ when diastolic blood pressure is 90mm Hg” | |
| <110-159 | Borderline systolic hypertension |
| 160 & above | Isolated systolic hypertension |
CAUSES OF SECONDARY HYPERTENSION
1. Coarctation of aorta
2. Renal disease-parenchyma renal disease
(1) Acute or chronic glomerulonephritis
(2) Pylonephritis
(3) Renal artery stensosis
(4) Polycystic kidney
3. Endocrine disorder
(a) Pheochromocytoma
(b) Cushings syndrome
(c) Cohn’s syndrome (primary aldosteronism)
(d) Hyper parathyroidism
(e) Acromegaly
(f) Primary hypothyroidism
(g) Congenital adrenal hyp0erplasia
4. Drugs: – Oral contraceptive, Anabolic steroid, cortip steroid.
NSAID<Carbenoxolone, Sympathomymetic agent.
5. Pregnancy:- Pre-eclampsia
PATH-PHYSIOLOGY OF HYPERTENSION
The primary hacmodynamic fault responsible for the persistence of higher blood pressure is and increased vascular tone & resistance. The mechanism likely to involve a constantly changing interaction between two sets of opposing forces, one contracting & other relaxing the resistance vessels. Each of those, in term, involves numerous hormonal & neural impulses that are transmitted into a smaller number of intracellular passages with free intracellular calcium as the final mediator. The specific change, both contraction & relaxation that may be involved in human hypertension remain unknown. However, considerable knowledge is gained concerning the way by which interactions between certain agonist and their member, which in term, may regulate the mobilization of second messenger for smooth muscle contraction.
Along with contraction, bio-chemical effects of various stimulants of vascular cells may be responsible for conversion of quick acting but transient and rather small pressure effects into long lasting and larger rises in blood pressure by the induction of vascular wall hypertrophy. Follow in 1950 propose that rise in pressure induce hypertrophy which in the tern, feedback raise further. Since hypertrophy or resistance vessels seems to come not after but either before or in parallel with the rise in blood pressure, lever proposes that various tropic mechanism of phosphoinostide with in the membrane of vascular smooth muscle cells leading through a series of steps to an increased cell alkalinity, which has been proposed as the signal of hyperplasia and hypertrophy via stimulation of DNA synthesis.
There are various specific tropics that could be responsible for the vascular hypertrophy that sustains the elevated blood pressure in certain known forms of secondary hypertension, growth hormone & catecholamine in pheochromocytoma; Aldesterzin primary aldosteronism. Although these may also be involved in essential hypertension, another potential candidate is insulin. Insulin receptors are found on blood vessels; Insulin causes proliferation of vascular smooth muscle in culture. Patients with primary (essential) hypertension have increased levels of plasma insulin and such increase levels may explain the communality of obesity and hypertension. High insulin could raise the blood in at least two other ways; by stimulation of sympathetic nervous system. And by renal retention of sodium.
Another new arena that is receiving attention in elevating blood pressure, are the forces that modulate the vascular. Vasodilatation induced by some endogenous neurotransmitters such as acetylcholine & 5 hydroxytryp0tamine involves the local release of and endothenlium-derived factor.
Other possible factors in the pathogenesis of essential hypertension include: –
Defect in transfer of sodium into cells. For sometime there has been strong evidence that hypetensive persons have increased sodium within their cells that may directly cause arise in free intracellular calcium levels which in turn are responsible for cell contraction.
There are loose of sensitivity of Baro-receptors in the progressively stiffening walls of the carotid sinus and aortic arch and with increasing levels of resting mean arterial pressure (Aars H 1968). Also sympathetic stimulation of juxtraglumerular mechanism changes the rennin angiotensin setting, (Davis C 1973). As hypetension progresses, increased releases of rennin by juxtaglumerular cells follows the increase in catecholamine (De Quarter V etal 1973) late with deterioration of the renal parenchyma and the juxtaglumerular cells, production of rennin my diminish possibily explaining lower levels found in aging persons. There is gradual build up that beings the subjects closer to the positive feed back state in which renal vascular damage combines with other positive feed back and in which the full blown clinical state of fixed hypertension gradually develops.
THE ROLE OF KIDNEY IN ESSENTIAL HYPERTENSION
Guyton states that kidney is of great importance in great determination of arterial pressure. His thesis states that if the arterial pressure rises, the kidney excretes more salts & water until it again reaches equilibrium at the original arterial pressure. A decrease in renal mass will need a higher arterial pressure to excrete the obligatory salty & water load imposed by the dietary intake.
Powerful evidence for the role of the kidney has been gathered from the elegant experiments on rats, which shown that the high blood pressure of selectively bred, spontaneously hypertensive rat can be lowered by transplanting the normotensive rat and vice versa. In humans there is some evidence that hypertension may regress after transplantation of kidney from a normotensive donor and vice versa (P. sleighy 1989).
CALCIUM MEMBRANE THEORY OF ESSENTIAL HYPERTENSION:
The membrane activity determines the calcium ion concentration in cytosol which depends upon the activity of calcium channel. An increase in the number of inward calcium channels induces an enhancement in calcium on concentration in the cytosol of the arterial smooth muscle. The increased concentration of calcium in the cytosol causes hyper contraction and incomplete relaxation of arterial smooth muscles, which leads to narrowing of arterial lumen. Narrowing of the lumen cause induce elevation of total peripheral resistance and hence hypertension mechanism of hypertension development is designed the calcium membrane theory of essential (K. Aoki, 1985). Lastly, sympathetic nerve hyperactivity with or without more stress my be involved. A decrease in central dopamingergic activity may be responsible. This fits with the blood pressure lowering effect from dopamine receptor agonist, such as fenoldopam (Schlant et-al, 1988).
RISK FACTORS FOR ESSENTIAL HYPERTENSION
Hypertension has its own risk factors though it is one of the major risk factors for most forms of cardiovascular diseases. A W H O Scientific group has recently reviewed the risk factors for essential hypertension. These are:
1. NON MODIFIABLE RISK FACTORS:
a) Age:
Blood pressure rises with age in both sexes. Hypertension is more around the age of 40-50 years. The risk of blood pressure with age is greater in those who have higher initial blood pressure. Some population has now been identified whose mean blood pressure does not rise with age. These communities are for the most part primitive societies with calories and often salt intake at subsistence level.
b) Genetic Factors:
Blood pressure levels are determined in part by genetic factors and that the inheritance in polygenic. Twin and family studies have confirmed the importance of genetic factors. Possibility of developing hypertension is 3% in children of two normotensive parents. Possibility is 45% in children of two hypertensive parents. Blood pressure level among first degree adult relative is noted statistically significant.
3. MODIFIABLE RISK FACTORS:
a) Obesity:
Greater the weight gain the greater the risk of blood pressure. Hypertension and obesity are closely linked. There is a continuous linear relationship between excess body fat, blood pressure and the prevalence of hypertension. The cause and effect of relationship between obesity and hypertension has been confirmed in randomized trails demonstrating falls in blood lipid abnormalities and impaired glucose tolerance, it has particular significant on coronary artery in hypertensive patients.
b) Smoking:
Smoking leads to and acute elevation of blood pressure within 15 minutes unless combined with strong coffee, when it may persist up to 2 hours. Contrary popular belief, regular smokers have slightly lower pressure than nonsmoker; largely they tend to be slimmer. Unfortunately, the small potential benefits of this effect are greatly outweighed by the adverse effect of smoking on coronary artery disease and the other pathologies. Heavy smoking may also be associated with increased incidence of malignant hypertension, secondary to renal stenosis.
c) Alcohol:
High alcohol intake is associated with an increased risk of high systolic blood pressure more than the diastolic. Generally blood pressure returns to normal with abstinence. So it is suggested that alcohol induced elevation may not be fixed and do not necessarily lead to sustained blood pressure elevation. Effects of alcohol consumption on blood pressure are addictive to those of obesity an in women to the pressure effects of oral contraceptive. Individuals who have three or more standard drinks per day. (i.e. Greater than 10-20 gm per day). Have a three fold increased prevalence of mild hypertension.
d) Physical activity:
Several population studies have suggested that individual who undertakes regular physical exercise have lower blood pressure than sedentary individuals.
e) Salt intake:
Approximately 60% of hypertensive is particualarity assumed that it is responsive to the level of sodium intake. The etiologic basis for this special sensitivity to salt varies, with primary aldosteronism, bilateral renal artery stenosis, renal parenchyma diseases.
f) Saturated and polyunsaturated fat diets:
Recent evidence suggests saturated fat raises blood pressure as well as serum cholesterol. Well controlled studies have shown that a vegan diet. Or a diet high in polyunsaturated fatty acid, may lower blood pressure by about 5mm of Hg.
g) Environmental stress and psychological factors:
Despite the extensive literature on psychological factors, it is not still clear whether they play a significant part in long term blood pressure regulation; though there is no doubt that emotional factors can induce pronounced but transient variation in blood pressure. The term hypertension it self implies a disorder initiated by tension or stress. Since stress is now the defined the hypothesis is in testable. However, it is and acceptable fact that psychological factors operate through mental process consciously or unconsciously to produce hypertension. Virtually all studies on blood pressure and catecholamine levels in young people reveled significantly higher noradrenalin level in hypertensive than in normotensive. This support the contention part to play in the pathogenesis of hypertension.
h) Other factors:
Noise, vibration, temperature and humidity require further investigation. Noisy environment, such as airport, communities in heavy industrial area have shown that raised noise level can raise blood pressure.
CLINICAL FEATURES OF HYPERTENSION
Hypertension occasionally causes headache or polyuria, but provided there is no complication, most patient remains asymptomatic accordingly the diagnosis is usually made at routine examination or when complication arises. There may be a family history of hypertension and prior history of renal disease. A careful history should identify those patient with drug or alcohol induced hypertension and those at increased risk from smoking, paroxysmal headache, palpitation and sweating should prompt a careful search for a peochromocytoma. Similarly recurrent back ache or urinary tract infection may be due to chronic pyelonephritis.
PHYSICAL FINDINGS OF HYPERTENSION
Most patients have no abnormal physical signs apart from the hypertension. Own specific signs may include left ventricular hypertrophy, accentuation of the aortic component of the second heart sound and possibly fourth heart sound. The optic funds are often abnormal.
The three main objectives of clinical examination in a hyp0ertensive patient are to identify any underlying causes, to recognize risk factors for the development of complication and to detect any complication already present.
Physical examination must include detection of the delay between radial & femoral pulses characteristic of coarctation of the aorta & examination for enlarged kidney in polycystic disease. The characteristic faces & habits of Cushing syndrome may be recognized & a bruit is sometimes audible over the abdomen in renal artery stensosis.
COMPLICATION OF HYPERTENSION
The adverse effect of hypertension principally involves the central nervous system. The retina, the heart and the kidneys.
TARGET ORGAN EFFECT:
Systemic hypertension is a disease manifested by elevated arterial blood pressure and if not corrected, is associated with impaired function of primary target organs; brain, heart, kidney and blood vessels (Edward D Frolish 1987).
IMPACT OF ARTERIAL HYPERTENSION ON THE HEART:
Hypertension involves the heart because of the demands imposed on the myocardium by the increased arterial pressure and the homodynamic after load of hypertensive disease. The heart initially responds by a period of hyper function until there is a structural adaptation of hypertrophy can no longer keep up with the after load imposed on it by the hypertensive disease, congestive heart failure supervenes. Hypertension imposes two cardiac response other than pressure overload. Left ventricular hypetrophy associated with hypertension confers an independent risk of cardiovascular morbidity and morality. This has been suggested to be related to cardiac dysrhythmias and sudden death. A second factor is the risk imposed by hypertension on the heart through the predisposition of patient with hypertension to accelerated epeirogenesis and thereby development of concomitant coronary heart disease (CHD) (Edward D. frohli8ch 1987).
LEFT VENTRICULAR HYPERTROPHY, ARRHYTHMIAS AND SUDDEN DEATH INSYSTEMIC HYPERTENSION:
Elevated blood pressure (systolic or diastolic) is a significant determinant of left ventricular hypertrophy. Prevalence rates of hypertrophy increase with elevated levels of blood pressure in men and women and in all age groups. The higher the level of blood pressure, the greater the probability of LV hypertrophy and greater the risk mortality. The risk of mortality associated with LV hypertrophy is independent of other risk factors. A logical explanation for the association between uncontrolled hypertension and sudden death is that some of the determinants of hypertension are also predictors of sudden cardiac death; these include sympathoneural stimulation as well as hypertensitivity and hyper tonicity of myocardium. For example increased levels of circulating catecholamine in-patient with hypertension cause a reduction of coronary reserve. This phenomenon in turn increases the potential for myocardial ischemia, making it vulnerable to sudden death, conversely, clinical trails on the efficacy of drug treatment of hypertension have shown that lowering blood pressure lead to a regressing o LV hypertrophy, a ventricular premature beats and a reduction in subsequent morality, including sudden death. Despite the demonstration, efficacy of antihyp0ertensive drug treatment in reducing mortality associated with uncontrolled hypertension there is a question weather some of the antihypertensive drugs in common use may cause sudden death, at least in a selected group of patient with hypertension. For example published results of multiple risk factor intervention trial (MRFIT) have caused concern among clinical about the use of thiazide diuretics in the treatment of hypertensive patient with minor abnormalities of the electrocardiogram.
Based on available clinical, laboratory and epidemiological evidence, it is to state that cigarette smoking and hypertension are the only two factors that consistently discriminate sudden death from other clinical manifestation of coronary heart disease. Hypertension assumes an even greater role in its contribution to sudden death when it is accompanied by LV hypertrophy. When acute myocardial infraction manifests itself in patients with established hypertension, LV hypertrophy is a common clinical finding. The probability of sudden death increase many fold in these patients. There are two explanations for this. One is the high incidence if ventricular arrhythias in hypertensive patients with LV hypertrophy. The other is a decrease coronary reserve. Which is a characteristic feature of pressure induced LV hypertrophy and which leads to myocardial ischemia. (Nemat O. Borhani 1987).
HYPERTENSION AND ISCHEMIC HEART DISEASE:
The potential mechanism for the development myocardial ischemia in hypertensive patients is due to development of LV hypetrophy which causes changes in the coronary circulation characterized by a reduction of coronary vascular reserve and acceleration of the atherosclerotic process (Julio F er al 1987).
In the Framinghan study (Kannel W B 1970) LV hypertrophy and stain was termed definite. LV hypertrophy and patients with theist abnormality held an 8 fold inverts in cardiovascular death and a 6 fold increase in coronary mortality. There have been a number of studies in recent year’s demonstrating the effects of cardiac hypertrophy on myocardial perfusion. The major epicedial coronary arteries are enlarged in a hypertrophied ventricle and this could have some effect on increasing coronary artery resistance. Of greater important would be, the effect on smaller coronary arteries. Although number of abnormalities in the peripheral coronary arterioles is suggested a recent study revealed no significant alterations in wall ratio over a large range of sizes. There does appear to be a decrease in the capillary density in hyperthorphy (murry P A 1981), this would lead to and alteration in diffusion distance of nutrients through the myocardium and hence lead to myocardial ischemia, although again the functional effects of this decrease in capillary density have not been clearly demonstrated. There is also good evidence of abnormalities in maximum coronary dilator capacity in animals with cardiac hypertrophy and of a definite decrease in coronary reserve in patients with systemic hypertension.
Structural changes in coronary arteries during the development of LV hypertrophy secondary to hypertension may predispose myocardial ischemia even in absence of obstructive epicedial coronary artery disease. During the development phase of LV hypertrophy the increase in myocardial mass is not always accompanied by commensurate augment ration in coronary blood supply when the hypertensive insult occur gradually, such as in the spontaneously hypertensive rats, there is decrease in capillary density, and total capillary surface which may be
responsible for a reduction of the coronary blood supply relative to LV mass. When the hypertensive process persists, structural changes in the coronary resistance vessels occur with hypertrophy of the media, which are responsible for an increase coronary vascular resistance and reduce coronary reserve. Finally, intraventricular compressive force may be responsible for impairment in coronary blood supply to the myocardium.
ARTERIAL DISEASE IN HYPERTENSION:
Chief arterial diseases which are known to occur with increased frequency with hypertension are:
1. Atherosclerosis
2. Dissection of the aorta
3. Fibrinoid necrosis of small arteries and arterioles.
4. Arteriolosclerosis
1. ATHEROSCLEROSIS:
Is a disease of large and medium size muscular arteries (e.g. coronary, carotid) and large elastic arteries such as the aorta? The basic lesion is atheroma, consists of a raised focal plaque within the intima, having a core of lipid (mainly cholesterol) and a covering fibrous cap. Of the various risk factors that predisposes to atherosclerclerosis four are considered of prime importance:
i) Hyperlipidemia
ii) Hypertension
iii) Cigarette smoking
iv) Diabetes.
Pick R, et al (1974) shown that hypertension appears to be the most important risk factors. The important of hypertension is localization of the atherosclerosis.
2. DISSECTION OF THE AORTA:
Hypertension is also the commonest risk factor for the dissection of the aorta in which the intima is interrupted so that the blood enters the wall of the aorta and separates its layers. Controversy exists about the pathogeneses of dissection of the aorta. Factored hypothesis is that intimal tears occurs owing to homodynamic factors accentuated by the hypertension and once the tear occurred, the increased blood pressure present in most of these patient enhances dissection in to the wall.
3. FIBRINOID NECROSIS OF SMALL ARTERIES AND ARTERIOLES:
This type of change occurs in malignant hypertension. Rupture of muscle fiber is followed by an enormous exudation of plasma with or without red cells into the arterial wall, with consequent stenosis or obliteration of lumen. Latter there may be an inflammatory reaction involving all the coats, especially the adventitia and fibroblast invade the exudates. The organ so affected are kidney, pancreas, adrenal, gut, brain, heart, liver in that order. Hence progressive renal failure occurs in malignant hypertension.
4. ARTERIOLOSCLEROSIS:
Arteriolosclerosis refers to thickening of walls and narrowing of the lumen of small arteries and arterioles. Two types are differentiated morphologically, hyaline arteriolosclerosis and hyperplasic arteriolosclerosis. Both forms are believed to be anatomic reflections of prolonged hypertension.
IMPACT OF SYSTEMIC HYPERTENSION ON THE BRAIN:
Hypertension induces hyaline arteriosclerosis, increased formation of atheroma, lacunae, multi-infarct dementia, hypertensive encephalopathy, binswangers, disease and intracerebral homorrhage.
Increase formation of atheroma:
Pathological studies indicate that 80-85% of acute stroke are due to cerebral infarction (J.A. Simpson 1987). Plaques of atheroma can produce cerebral infarction either by causing narrowing of complete occlusion of and artery or its branches, or by causing as a source of emboli. The territory of the middle cerebral artery is the most frequently involved. Infarcts may also often seen in the boundary zones (watersheds between defined arterial territories. The deficits resulting from cerebral infraction depends on the region and volume of brain involved.
Hemiperesis and aphaisa:
It suggests the involvement of middle cerebral artery territory of the dominant hemisphere. A sudden disturbance of visual field suggests the involvement of posterior cerebral artery territory.
Stupor or coma:
It is not associated with bland or non-hemorrhagic cerebral infarction but exception occur if oedema follows infarction in the cerebral hemisphere.
Transient ischemic attracts:
They are usually recurrent episodes of temporary and focal cerebral dysfunction of vascular origin. Hypertension is the mainly responsible for their evolution to complete strokes and reduction of art with efficient hypertensive agent can prevent the appearance and limit the extent of many such strokes (MRC trail, 1985).
Intracerebral hemorrhage:
The most common type of intracerebral hemorrhage is that associated with hypertension. Within the cestartsmost often in basal ganglia, or the thalamus. The haematoma may increase in size rapidly to cause serve local destruction. About 80% of hemorrhage occur in the cerebral hemisphere (Ross Russel R W 1963), 10% in the pons and 10% in the remaining brain stem area and cerebellum. In malignant hypertension, there is fibrinoid necrosis of arterioles and vessels, so affected rupture causes bleeding into the brain. Patients with long standing hypertension develop hyaline changes in the muscular and elastic arterial layers which give rise to small aneurysm (charcot Bouchard aneurysm) that are liable to rupture. The penetrating branches of the middle cerebral artery, notably the lanticulostriate arteries, are particularly prone to develop such micro aneurysm and the majority or intracerebral hemorrhage occur in the region of internal capsule (Simpson JA, 1987).
Hypertensive encephalopathy:
In brain disease of the nervous system, this is defined as an acute and largely reversible disorder of cerebral function occurring in association with severe arterial hypertension. The most common cause of hypertensive encephalopathy is malignant hypertension but it may also be seen in some patients with nephritis and ecclamsia.
KIDNEY AS TARGET ORGAN:
Most common and most characteristic effect of hypertension on kidney is nepllrosclerosis, which is realy the pathological hallmark of the disease from the stand point of kidney. Clinically and pathologically nephrosclerosis can be classified as benign and malignant.
Benign nephrosclerosis:
Benign nephrosclerosis is most commonly seen in association with essential hypertension. However vascular change of hephrosclerosis can be associated with hypertension of any cause.
Malignant hypertension:
Malignant hypertension is associated with malignant nehprosclero and characterized by rapid deterioration of renal function. Two different renal lesions are described in malignant hypertension, febrinoid necrosis and proliferate arteritis. Fibrinoid necrosis is the most characteristic lesion and presumably result from leakage of fibrin and other plasma elements on to the aertiolar wall. This lesion is recognized by a fibrin, homogeneous esonophlic material composed of fibrin in the walls of the blood vessel.
The second lesion is proliferate arteritis characterized by marked thickening of the intima due mainly to the presence of smooth muscle cells, basement membrane material and acid mucopolusacande, as a result the vascular lumen progressively narrows.
CLINICAL CONSIDERATION:
Benign nephrosclerosis along rarly produces renal insufficiency. It can be assumed that most patients who have uncontrolled hypertension for more than five years show microscopic evidence of nephrosclerosis. There are usually moderate reductions in renal plasma flow, but GFR is normal or slightly reduced. Occasionally
there is mild proteneuria. Renal failure develops in 1-5% of patients with sever prolonged hypertension (Ramzi S Cotran 1989).
Malignant nephrosclerosis is usually associated with marked preternuria, gross or microscopic haematuria and a rapid rise of BUN and creatinine. The degree of protenuria associated with malignant nephrosclerosis is often impressive and occasionally may reach the nephriatic range.
EYE-AS A TARGET ORGAN:
The effects of blood pressure of the retinal vessels depend upon both its absolute level and duration. Essential hypertension may exist as a chronic or intermittent disease for many years without observable changes in the alterations such as generalized and localized narrowing of the arterioles, hemorrhages, oedema residues and cotton wool patches. A more fulminating course may be followed in malignant hypertension in which papilloedema is found in addition to hemorrhages and exudates.
Changes in chronic hypertension:
In early moderate hypertension changes are rarely detectable, but sclerosis invariably occur in persistent moderate or severe hypertension.
The earliest opthalmoscopic sign sclerosis is a change in the arteriolar light reflex. Normally blood column is visible with opthalmoscope. The normal light reflex of the ophalmoscope forms a bright stripe along the center of the blood column. This is produced by reflexion of light from the interface between the column of blood and the vessel wall. Arteriolosclerosis alters the density of the vessel wall, therefore the reflexion of light, so that the central reflex is less bright and more diffused.
Light reflex becomes even more diffused and the arteriolar color changes to reddish brown color. These are due to increasing sclerosis of the wall of the arteriole with hyalinization of the media.
In long standing hypertension, advanced sclerosis gradually becomes evident with crossing changes. One of the earliest sign of this change is nicking.
A second important sclerotic crossing change is deflection of the veins, is important for the diagnosis of sclerosis. Retinal vascular sclerosis can lead to gradual atrophy of the retina, reduction in number and size of the cells function. Oedema and hemorrhages are not characteristic of this type of retinopathy.
ASSESSMENT OF PATIENTS
The measurement of patients should be considered in three stages: assessment, non-pharmacological treatment and drug treatment. During the assessment period, secondary causes of hypertension should but excludes, the target effect of the blood pressure should be evaluated and any concomitant conditions (e.g. syslipidaemia or diabetes) identified.
HISTORY
The patient with mild hypertensions usually asymptomatic. Features in the history such as attacks of sweating and palpitations in phaeochromocytoma might suggest secondary hypertension. Higher levels of blood pressure may be associated with headaches, epistaxis or nocturia.
Breathlessness may be present owing to left ventricular hypertrophy or cardiac failure, whilst angina or peripheral claudianting may represent atheromatous disease. Malignant hypertension may present with severe headaches, visual disturbances, fits, transient loss of consciousness or symptoms of heart failure.
EXAMINATION
The elevated blood pressure is usually the only abnormal sign. Signs of an underlying cause should be sought, such as renal artery bruit in Reno vascular hypertension or radio-femoral delay in coarctation of the aorta. The cardiac examination may also reveal features of left ventricular hypertrophy and a loud aortic second sound. If cardiac failure develops there may be a sinus tachycardia and a third heart sound.
Fundoscopy is and essential part of the examination of any hypertensive patient. The abnormalities are graded according to the Keith-Wagener classifications:
Ø Grade 1- Tortuosity of the retinal arteries with increased reflectiveness (silver wiring)
Ø Grade 2- grade 1 plus the appearance of arterovenous nipping produced when thickened retinal arteries pass over the retinal veins.
Ø Grade 3- grade 2 plus flame –shaped hemorrhages and soft (cotton wool) exudates actually due to small infarcts.
Ø Grade 4- grade 3- plus papilloedema (blurring of the margins of the optic disc)
Grade 3 and Grade 4 are diagnostic of malignant hypertention.
INVESTIGATION OF HYPERTENSION: ALL PATIENTS
Ø Urine analysis: protein, glucose, haematuria
Ø CBC
Ø Plasma urea / creating
Ø Chest X-ray P/A view (cardiomegaly, heart failure rib notching)
Ø ECG (left ventricular hypertrophy, ischaemia)
Ø RBS
Ø Plasma electrolysis (hypokalaemic alkalosis may Indicate primary or secondary hyperaldosteronism)
Ø Lipid profile.
INVESTIGATION OF HYPERTENSION: HIGH RISK PATIENTS
· Intravenous urogram, ultrasound
————- If renal disease suspected
· Raionuclide renography or renal arterography
————- If there is evidence or renal artery stenosis
· 24-hour urine catecholamines
————- If history suggests phaeochromocytoma
· Plasma rennin activity & aldosterone
————- If Conn’s syndrome suspected
· Urinary cortisol, dexamethasone suppression test
————- If signs of cushing syndrome
· Angiograhpy / MRI
————- If coarctation suspected.
MANAGEMENT
Unless the patient has severe or malignant hypertension, there should be a period of assessment with repeated blood pressure measurement, combined with advice and non-pharmacological measures prior to the initiation of drug therapy.
GENERAL MEASURES IN THE MANAGEMENT OF HYPERTENSION:
Ø Diet: Weight reduction in obese and over –weight patient reduce heavy alcohol consumption. Avoid excess salt consumption.
Ø Exercise
Ø Encourage regular exercise program
Ø Smoking
Ø Stop smoking
Ø Hyperlipisaemia: Test cholesterol (including HDL < LDL) and triglycerides Treat according to guidelines.
Ø Consider renal / endocrine causes investigations and management.
ANTI-HYPERTENSIVE DRUG THERAPHY:
STRATEGY
i. Confirm that hypertension is present on repeat measurement.
ii. Determine whether drug therapy is required directly (e.g. cardiovascular, cerebrovascular or renal complication) or whether general measures are appropriate.
iii. Thiazide diurectic: a first line treatment, especially in the elderly.
iv. Beta – adrenoceptor antagonists can be used in combination with a thiazed especially relevant in the presence of angina.
v. Calciuma antagonists: Where b-adrenoceptor antagonists contraindicated or not tolerated: can be used in combination with thiazed.
vi. Angiotensin – converting enzyme inhibitors may be used where first line treatment fails, or may be used as an alternative to b-adrenocept antagonists or calcium antagonist. Most effective in combination with thiazide diuretic.
vii. Aspirin indicated to reduce cardiac and stroke complications.
viii. Resistant hypertension: Examine drug compliance and consider referral to specialist clinic.
Available Drugs:
Several classes of drugs are available to treat hypertension. The most appropriate line treatment depends on the individual patient.
Diuretics:
Thiazide diurectics such as bendrofluazide (2.5 – 5 mg daily) and cyclopenthiazide (0.5 mg daily) are well established agents which have been shown to reduce stroke in hypertension. The lower doses seem to be as effective as higher dose reduction of blood pressure and most have duration of 12 –24 hours. To concern with these agents is their adverse metabolic effects, and in part increased serum cholesterol, impaired glucose intolerance, heyperuricemia Hypokalaemia.
Loop diuretics such as frusemide (40 mg daily) do have a hypertensive effect, but are not routinely used in the treatment of essential hypertension. Potassium – sparing diureties such as amiloride (5 –10 mg daily) or spionolactone (50 – 200 mg) are not effective agents when used alone, with the exception of spironolactone in hyperaldosteronism.
b-BLOCKERS:
The b-blockers have been shown to improve the prognosis of hypertensive, although their mechanism of action remains unclean. They reduce the force of cardiac contraction, some reduce rennin secretion and some reduce anxiety. There is major difference between the agents.
MAIN PROPERTIES OF THE b-BLOCKERS COMMONLY USED FOR HYPERTENSION:
| Cardiac Selectivity | Intrinsic Sympathomimetic Acitvity | Lipid Solubility | Plasma half Life (hours) | Usual Doses | ||
| Actubutratol | + | + | 0 | 5 | 400mg once or twice per day | |
| Atenonol | + | 0 | 0 | 6 | 50mg once daily | |
| Bisoprolol | ++ | 0 | 0 | 10-12 | 10-12mg once daily | |
| Oxeprenolol | 0 | ++ | + | 1.5 | 20-80mg trice daily | |
| Propranolol | 0 | 0 | ++ | 5 | 80-160mg twice daily | |
| Timolol | 0 | 0 | + | 5 | 5-20mg twice daily |
The major side effects of this class of agents are bradycardia, bronchospasom, cold extremities, fatigue, bad failure dreams and hallucinations. They initially aggravate cardiac failure but this is usually short-term. They also have adverse metabolic effects and in particular an increase in triglycerides and a reduction in HDL cholesterol. These agents are especially useful in-patient with both hypertension and angina.
Angiotension-converting enzyme (ACE) inhibitors:
These drugs block the conversion of angiotensin 1 to angiotensin 11 which is a potent vasoconstrictor. They also block the degradation of bradykinin, a potent vasodilatior. Although there are no long-term trials to demonstrate a reduction in complicantions. There is also some evidence that the African population do not respond as well to ACE inhibitors. They are particularly useful un diabetics with nephropathy where they have been shown to slow disease progression and in diabetics with depressed left ventricular function, where they improve survival.
Angiotensin 11 receptor antagonists: