Hypertension, often known as high blood pressure, is a highly common and serious illness that may lead to or worsen a variety of health problems Hypertension is a chronic medical disorder characterized by excessive blood pressure in the arteries. Systolic and diastolic blood pressure measures are used to determine whether the heart muscle is contracting (systole) or relaxing between beats (diastole). This is equal to the maximum and minimum pressures. The normal systolic and diastolic blood pressures during rest are 100-140 mmHg and 60-90 mmHg,
Types Of Hypertension
It is divided into two types:
Primary hypertension (Essential hypertension)
Secondary hypertension (Non-essential hypertension)
1) Primary hypertension
It occurs when arterial blood pressure rises as a result of increased peripheral resistance. It is further divided into two types namely: benign and malignant hypertension.
Here, there is a moderate increase in blood pressure with a systolic pressure of 200 mm Hg and a diastolic pressure of above 100 mm Hg. However, in resting condition and sleep, the blood pressure returns to normal levels. Later, if there is an increase in blood pressure it will not come back to normal level in resting conditions.
Here, the blood pressure elevated to a great extent of about 250 mm Hg of systolic pressure
and 150 mm Hg of diastolic pressure. It produces severe symptoms like renal disease and retinal disease, and being a fatal disease, it causes death within a few years.
The following are some of the characteristics of primary or essential hypertension:
1) The average arterial pressure is raised by 40-60%..
2) The renal blood flow in the later stages is decreased by about one-half of normal.
3) Blood flow resistance through the kidney is increased 2-4 times..
4) The kidneys will not excrete adequate amounts of salt and water unless the arterial pressure is high.
2) Secondary Hypertension
The different forms of secondary hypertension are:
Cardiovascular hypertension: It is produced due to
a) Atherosclerosis is defined as the hardening and narrowing of blood arteries.
b) Aortic coarctation causes narrowing of the aorta.
Renal hypertension: It is produced due to
a) Stenosis of renal arteries- narrowing of one or both renal arteries, so that the renal function is impaired.
b) Glomerulonephritis- nephritis with inflammation of the capillary loops in the renal glomeruli.
Endocrine hypertension: It occurs due to
a) Pheochromocytoma- tumor in adrenal medulla
b) Hyperaldosteronism- excess secretion of aldosterone from the adrenal cortex Conn’s
c) Cushing’s syndrome- excess secretion of cortisone.
d) Gigantism or Acromegaly- excess secretion of growth hormone.
Acute hypertension: It can be caused by strong stimulation of the sympathetic nervous system.
a) Section of the baroreceptors nerves.
b) Lesions in tractus solitarius.
c) Increased intracranial pressure
|Category pressure||Systolic pressure mm Hg||Diastolic pressure mm Hg|
|Stage 1 hypertension||140-159||90-99|
|Stage 2 hypertension||≥160||≥100|
|Isolated systolic Hypertension||≥140||<90|
Causes Of Hypertension
Although hypertension may occur secondary to other disease processes, more than 90% of patients have essential hypertension, a disorder of unknown origin affecting blood pressure regulating mechanisms. A family history of hypertension increases the likelihood that an individual will develop hypertensive disease. Essential hypertension is four times more common in blacks than in whites, and it is more common in middle-aged males than in middle-aged females. Environmental factors such as a stressful lifestyle, a high sodium intake in the diet, obesity, and smoking all contribute to the development of hypertension.
Pathophysiology Of Hypertension
Hypertension is a chronic increase in blood pressure that, over time, causes end-organ damage and increases morbidity and mortality. Blood pressure is calculated as the sum of cardiac output and systemic vascular resistance. As a result, patients with arterial hypertension may experience an increase in either cardiac output or systemic vascular resistance, or both. In younger patients, cardiac output is frequently elevated, whereas in older patients, increased systemic vascular resistance and vasculature stiffness play a dominant role. Vascular tone may be elevated because of increased adrenoceptor stimulation or increased release of peptides such as angiotensin or endothelins. The final pathway results in vasoconstriction due to an increase in cytosolic calcium in the vascular smooth muscle. Several growth factors, including angiotensin and endothelins, increase vascular smooth muscle mass, a process known as vascular remodeling.
Symptoms Of Hypertension
The common organs damage by long-standing hypertension is the heart, blood vessels, retina, and central nervous system.
- CVS: Increased myocardial work leads to concentric hypertrophy of the left ventricle, angina pectoris, and accelerated coronary artery diseases. There are systolic as well as diastolic dysfunction.
- Kidneys: Progressive arteriosclerosis involves both the efferent and afferent renal arterioles and capillaries of the glomerular tuft. This leads to compromise in renal function, shrinkage of kidneys, and proteinuria.
- CNS: Hypertension can lead to the formation of micro-aneurysms, which can rupture and cause cerebral hemorrhage. Accelerated atherosclerosis may cause cerebral thrombosis, embolism, and infection. Hypertensive encephalopathy can be caused by cerebral arteriolar spasm.
- Fundus: The following changes may occur:
- Grade I: Arteriolar narrowing leading to copper wire and silver wire appearance.
- Grade II: Arteriovenous nipping where arteries cross the vein.
- Grade III: In addition to Grade II changes, superficial flame-shaped and deep dot-like hemorrhage and cotton wool exudates.
- Grade IV: Grade III change with papilledema.
Complications Of Hypertension
Hypertension has two cardiac consequences: left ventricular hypertrophy and coronary artery disease. Pressure overload causes concentric left ventricular hypertrophy. Muscle mass and wall thickness increase, but ventricular volume does not. Diastolic function is hampered by left ventricular hypertrophy, which slows ventricular relaxation and delays filling. Left ventricular hypertrophy is a risk factor in and of itself for cardiovascular disease, particularly sudden death. The consequences of hypertension depend on its severity. There is no threshold for complications to occur because elevated blood pressure is associated with increased morbidity across the entire blood pressure range. Chronic arterial hypertension is associated with and accelerates coronary artery disease, resulting in myocardial ischemia and myocardial infarction.
Myocardial ischemia is caused by two major factors: a pressure-related increase in oxygen demand and a decrease in coronary oxygen supply caused by atheromatous lesions. Hypertension is a significant risk factor for coronary artery disease-related death. Chronic pressure overload leads to heart failure. It could begin with diastolic dysfunction and progress to overt systolic failure with cardiac congestion. Strokes are major hypertension complications caused by thrombosis, thrombo-embolism, or intracranial hemorrhage. Renal disease, which is initially detected by microalbuminaemia, may progress slowly and become apparent later in life.
All anti-hypertensive drugs must act by decreasing the cardiac output, the peripheral vascular resistance, or both. The classes of drugs most commonly used include thiazide diuretics, β-blockers, ACE inhibitors, angiotensin II receptor antagonists, calcium channel blockers, αadrenoceptor blockers, combined α- and β-blockers, direct vasodilators, and some centrally acting drugs such as α2-adrenoceptor agonists and imidazoline I1 receptor agonists. Lifestyle modification is the first step in the treatment of hypertension; it includes moderate sodium restriction, weight reduction in the , decreased alcohol intake, and an increase in exercise. Drug therapy is necessary when the above measures have not been successful or when hypertension is already at a dangerous stage (Stage 3) when first recognized.
Low-dose diuretic therapy is effective in lowering the risk of stroke, coronary heart disease, congestive heart failure, and death. While thiazides are the most commonly used, loop diuretics are also used successfully, and when combined with a potassium-sparing diuretic, the risk of hypokalaemia and hypomagnesemia is reduced. Diuretics, even in low doses, enhance the effects of other antihypertensive medications. When potassium-sparing diuretics are used, the risk of sudden death is reduced. Spironolactone reduces morbidity and mortality in patients with heart failure, which is a common complication of long-term hypertension.
Calcium Channel Blockers
Calcium channel blockers are classified as dihydropyridines (such as nifedipine, nimodipine, and amlodipine) or non-dihydropyridines (such as verapamil and diltiazem). Although both groups reduce peripheral vascular resistance, verapamil and diltiazem have inotropic and chronotropic effects. Short-acting dihydropyridines like nifedipine cause reflex sympathetic activation and tachycardia, whereas long-acting dihydropyridines like amlodipine and slow-release nifedipine cause less sympathetic activation. Calcium channel blockers are often associated with b-blockers, diuretics, and/or ACE inhibitors.
Angiotensin II Receptor Blockers
As angiotensin II stimulates AT1-receptors that cause vasoconstriction, angiotensin AT1- receptor antagonists are effective antihypertensive drugs. Losartan, valsartan, and candesartan are more effective than ACE inhibitors and cause less coughing.
High sympathetic tone, angina, and a history of myocardial infarction are all reasons to use -blockers. Because a low dose reduces the risk of fatigue, the addition of a diuretic or calcium channel blocker is frequently beneficial. However, -blockade therapy has been linked to depression, fatigue, and sexual dysfunction. These side effects must be taken into account when weighing the benefits of treatment. Blockers have been used more frequently in the management of heart failure, a known complication of arterial hypertension, in recent years. They are effective, but their use in the presence of heart failure must be done with extreme caution, beginning with very low doses to avoid an initial worsening of heart failure.
These drugs, which have no metabolic side effects, lower blood cholesterol and peripheral vascular resistance. Prazosin has a shorter duration of action than doxazosin, indoramin, and terazosin. These drugs have a high affinity for 1adrenoceptors. Drowsiness, postural hypotension, and, on rare occasions, tachycardia can be problematic. Fluid retention may necessitate the use of a diuretic. Phenoxybenzamine is a non-competitive a-adrenoceptor agonist used (in association with a β-blocker) in the management of patients with phaeochromocytoma, though recently doxazosin has been used successfully.
ACE (Angiotensin converting enzyme) Inhibitors
ACE inhibitors are becoming more popular as first-line therapy. They have relatively few side-effects and contraindications except bilateral renal artery stenosis. Though ACE inhibitors are effective in unilateral renovascular hypertension, there is risk of ischemic atrophy. As a result, angioplasty or surgical renal artery reconstruction are preferable to long-term medical treatment. Because they slow the progression of renal dysfunction, ACE inhibitors are first-line therapy in diabetic hypertensive patients. ACE inhibitors are also first-line treatments for hypertension with heart failure. As a result, this ACE inhibitor may provide protection through mechanisms other than blood pressure reduction.
Central adrenergic inhibitors
Methyldopa is a false neurotransmitter as well as a 2-adrenoceptor agonist. Clonidine and dexmedetomidine bind to centrally located 2-adrenoceptors and act as agonists. The selectivity for α2- vs α1-adrenoceptors is greatest for dexmedetomidine, followed by clonidine, and least for a- methyldopa. Dexmedetomidine is now used for sedation because it causes sedation, increases circulation stability, and decreases catecholamine release in response to stress in intensive care units. Moxonidine is representative of a new class of antihypertensive agents acting on imidazoline1 receptors (I1). Moxonidine reduces sympathetic activity by acting on centers in the rostral ventral lateral medulla, thereby reducing peripheral vascular resistance.
Hydralazine and minoxidil are directly acting vasodilators. Because of the possibility of serious side effects, their use has declined.
Natriuretic peptides regulate vascular tone by interacting with the renin-angiotensin-aldosterone system. Peptidase inhibitors increase the effectiveness of naturally occurring peptides by inhibiting their degradation, reducing vascular resistance.
|1.||Angiotensin Converting Enzyme (ACE) Inhibitors||Captopril|
|2.||Angiotensin (AT1 Receptor) Antagonists||Losartan|
|3.||Calcium Channel Blockers||Verapamil|
|5.||β- Adrenergic blockers||Propranolol|
|6.||β + α Adrenergic blockers||Labetalol|
|7.||α Adrenergic blockers||Prazosin|
Non Pharmacological Management Of Hypertension
Non-pharmacological measures can lower blood pressure in the early stages of hypertension (high, normal, or mild hypertension), in most of individuals. in some patients, who do not show any reduction even after 4-6 months need drug therapy. it is harmless treatment and helpful either to eliminate the requirement of drug or reduce the dose as well as dose regimen. Non-pharmacological approaches to blood pressure reduction are generally recommended as the first line of treatment for patients with diastolic blood pressures of 90 to 95 mmHg.
Furthermore, these approaches will improve the efficacy of pharmacological therapy in patients with high blood pressure. Non-pharmacological methods of lowering blood pressure allow the patient to actively participate in disease management. Weight loss, salt restriction, and moderation in alcohol consumption may lower blood pressure and improve the effect of drug treatment. Furthermore, regular isotonic exercise reduces blood pressure in hypertensive patients.
Reduction of body weight
Obesity and hypertension are inextricably linked, and the degree of obesity is positively related to the occurrence of hypertension. Higher weight hypertensives may lower their blood pressure by losing weight regardless of a change in salt consumption. The mechanism by which obesity causes hypertension is unclear, but increases the secretion of insulin in obesity could result in insulin mediated enhancement of renal tubular reabsorption of Na+ and an expansion of extracellular volume. Obesity is also associated with increased activity of the sympathetic nervous system. A combination of aerobic physical exercise and dietary counseling may enhance compliance.
Severe restriction of salt will lower the blood pressure in most hospitalized hypertensive patients; this treatment method was advocated prior to the development of effective antihypertensive drugs. Several studies have shown that moderate restriction of salt intake to approximately 5 g per day (2 g Na+) will, on average, lower blood pressure by 12 mm Hg systolic and 6 mm Hg diastolic. An additional benefit of salt restriction is improved responsiveness to some antihypertensive drugs.
Alcohol consumption can raise blood pressure, but it is unclear how much alcohol is required to see this effect. Heavy alcohol consumption raises the risk of cerebrovascular accidents but not coronary heart disease. In the fact, small amount of ethanol have been found to protect against the development of coronary artery disease. The mechanism by which alcohol raises blood pressure is unknown, but it may involve increased transport of Ca2+ into vascular smooth muscle cells. Excessive intake of alcohol also may result in poor compliance with antihypertensive regimens. All hypertensive patients should be advised to limit their ethanol consumption to less than 30 mL per day.
Increased physical activity reduces the prevalence of cardiovascular disease in men. It is unknown whether this beneficial effect is a result of an antihypertensive response to exercise. A lack of physical activity is linked to an increased risk of hypertension. Regular isotonic exercise reduces blood volume and plasma catecholamines while increasing plasma atrial natriuretic factor concentration. Exercise can be beneficial even when there is no change in body weight or salt intake during the training period.
Relaxation and biomedical therapy
It is possible that relaxation therapy will lower blood pressure in some hypertensive patients because long-term stressful stimuli can cause sustained hypertension in animals. Only those few patients with mild hypertension who wish to use this method should be encouraged to try, and these patients should be closely followed and receive pharmacological treatment if necessary.
Due to the high potassium content and high fiber content of a vegetable diet, a lacto vegetarian diet and a high intake of polyunsaturated fish oils lower blood pressure. Natural vegetables with high potassium content reduce blood pressure by:
- Increased sodium excretion.
- Decreased sympathetic activity.
- Decreased renin angiotensin secretion and direct dilation of renal arteries.