HTN or Hypertension Diagnosis Treatment Drug Medicine and Cure

What is Hypertension? Diagnosis Causes Treatment Medicines

HTN or Hypertension is one of the most common diseases in internal medicine. According to the census data of China in 1979, the incidence of hypertension is 3-9%. Compared with the incidence of 10-20% in most European and American countries, the incidence is relatively low. The 1982 national census showed that there are about 50 million people with hypertension in China, with obvious regional differences between high north and low south. Those with unknown etiology are called primary hypertension or secondary hypertension. In 1979, China adopted the blood pressure discrimination standards recommended by the World Health Organization in 1979:

   1.   Normal blood pressure, systolic blood pressure ≤ 18.64Kpa (140mmHg), and diastolic blood pressure ≤ 12.1Kpa (90mmHg).

   2.   Hypertension in adults, systolic blood pressure ≥21.3Kpa (160mmHg), diastolic blood pressure ≥12.65Kpa (95mmHg).

   3.   Critical hypertension refers to blood pressure between the above two, and systolic blood pressure 18.8-21.2Kpa (141-159mmHg). Diastolic blood pressure between 12.12-12.52Kpa (91-94mmHg).


What are the Causes of Hypertension?

The cause of hypertension is unknown, and the factors related to the onset are:

(i) Age Incidence tends to increase with age, and the incidence is higher in people over 40 years of age.

(ii) People who eat too much salt have a high incidence of hypertension. Some people think that salt is less than 2g / day, and almost no hypertension occurs; 3-4g / day, the incidence of hypertension is 3%, and 4-15g / day, the incidence is high. The rate is 15%, and the incidence rate is> 20g / day and 30%.

(iii) The incidence of body weight and obesity is high.

(iv) Genetics Approximately half of patients with hypertension have a family history, which may be related to hereditary renal sodium deficiency.

(v) Environment and Occupation Noisy working environments, excessively intense mental labor are prone to high blood pressure, and the incidence of high pressure is higher in urban areas than in rural areas.


What is Pathogenesis of Hypertension HTN?

The pathogenesis of hypertension is unknown. The main theories are:

1. The theory of sympathetic adrenergic system hyperfunction The research on the relationship between sympathetic adrenergic system and the onset of hypertension has received great attention. The catecholamines in patients with hypertension are significantly higher than those in normal subjects, and the increase in norepinephrine is more pronounced than that in epinephrine. The sympathetic nerve activity of borderline hypertension is significantly enhanced, while the stability of hypertension may be covered by the maintenance mechanism and various feedback mechanisms, concealing its relationship with hypertension. Therefore, the sympathetic nerve activity has a greater effect on the initiation mechanism of hypertension than the maintenance mechanism.

Before the blood pressure has not increased significantly, cardiomyocytes and vascular smooth muscle cells are more prone to hypertrophy, proliferation, and related enzymatic changes, suggesting that it is not entirely the result of increased blood pressure. This may be the cause of increased sympathetic nerve activity.

Long-term excessive tension or trauma causes hyperfunction of the sympathetic adrenergic system, contraction of vasospasm, and increased blood pressure.


2. Second, the theory of nephron glomerular cells secrete renin. Renin can decompose angiotensinogen into angiotensin I, and then convert it into angiotensin II through the action of converting enzymes in the pulmonary circulation.

Angiotensin II acts on the central nervous system, increasing the sympathetic nerve impulse or directly contracting blood vessels. It also stimulates the adrenal gland to secrete aldosterone, causing water and sodium retention.

The renin-angiotensin-aldosterone system can regulate extracellular fluid and vascular resistance.

Angiotensin and aldosterone are important factors determining blood pressure.

During renal ischemia, the perfusion pressure of the glomerular cells is low, and the secretion of renin increases, which increases the blood pressure.


3. Atrial natriuretic peptide theory: Experiments have found that atrial natriuretic peptides are contained in the atria, kidneys, and blood vessels.

 The main physiological effects are diuresis, expelling sodium, dilating blood vessels, lowering blood pressure, and increasing myocardial blood flow. Can inhibit the angiotensin-promoting effect of aldosterone, and counteract the vasoconstrictive effect of catecholamines.

 The plasma atrial natriuretic peptide is significantly reduced in patients with hypertension. The heavier the hypertension is, the lower the atrial natriuretic peptide is, suggesting that the occurrence and maintenance of hypertension may be related to atrial natriuretic peptide deficiency.


4. The ion theory: The relationship between cell membrane ion transport and hypertension has become one of the latest advances in hypertension research in the 1980s, which indicates that the study of the pathogenesis of hypertension has reached the level of cellular molecules.

Hypertensive patients have higher levels of sodium in red blood cells, white blood cells, and lymphocytes. The sodium content of cardiovascular tissue in experimental hypertensive rats was also higher than that in normal control group. This shows that the changes in cell sodium are not only found in blood cells, but also in vascular smooth muscle cells. Changes in blood cell sodium positively correlate with blood pressure.

Those with normal blood pressure who have a family history of hypertension in the early stage of hypertension also have increased intracellular sodium, suggesting that changes in cellular sodium are not a consequence of increased blood pressure and may relate to some genetic factors of primary hypertension. Sodium pump inhibition theory, hypertension has hereditary renal sodium excretion disorder.

When the sodium intake increases, the sodium excretion disorder worsens.

In order to excrete the retained sodium, the body releases sodium transport inhibitors, row of sodium. It also inhibits the sodium pump of arterial smooth muscle cells, which leads to increased blood pressure.

The possible mechanisms of sodium pump inhibition leading to elevated blood pressure are:

1. Partial depolarization of vascular smooth muscle cell membranes and increased sensitivity to pressurized substances.

2. Cell sodium increases, and free calcium in cells increases through Na1 + -Ca2 + exchange.

3. Norepinephrine uptake at the end of sympathetic nerves decreases, and release increases. Patients with hypertension may have different ion transport defects, some of which are shown to be inhibited by sodium pumps, which are related to an increase in plasma endogenous digitalis-like substances. The  are obstacles in sodium pump transport. There  is increase in Na1 + concentration in cells.

Some patients have abnormal calcium metabolism, increased plasma membrane permeability to calcium, or decreased Ca2 + transport capacity, increase in intracellular calcium concentration, increase in vascular smooth muscle tension, and increase in blood pressure.


In recent years, the relationship between insulin resistance and hypertension has attracted attention.


What is Clinical Manifestations of Hypertension?

According to the onset of the onset and the course of the disease, it can be divided into the slow-onset and the rapid-onset, and the slow-onset is more common.


I. What is Slow-onset Hypertension?

(1) Early manifestations are mostly asymptomatic, occasionally increased blood pressure during physical examinations, or feeling dizzy, headache, dazzling, tinnitus, insomnia, fatigue, lack of concentration, etc. may be advanced Caused by mental dysfunction. Early blood pressure increased only temporarily, as the disease progressed, blood pressure continued to rise, and organs were affected.


(2) Brain manifestations: Headache and dizziness are common, which may be caused by high carotid artery dilatation, swelling and increased pulse. Peripheral arterioles have a temporary and intense spasm, leading to a sudden rise in blood pressure that can cause a hypertension crisis. It is usually caused by emotional excitement, excessive fatigue, climate change, or discontinuation of antihypertensive drugs. Sudden increase in blood pressure. > 26.16Kpa (200 / 120mmHg), severe headache, blurred vision, palpitations, shortness of breath, pale complexion, tinnitus, dizziness, hyperhidrosis, and acute heart, brain, and renal insufficiency may occur, and should be treated with antihypertensive pressure.

If the sudden rise in blood pressure causes acute cerebral circulation dysfunction, which causes cerebral vasospasm, cerebral edema, and increased intracranial pressure, it is called hypertensive encephalopathy, which is a subacute attack.

It takes about 24-48 hours from the onset of symptoms to symptoms.

The pathogenesis may, when the mean arterial pressure is > 21.3Kpa (160mmHg), it causes cerebrovascular regulation dysfunction, resulting in cerebrovascular spasm, cerebral edema or spotted bleeding.

Hypertensive encephalopathy can also be seen in a variety of secondary hypertension, more common in acute nephritis. Severe headache, visual impairment, nausea, vomiting, convulsions, coma, transient hemiplegia, aphasia, etc.

Fundus arteriolar spasm, optic nerve papillary edema, bleeding and exudate can be seen.

There is increase in Cerebrospinal fluid pressure.

After 1 to 2 hours of antihypertensive treatment, headache and disturbance of consciousness could be significantly improved.


(3) Cardiac manifestations: Plasma catecholamine concentration in hypertensive patients increases, and norepinephrine can induce myocardial protein synthesis and cause myocardial hypertrophy.

Ventricular septum is more sensitive to norepinephrine than the right ventricle and the posterior wall of the left ventricle, which may be one of the reasons that the ventricular septum thickens earlier than the posterior wall of the left ventricle.

Long-term elevated blood pressure and excessive left ventricular systolic load are also causes of myocardial hypertrophy.

Hypertrophic heart disease is formed by myocardial hypertrophy and cardiac dilatation.

 In the early stage, the cardiac function is compensated and the symptoms are not obvious. In the later stage, the cardiac function is decompensated and heart failure occurs.

Physical examination revealed that the apical pulsation was lifting, and the heart dullness circle expanded to the lower left.

Aortic valve auscultation area with second hyperphonic sound, apical region hairy systolic murmur due to left ventricular enlargement relative mitral regurgitation, or due to accompanying myocardial ischemia, papillary muscle insufficiency, aortic valve auscultation, regional systolic murmurs reflect aortic dilatation and relative aortic stenosis.

A few aortic valve auscultation areas can be heard with water-like diastolic murmurs, which are caused by aortic dilatation and relative insufficiency of the aortic valve.

When heart failure occurs, pathological third heart sounds and / or pathological four heart sounds, second heart sound enhancement in the pulmonary valve area, blisters sound at the bottom of the lung, left ventricular hypertrophy and strain on the electrocardiogram, and various types of arrhythmia may be present.

Sometimes ST segment decline, which is not caused by coronary heart disease, should pay attention to identification. On X-ray examination, left ventricular hypertrophy was dilated and the aortic arch was extended and bent.

 The positive rate of echocardiography was higher than that of electrocardiogram and X-ray examination, and early changes were found such as early left atrial enlargement, thickened ventricular septum.

Also a typical change in hypertensive heart disease is thickening of the left ventricle wall. This may be accompanied by left ventricle and left atrium dilation.

Patients with borderline hypertension may have thickened ventricular septum and enlarged left atrium.


(4) Renal manifestations: Renal arteriosclerosis due to long-term hypertension. When renal function declines, it can cause nocturia, polyuria, protein in urine, cast and red blood cells.

Low urine concentration, phenol red excretion and urea clearance disorder. Nitroemia and uremia appear.


(5) Arterial changes: Sustained blood pressure rises can cause thoracic aorta dilation and prolonged flexion.

When the intima of the aorta ruptures, extravasation of blood can form aortic dissection aneurysms. It is one of the rare and serious complications of hypertension.

Hypertension promotes aortic atherosclerosis, which in turn can form aortic aneurysms. Atherosclerosis of the lower limbs can cause intermittent claudication, and severe diabetic lesions can cause limb anthrax.


(6) Fundus changes: The incidence of fundus changes is parallel to age, course of disease, blood pressure level, heart and kidney changes.

What 4 levels are Fundus changes divided into?
  1. Early retinal arterial spasm, arterial thinning is a grade I fundus change.
  2. Later it may develop into retinal arterial stenosis and sacral arteriovenous cross compression, which is a grade II change.
  3.  Fundus hemorrhage or cotton-like exudation is grade III.
  4.  Optic nerve papillary edema was grade IV.


II. What is Rapid-onset hypertension?

Rapid-onset hypertension, also known as malignant hypertension, accounts for 1% of hypertension.

 This can be suddenly changed from the slow-moving type, or onset is malignant.

 Its pathological characteristics are small arteries In particular, the changes in the small arteries of the kidney are mainly fibrous necrosis and there is significant intimal thickening, which leads to proliferative endometritis.


The pathological basis for this change is elevated blood pressure. Malignant hypertension can occur at any age, but is most common in 30-40 years.


 The blood pressure increased significantly, and the diastolic blood pressure was more than 17.3Kpa (130mmHg). He had weakness, thirst and polyuria.

Vision is rapidly deteriorating, retinal hemorrhage and exudation are present in the fundus, and bilateral optic nerve papillary edema is often present. Rapid development of proteinuria, hematuria and renal insufficiency.

Heart failure, hypertensive encephalopathy, and hypertensive crisis can also occur, and the course of the disease progresses more rapidly than death from uremia.

 The diagnosis of malignant hypertension can be divided into two groups:

Group A should have four conditions:

1.  Diastolic blood pressure continues to be above 17.3Kpa (130mmHg)

2. The fundus changes four levels

3. Rapidly progressing renal dysfunction (progression to renal failure within six months).

4. At the same time as blood pressure and renal function worsen, most of them have brain symptoms and heart failure.

Group B:

  1.     The diastolic pressure was 16Kpa (120-130mmHg)
  2.        Third level of the fundus
  3.        Renal dysfunction.
  4.         The remaining conditions are the same as group A


What are the Stages of Hypertension?

In the first stage, the blood pressure reached the diagnosed hypertension level, and there was no clinical signs of heart, brain and kidney damage.


In the second stage, the blood pressure reaches the confirmed level of hypertension, and one of the following:

   1.   Physical examination, X-ray, electrocardiogram or echocardiogram shows left ventricular enlargement

   2.   Fundus examination, fundus arteries are common or local stenosis

   3.   Proteinuria or plasma creatinine concentration increased slightly.


In the third stage, the blood pressure reaches the confirmed level of hypertension, and one of the following:

  1.   Cerebral hemorrhage or hypertensive encephalopathy

  2.   Heart failure

  3.   Renal failure

  4.   Fundus hemorrhage or exudation, with or without optic nerve papillary edema

  5.   Angina pectoris, myocardial infarction, and cerebral thrombosis


Diagnosis and Differential Diagnosis

   a.   Determine the presence or absence of hypertension. Blood pressure measurement should be performed in a quiet situation. Generally, take a seated position, measure the blood pressure of the right upper limb, and measure the blood pressure of the left upper limb and lower limb at the same time if necessary. The measurement should be repeated several times until the blood pressure measurement is relatively stable. Diastolic blood pressure shall prevail. If the sound persists, the tone value can be used and noted. Sometimes the examiner may have a temporary pressure response due to nervousness or emotional excitement. The blood pressure rise should be measured several times for several days in a row, and the blood pressure can be described as high blood pressure more than twice.


   b.   Identify the cause of high blood pressure. When encountering patients with high blood pressure, they should inquire about the medical history in detail and conduct a comprehensive systemic examination to rule out symptomatic hypertension.


(A) Kidney Disease: Hypertension caused by kidney disease is called renal hypertension. It is the most common type of symptomatic hypertension, including renal parenchymal disease and renal artery stenosis.


   1.   Renal parenchymal lesions: glomerulonephritis, pyelonephritis, polycystic kidney, renal tuberculosis, kidney stones, etc. cause renal damage, cause renal ischemia, and lead to hypertension.

a.   Acute nephritis is more common in adolescents, with a history of streptococcal infection, edema, hematuria, and proteinuria before onset. Fundus examination showed retinal arterial spasm

b.   Chronic nephritis and advanced hypertension combined with impaired renal function are sometimes difficult to distinguish, younger, have a history of acute nephritis or repeated edema, proteinuria appeared before hypertension, marked anemia, decreased plasma protein and azotemia. There is relatively mild increase in blood pressure, etc., mostly chronic nephritis

c.    Chronic pyelonephritis is more common in women and has a history of urinary tract infection. Urinary protein, red blood cells, pus cells, and urine bacterial cultures are positive, supporting chronic pyelonephritis

d.   Polycystic kidney disease often has a family history, kidney area swollen and swollen kidney, ultrasound examination can confirm the diagnosis.


   2.   Renal artery stenosis is unilateral or bilateral. Young people are mostly caused by Takayasu’s arteritis. Older people over 50 years of age are mostly renal atherosclerosis. Renal artery stenosis and hypertension have the following clinical manifestations:

a.   a shorter history

b.   Suddenly developed high blood pressure, or sudden increase in hypertension

c.    No family history of hypertension

d.   Antihypertensive drugs are not effective

e.   Vascular murmur can be heard in the upper abdomen or lumbar spine and rib area

f.      History of lumbar trauma Examination can be done by intravenous pyelography, radionuclide nephrogram, renal vein renin activity measurement, and confirmed by renal arteriography.


(B) Endocrine Diseases

1. 90% of pheochromocytoma occur in the adrenal medulla, and the rest occur in sympathetic ganglia and other parts of the body. Because catecholamines are secreted by tumor cells, they can cause high blood pressure and metabolic disorders, manifested as paroxysmal or persistent hypertension with exacerbations.

There is sudden increase in blood pressure, severe headache, palpitations, shortness of breath, sweating, pale, tachycardia, elevated blood sugar, nausea, fatigue, lasting for several minutes or days, intermittent seizures and normal blood pressure.

Adrenaline, norepinephrine or its metabolite, 3-methyl-4hydroxyamandelic acid (VMA), are measured during the period of increased blood pressure, indicating a significant increase in pheochromocytoma.

 Phtotoxamine hypotensive test can be done during the period of increased blood pressure.

With phentolamine 5mg, diluted with 90ml glucose solution, the systolic blood pressure fell more than 4.66Kpa (35mmHg), the diastolic blood pressure fell more than 3.33Kpa (25mmHg), and those who could maintain for 3 to 5 minutes were positive.

In normal people and patients with hypertension, the blood pressure drop after using phentolamine is generally not more than 4Kpa (30mmHg). Intermittent seizures, normal blood pressure, can be used for histamine challenge test, 0.01-0.02mg intravenous injection of histamine phosphate, if there is no response, increase the dose.

After the injection, blood pressure was measured every minute for 15 minutes. Patients with this disease can increase blood pressure within 2 minutes after injection.

If the systolic blood pressure rises more than 8Kpa (60mmHg) above the original level, the diastolic blood pressure rises more than 5.3Kpa (40mmHg), and it is positive for more than 5 minutes. Food, intravenous injection of glucagon 1mg, and then blood pressure measurement every minute for 15 minutes, the judgment criteria are the same as the tissue test. This method has fewer side effects and fewer false positives.

Intravenous pyelography and retroperitoneal inflation can reveal the tumor site.

B-ultrasound or computed tomography (CT) has value in determining diagnosis and tumor localization.


2. Primary aldosteronism: This disease is more common in adult women, with long-term elevated blood pressure accompanied by refractory hypokalemia.

Due to adrenal hyperplasia or increased tumor secretion of aldosterone, which causes hypertension, the kidneys excrete a large amount of potassium and hypokalemia occurs.

Neuromuscular dysfunction, paroxysmal or persistent muscle weakness or paralysis. Long-term massive potassium loss can lead to tubule vacuole-like degeneration, renal concentrating dysfunction, polyuria, nocturia, polydipsia, and drinking.

Blood potassium ≤ 33.24mmol / 24h (12ug / 24h), 17 steroids are normal, plasma renin activity is reduced, spiron test is positive, adrenal scan or CT examination, can find adrenal gland occupying lesions, giving the diagnosis provided objective evidence.


3. Cortisolism: due to adrenal hyperplasia or tumors, excessive secretion of glucocorticoids, retention of water and sodium caused increased blood pressure, concentric obesity, full moon face, hairy, thin skin, purple stripes, and increased blood sugar.

It has the following special manifestations, and the general diagnosis is not difficult.

To confirm the diagnosis, it is necessary to further prove that cortisol secretes too much or loses its normal circadian rhythm, that is, the secretion in the morning is higher than normal, and the secretion in the evening and midnight is not lower than normal or higher than afternoon secretion levels.

In the 24-hour urine, 17-hydroxysteroids and 17-ketosteroids increased. Dexamethasone inhibition test and adrenocorticotropic hormone test were positive.

X-ray skull examination of some hyperplastic cases showed enlarged pteramide. Peripheral renal angiography can also be used to assist diagnosis.


Pregnancy toxemia occurs within 3 to 4 months in the third trimester or during childbirth and within 48 hours after delivery. It is characterized by hypertension, edema and proteinuria. Severe convulsions and coma. If elevated blood pressure is found early in pregnancy, it may be hypertension or secondary hypertension with pregnancy.

If one has a history of hypertension, light urine protein, can be identified. However, in patients with hypertension, during the pregnancy, there may often be worsening of hypertension and urinary changes.

There are also statistics that show that about 30% of patients with hypertension have pregnancy, and that pregnancy toxemia occurs, which can be considered during diagnosis.


   3.   Vascular lesions: congenital aortic constriction, more common in adolescents, more men than women.

   The clinical manifestations are high blood pressure in the upper extremities, lower blood pressure in the lower extremities, and an abnormal phenomenon of upper and lower blood pressure.

   Due to inadequate blood supply to the lower limbs, there may be weakness and coldness in the lower limbs.

   Vascular murmurs can be heard in the auscultation area and the interscapular region, and chest radiographs can show notches caused by erosion of the intercostal collateral circulation arteries. Aortic angiography can confirm the diagnosis.

   4.   Polyarteritis is a non-specific inflammation of the aorta and its branches, which can cause stenosis of the lumen of diseased blood vessels.

   If the disease spreads to the aorta, high blood pressure in the upper limbs and low in the lower limbs may also occur.

   If the lesion spreads to the renal arteries, it can cause renal vascular hypertension, vascular murmurs can be heard in the corresponding parts of the narrowed blood vessels, and angiography can confirm the diagnosis.


5. Craniocerebral diseases: Intracranial tumors, encephalitis, and craniocerebral trauma, which cause increased intracranial pressure, can cause hypertension. Due to the manifestations of the nervous system, it is generally not difficult to diagnose.


What is Treatment of HTN or Hypertension?

Hypertension is a chronic disease that is prone to recurrence. Long-term reasonable treatment should be adhered to stabilize blood pressure at a near-normal level to prevent further damage to the organs by hypertension.

As to how high blood pressure is needed for treatment? Which  method is better?

 There is no unified opinion on these issues.


Do you need treatment for critical hypertension?

At present, most people believe that critical hypertension can cause target organ damage and should be taken seriously. For patients with critical hypertension, follow-up for six months should be followed to observe changes in blood pressure.

If blood pressure becomes normal, no treatment will be given. If blood pressure changes to a confirmed hypertension level, it should be treated.

For those still fluctuating at critical hypertension levels, non-drugs can be used first. If the treatment is not effective, then medication is used.


I. What is General HTN Treatment?

The onset of hypertension is related to central nervous system dysfunction. Attention should be paid to work and rest to ensure adequate sleep, avoid excessive mental stress, and prevent physical exertion.

Perform appropriate physical exercises, such as walking, gymnastics, tai chi, qigong, etc.

Patients with significantly elevated blood pressure, many symptoms or complications should be appropriately relieved from work and rested according to the condition and nature of work.

Diet should be light, eat less salt and cholesterol-rich foods, eat more potassium and magnesium foods. Eat so as not to overweight. Stop smoking and avoid excessive alcohol consumption.

Sedatives such as diazepam, linomine, mianertong and phenobarbital can be used for those with poor sleepiness and nervousness.


II. What is Antihypertensive drug treatment?

(i.) Angiotensin-converting enzyme inhibitors: Captopril is the most commonly used. The mechanism of action, inhibits the transition of angiotensin I to angiotensin II, inhibits the degradation of bradykinin, inhibits the synthesis of aldosterone, reduces the secretion of catecholamines, dilates blood vessels and lowers blood pressure.

Due to reduced aldosterone secretion, sodium retention is prevented. It can also promote the synthesis of prostacyclin and dilate blood vessels. There is also an antiarrhythmic effect. It can be used in various stages of hypertension, the dosage is 6.25mg-25mg orally, three times a day.

The hypotensive effect of this product can be enhanced by limiting sodium salt intake.

If combined with diuretics, the antihypertensive effect can be significantly enhanced. Side effects: low fever, rash, pruritus, dizziness, and decreased white blood cells.

Those with original renal insufficiency can aggravate renal insufficiency. Enalapril (MK-421) ‘s antihypertensive mechanism reduces the concentration of angiotensin II in plasma, enhances the hypotensive effect of bradykinin, and reduces sympathetic tone.

Very large doses can directly interfere with the transmission of sympathetic nerve media.

Dosage: 5mg, orally, twice daily. Increase the dose once a week until the maximum dose is 40mg / day or effective.

Antihypertensive effect began to occur 1-2 hours after oral administration, and peaked at 4-6 hours.

After the effect is gradually reduced, once a day to maintain the effect. Inosin anti-pressin (Saralasin) is an angiotensin II antagonist and has a competitive antagonistic effect on angiotensin II. It has antihypertensive effect on hypertension caused by increased angiotensin II and can also be used for malignant hypertension.

For low renin type and normal renin type hypertension, instead of lowering blood pressure, it can increase hypertension. This is because this product is an analogue of angiotensin II and has certain intrinsic excitement for angiotensin II receptor effect.


(ii.) Calcium antagonists: a group of drugs with different chemical structures and different mechanisms of action. Because it inhibits the influx of calcium ions through the calcium channels on the cell membrane, it is called a calcium channel antagonist.

Calcium antagonists reduce the concentration of free calcium in vascular smooth muscle cells, dilate blood vessels and lower blood pressure.

It also has the advantages of inhibiting platelet aggregation, enhancing the ability of red blood cells to deform under hypoxia, and has no adverse effects on lipid metabolism. Isoptin, thiazezone and nifedipine.

Nifedipine (Nifedipine) has a strong vasodilator effect and plays an important role in the treatment of hypertension. Nifedipine has the following characteristics for lowering blood pressure:

1. It acts quickly, and the sublingual content is effective for 1-5 minutes, and it takes effect for 10-20 minutes after oral administration.

2. The curative effect is significant. The magnitude of blood pressure reduction is related to the height of the original blood pressure. The higher the blood pressure, the greater the blood pressure reduction, and rarely a severe hypotension reaction.

3. It is convenient to apply, can be taken orally and can be contained, and coma patients can be contained under the tongue.

4. One drug is multi-effect, that is, dilating peripheral blood vessels to lower blood pressure, and also expanding coronary arteries to treat angina pectoris. It can treat heart failure because it increases the blood output of the heart and dilates the renal vessels. Dosage: 10-20mg, 3-4 times a day.

Side effects are small, sometimes with mild dilated headaches, swelling of the head, and flushing. The significant antihypertensive effect is often accompanied by increased heart rate, which may be due to hyperreflexive sympathetic nerve function due to peripheral vasodilatation.

When this product is used in combination with meproprolic acid, it can enhance the effect of lowering blood pressure.

The advantages of verapamil in the treatment of hypertension are high, with few side effects, and the advantages of verapamil in lowering blood pressure.

1. The expansion of peripheral arteries has a strong effect on lowering blood pressure. There is no obvious antihypertensive effect. Hypertensive crisis can be injected intravenously, and the effect is rapid.

2. Dilation of coronary arteries to treat angina pectoris and protect ischemic myocardium, especially suitable for patients with hypertension and coronary heart disease.

3. It can slow the atrioventricular conduction velocity, prolong the effective refractory period, reduce the electrophysiological effect of autonomy, and is suitable for those with hypertension and tachyarrhythmia.

4. Due to the expansion of peripheral arteries, it can be used in patients with hypertension and peripheral arterial obstructive disease. The side effects include: sinus bradycardia, atrioventricular block, and negative muscle strength. And heart failure were banned, the dose was 40-80mg, 3 times a day, if necessary, 0.075mg / kg, intravenous injection.

Thiazemone (Diltiazem) has a certain antihypertensive effect, but it is not as good as nifedipine, and it also inhibits the AV node conduction velocity and prolongs the AV node refractory period. Hypertension and supraventricular tachyarrhythmias are more suitable.

The dose is 30-60mg, orally, three times daily. Nitrendipine reduces blood pressure and reduces blood pressure. It has little effect on normal blood pressure. It will start to lower blood pressure one hour after taking the medicine. The effect can be maintained for 24 hours.

It has no adverse effects on blood glucose and lipids. Dose 10mg, orally 1-2 times a day, Nimododipine easily penetrates the blood-brain barrier, and is a powerful cerebral vasodilator that can lower blood pressure.

It also has the effect of preventing strokes. The dose is 10-30mg, 2-3 times a day. Nicardipine (Nicardipine) has a strong effect on dilating the cerebral blood vessels.

It is suitable for patients with hypertension and cerebrovascular disease. The dose is 10-20 mg orally, 3 times a day.


(iii.) Vasodilators directly relax vascular smooth muscle, dilate blood vessels, and lower blood pressure. Commonly used drugs are:

1. Sodium Nitroprusside can directly dilate small arteries and veins, which can reduce both the preload and postload of the heart.

It reduces both the amount of returning blood and the forward stroke volume. The effect time is short and continuous intravenous drip is required. Mainly used for hypertensive emergencies and hypertension with heart failure.

Usage: Start with 10-20ug / min, and adjust the infusion dose according to blood pressure level, the maximum does not exceed 300ug / min. Side effects: orthostatic hypotension, lethargy, fatigue, nausea, vomiting, sweating, headache, etc.

Continuous intravenous infusion generally does not exceed 48 hours.

Sodium nitroprusside is converted to thiocyanate in the body. Those who continue to use the drug for more than 72 hours should measure the thiocyanate concentration in the blood every other day.

If it exceeds 10%, the concentration is toxic. This should be discontinued.


2. Minoxidil directly acts on arteriolar vascular smooth muscle, has a strong antihypertensive effect and lasts a long time. For severe or refractory hypertension, resistance to other drugs or poor efficacy.

This product does not reduce renal vascular flow, so it is suitable for those with hypertension and renal dysfunction.

Usage: 25mg, orally, 2 to 4 times a day, can gradually increase the dose, the maximum daily dose does not exceed 40mg, common side effects, edema, hairy, hypercardia, nausea, stomach upset and so on.

3. Hydrazine (Hydrolazine) has a chelating effect on certain trace metals such as copper, which are necessary for vasoconstriction in the body, and also has an inhibitory effect on histamine and dihydroxyphenylalanine dehydroxylase, which is related to norepinephrine in the body.

The synthesis of voxels is closely related. In addition, it can also inhibit the activity of two peptides, namely blood pressure propenin and angiotensin, to achieve the purpose of lowering blood pressure through various ways.

This product enhances myocardial contractility, speeds up heart rate, increases cardiac blood flow, increases renal blood flow, and increases myocardial oxygen consumption. Therefore, patients with coronary heart disease should be used with caution.

For patients with hypertension and renal insufficiency, this product can be used in combination with diuretics.

The usual dose is 10-25mg, taken orally, 4 times a day, which can be gradually increased.

The daily dose is preferably not more than 250mg. Currently, diazepam is commonly used.

The usual amount is 25-50 mg, taken orally, 3 times a day. Side effects: tachycardia, headache, nausea, vomiting, fatigue, decreased whole blood cells, polyneuritis, and lupus erythematosus-like symptoms.


(iv.) Antihypertensive drugs acting on the sympathetic nervous system


1. What are Central sympathetic inhibitors?

(i) Clonidine (Clonidine) can inhibit the cerebrum vascular motor center, reduce the activity of sympathetic nerves, reduce peripheral resistance and reduce blood pressure. It can also increase vagus nerve activity, reduce heart rate, lower blood pressure, and can directly expand.

The peripheral blood vessels reduce blood pressure and have a sedative effect.

It is more suitable for patients who are prone to agitation and nervousness, and can also be used for those with high renin type. Start with 75ug orally, 2-3 times a day.

If it doesn’t work, gradually increase the dose to 300ug, 3 times a day. The drug has a rapid effect, and it can lower blood pressure after half an hour after oral administration, and the maximum effect is achieved in 2-3 hours.

Side effects are dry mouth, nausea, fatigue, lethargy, palpitation, headache, dizziness.

Sudden discontinuation of medication can cause rebound blood pressure, headache, palpitations, sweating, and should be gradually reduced before discontinuation of medication.

To reduce water and sodium retention, it should be used with diuretics.


(ii) Methyldopa can competitively block the decarboxylation of dopamine to dopamine in the process of norepinephrine synthesis, prevent the synthesis of norepinephrine and lower blood pressure.

It has little effect on heart rate and cardiac output, and can maintain the same renal blood flow and glomerular filtration rate.

This can also dilate the internal renal artery and reduce the renal vascular resistance.

It is suitable for hypertension with renal insufficiency By. Hepatic insufficiency is disabled.

Usage: 250mg orally, 2-3 times a day, can be gradually increased to 1000mg, 3 times a day. Side effects: lethargy, dry mouth, fatigue, fever, etc.


2. What are Sympathetic ganglion blockers?

These block the transmission of excitatory sympathetic nerves, dilate small arteries, reduce vascular resistance, and also dilate small veins, which can easily cause orthostatic hypotension.

Commonly used are Alfonate 500mg, dissolved in 50% glucose solution 500ml Intravenous infusion for the treatment of hypertensive encephalopathy.


3. What is Post-sympathetic ganglion blocker?

This depletes the storage of norepinephrine in the sympathetic nerve endings and achieves the purpose of lowering blood pressure.


(i) Guanethidine can prevent the norepinephrine from being released from the sympathetic nerves, and deplete the storage of norepinephrine, thereby interfering with the nerve transmission from the nerve endings after the adrenergic ganglia, reducing peripheral resistance and lowering blood pressure.

It slows down the heart rate and reduces the amount of cardiac output.

The dose is 10 mg, taken orally, 2-3 times a day, and can gradually increase to 75 mg / day.

It has a strong antihypertensive effect and many side effects, including orthostatic hypotension, dry mouth, diarrhea, nasal congestion, and impotence.

Currently only used for severe hypertension, other antihypertensive drugs are not effective.


(ii) Reserpine is a lovacea, which can reduce the levels of catecholamines in the brain and internal organs, thereby inhibiting and depleting the nerve-transmitting substances at the end of sympathetic nerves, reducing peripheral resistance and lowering blood pressure.

Decreased serotonin levels in the brain have a central sedative effect. The effect of this product is mild, and the effect is slow.

Usually, it only gradually takes effect within 1-2 hours after the first medication, and the effect lasts for 24-48 hours.

The peak of the drug effect is 1-2 weeks after the medication. Dosage: 0.25mg, orally, three times a day.

Due to the central inhibitory effect, disabled patients with depression can promote gastric secretion and cause gastrointestinal bleeding.

Those with original ulcers should be used with caution. Side effects include nasal congestion, bradycardia, and fatigue.

Long-term use can lead to elevated blood lipids. Due to many side effects, it is no longer the first choice for antihypertensive drugs.


4. Whataare Adrenergic blockers?

(i) β-blocker; This drug competes with catecholamines and β-receptors to reduce sympathetic nerve tension and increase the sensitivity of vascular smooth muscle to vasodilator drugs.

It has negative muscle strength and negative frequency effect, which slows down the heart rate and reduces the cardiac output. Beta blockers in the kidney can inhibit renin secretion. Blocks the central nervous system beta receptors and produces bradycardia and hypotension.


1. Young patients with hypertension

2. High renin type hypertension (malignant hypertension, renal vascular hypertension, high renin type primary high Blood pressure)

3. High cardiac output type hypertension

4. Hypertension with tachycardia

5. Hypertension with labor-type angina pectoris and arrhythmia, commonly used propranolol 10-80mg, orally, each 3 times a day, the dose should be individualized, from small to large, effective.

Propranolol can increase serum triglycerides, very low density lipoprotein, and high density lipoprotein.

Due to its adverse effects on blood lipids, it is no longer the drug of choice for antihypertensive use. It is contraindicated in patients with bronchial asthma.

Labetalol is a recommended antihypertensive drug recommended by WHO. It is an analog of propranolol and has α and β. This has receptor combined block effect.

It can antagonize the vasoconstrictive effect of norepinephrine, antagonize the pressure-increasing effect of alpha receptor excitement, antagonize the vasodilator effect of isoproterenol, and antagonize the heart rate acceleration effect of beta receptor excitement.

 Blocking beta receptors> Blocking alpha receptors. The dosage is 100-200mg, taken orally, 3 times a day, if necessary, 1.5-2mg / kg intravenous drip, combined with diuretics, can enhance the efficacy.

Side effects: bradycardia, orthostatic hypotension, dry mouth, lethargy, nausea, vomiting, diarrhea, etc.

Acebutolol has a good antihypertensive effect on mild and moderate hypertension, has a milder effect on slowing heart rate, and has no adverse effect on blood lipids.

 The dose is 400-800mg / day, and it is taken orally twice. In addition, metoprolol and aminoacid are also effective in reducing blood pressure.


(2) Alpha blockers block the effects of epinephrine, norepinephrine, and sympathetic nerves on blood vessels, reduce peripheral resistance and lower blood pressure.

Prazosin is commonly used to block α1 receptors. Cardiac blood output, heart rate, and plasma renin activity have a small effect. Try to take 0.5-1mg. If there is no response, take 1mg, 3 times a day, and gradually increase to 5mg, 3 times a day.

This product has a strong vascular effect. Orthostatic hypotension and even syncope may occur 30-60 minutes after the first dose, and it should be started from a small dose.

Doxazosin has a stronger antihypertensive effect than prazosin and is convenient to use.

 2.4mg once daily, phentolamine (Phentolamine) blocks α1 and α2 receptors, reduces afterload, increases cardiac output, increases renin release, increases heart rate.

Dose 25-50mg orally daily 3 Or 10 mg diluted in 250 ml of 5% dextrose intravenously, intravenously, benzylamine (Didenzyline) blocks α1 and α2 receptors.

Dose 10-20mg orally, 3 times a day.

 Side effects include dizziness, fatigue, edema


5. Diuretic and Antihypertensive Drugs

1. Thiazines are the most widely used oral diuretic and antihypertensive drugs. Dihydrochlorothiazide 25mg, 2-3 times a day, has a good antihypertensive effect on mild and moderate hypertension.

Because of lowering blood volume, lowering blood pressure, and increasing blood viscosity, there is a risk of inducing cerebral ischemia in patients with cerebrovascular disease.

The elderly should be used with caution if they have a short history of cerebral ischemia.

 This product inhibits the excretion of uric acid by the kidneys, increases the serum uric acid concentration, and can induce gout.

Inhibition of insulin release and impaired glucose utilization in surrounding tissues can lead to elevated blood sugar.

 People with diabetes should use it with caution. It can also increase serum cholesterol and triglycerides, adversely affect coronary heart disease, and can cause low potassium and low magnesium.

Due to the many side effects, it should not be used as the first choice.


2. Chlorthalidone has a long-lasting effect, the dose is 50mg, once a day. This product also increases serum cholesterol and triglycerides, which is not good for coronary heart disease.


3. Fasting urine has a strong effect and a short effect. The dose is 40mg, twice a day. Severe hypertension can be injected intravenously.


4. Ampicillin has a weak antihypertensive effect, excretion of sodium, potassium, and potassium at a dose of 50 mg once daily.


Principles of drug treatment

(1) Individualized: According to the pathophysiological characteristics, course progression and complications of different patients, different doses of different drugs are used.

Except in emergency situations, it is generally not necessary to sharply lower blood pressure, especially in the elderly, and it is advisable to gradually lower blood pressure.

 Those without complications can lower blood pressure to 18.7 / 12Kpa (140 / 90mmHg), and those with insufficient blood supply to the heart, brain, and kidneys.

Excessive hypotension can aggravate ischemia, drug antihypertensive, not the cause of the disease, long-term medication. Or, for life-long treatment, take the smallest effective amount and persist for a long time.


(2) Combined drugs: Combined drugs can produce synergistic effects and offset side effects. Such as vasodilators often secondary to sympathetic nerve excitement, increase heart rate, increase cardiac output, and the use of β-blockers can accelerate heart rate.

Vasodilators can secondary to aldosterone increase, water and sodium retention. With diuretics, it can be eliminated.


(3) Graded treatment: For general hypertension, first use drugs with few side effects. If satisfactory results are not achieved, one or more drugs with different mechanisms of action can be gradually added. Consider tiered treatment.


First-grade diuretics, beta-blockers, calcium antagonists and angiotensin-converting enzyme inhibitors. One drug can be used, and one that is ineffective can be switched to another.


Combined use of second-grade thorium, two drugs, starting from a small amount, until effective, and transferred to third-level if ineffective.


Three levels of tincture are used in combination, and three drugs are used in combination.


For patients with poor treatment of Grades 4 and 3, guanethidine or clonine can be used.


What is Treatment of Hypertensive Encephalopathy?

1. Rest in bed: Raise the head of the bed, inhale oxygen, and calm.


2. Quickly lower blood pressure nifedipine 10-20mg, sublingual administration, intravenous infusion of sodium nitroprusside, intramuscular injection of magnesium sulfate or intravenous injection.


3. Reduce cerebral pressure, mannitol, fast urine injection.


HTN Prognosis

Slow-onset hypertension, which develops slowly, can be asymptomatic for a long time, and has a good prognosis. With proper treatment, the existing cardiovascular damage can be terminated or recovered, and those who are not treated or undertreated are prone to heart and brain renal comorbidities.

The most common cause of death was cerebral blood vessels, followed by heart failure and uremia. Radical hypertension has a poor prognosis, and those who do not treat often die within 1-2 years. Active treatment, if severe renal failure has not formed, there is a possibility of survival.


Prevention of Hypertension

Hyprtension Prevention: Extensive promotion of knowledge about hypertension, attention to work and rest, proper physical exercise, light diet, low salt, etc. to prevent overweight. Organize a general survey of hypertension.

Those with critical hypertension and those with a high prevalence of stressful work, such as drivers and operators, should be listed as the focus of the general survey of hypertension to facilitate early detection and early treatment to prevent target tube damage.


See Also:




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