TREATMENT Medical Assignment Help

In the young, the secondary causes of hypertension should be excluded before treatment is commenced. When the blood pressure is only mildly or moderately elevated, it may be difficult to persuade an asymptomatic patient that treatment is necessary. However, there are definite advantages from treating diastolic blood pressures in excess of 100 mmHg. If the diastolic blood pressure is between 90 and 100 mmHg it should be carefully reassessed on several occasions with the patient in a comfortable, relaxed position. If it is truly elevated (above 90 mmHg) it should be actively treated, especially in young men, and particularly so if there is any vidence of retinal, cardiac or renal end-organ damage. There is no evidence to support treating mild to moderate blood pressure elevation in the very old (>80 years). However, patients between 65 and 80 years with a diastolic pressure above 90 mmHg or a systolic blood pressure above 160 mmHg or both do benefit from treatment. The Framingham studies have shown that the systolic blood pressure in this group is as important as the diastolic blood pressure and is the best guide to the risk of peripheral arterial disease. Thus, a man with a systolic pressure of 170 mmHg has twice the risk of dying compared with a man with a systolic pressure of 120 mmHg. Only in the elderly has it been demonstrated that isolated systolic hypertension is associated with an increased risk of cardiovascular events. Nevertheless it is recommended that patients of all ages with a persistent systolic pressure above 160 mmHg should be treated. The thresholds for drug treatment of hypertension which have been recommended by the British Hypertension Society are illustrated.

General measures

A review of the patient’s life-style and diet may suggest modifications that could lead to some reduction of blood pressure, such as:
WEIGHT REDUCTION. Obese patients should lose weight. This leads to a true fall in blood pressure as well as to a reduction of artefactually increased cuff measurements.
REDUCTION OF HEAVY ALCOHOL CONSUMPTION.
This also leads to a small reduction in blood pressure of around 5-10 mmHg.
SALT RESTRICTION. This is generally of little effect except in some individuals. Usually, the patient is advised not to add salt at the table.
REGULAR EXERCISE, MEDITATION AND BIOFEEDBACK. These are all techniques that have been claimed to lead to blood pressure reduction. An attempt should be made to reduce stress and anxiety.
Young people should jog for 30 min three times per week and elderly patients should walk longer distances than usual.
Patients should also be told to stop smoking to reduce their overall coronary risk. It is doubtful whether cessation of smoking reduces the blood pressure except in malignant hypertension. Hyperlipidaemia should also be corrected to reduce the risk of atheroma.

Drug treatment

A large number of drugs are used to treat hypertension. This reflects the difficulty in finding a single drug that effectively lowers blood pressure without producing side-effects that may be more troublesome or more dangerous than the hypertension itself. Compliance is a problem as the side-effects of drug therapy are frequent and the immediate benefits of treatment are not obvious to the patient.

Available drugs

DIURETICS. Loop diuretics (e.g. frusemide 40 mg daily or bumetanide 1-2 mg daily) and thiazide diuretics (e.g. bendrofluazide 5 mg daily or cyclopenthiazide 0.5 mg daily) are equally effective at lowering the blood pressure. Thiazides are usually preferred because the duration of action is longer, the diuresis is not so severe, and they cost less. Loop diuretics are restricted to those with cardiac or renal impairment for whom an additional diuretic effect is required.
Although diuretics may lower blood pressure transiently by sodium and water excretion, they also act by directly dilating arterioles. Oral potassium supplements are often not required. Occasionally, hypokalaemia occurs and this is most effectively treated with a potassiumsparing diuretic.

Thresholds for treatment of diastolic

Thresholds for treatment of diastolic

Advantages and disadvantages of hypotensive drugs with respect to associated conditions (modified from British Hypertension Society).

Advantages and disadvantages of hypotensive drugs with respect to associated conditions (modified from British Hypertension Society).

Potassium-sparing diuretics (e.g. triamterene 150- 250 mg daily, spironolactone 50-200 mg and amiloride 5-10 mg daily) are not effective hypotensive agents, with the exception of spironolactone in primary or secondary aldosteronism. These diuretics are combined with others to treat hypokalaemia, which very occasionally occurs in hypertensive patients on diuretics. Thiazide diuretics may cause hyperuricaemia and may precipitate gout. They may worsen glucose intolerance. Thiazide diuretics increase the serum renin level. Unlike other hypotensives, their effect is not postural. f3-ADRENERGIC ANTAGONISTS. The mechanism by which f3-blockers reduce hypertension is unclear. Although they reduce the force of cardiac contraction and renin production, they probably act predominantly via the central nervous system. f3-Blockers also reduce anxiety. Propranolol 80 mg twice daily, ateno- 101 50-100 mg daily and oxprenolol 80 mg twice daily have been most widely used for the treatment of blood pressure, but there is a wide range of f3-blockers with  different properties:
CARDIOSELECTIVITY implies a greater effect on 131- receptors (cardiac receptors) than on f32-receptors. Such a selective effect is preferred when bronchospasm, intermittent claudication or diabetes is present. Metoprolol, atenolol and acebutolol are cardioselective 13- blockers.
INTRINSIC SYMPATHOMIMETIC ACTIVITY is necessary if bradycardia complicates therapy with 13- blockade. Pindolol has the largest degree of ISA. POOR LIPID SOLUBILITY (e.g. sotalol) is an advantage  if central nervous system side-effects are prominent. The complications of f3-blockade include aggravation of ventricular failure, bradycardia, cold extremities, aching muscles, fatigue, weakness, bad dreams and hallucinations. Non-selective f3-blockade may lead to elevation of serum potassium and may mask or prolong the effects  of hypoglycaemia. f3-Blockers can, however, usefully be used in patients with both hypertension and angina.
VASODILATORS. Dilatation of the peripheral arterioles leads to a fall in blood pressure. There are many mechanisms by which vasodilatation can be achieved.
CALCIUM ANTAGONISTS such as nifedipine (20 mg twice daily), diltiazem (60 mg three times daily), verapamil (120-240 mg daily in divided doses) and amlodipine (5-10 mg once daily) reduce blood pressure predominantly by arteriolar dilatation but also by reducing the force of cardiac contraction. They have proved to be effective antihypertensive agents with only a few side-effects; those that do occur include bradycardia and conduction defects (verapamil and diltiazem), headaches, constipation, flushing and fluid retention. The routine use of calcium antagonists in the treatment of hypertension has been increasing as they prove to be safe and effective drugs.

Main properties of /3·blockers.

Main properties of /3·blockers.

ai-ADRENERGIC ANTAGONISTS such as prazosin (500 J.tg to a maximum of 20 mg daily) and doxazosin (1-4 mg daily) are postsynaptic a-blockers that produce vasodilatation and are very effective hypotensive  drugs. Their main complication is marked hypotension following the first dose, especially when the patient is salt-depleted because of previous diuretic therapy. Presynaptic (a,-adrenergic) antagonists such as phentolamine are now used only in combination with f3-blockers in the treatment of phaeochromocytoma. Labetolol (300-600 mg daily in divided doses) is a combined 13- and a-blocker but it has little advantage over 13- blockers.
ACE INHIBITORS such as captopril (50-150 mg daily in divided doses), lisinopril (10- 20 mg daily) and enalapril (10-20 mg daily) block the conversion of angiotensin I to angiotensin II, which is a more powerful vasoconstrictor. ACE inhibitors also block the degradation of bradykinin, which is a vasodilator. Their side-effects include first-dose hypotension and cough. A metallic taste, proteinuria, skin rashes and leucopenia occur generally when they are given in very high doses. The use of ACE inhibitors is increasing as they prove to be safe and effective drugs in the treatment of high blood pressure. ACE inhibitors are particularly useful in diabetics with secondary nephropathy where there is some evidence that proteinuria may be attenuated and they are now the drugs of choice. ACE inhibitors should not be used in the  presence of renal artery stenosis since in this situation the renin-angiotensin system is critical to the maintenance of renal blood flow. Blockade of the production of angiotensin II may result in loss of renal blood flow and infarction of the kidney.
NON-DIURETIC THIAZIDES, including indapamide (2.5 mg daily in the morning) and diazoxide (250- 600 mg i.v. in divided doses), produce vasodilatation but are seldom used. They produce fluid retention and may provoke glucose intolerance.
HYDRALAZINE (up to 150 mg daily in divided doses) and minoxidil (10 mg or more daily; maximum 50 mg) directly dilate the peripheral arterioles, leading to a fall in blood pressure. Hydralazine, when given in doses  greater than 200 mg daily, may provoke a lupus erythematosus- like syndrome, and minoxidil produces fluid retention and an increase in facial and body hair (hypertrichosis) that renders it unsuitable for women. Both drugs are complicated by sinus tachycardia, which may cause uncomfortable palpitations. They are therefore often combined with {3-blockade for the resistant case.
SODIUM NITROPRUSSIDE is effective as an arterial and venous dilator when given intravenously. However, it is inconvenient to use because it must be protected from light to prevent degradation. It is occasionally used for the treatment of hypertensive emergencies
such as disse cting aneurysm.
CENTRALLY ACTING DRUGS such as methyldopa (a false adrenergic transmitter) (750 mg daily in divided doses) and clonidine (an (X2-agonist) (0.1-0.3 mg daily in divided doses) reduce the degree of vasomotor tone.  Both drugs are complicated by tiredness, fluid retention and mild postural hypotension. Methyldopa may also cause a dry mouth, impotence, pyrexia and a positive Coombs’ test. Very rarely, a haemolytic anaemia may be produced. It can also rarely cause chronic active hepatitis. Clonidine may cause depression and it is important that it is not stopped suddenly because severe rebound hypertension may occur.
DEBRISOQUINE, BETHANIDINE AND GUANETHIDINE block postsynaptic adrenergic neurones and are powerful hypotensive drugs. Side-effects include marked postural  hypotension, bradycardia, diarrhoea, nasal congestion, salivary gland pain and inability to ejaculate. Centrally acting drugs and ganglion blockers are rarely used nowadays.

Stepped care for the control of hypertension

The majority of patients with mild or moderate hypertension can be treated as outpatients. The usual practice is to attempt to reduce the blood pressure to about 150/95 mmHg. If general adjustment to life-style and diet have not led to an adequate fall in the blood pressure, it is conventional to prescribe either a {3-blocker or a diuretic. Diuretics (e.g. bendrofluazide 5-10 mg daily) are preferred if heart failure or peripheral vascular disease is present, but {3-blockers (e.g. propranolol 80 mg twice daily or atenolol 100 mg daily) are more suitable if the patient complains of angina. Calcium antagonists such as nifedipine 10 mg twice daily have also been used as a firstline therapy.
If single drug treatment is unsuccessful, it is appropriate to prescribe both a {3-blocker or a calcium antagonist in combination with a diuretic. The combination of {3- blockers and diuretics is particularly attractive because some of their side-effects are partially antagonistic. For example, {3-blockers lead to potassium retention, aggravation of heart failure and decreased renin secretion, whilst thiazide diuretics induce the opposite changes. If these combined therapies are insufficient, more powerful vasodil tors such as hydralazine, prazosin or nifedipine are added to the regimen. ACE inhibitors may be used if these prove inadequate and should always be used with associated diabetes. The hypotensive effect of ACE inhibitors is increased by their use with a diuretic. It is essential that the patient understands that high blood pressure does not go away after a single course of treatment. It is necessary to continue treatment for many years or for life. In addition, the patient’s blood pressure must be checked at regular intervals. Since treatment is lifelong the physician must attempt to simplify treatment regimens to improve compliance. Evidence suggests that poor treatment is better than no treatment at all. Hypertension that is unresponsive to treatment is usually due to the patient not taking the drugs prescribed or to the presence of an underlying primary cause such as coarctation or renal artery stenosis. Such underlying causes must be discovered and corrected before therapy will succeed.

The management of severe or malignant hypertension Patients with severe hypertension (diastolic pressure >130 mmHg), hypertensive encephalopathy or severe complications of hypertension such as left ventricular failure or aortic dissection should be admitted to hospital for urgent treatment of their hypertension under close supervision. It is unwise to reduce the blood pressure too rapidly because cerebral, myocardial or renal infarction may result. The majority of hypertensive emergencies can be treated by slowly (over about 24 hours) bringing the diastolic blood pressure back to 100-110 mmHg. This can normally be achieved by using oral nifedipine (10-20 mg) and {3-blockade, e.g. atenolol 50 mg. When a more rapid fall of blood pressure is needed, e.g. when managing an aortic dissection, intravenous nitroprusside (0.3 f.Lgkg’ min-I) is the agent of choice. Alternatively, chewable nifedipine (5-10 mg), oral captopril (12.5 mg), intravenous diazoxide (bolus of 50 mg over 1 min) or a labeta- 101 infusion (initially 1 mg min-I) may be used.
The management of hypertension during pregnancy Mild hypertension in pregnancy is usual, but more severe hypertension (>140/90 mmHg), associated with proteinuria and peripheral oedema, may be a prelude to eclampsia. Pre-eclampsia is treated with bed rest and hypotensive drugs known to be safe in pregnancy.
Methyldopa, propranolol, atenolol, nifedipine and hydralazine are usually used. Full-blown eclampsia is treated as a hypertensive emergency with intravenous hydralazine. If the high pressure cannot be reduced, the pregnancy may need to be terminated, and this universally reduces the high blood pressure unless the patient had prior high blood pressure.

PROGNOSIS

Patients with untreated malignant or accelerated hypertension have a very poor prognosis-more than 90% will die within the first year. Effective reduction in the blood pressure leads to a dramatic improvement of prognosis. In general, the risk from hypertension depends on:
• Level of blood pressure
• Presence of retinal changes
• Presence of cardiac or renal complications
• Sex of the patient (men are more at risk than women)
• Coexistence of coronary disease and risk factors for
coronary disease such as high plasma lipids, diabetes and smoking
• Age of the patient (young patients fare worse than
the old) The cause of death in hypertensive patients is usually myocardial infarction, cardiac failure, renal failure or cerebrovascular accident. Effective treatment of moderate hypertension clearly improves the prognosis for each of these causes of death. The treatment of even mild hypertension reduces the likelihood of stroke or cardiac failure.

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