Antihypertensives Prescribing Notes

Lowering of even mildly or moderately elevated blood pressure significantly reduces cardiovascular morbidity.

Assessment

Blood Pressure :

The British Hypertension Society recommends that all adults should have their blood pressure measured at least every 5 years until the age of 80. Those with high normal values (135-139 over 85-89) or a history of high readings should be remeasured annually. Patients with elevated readings but non life- threatening hypertension, ie untreated blood pressure should be observed for 1 to 12 months, depending upon the initial measurement. All hypertensive patients should be monitored indefinitely, irrespective of treatment, to ensure target blood pressure is maintained.

Evaluation :

Note family and personal history of symptoms suggestive of ischaemic heart disease, cardiac failure or transient cerebral ischaemic episodes. History of kidney disease, bronchospasm, previously elevated blood pressure should also be recorded, together with details of lifestyle education and sociological background. Urinalysis and serum creatinine, urea, glucose, electrolytes ad lipids should be investigated and electrocardiogram may also be useful in assessment of target organ damage. Evaluation should also include an estimate of the 10 year cardiovascular risk assessed using the Joint British Societies' scheme(www.bhsoc.org).

Major Risk Factors:

The presence of one or more of the following should strongly influence the decision to initiate treatment: target organ damage, diabetes, cardiovascular disease or 10 year CV risk >20%.

Other Risk Factors:

Additional pre-existing factors should also be taken into account when considering therapy:

• age - blood pressure rises with age and trials have consistently confirmed the benefits of reduction up to 84 years of age, benefits of treatment are not so clear for the very elderly. More frequent monitoring and gradual reduction of blood pressure is necessary in the elderly.
• gender - the risk of cardiovascular disease is greater in men, and the evidence of benefit from treatment is stronger than for women.
• cardiovascular/renal signs -evidence of left ventricular hypertrophy, ischaemic heart disease, cerebrovascular disease, or signs of renal disease are all indications for drug treatment,
• behavioural risks - smoking, obesity and lack of regular exercise.
• biochemical analysis - elevated fasting glucose, elevated serum cholesterol orcreatinine, require early drug treatment.
• poor diet.

Lifestyle Measures

Advise all patients to stop smoking, reduce weight, dietary saturated fat and salt, increase fish, fruit and vegetable intake, limit alcohol and take regular aerobic exercise. Avoid oestrogen-containing oral contraceptives: a progestogen-only pill or non-hormonal contraceptive may be preferable. Such lifestyle changes should be continued even if blood pressure remains elevated and drug treatment is initiated.

Drug Treatment

The objective is to decrease diastolic blood pressure to below 85 mmHg and/ or to reduce systolic blood pressure to below 140 mmHg (130/80 in patients with diabetes or high cardiovascular risk). Management and intervention strategies should be discussed with the patient and the decision to treat, made on an individual basis. Treatment of malignant phase hypertension should be initiated without delay. Treatment following consistently raised blood pressure recordings, should be commenced at the lowest dose and titrated as necessary. A single once daily dose is preferable. The British Hypertension Society recommendations for treatment are:

Step1:- ACE inhibitor/angiotensin II antagonist or b-blocker for non-black patients and those under the age of 55 years (high renin hypertension). Calcium channel blocker or diuretic for patients over 55 years of age or of African origin (low renin hypertension). Where initial monotherapy fails to control blood pressure adequately,

Step2:- Combination therapy using an ACE inhibitor/ angiotensin II antagonist or b-blocker plus a calcium channel blockeror diuretic. Where further treatment measures are necessary, triple therapy.

Step 3:- ACE inhibitor/angiotensin II antagonist or 1-t-blocker plus a calcium channel blocker plusdiuretic. For patients with resistant hypertension, quadruple therapy and the need for secondary referral reviewed,

Step 4:- ACE inhibitor/angiotensin II antagonist plus b-blocker plus a calcium channel blocker plus diuretic or add on a selective b-blocker or spironolactone. If combination therapy is required, it should be remembered that combinations involving b-blockers and diuretics are more diabetogenic than other combinations and caution is advised in patients at high risk of diabetes. It may also be appropriate to add low dose aspirin or a statin at any stage of the treatment regimen for those with increased cardiovascular risk or hyperlipidaemia respectively.

ACE INHIBITORS Blockade of angiotensin converting enzyme (ACE) prevents the formation of angiotensin II, a powerful vasoconstrictor and indirect tacilitator of the sympathetic nervous system. This results in arteriolar and venous dilatation, reducing total peripheral resistance and arterial blood pressure. ACE inhibitors also suppress aldosterone secretion, increase renal blood flow (and hence natriuresis). and increase circulating levels of the vasodilating cytokine, bradykinin. The antihypertensive effect is dose-related and dose titration may be required. The most common adverse effect is a chronic dry cough which may be improved by dose reduction. ACE inhibitors are generally free of metabolic side effects, and have little effect on heart rate or airway resistance. They are therefore useful in patients with cardiac failure, asthma. COPD, peripheral vascular disease and in diabetes. ACE inhibitors can cause taste disturbance and rash and are confraindicated in pregnancy. First-dose hypotension is a potential problem in patients on diuretics or those who are fluid-depleted.

In patients with renal arterial stenosis, ACE inhibitors may precipitate acute renal failure, and with renal insufficiency they may induce hyperkalaemia. Serum creatinine levels should be measured before and during ACE inhibitor therapy. Co-prescription of potassium supplements or potassium-sparing diuretics should be avoided unless specifically indicated. As with b-blockers, ACE inhibitors are less effective in those of African origin, unless combined with thiazides.

Angiotensin II Antagonists

Candesartan, eprosartan, irbesartan, losartan, olmesartan, telmisartan and valsartan produce a fall in blood pressure by direct antagonism of the vasoconstrictor angiotensin II at its AT,-receptor site. Unlike ACE inhibitors. they do not increase bradykinin levels and do not therefore produce the dry cough or angioedema associated with the ACE inhibitors.

Beta-Blockers

The antihypertensive effect of b-blockers is not fully understood, b1-blockers competitively inhibit receptors in the heart, b2-blockers inhibit receptors in the peripheral vasculature, bronchi, pancreas, kidney and liver. b-blockers decrease cardiac rate, force of contraction and output, and renin secretion. Some are believed to have direct CNS activity, although this is unlikely to account for any antihypertensive effect. Their efficacy as monotherapy is equivalent to thiazides although their antihypertensive effect is greatest in young and white patients. The major advantage of b-blockers is m the treatment of hypertensive patients with concurrent angina or rhythm disturbances. They are also less likely to cause impotence than thiazides.

First generation b-blockers (e.g. oxprenolol, propranolol) are non-cardioselective and generally well tolerated, although they may produce peripheral ischaemia, CNS disturbance or bronchospasm, exacerbate congestive heart failure and reduce exercise tolerance. Metabolically, they adversely affect plasma lipids and reduce hepatic glucose mobility. Second generation b-blockers (e.g. atenolol, bisoprolol, metoprolol) have greater cardioselectivity and a less, but still demonstrable, adverse effect on triglycerides and HDL cholesterol. In addition to cardioselectivity. third generation b-blockers (e.g. celiprolol, nebivolol) have a peripheral vasodilating effect and have not been shown to affect plasma lipid levels adversely.

As with the more selective drugs, those with intrinsic sympathomimetic activity (e.g. acebutolol, oxprenolol, pindolol) are less likely to cause coldness of the extremities and produce less effect on resting heart rate and cardiac output. Low lipid soluble b-blockers (e.g. atenolol) may be less likely to cause CNS side effects. Combined receptor antagonists (e.g. carvedilol, labetalol) have both a and b receptor antagonist activity. In contrast to b-blockers, their a-blocking activity helps offset the rise in the peripheral vascular resistance and the adverse effect on plasma lipid profile produced by b-blockade. Although non-cardioselective b-blockers are contraindicaled for hypertensive patients with obstructive airway diseases or insulin-dependent diabetes, other drugs such as ACE inhibitors or calcium channel blockers may be used.

Ca++ Antagonists

These act by blocking the voltage-dependent calcium channels on the surface of cell membranes. This prevents the inward flow of calcium ions into the cell which in turn reduces the availability of intracellular calcium for muscle contraction. In the vasculature. this leads to a reduction in vascular tone, a decrease in the peripheral vascular resistance and hence a fall in blood pressure. At least 6 different types . of calcium channel have been identified. In the cardiovascular system, the most important are the L type or long-lasting channels which are found in all excitable cells including the vasculature, myocardium and the heart's conducting tissue. L-type channel calcium antagonists can be subdivided into three classes. Class 1. the phenylalkylamines, include verapamil. Class II, the dihydropyridines include amiodipine, felodipine, isradipine. lacidipine, lercanidipine, nicardipine, nifedipine andnisoldipine. Class III, the benzothiazepines, include diltiazem. Class I agents have the most potent negative inotropic effect. Their y; depressant effect on cardiac conduction,'. may precipitate heart failure if there is AV or SA node dysfunction, or it b-blockers are prescribed concurrently.

Class II agents are relatively selective for the vasculature. They do not depressl-conduction or contractility and therefore the risk of precipitating cardiac failure in, patients with conduction disorders is r reduced. In fact. they may be used in combination with b-blockers to reverse some of the negative inotropic effects of b-blockade or, conversely, to oppose the reflex tachycardia induced by the calcium antagonist. Vasodilator side effects such as headache, flushing, palpitations and ankle oedema can be troublesome. These can largely be avoided by dose titration or the use of slow-release or slow onset, long-acting drugs such as amiodipine. lacidipine or lercanidipine.

Class III agents have a negligible or slightly negative inotropic effect and cause virtually no reflex tachycardia.

Ca++ antagonists do not adversely affect plasma lipids, glucose metabolism, cause sodium/water/uric acid retention, or activate the renin-angiotensin system. They are appropriate for use in elderly patients and those of African origin. They are also suitable for patients suffering from co-existing asthma, diabetes, renal impairment, claudication and Raynaud's phenomenon.

N.B. Bioavailability

Sustained-release preparations containing the same quantity of a given calcium antagonist are unlikely to have the same pharmacokinetic profiles. It is therefore essential that such preparations are prescribed by brand name and patients are not transferred from one preparation to another without full clinical assessment and retitration.

Thiazides And Related Diuretics

These include bendroflumethiazide, cyclopenthiazide, hydrochlorthiazide, hydroflumethiazide and polythiazide. The hypotensive effect of this group is mediated by arteriolar vasodilatation. In part. this is a consequence of the natriuretic action of thiazides and subsequent reduction in plasma volume and loss in arteriolar tone. The thiazide antihypertensive dose-response is flat, therefore most of the effect will be attained at a low dose. Although the duration of diuretic action varies, this does not reflect the duration of antihyperfensive activity. Thiazides are generally well tolerated and enhance the efficacy of other antihypertensive agents.

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