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At the heart of general practice since 1960

Simple questions could spot hep C


GPs put their burning questions on a particular topic to an expert. This week, Professor Gareth Beevers answers questions from Dr Melanie Wynne-Jones

1. When should we suspect secondary rather than primary hypertension: how should we investigate suspect patients?

Each GP has around half a dozen patients with secondary hypertension. In most, it is due to primary renal disease but there is increasing awareness that primary hyperaldo-steronism (Conn's syndrome) is commoner than originally thought and it is probable that each GP has about two cases.

It is assumed all hypertensive patients will undergo a simple dipstick urine test and routine check for serum creatinine, urea and electrolytes (as well as serum total cholesterol and HDL levels). If dipstick urine testing is normal then primary renal disease is unlikely.

Patients who have proteinuria or haematuria or a raised serum creatinine do need further investigation, including renal ultrasound scans and where relevant 24-hour urine total protein estimation.

The value of renal ultrasound scans in the absence of proteinuria or haematuria and with a normal serum creatinine level is debatable. It is usual to perform this investigation in patients under the age of 30 as a routine. Patients with hypertension resistant to triple therapy should also undergo renal imaging and possibly renal MR angiography.

Detailed investigation is also necessary in patients with severe hypertension (diastolic BP>120mmHg).

If first-line tests suggest the presence of an underlying cause for high blood pressure further investigation is necessary. In particular, patients with hypokalaemia need

detailed investigation, as do patients with intermittent symptoms including tachycardia and variable hypertension, which can occasionally be due to phaeochromocytoma.

2. How much effect (in terms of mmHg) do each of the following lifestyle changes have: lowering salt intake, lowering alcohol intake, stopping smoking, taking more exercise?

This is summarised in the box above.

3. When should we measure renin and aldosterone levels in hypertensive patients and what should we do if they are raised?

An estimation of random levels of plasma renin activity and plasma aldosterone concentration should be performed in patients who have unexplained hypo-kalaemia where Conn's syndrome is a possibility. Patients whose serum potassium is persistently in the lower half of the normal range should also undergo investigation.

In Conn's syndrome plasma renin activity is low while plasma aldosterone concentration is raised. Unfortunately, many anti-

hypertensive drugs affect renin and aldosterone levels.

All forms of diuretic therapy need to be stopped for four weeks and ß-blockers and angiotensin blocking drugs should be stopped for one or two weeks. Raised plasma renin levels are usually seen in patients on diuretic therapy or those with underlying renal disease (see question 1).

4. If the patient's treated blood pressure meets the QOF standard of less than 150/90mmHg, should we treat more vigorously to reach the BHS target of less then 140/90?

On the basis of the Hypertension Optimal Treatment (HOT) study we should try to reduce the blood pressure to below 140/85. But this is often difficult to achieve and necessitates the use of several antihypertensive drugs, which may adversely affect quality of life.

The audit standard of 150/90mmHg is mandatory and we should strive to reduce blood pressure even further in patients with significant other medical problems including ECG left ventricular hypertrophy and diabetes. There may be times when the patient is taking so many pills for hypertension and other medical problems that clinicians might argue that having reached the audit standard further drugs cannot be justified in view of the relatively small benefits from further reduction.

Such decisions must be made on the basis of the patient's quality of life and their feelings about the number of tablets they take and their motivation to take even more.

5. If we use patients' home readings to decide whether treatment is effective, what are the pitfalls and should we recommend any particular machine?

Patients should be encouraged to measure their blood pressure at home, although they should only use measuring systems that rely on the upper arm cuff. Wrist and finger machines should be discouraged. There are reports of patients deceiving their doctors by only recording their good BP readings and ignoring the bad ones.

It is best to monitor ambulatory blood pressure over 24 hours. If this shows the daytime average blood pressure is similar to average home readings then these can be used. A lot depends on the patient.

This brings us to ‘white coat' hypertension. There remains uncertainty over the prognostic significance of blood pressure which is only raised in the clinical setting. Evidence suggests such patients have a clinical outlook somewhere between persistent normotensives and persistent hypertensives. They need to be followed up carefully once or twice per year as many will eventually require antihypertensive treatment.

Some GPs adjust the patient home figure by 10/5 but there are too many exceptions for this rule to be applied across the board. Clinical decisions must be made on the basis of clinic BP readings, as long as they are taken carefully in a quiet environment with at least three measures.

6. We usually record a baseline ECG when hypertension is diagnosed. Should ECGs be repeated in the well-controlled asymptomatic hypertensive and, if so, how often?

All hypertensive patients should undergo an ECG when first diagnosed. If this shows no evidence of left ventricular hypertrophy (S-wave in V1 plus the R-wave in V5 or V6 less then 35mm) then it is not necessary to

repeat this.

If the ECG does meet the criteria for LVH then it is best to repeat this after about one year to see whether there has been regression. Otherwise follow-up ECGs are not useful unless there is chest pain. The ECG is a very insensitive test for LVH, particularly in obese patients. If a severe hypertensive has no ECG evidence of LVH, echocardiography may be useful.

7. Side-effects, particularly postural hypotension and falls, are more prevalent in elderly patients. How can these be minimised and should we always treat to a target of 150/90mmHg in order to minimise the risk of heart attack or stroke?

Postural hypotension can be minimised by the use of long-acting antihypertensive drugs including the thiazide diuretics and the long-acting calcium channel blockers. In such patients, a-blockers like doxazosin should not be used (they also cause stress incontinence in 50 per cent of women).

Up to the age of 80 there is good evidence that we should lower the seated blood pressure to below 140/80mmHg. Quite often symptoms, including postural hypotension, render this difficult to achieve. It is up to the clinician to make judgments on the basis of individual patients.

In the elderly it is sometimes sensible to escalate antihypertensive drug doses at a very slow rate so the cardiovascular system can get used to lower levels of pressure. Patients may be discouraged if they are put on high doses early on in their treatment and then develop symptoms and side-effects.

8. Medication, as well as hypertension itself, can affect renal function. We often end up trying to reconcile BP control, a raised creatinine and the patient's willingness/ability to tolerate various drugs. Any tips?

Angiotensin-blocking drugs (ACE inhibitors and ARBs) can cause a 20 per cent rise in serum creatinine which is of no significance.

These drugs reduce intragromerular pressure and can, on a short-term basis, reduce filtration. This effect is reversible.

On a long-term basis these drugs protect renal function by preventing gromerular damage. If in response to angiotensin blocking drugs the serum creatinine rises by more than 20 per cent then there are several possibilities.

There may be underlying renal artery stenosis or the patients may be receiving too much diuretic, in particular frusemide (this should not be used in hypertension unless there is concomitant heart failure).

If the serum creatinine is below 200µmol/L and stable then nephrological referral may not be necessary except in young patients.

If serum creatinine is greater than 200µmol/L then patients need renal imaging and detailed investigation. In some cases renal biopsy may be necessary.

Patients under the age of about 30 who have any renal abnormality should be referred for detailed investigation. Nephrologists usually use angiotensin-blocking drugs, initially in low doses with monitoring of serum creatinine.

Angiotensin blocking drugs are not nephrotoxic.

Gareth Beevers is honorary consultant physician, City Hospital, Birmingham – he is editor of the Journal of Human Hypertension and a past-president of the British Hypertension Society

Melanie Wynne-Jones is a GP in Marple, Cheshire, and a GP trainer

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