How we improved our treatment of hypertensionBMJ 2000; 320 doi: https://doi.org/10.1136/bmj.320.7230.309 (Published 29 January 2000) Cite this as: BMJ 2000;320:309
In my early years of general practice I was enthusiastic about controlling blood pressure. One particular patient, a retired civil servant, presented with a sore throat, and an incidental finding showed a blood pressure of 200/130.
I was not sure how much of this was caused by meeting a new doctor so I took his blood pressure several times and it continued to be high. A general physical examination was unremarkable apart from a soft ejection systolic murmur at the left sternal edge. In particular, he had no protein in his urine and his fundi showed only grade 1 retinopathy. Baseline investigation showed his renal function was normal, mid—stream urine specimen was negative, and serum urate was normal. I initially started him on bendrofluazide at a dose of 5 mg a day, which was the accepted starting dose in those days in our practice. His blood pressure came down to only 200/120 after five weeks of treatment and necessitated an addition of atenolol 50 mg a day. His blood pressure came down a little further to 170/100. However, as he had no side effects from his medication, I increased the dosage of bendrofluazide but omitted to check his electrolytes. He developed cold fingers at this stage although his blood pressure was normal. I stopped his atenolol and prescribed nifedipine.
Two months after the increased dose of bendrofluazide he collapsed. His wife described this as him going very grey, nearly blacking out, and then being profusely sick. He did not have any obvious seizure. He was seen by a local GP who found nothing abnormal but advised that someone else should drive him home. He had another similar turn later in the day and was admitted to hospital. He was found to have hypokalaemia—his potassium level was only 2.7. He was treated with intravenous potassium and his diuretic dose was reduced to 2.5 mg of bendrofluazide.
I have seen this patient frequently since then as his blood pressure has proved quite difficult to control and has necessitated use of different ACE inhibitors. A referral to the cardiologist has shown that his heart murmur was not due to any structural abnormality as an echocardiogram was normal.
Over the years I have built up quite a strong relationship with him and I am always interested to hear about his trips to Italy where he visits his daughter and grandchildren.
I have always felt responsible for inducing his hypokalaemia. However, I have subsequently written various protocols for the practice to follow in controlling hypertension, including the suggestion of a starting dose for bendrofluazide of 2.5 mg a day1 and not increasing this dose because of the increased risk of side effects. Ideally, serum electrolytes should be checked both before and after starting treatment and on an annual basis while on treatment. I have also been involved in searching our practice database for patients who are on high doses of thiazide diuretics and have changed them all to the maintenance dose of 2.5 mg bendrofluazide. We are also scrutinised by our local prescribing department of the Prescription Pricing Authority, which as one of its quality markers of prescribing provides the ratio of bendrofluazide 2.5mg to 5 mg a day. We are now one of the better performing practices in the Exeter area at maintaining this ratio.
I hope that through my overzealous use of diuretics we now have a better control of patients with hypertension and certainly have fewer episodes of drug induced hypokalaemia.
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