Chapter 86: Hypertension

Hypertension is a serious community disorder and the most common condition requiring long-term drug therapy in Australia. It is a silent killer because most people with hypertension are asymptomatic and unaware of their problem. Epidemiological studies have demonstrated the association between hypertension and stroke, coronary heart disease, kidney disease, heart failure and atrial fibrillation. Treatment may be lifelong, hence the need for careful work-up.

• Target organs that can be damaged by hypertension include the heart (failure, LVH, ischaemic disease), kidney (kidney insufficiency), retina (retinopathy), blood vessels (peripheral vascular disease, aortic dissection) and brain (cerebrovascular disease).

• Deaths in hypertensive patients have been shown to be due to stroke 45%, heart failure 35%, kidney failure 3% and others 17%.¹

• Almost half of the Australian cardiovascular disease burden is due to hypertension.²

• Factors increasing the chances of dying in hypertensive patients are: male, onset at a young age, family history, increased diastolic pressure.²

• The various categories of BP are arbitrarily defined according to BP values for both diastolic and systolic readings (see TABLE 86.1).^4,5

• Isolated systolic hypertension is that of ≥140 mmHg in the presence of a diastolic pressure <90 mmHg.

• Hypertension is either essential or secondary (see TABLE 86.2).

• Essential hypertension is the presence of sustained hypertension in the absence of underlying, potentially correctable kidney, adrenal or other factors.

• Malignant hypertension is that with a diastolic pressure >120 mmHg and exudative vasculopathy in the retinal and kidney circulations.

• Refractory hypertension is a BP >140/90 mmHg despite maximum dosage of two drugs for 3–4 months.

Treatment of hypertension is generally indefinite (or until old age and frailty render the risks of treatment greater than the benefits). It is important to establish the risk status and the prognosis prior to commencing therapy, especially if hypertension is an isolated factor. The World Health Organization–International Society of Hypertension (WHO–ISH) recommendation is that decisions about management of patients with hypertension should not be based on BP alone but also on the presence or absence of other risk factors, including age, diabetes and smoking. This is because the benefits of treatment are less in those with low cardiovascular risk. CV risk should be stratified according to the BP level and the presence of:

• absolute cardiovascular risk factors

• associated clinical conditions

• target organ damage (see TABLE 86.3)

A practical approach to stratifying total cardiovascular risk is proposed in TABLE 86.4. The terms ‘low’, ‘moderate’ (medium), ‘high’ and ‘very high’ added risk are calibrated to indicate an absolute 5-year risk of cardiovascular disease of <10%, 10–15%, 15–20% and >20% respectively (based on Framingham criteria).⁶ For example, ‘low risk’ indicates consideration of treatment and monitoring; ‘high risk’ indicates treating immediately.

Risk estimation can be determined by referring to various cardiovascular risk tables on the website (and in CHAPTER 85). A commonly used tool in Australasia is the modified New Zealand Cardiovascular Risk Charts (www.nzgg.org.nz or www.heartfoundation.com.au). See CHAPTERS 20 and 85.

It is important to collaborate with patients in decision making, and thus discussing cardiovascular risk assessment and blood pressure (BP) level should be the starting point when discussing the risks and benefits of treatment.

Secondary hypertension may be suggested in patients below 40 years by the history (see TABLE 86.5), physical examination, severity of hypertension or the initial laboratory findings. It is also more likely where BP is responding poorly to drug therapy, and in patients with accelerated or malignant hypertension.⁵

The most common causes of secondary hypertension are various kidney diseases, such as renovascular disease, chronic glomerulonephritis, and chronic pyelonephritis (often associated with reflux nephropathy).¹ There will often be no physical findings to suggest the existence of such kidney diseases, but an indication will generally be obtained by the presence of one or more abnormalities when the urine is examined. Clinical pointers include proteinuria, an abnormal urine sediment, general atheroma, smokers and abdominal bruit. Consider sleep apnoea, and take a comprehensive medication history, including illicit drugs and alternative remedies.

Physical findings that may suggest secondary hypertension include epigastric bruits (indicating possible kidney artery stenosis) and abdominal aortic aneurysm. Less common findings include abdominal flank masses (polycystic kidneys), delayed or absent femoral pulses (coarctation of the aorta), truncal obesity with pigmented striae (Cushing syndrome), and tachycardia, sweating and pallor (phaeochromocytoma). Endocrine causes are presented in CHAPTER 23.

Further investigation will be required to confirm or reveal secondary hypertension.

Renal artery stenosis

Atherosclerotic kidney artery stenosis accounts for the majority of cases, while fibromuscular dysplasia remains an important cause. Doppler ultrasound is a highly sensitive and specific investigation.

Hypertension can only be detected when BP is measured. Therefore frequent opportunities should be taken to measure BP: every 6–12 weeks in high-risk patients; every 6–12 months in moderate-risk patients.⁷

Diagnosis should not be made on the basis of a single visit. Initial raised BP readings should be confirmed on at least two other visits within the space of 3 months; average levels of 90 mmHg diastolic or more, or 140 mmHg systolic or more, are needed before hypertension can be diagnosed. This will avoid the possibility of an incorrect diagnosis, committing an asymptomatic, normotensive individual to unjustified, lifelong treatment.

Measurement guidelines^4,5

BP varies continuously and can be affected by many outside factors. Care should therefore be taken to ensure that readings accurately represent the patient’s usual pressure.

Recording

On each occasion when the BP is taken, two or more readings should be averaged. Wait at least 30 seconds before repeating the procedure. If the first two readings differ by more than 6 mmHg systolic or 4 mmHg diastolic, more readings should be taken.

Both systolic and diastolic levels should be recorded. For the diastolic reading the disappearance of sound (Phase 5)—that is, the pressure when the last sound is heard and after which all sound disappears—should be used.⁸ This is more accurate than the muffling of sounds (phase 4) (see FIG. 86.2), which should only be used if the sound continues to zero.

Heart rate and pulse

At the same time the BP is measured, the heart rate and rhythm should be measured and recorded. A high heart rate may indicate undue stress that is causing the associated elevated BP reading. An irregular heart rhythm may cause difficulty in obtaining an accurate BP reading.

BP modifying factors

Strategies for high initial readings

If the initial reading is high (DBP >90 mmHg, SBP >140 mmHg) repeat the measures after 10 minutes of quiet rest. The ‘white coat’ influence in the medical practitioner’s office may cause higher readings so measurement in other settings such as the home or the workplace should be managed whenever possible.

Confirmation and follow-up¹

Repeated BP readings will determine whether initial high levels are confirmed and need attention, or whether they return to normal and need only periodic checking. Particular attention should be paid to younger patients to ensure that they are regularly followed up.

Initial diastolic BP readings of 115 mmHg or more, particularly for patients with target organ damage, may need immediate drug therapy.

Once an elevated level has been detected, the timing of subsequent readings should be based on the initial pressure level, as shown in TABLE 86.6.

If mild hypertension is found, observation with repeated measurement over 3–6 months should be followed before beginning therapy. This is because levels often return to normal.

Ambulatory 24-hour monitoring

This is required for the diagnosis and follow-up of patients with fluctuating levels, borderline hypertension or refractory hypertension (especially where the ‘white coat’ effect may be significant). Studies have shown that this method provides a more precise estimate of BP variability than casual recordings.

Guidelines for ambulatory BP measurement:

• unusual variability of office BP

• marked discrepancy between office and home BP

• resistance to drug treatment

• suspected sleep apnoea

• when two BP readings >140/90

‘White coat’ hypertension

This group may comprise up to 25% of patients presenting with hypertension. These people have a type of conditioned response to the clinic or office setting, yet their home BP and ambulatory BP profiles are normal. They appear to be at low risk of cardiovascular disease but may progress to sustained hypertension. Ambulatory 24-hour monitoring can be useful.

Masked hypertension

This is where office measurements are normal but ambulatory BP is elevated. Prognosis is relatively poor. Suspect it if evidence of end organ damage but normal office BP.

Isolated systolic hypertension

Isolated systolic hypertension is most frequently seen in elderly people. It is not benign.

If a trial of non-pharmacological therapy fails, then drugs are used to cautiously reduce the systolic BP to between 140 and 160 mmHg.

As well as defining the BP problem, the clinical evaluation for suspected hypertension should also determine:

• whether the patient has potentially reversible secondary hypertension

• whether target organ damage is present

• whether there are other potentially modifiable cardiovascular risk factors present, and

• what comorbid factors exist

These factors markedly influence the weighing up of benefit versus risk when deciding whether to commence (or increase) antihypertensive medication. That decision needs to take into account more than just the BP reading.

The following should be included in the medical history of the patient.

History of hypertension

• Method and date of initial diagnosis

• Known duration and levels of elevated BP

• Symptoms that may indicate the effects of high BP on target organ damage, such as headache, dyspnoea, chest pain, claudication, ankle oedema and haematuria

• Symptoms suggesting secondary hypertension (see TABLE 86.5)

• The results and side effects of all previous antihypertensive treatment

Presence of other diseases and risk factors

• A history of cardiovascular, cerebrovascular or peripheral vascular disease, kidney disease, diabetes mellitus or recent weight gain

• Other cardiovascular risk factors, including obesity, hyperlipidaemia, carbohydrate intolerance, smoking, salt intake, alcohol consumption, exercise levels and analgesic intake

• Other relevant conditions, such as asthma or psychiatric illness (particularly depressive illness)

Family history

Particular attention should be paid to the family history of hypertension, cardiovascular or cerebrovascular disease, hyperlipidaemia, obesity, diabetes mellitus, kidney disease, alcohol abuse and premature sudden death.

Medication history

A history of all medications, including over-the-counter products, should be obtained because some can raise BP or interfere with antihypertensive therapy. Prohypertensive substances include:

• alcohol

• oral and depot contraceptives

• hormone replacement therapy

• steroids/corticosteroids

• NSAIDs/COX–2 inhibitors

• sympathomimetics, nasal decongestants and other cold remedies, pseudoephedrine

• appetite suppressants

• stimulants, e.g. amphetamines

• irreversible monoamine oxidase inhibitors

• analgesics

• ergotamine

• cyclosporin

• tacrolimus

• natural liquorice

• bupropion/clozapine

• SNRIs, e.g. venlafaxine (dose-related)

Alcohol intake¹

Alcohol has a direct pressor effect that is dose-related. An assessment of the average daily number of standard drinks is important—more than two standard drinks (20 g alcohol) a day is significant.

The approach to the physical examination is to detect possible target organ damage and possible causes of secondary hypertension. The main features to consider are illustrated in FIGURE 86.3.

The four grades of hypertensive retinopathy are illustrated in FIGURE 86.4.

Leg pulses and pressure

To assess the remote possibility of coarctation of the aorta in the hypertensive patient, perform at least one observation comparing:

1. the volume and timing of the radial and femoral pulses

2. the BP in the arm and leg

3. comparison of BP in the two arms

Blood pressure measurement in the leg

• Place the patient prone.

• Use a wide, long cuff at mid-thigh level.

• Position the bladder over the posterior surface and fix it firmly.

• Auscultate over the popliteal artery.

Recommended tests

• Chest X-ray

• Plasma glucose (preferably fasting)

• Serum total and high-density lipoprotein (HDL) cholesterol, fasting serum triglycerides

• Serum creatinine/eGFR/ACR

• Serum uric acid

• Serum potassium and sodium

• Haemoglobin and haematocrit

• Urinalysis (dipstick test and urinary sediment)

• Electrocardiogram

Other tests to consider

• Echocardiogram

• Carotid (and femoral) ultrasound

• HbA1c (when fasting glucose ≥6.1 mmol/L or 110 mg/dL)

• Fundoscopy (in severe hypertension)

These other investigations, including echocardiography, kidney imaging studies (especially kidney doppler ultrasound), 24-hour urinary catecholamines, aldosterone and plasma renin, are not routine and should be performed if specifically indicated (e.g. suspected primary hyperaldosteronism). A chest X-ray may serve as a baseline against which to measure future changes. However, if a chest X-ray shows the heart is enlarged, it is more likely to represent chamber dilatation than increased ventricular wall thickness.¹ Specific kidney studies now favoured include isotope scans, duplex ultrasound studies of kidney arteries and kidney arteriography.

A correct diagnosis is the basis of management. Assuming that the uncommon secondary causes are identified and treated, treatment will focus on essential hypertension.

Benefits of treatment

Trials have shown that lowering BP reduces:

• cardiovascular and total mortality

• stroke

• coronary events

Benefits have been proven:

• in patients with systolic/diastolic hypertension

• in elderly patients with isolated systolic hypertension

Principles of management³

• The overall goal is to improve the long-term survival and quality of life.

• Promote an effective physician–patient working relationship.

• Aim to reduce the levels to 140/90 mmHg or less (ideal).

• Undertake a thorough assessment of all cardiovascular risk factors.

• Instruct all patients in the use of non-drug treatment strategies and their potential benefits. The benefits of exercise and healthy diet go far beyond what will be measurable by merely observing their effect on hypertension.

• In patients with mild-to-moderate hypertension and no target organ damage, consider ambulatory or home BP monitoring before deciding to start medication.

• Drug therapy should be given to those with:

  • – sustained high initial readings (e.g. DBP 100 mmHg)

  • – target organ damage

  • – failed non-drug measures

• Make a careful selection of an antihypertensive drug and an appraisal of the side effects against the benefits of treatment.

• Avoid drug-related problems such as postural hypotension.

• Avoid excessive lowering of BP—aim for steady and graduated control.

• Aim to counter the problem of patient non-compliance.

• Be aware of factors that may contribute to drug resistance.

Patient education should include appropriate reassurances, clear information and easy-to-follow instructions. It is important to establish patients’ understanding of the concept of hypertension and its consequences by quizzing them about their knowledge and feelings.

Correction of patients’ misconceptions¹

Patients are likely to have several misconceptions about hypertension that may adversely affect their treatment.

For example, they might believe that:

• hypertension can be cured

• they do not need to continue treatment once BP is controlled

• they do not have a problem because they do not have symptoms

• they need to take additional pills, or stop treatment in response to symptoms they believe are caused by high or low BP levels

• they need not take prescribed pills if they attend to lifestyle factors such as exercise and diet

• they can gauge their BP by how they feel

Tips for optimal compliance

• Establish a good, caring rapport.

• Give advice about pill-taking times.

• Set therapeutic goals.

• Establish a recall system.

• Provide patient education material.

On review:

• Ask if any pills were missed by accident.

• Attempt to reduce waiting time to a minimum (e.g. direct a patient to a spare room on arrival).

• Review all cardiovascular risk factors.

• Enquire about any side effects.

If the average diastolic BP at the initial visit is 90–100 mmHg, and there is no evidence of end organ damage, non-pharmacological therapy is indicated for a 3-month period without use of antihypertensive drugs. Remember to remove, revise or substitute drugs that may be causing hypertension (e.g. NSAIDs, corticosteroids, oral contraceptives, hormone replacement therapy).

Behaviour intervention measures

• Weight reduction

  There is considerable evidence that weight loss and gain are linked to a corresponding fall and rise in BP. Hovell has estimated that for every 1 kg of weight lost, BP dropped by 2.5 mmHg systolic and 1.5 mmHg diastolic.¹⁰ The BMI should be calculated for all patients and where appropriate a weight loss program organised to target waist measurement to <94 in males and <80 in females or reduce the BMI to around 25.

• Reduction of excessive alcohol intake¹

  The direct pressor effect of alcohol is reversible. Drinking more than 20 g of alcohol a day raises BP and makes treatment of established hypertension more difficult. People with hypertension should limit their alcohol intake to one or two standard drinks (10–20 g) per day. Reduction or withdrawal of regular alcohol intake reduces BP by 5–10 mmHg.

• Reduction of sodium intake to ≤4 g/day

  Some individuals seem to be more sensitive to salt restriction. Advise patients to put away the salt shaker and use only a little salt with their food. Reduction of sodium intake to less than 100 mmol sodium per day is advised. Special care should be taken with processed and take-away foods.

• Increased exercise and regular physical activity

  Regular aerobic or isotonic exercise helps to reduce BP.⁹ Hypertensive patients beginning an exercise program should do so gradually. Walking is an appropriate exercise, ideally 150–300 minutes each week.

• Reduction of particular stress

  If avoiding stress or overwork is difficult, recommend relaxation and/or meditation therapy.

• Other dietary factors for a healthy eating plan

  There is evidence that lacto–vegetarian diets and diets high in vegetables, fruits and whole grains can reduce BP.³ A diet high in calcium, and low in fat and caffeine, may also be beneficial. Avoid or minimise liquorice.

• Smoking

  Smoking causes acute rises in BP but does not appear to cause sustained hypertension. However, the elimination of smoking is important as it is a strong risk factor for cardiovascular disease and continuing to smoke may negate any cardiovascular benefits of antihypertensive therapy.¹

• Management of sleep apnoea

  A 2014 systematic review found that CPAP reduces BP in those with obstructive sleep apnoea and hypertension, although only by a small amount (2–3 mmHg).¹¹

The benefits of drug therapy appear to outweigh any known risks to individuals with a persistently raised diastolic pressure >95 mmHg. Although the ideal antihypertensive drug has yet to be discovered, there are many effective drugs available from all the major classes of antihypertensive drugs.¹² Deciding which one to use first involves an assessment of the patient’s general health, the medication’s known side effects, the simplicity of its administration and its cost. A useful plan is outlined in FIGURE 86.5.

Various disorders such as diabetes, asthma, COPD, Raynaud phenomenon, heart failure, and elevated serum urate and/or lipid levels may restrict the use of some classes of drugs.

When to treat

• Failed genuine non-pharmacological trial

• For those with >10% 5-year CV risk, treat if SBP >140 mmHg or DBP >90 mmHg

• For those with <10% 5-year CV risk, treat if SBP >160 mmHg or DBP >100 mmHg (see TABLE 86.7)

Guidelines¹³

• Start with a single drug at low dose.

• A period of 4–6 weeks is needed for the effect to become fully apparent.

• If ineffective, consider increasing the drug to its maximum recommended dose, or add an agent from another compatible class, or substitute with a drug from another class.

• Use only one drug from any one class at the same time.

• A summary of first-line therapy options and the uses of the various pharmacological agents is shown in TABLE 86.8.

• Measure the BP at the same time each day.

• Consider asking patients to self-measure.

• Patients commonly require two or more agents to reach BP targets.

Starting regimens

In patients with uncomplicated hypertension, ACE inhibitors or ARBs, calcium channel blockers and thiazides are all suitable first-line antihypertensive drugs, either as monotherapy or in some combinations unless contraindicated.

The traditional method has been to use stepwise therapy until ideal control has been reached, commencing with:

The following are useful combinations:^9,15

Relatively ineffective combinations⁹

• Diuretic and calcium channel blocker

• Beta blockers and ACE inhibitors

Undesirable combinations^9,13

• More than one drug from a particular pharmacological group:

  • – beta blockers and verapamil (heart block, heart failure)

  • – potassium-sparing diuretics and ACE inhibitors or ARB (hyperkalaemia)

  • – ACEI and ARB

Diuretics^9,16

• Thiazides are good first-line therapy for hypertension.

• Hypokalaemia can be corrected with potassium-sparing diuretics or by changing to another first-line drug.

• Loop diuretics are less potent as antihypertensive agents but are indicated where there is concomitant cardiac or kidney failure and in resistant hypertension.

• Thiazides are less effective where there is kidney impairment.

• Thiazides may precipitate acute gout.

• NSAIDs may antagonise the antihypertensive and natriuretic effectiveness of diuretics.

• A diet high in potassium and magnesium should accompany diuretic therapy (e.g. lentils, nuts, high fibre).

• Avoid use if significant dyslipidaemia.

• Indapamide has different properties to the thiazide and loop diuretics and has less effect on serum lipids.

Beta blockers

• NSAIDs may interfere with the hypotensive effect of beta blockers.

• If BP is not reduced by one beta blocker it is unlikely to be reduced by changing to another.

• Verapamil plus a beta blocker may unmask conduction abnormalities causing heart block.

• In patients with ischaemic heart disease, or susceptibility to it, treatment must not be stopped suddenly—this can precipitate angina at rest.

Calcium channel blockers

• These drugs reduce BP by vasodilatation.

• The properties of individual drugs vary, especially their effects on cardiac function.

• The dihydropyridine compounds (nifedipine and felodipine) tend to produce more vasodilatation and thus related side effects.

• Unlike verapamil or diltiazem (which slow the heart), dihydropyridine drugs can be used safely with a beta blocker.

• Verapamil is contraindicated in second and third degree heart block.

• Verapamil and diltiazem should be used with caution in patients with heart failure.

• These drugs are efficacious with ACE inhibitors, beta blockers, prazosin and methyldopa.

ACE inhibitors

Angiotensin-converting enzyme (ACE) is responsible for converting angiotensin I to angiotensin II (a potent vasoconstrictor and stimulator of aldosterone secretion) and for the breakdown of bradykinin (a vasodilator). ACE inhibitors are effective in the elderly; improve survival and performance status in cardiac failure; are protective of kidney function in diabetes; and are cardioprotective after myocardial infarction.

Disturbance in taste is usually transitory and may resolve with continued treatment. Cough, which occurs in about 15% of patients, may disappear with time or a reduction in dose but it often persists and requires a change in drug in some patients. Angioedema, a potentially life-threatening condition, may occur in 0.1–0.2% of subjects. Like cough, it is a class effect and will mitigate against use of any ACE inhibitor in patients with such an adverse effect. The Heart Outcomes Prevention Evaluation (HOPE)¹⁷ trial demonstrated that the ACE inhibitor ramipril reduces the number of cardiovascular deaths, non-fatal myocardial infarctions, non-fatal strokes and instances of new onset heart failure in a high-risk population. The data also indicated that all diabetic patients with microalbuminuria or pre-existing vascular disease will benefit from ACE I treatment, even if normotensive.^15,17

Angiotensin II receptor antagonists (sartans)

These agents competitively block the binding of angiotensin II to type I angiotensin receptors and block the effects of angiotensin more selectively than the ACE inhibitors. This reduces angiotensin-induced vasoconstriction, sodium reabsorption and aldosterone release. The action of the ACEIs and ARBs on the renin–angiotensin–aldosterone pathway system is illustrated in FIGURE 86.7. They have a similar adverse kidney and other effects to the ACE inhibitors but cough does not appear to be a significant adverse effect. This group is used for mild-to-moderate hypertension alone or with other antihypertensive agents. They are useful alternatives for patients who discontinue an ACE inhibitor because of cough. They may be used in combination with thiazide diuretics.

Alpha blockers: prazosin and terazosin

Not recommended as first-line therapy.

A specific problem of alpha blockers is the ‘first-dose phenomenon’; this involves acute syncope about 90 minutes after the first dose, hence treatment is best initiated at bedtime. Prazosin potentiates beta blockers and works best if used with them. It is a useful second-line therapy in patients who are unsuitable for diuretic or beta blocker therapy (e.g. those with diabetes, asthma or hyperlipidaemia).

Vascular smooth muscle relaxants

Other than calcium channel blockers these include hydralazine, minoxidil and diazoxide, which are not used for first-line therapy but for refractory hypertensive states and hypertensive emergencies.

Sympathetic nervous system inhibitors

A newer class of antihypertensive agents has been developed to reduce peripheral sympathetic activity by inhibiting the sympathetic nervous system. Methyldopa and clonidine may be used during pregnancy.

A hypertensive emergency occurs when high BP causes the presenting cardiovascular problem. Typical presentations of hypertensive emergencies (which are rare) include hypertensive encephalopathy, acute stroke, heart failure, dissecting aortic aneurysm and eclampsia. Symptomatically patients may present with headache and confusion.

In all such cases referral to an emergency department is essential and the patient should be hospitalised immediately for monitoring and treatment. Treatment must be individualised, mindful of the nature of the underlying problem and associated disorders.

The BP lowering must be gradual because a sudden fall can precipitate a stroke. Aim to reduce the BP by no more than 25% within the first 2 hours then towards 160/100 mmHg within 2 to 6 hours.¹³

Treatment is with a dihydropyridine CCB and/or an ACE inhibitor. Otherwise, sodium nitroprusside IV in an intensive care setting is the optimal treatment.

Magnesium sulphate reduces the risk of eclampsia and maternal death in women with pre-eclampsia (see CHAPTER 108).

Refractory hypertension exists where control has not been achieved despite reasonable treatment for 3–4 months. A review of a possible secondary causes is appropriate. Consider non-compliance, sleep apnoea, hypertensive effects of other drugs, undisclosed use of alcohol and recreational drugs, and also spurious factors (e.g. instrument factors such as small cuff, ‘white coat’ hypertension).

When adequate control is not possible and the cause is not obvious, the patient should be referred to a specialist. Measurement outside the clinic may help in the assessment of such people, as may 24-hour ambulatory monitoring.

BP is less frequently measured in children for a number of reasons, including the lower chances of finding any abnormality, the unavailability of an appropriately sized cuff or difficulty in measuring BP in the infant or toddler.

The children of parents with hypertension should be closely watched. Those at risk of secondary hypertension (e.g. kidney or cardiovascular disease, urological abnormalities and diabetes mellitus) should have routine measurements. Children with visual changes, recurrent headache or abdominal pain, seizures, and those on drugs such as corticosteroids or oral contraceptives, should have their BP checked regularly.

Although secondary causes of hypertension are proportionally more common in children than in adults, young people are still more prone to developing essential rather than secondary hypertension. Kidney parenchymal disease and kidney artery stenosis are the major secondary causes.

The upper limits of normal BP for children in different age groups are:¹

The proper cuff size is very important to avoid inaccurate readings and a larger rather than a smaller cuff is recommended. The width of the bladder should cover 75% of the upper arm. In infants and toddlers, use of an electronic unit may be necessary. Although cessation of sound (phase 5) is the better reflection of true diastolic pressure, there is often no disappearance of sound in children and so estimation of the point of muffling (phase 4) is recorded instead.

Diagnostic evaluation and drug treatment for children are similar to those for adults. Strongly consider specialist referral. When a child is obese, reduction in weight may adequately lower BP. ACE inhibitors or calcium channel blocking agents are preferable in the young hypertensive, with diuretics a second agent. ACE inhibitors should be avoided in postpubertal girls.

BP shows a gradual increasing linear relationship with age.

Guidelines for treatment

• Isolated systolic hypertension is worth treating.¹⁸

• Older patients may respond to non-pharmacological treatment.

• Reducing dietary sodium is more beneficial than with younger patients.

• If drug treatment is necessary, commence with half the normal recommended adult dosage—‘start low and go slow’.

• Patients over 75 years and in good health should be treated the same as younger patients. Studies indicate that benefits are still significant. However, weigh this against the fact that harms (e.g. falls risk) may be greater.

• A gradual reduction in BP is recommended.

• Drug reactions are a limiting factor.

• Drug interactions are also a problem: these include NSAIDs, antiparkinson drugs and phenothiazines.

Specific treatment

• First-line choice: indapamide (preferred) or thiazide diuretic (low dose);¹ check electrolytes in 2–4 weeks: if hypokalaemia develops add a K-sparing diuretic rather than K supplements. Diuretics may aggravate bladder difficulties (e.g. incontinence).

• Second-line choice: ACE (or ARB) inhibitors (especially with heart failure)

Other effective drugs (especially for isolated systolic hypertension):

• beta blockers (low dose) where diuretic cannot be prescribed or if angina

• calcium channel blockers

Both these groups are generally well tolerated but constipation may be a problem with verapamil.

Kidney function and electrolytes should be monitored when ACE inhibitors are started.

These conditions are summarised in TABLE 86.9.

This is an important concept that recognises that drug treatment need not necessarily be lifelong. If BP has been well controlled for several months to years it is often worth reducing the dosage or the number of drugs.

The general ‘deprescribing’ rule of thumb is that a drug (or its specific dosage) should only be continued if the expected benefits justify its continuation.

A ‘drug holiday’ (cessation of treatment) can be hazardous, however, because satisfactory control may be temporary and hypertension will re-emerge. Careful monitoring under such circumstances is mandatory.

• Refractory hypertension—adequate control not possible and cause not obvious

• Suspected ‘white coat’ hypertension—for ambulatory BP monitoring

• Severe hypertension—diastolic BP >115 mmHg

• Hypertensive emergency

• Evidence of ongoing target organ impairment and BP inadequately controlled

• Significant kidney impairment eGFR <30 mL/min

• A treatable cause of secondary hypertension is found

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Hypertension