Hypertension, HHD and Complications .pptx

This slide discusses the prevalence of hypertension, its epidemiology and attributable risks

1. SYSTEMIC HYPERTENSION

2. INTRODUCTION The 2024 Guidelines define hypertension as a confirmed office systolic BP of ≥140 mmHg or diastolic BP of ≥90 mmHg. confirmation is recommended with out-of-office measurements (HBPM or ABPM) or at least one repeat office measurement at a subsequent visit. Second, most adults with BP above this threshold are at increased CVD risk, typically with 10-year risk estimates of ≥10% for fatal and non-fatal CVD events.

3. Current global guidelines recommend treating hypertension based on 24-h ambulatory blood pressure monitoring (ABPM) and home blood pressure (BP) measurements rather than measurement in the clinical setting.

4. Hypertension is defined as office SBP values >_140 mmHg and/or diastolic BP (DBP) values >_90 mmHg. This is based on evidence from multiple RCTs that treatment of patients with these BP values is beneficial. The same classification is used in younger, middle-aged, and older people, whereas BP centiles are used in children and teenagers

5. Prevalence of hypertension the global prevalence of hypertension was estimated to be 1.13 billion in 2015, with a prevalence of over 150 million in central and eastern Europe. The overall prevalence of hypertension in adults is around 30 - 45%, with a global age standardized prevalence of 24 and 20% in men and women, respectively, in 2015. This high prevalence of hypertension is consistent across the world, irrespective of income status, i.e. in lower, middle, and higher income countries.

6. Hypertension is more common with advancing age, with a prevalence of >60% in people aged >60 years. It is estimated that the number of people with hypertension will increase by 15–20% by 2025, reaching close to 1.5 billion

7. Demographic characteristics and laboratory parameters Sex (men >women) Age Smoking (current or past history)a Total cholesterol and HDL-C Uric acid Diabetes Overweight or obesity Family history of premature CVD (men aged

8. Early-onset menopause Sedentary lifestyle Psychosocial and socioeconomic factors Heart rate (resting values >80 beats/min)

9. EPIDEMIOLOGY Worldwide prevalence is around 20% , and approximately 7.1 million deaths per year may be attributable to hypertension The WHO reports that suboptimal BP (>115 mmHg SBP) is responsible for 62 percent of cerebrovascular disease and 49 percent of ischemic heart disease (IHD) Suboptimal BP is top attributable risk factor for death throughout the world Hajjar I, Kotchen TA. Trends in prevalence, awareness, treatment, and control of hypertension in the United States, 1988- 2000. JAMA 2003;290:199-206

10. Global Burden of Hypertension: Analysis of Worldwide Data Kearney PM et al. Lancet 2005; 365:217-223 In 2000 , 26.4% (95% CI 26.0-26.8%) of the adult population had hypertension, 26.6% of men & 26.1% of women. By 2025 , 29.2% (28.8-9.7%) were projected to be hypertensive, 29.0% of men & 29.5% of women.

11. HYPERTENSION PREVALANCE - AFRICA Increasing prevalence rates Prevalence in Nigeria is reported to be 12%-22% in people above 15 years Kenya (1929) – no hypertension in 1800 admissions Ghana (urban) – increase from 8% (1990) to 28% (2004) Tanzania (1997) -26% (rural), 37% (urban) S.Africa up to 50-60% above 65years

12. Attributable Risk Only half of the burden seen in people with hypertension (BP > 140 mmHg); remainder in prehypertensives (BP > 115mmHg) > 80% of the burden seen in low-income and middle-income regions Over half occurred in people aged 45-69 yrs 54% stroke 47% IHD 25% other CVD 13.5% Total mortality Study by Int Society of hypertension; Lancet May 2008;371:1513-8

13. Classification of BP in European and US Adults: ESH ESC and JNC 7 Guidelines BP category Systolic (mmHg) Diastolic (mmHg) BP category Systolic (mmHg) Diastolic (mmHg) Optimal <120 & <80 Normal 120–129 &/or 80–84 Normal <120 & <80 High normal 130–139 &/or 85–89 Pre-HTN 120–139 or 80–89 Grade 1 (mild) 140–159 &/or 90–99 Stage 1 140–159 or 90–99 Grade 2 (moderate) 160–179 &/or 100–109 Stage 2 ≥160 or ≥100 Grade 3 (severe) ≥180 &/or ≥110 Isolated systolic HTN 140 & <90 JNC 7 2 ESH ESC 1 1 Task Force of ESH–ESC. J Hypertens 2007;25:1105–87 2 Chobanian et al. JAMA 2003;289:2560 7 2

14. Hypertension classification (Hypertension. 2020;75:1334-1357. DOI: 10.1161/HYPERTENSIONAHA.120.15026 14

15. Nigeria Hypertension Society Risk factors for the development of primary hypertension include: • Heredity • High salt intake • Obesity • Physical inactivity • Excessive alcohol intake • Low potassium diet • Low vegetables or fresh fruits content in the diet • High saturated fats content in the diet. • Low birth weigh 15

16. In 2000 , 972 million adults had hypertension; 333 million (329-336 million) in economically developed countries & 639 million (625-654 million) in economically developing countries. By 2025 , the number of adults with hypertension was predicted to increase by about 60% to a total of 1.56 billion .

17. Epidemiology in Nigeria 18 Overall prevalence 38.1% NC-20.9%. SW-42.1% NW-26.8%. SS-44.6% NE-27.5%. SE-52.8%

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19. May Measurement Month 2021: an analysis of blood pressure screening results from Nigeria European Heart Journal Supplements (2024) 26 (Supplement 3), iii65–iii67. https://doi.org/10.1093/eurheartjsupp/suae053 1/3 rd of people screened were hypertensives. Approximately half of the screened population were not aware about the diagnosis of Hypertension T wo out of every five on antihypertensive medications had controlled BP 20

20. Causes The majority (80–90%) of patients with hypertension have primary elevation of blood pressure, i.e. essential hypertension of unknown cause. Essential hypertension has a multifactorial aetiology .

21. Genetic factors Blood pressure tends to run in families and children of hypertensive parents tend to have higher blood pressure than age-matched children of parents with normal blood pressure. This familial concordance of blood pressure may be explained, at least in part, by shared environmental influences.

22. Fetal factors Low birth weight is associated with subsequent high blood pressure. This relationship may be due to fetal adaptation to intrauterine undernutrition with long-term changes in blood vessel structure or in the function of crucial hormonal systems.

23. Environmental factors Amongst the several environmental factors the following are significant: Obesity. Fat people have higher blood pressures than thin people. There is a risk of overestimation if the blood pressure is measured with a small cuff. Sleep disordered breathing often seen with obesity may be an additional risk factor.

24. Alcohol intake. Most studies have shown a close relationship between the consumption of alcohol and blood pressure level. However, subjects who consume small amounts of alcohol seem to have lower blood pressure level than those who consume no alcohol.

25. Sodium intake. A high sodium intake has been suggested to be a major determinant of blood pressure differences between and within populations around the world. Populations with higher sodium intakes have higher average blood pressures than those with lower sodium intake. Migration from a rural to an urban environment is associated with an increase in blood pressure that is in part related to the amount of salt in the diet.

26. Stress. Whilst acute pain or stress can raise blood pressure, the relationship between chronic stress and blood pressure is uncertain.

27. Humoral mechanisms The autonomic nervous system, the renin– angiotensin, natriuretic peptide and kallikrein – kinin system, plays a role in the physiological regulation of short-term changes in blood pressure and have been implicated in the pathogenesis of essential hypertension. A low renin, salt sensitive, essential hypertension in which patients have renal sodium and water retention has been described.

28. Insulin resistance An association between diabetes and hypertension is recognized and a syndrome has been described of hyperinsulinaemia , glucose intolerance, reduced levels of HDL cholesterol, hypertriglyceridaemia and central obesity (all of which are related to insulin resistance) in association with hypertension. This association (also called the ‘metabolic syndrome is a major risk factor for cardiovascular disease.

29. Secondary hypertension Secondary hypertension is where blood pressure elevation is the result of a specific and potentially treatable cause. Secondary forms of hypertension include the following: Renal diseases These account for over 80% of the cases. The common causes are: diabetic nephropathy chronic glomerulonephritis adult polycystic disease ■ Chronic tubulointerstitial nephritis ■ renovascular disease.

30. Hypertension can itself cause or worsen renal disease. The mechanism of this blood pressure elevation is due to sodium and water retention, although there can be inappropriate elevation of plasma renin levels.

31. Endocrine causes These include: Conn’s syndrome adrenal hyperplasia phaeochromocytoma Cushing’s syndrome acromegaly. Congenital cardiovascular causes is coarctation of the aorta.

32. Drugs Many drugs may cause or aggravate hypertension, or interfere with the response to some antihypertensive agents: NSAIDs, oral contraceptives, steroids carbenoxolone , liquorice , sympathomimetics and vasopressin. Patients taking monoamine oxidase inhibitors who consume tyramine-containing foods may develop paroxysms of severe hypertension.

33. Pathophysiology The pathogenesis of essential hypertension is unclear. In some young hypertensive patients, there is an early increase in cardiac output, in association with increased pulse rate and circulating catecholamines . This could result in changes in baroreceptor sensitivity, which would then operate at a higher blood pressure level. In chronic hypertension , the cardiac output is normal and it is an increased peripheral resistance that maintains the elevated blood pressure.

34. The resistance vessels (the small arteries and arterioles) show structural changes in hypertension with an increase in wall thickness and a reduction in the vessel lumen diameter. There is also some evidence for rarefaction (decreased density) of these vessels. These mechanisms would result in an increased overall peripheral vascular resistance.

35. Hypertension also causes changes in the large arteries. There is thickening of the media, an increase in collagen and the secondary deposition of calcium. These changes result in a loss of arterial compliance, which in turn leads to a more pronounced arterial pressure wave. Pulse wave velocity is a measure of arterial stiffness and is inversely related to distensibility . With each systolic contraction a pulse wave travels down the arterial wall before the flow of blood.

36. Thus, the more rigid the arterial wall, the faster the wave travels. It can be measured but is not in routine use. Atheroma develops in the large arteries owing to the interaction of these mechanical stresses and low growth factors. Endothelial dysfunction with alternations in agents such as nitric oxide and endothelins appear to be involved

37. Changes in the renal vasculature eventually lead to a reduced renal perfusion, reduced glomerular filtration rate and, finally, a reduction in sodium and water excretion. The decreased renal perfusion may lead to activation of the renin–angiotensin system (renin converts angiotensinogen to angiotensin I, which is in turn converted to angiotensin II by angiotensin-converting enzyme) with increased secretion of aldosterone and further sodium and water retention.

38. Complications Cerebrovascular disease coronary artery disease renal failure and peripheral vascular disease. Hypertensives have a sixfold increase in stroke (both haemorrhagic and atherothrombotic ). There is a threefold increase in cardiac death (due either to coronary events or to cardiac failure). Furthermore, peripheral arterial disease is twice as common.

39. EVIDENCE OF TARGET ORGAN DAMAGE AND CARDIOVASCULAR DISEASE Cardiac  LVH (moderate to severe) Systolic or diastolic dysfunction Ischemic heart disease Vasculature  Peripheral arterial disease Carotid arterial disease Aortic aneurysm Renal  Albuminuria (urinary albumin >300 mg/day) CKD (estimated GFR <60 mL/min) or Cerebrovascular  Stroke /Transient ischemic attack

40. TOD Heart Left ventricular hypertrophy Angina or prior myocardial infarction Prior coronary revascularization Heart failure Brain Stroke or transient ischemic attack, cognitive disturbances Chronic kidney disease Peripheral arterial disease Retinopathy PWV

41. Malignant hypertension Malignant or accelerated hypertension occurs when blood pressure rises rapidly and is considered with severe hypertension (diastolic blood pressure > 120 mmHg). The characteristic histological change is fibrinoid necrosis of the vessel wall and, unless treated, it may lead to death from progressive renal failure, heart failure, aortic dissection or stroke. The changes in the renal circulation result in rapidly progressive renal failure, proteinuria and haematuria .

42. There is also a high risk of cerebral oedema and haemorrhage with resultant hypertensive encephalopathy. In the retina there may be flame-shaped haemorrhages , cotton wool spots, hard exudates and papilloedema . Without effective treatment there is a 1-year survival of less than 20%.

43. Assessment Management should be considered in three stages: assessment, non-pharmacological treatment and drug treatment . During the assessment period, secondary causes of hypertension should be excluded, target-organ damage from the blood pressure should be evaluated and any concomitant conditions (e.g. dyslipidaemia or diabetes) that may add to the cardiovascular burden should be identified.

44. History The patient with mild hypertension is usually asymptomatic. Attacks of sweating, headaches and palpitations point towards the diagnosis of phaeochromocytoma . Higher levels of blood pressure may be associated with headaches, epistaxis or nocturia . Breathlessness may be present owing to left ventricular hypertrophy or cardiac failure, angina or symptoms of peripheral arterial vascular disease suggest the diagnosis of atheromatous renal artery stenosis.

45. Fibromuscular disease of the renal arteries encompasses a group of conditions in which fibrous or muscular proliferation results in morphologically simple or complex stenosis and tends to occur in younger patients. Malignant hypertension may present with severe headaches, visual disturbances, fits, transient loss of consciousness or symptoms of heart failure.

46. Examination Elevated blood pressure is usually the only abnormal sign. Signs of an underlying cause should be sought, such as renal artery bruits in renovascular hypertension, or radiofemoral delay in coarctation of the aorta. The cardiac examination may also reveal features of left ventricular hypertrophy and a loud aortic second sound. If cardiac failure develops, there may be a sinus tachycardia and a third heart sound. Fundoscopy is an essential part of the examination of any hypertensive patient. The abnormalities are graded according to the Keith–Wagener classification:

47. Grade 1 –tortuosity of the retinal arteries with increased reflectiveness (silver wiring). Grade 2 – grade 1 plus the appearance of arteriovenous nipping produced when thickened retinal arteries pass over the retinal veins. Grade 3 – grade 2 plus flame-shaped haemorrhages and soft (‘cotton wool’) exudates actually due to small infarcts Grade 4 – grade 3 plus papilloedema (blurring of the margins of the optic disc). Grades 3 and 4 are diagnostic of malignant hypertension.

48. Ambulatory blood pressure monitoring Indirect automatic blood pressure measurements can be made over a 24-hour period using a measuring device worn by the patient. The clinical role of such devices remains they are used to confirm the diagnosis in those patients with ‘white-coat’ hypertension, i.e. blood pressure is completely normal at all stages except during a clinical consultation. These patients do not have any evidence of target-organ damage, and unnecessary treatment can be avoided.

49. These devices may also be used to monitor the response of patients to drug treatment and to determine the adequacy of 24hour control with once-daily medication. Ambulatory blood pressure recordings is a better predictor of cardiovascular risk than clinic measurements. Analysis of the diurnal variation in blood pressure suggests that those hypertensives with loss of the usual nocturnal fall in blood pressure (‘non-dippers’) have a worse prognosis than those who retain this pattern.

50. Investigations Routine investigation include: ECG urine stix test for protein and blood fasting blood for lipids (total and HDL cholesterol) and glucose Serum urea, creatinine and electrolytes

51. If the urea or creatinine is elevated, more specific renal investigations are indicated – creatinine clearance, renal ultrasound (in case of polycystic kidney disease, or parenchymal renal artery disease) and a renal isotope scan or renal angiography if renovascular disease (either atheromatous or fibromuscular dysplasia) is suspected. A low serum potassium may indicate an endocrine disorder (either primary hyperaldosteronism or glucocorticoid excess), and aldosterone, cortisol and renin measurements must then be made, preferably prior to initiating pharmacological therapy. Clinical suspicion of phaeochromocytoma should be investigated further with measurement of urinary metanephrines and plasma or urinary catecholamines .

52. If the ECG shows evidence of coronary artery disease the coronary vascular status should be assessed. If left ventricular hypertrophy is suspected echocardiography (or MRI) should be undertaken. A chest X-ray is indicated if cardiac involvement or aortic coarctation is likely.

53. Benefits of Therapy Reductions in (1) stroke incidence- 35–40 % (2) Myocardial infarction (MI)- 20–25 % (3) HF averaging >40 % Blood Pressure Lowering Treatment Trialists' Collaboration. Lancet 2000

54. Treatment There should be a period of assessment with repeated blood pressure measurements, combined with advice and non Pharmacological measures prior to the initiation of drug therapy. Use of non-pharmacological therapy in include ■ weight reduction – BMI should be < 25 kg/m2 ■ low-fat and saturated fat diet ■ low-sodium diet – < 6g sodium chloride per day ■

55. Limited alcohol consumption – ≤ 21 units/week for men and ≤ 14 units/week for women Dynamic exercise – at least 30 minutes’ brisk walk per day increased fruit and vegetable consumption reduce cardiovascular risk by stopping smoking and increasing oily fish consumption.

56. Pharmacological therapy The initiation of antihypertensive therapy in subjects with sustained systolic blood pressure (BP) ≥ 160 mmHg, or sustained diastolic BP ≥ 100 mmHg. Decide on treatment in subjects with sustained systolic blood pressure between 140 and 159 mmHg, or sustained diastolic BP between 90 and 99 mmHg, according to the presence or absence of target organ damage or a 10-year cardiovascular disease risk > 20%. ■

57. In patients with diabetes mellitus, the initiation of antihypertensive drug therapy if systolic BP is sustained ≥ 140 mmHg, or diastolic BP is sustained ≥ 90 mmHg. ■

58. Target blood pressure For most patients a target of ≈ 140 mmHg systolic blood pressure and ≈ 85 mmHg diastolic blood pressure is recommended. For patients with diabetes, renal impairment or established cardiovascular disease a lower target of ≈ 130/80 mmHg is recommended. When using ambulatory blood pressure readings, mean daytime pressures are preferred and this value would be expected to be approximately 10/5 mmHg lower than the clinic blood pressure equivalent for both thresholds and targets.

59. What are the goals of therapy? <140/90 for patients without diabetes or renal disease Most patients who achieve their systolic goal will also achieve their diastolic goal <130/80 for patients with diabetes or renal disease JNC 7

60. ESH  ESC and JNC 7 Summary: Target BP Goals Type of hypertension BP goal (mmHg) Uncomplicated <140/90 Complicated Diabetes mellitus <130/80 Kidney disease <130/80* Other high risk (stroke, myocardial infarction) <130/80 Task Force of ESH–ESC. J Hypertens 2007;25:1105 87 Chobanian et al. JAMA 2003;289:2560 7 2 *Lower if proteinuria is >1 g/day

61. All of the drugs used to treat hypertension have side-effects and, since the benefits of drug treatment are not immediate, compliance may be a major problem. Several classes of drugs are available to treat hypertension. The usual are: (a) ACE inhibitors or angiotensin receptor antagonists; (b) beta-blockers; (c) calcium-channel blockers; or (d) diuretics.

62. Drug classes DIURETICS: Thiazide e.g bendrofluathizide 1.25- 5 mg CENTRALLY ACTIING DRUGS: Reserpine in BRINERDIN . ALPHA RECEPTORS BLOCKERS eg prasosin in MINIPRES BETA-RECEPTOR BLOCKERS: Atenolol in TERNOMIN CALCIUM ANTAGONISTS: e.g Nifedipine in ADALAT ACE INHIBITORS: e.g Lisinipril in ZESTRIL ACE RECEPTOR BLOCKERS: e.g Telmisartan in DIOVAN CENTRALLY ACTING SYMPATETIC AMINES : Methyldopa 250-2000mg daily in 1-4 divided doses. (Avoid large doses because of adverse reaction on the liver. VASODILATORS : Hydralazine 25-200 mg in up to 4 divided doses-useful in resistant hypertension. Newer drugs Vasopeptidase inhibitors Oral anti renin drugs Endothelin inhibitors

63. Diuretics Thiazide diuretics such as bendroflumethiazide (2.5–5mg daily) and cyclopenthiazide (0.25–0.5 mg daily) are well established agents which have been shown to reduce the risk of stroke in patients with hypertension. The lower doses seems to be equally effective as higher doses in the reduction of blood pressure and most have a duration of up to 24 hours. The major concern with these agents is their adverse metabolic effects, particularly increased serum cholesterol, impaired glucose tolerance, hyperuricaemia (which may precipitate gout) and hypokalaemia . These tend to occur with higher doses of thiazide diuretics.

64. Loop diuretics such as furosemide (40 mgdaily ) do have a hypotensive effect, but are not routinely used in the treatment of essential hypertension. Potassium-sparing diuretics such as amiloride (5–10 mg daily)or spironolactone (50– 200 mg daily) are not effective agents when used alone, with the exception of spironolactone in the treatment of hypertension and hypokalaemia associated with primary hyperaldosteronism.

65. Beta- adrenoceptor blockers Beta-blockers are no longer a preferred initial therapy for hypertension. beta-blockers are used in younger people, particularly those with an intolerance or contraindication to ACE inhibitors and angiotensin-II receptor antagonists; women of child-bearing potential; or patients with evidence of increased sympathetic drive. In these circumstances, if therapy is initiated with a beta-blocker and a second drug is required, add a calcium-channel blocker Rather than a thiazide-type diuretic to reduce the patient’s risk of developing diabetes.

66. Beta-blockers exert their effects by attenuating the effects of the sympathetic nervous and the renin–angiotensin systems. The major side-effects of this class of agents are bradycardia, bronchospasm, cold extremities, fatigue, bad dreams and hallucinations. These agents are especially useful in the treatment of patients with both hypertension and angina. The drugs include atenolol (50 mg daily), bisoprolol (10–20mg daily), metoprolol (100– 200mg in divided doses daily) and propranolol (160–320 mg in divided doses daily). Atenolol has been shown to reduce brachial arterial pressure but not aortic pressure, which is more significant in causing strokes and heart attacks.

67. Angiotensin-converting enzyme (ACE) inhibitors These drugs block the conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor. They also block the degradation of bradykinin, a potent vasodilator. There is evidence that black African patients respond less well to ACE inhibitors unless combined with diuretics. They are useful in diabetics with nephropathy, where they have been shown to slow disease progression, and in those patients with symptomatic or asymptomatic left ventricular dysfunction, where they have been shown to improve survival.

68. The major potential side-effects are profound hypotension following the first dose, which is usually seen in sodium depleted patients or in those on treatment with large doses of diuretics, and deterioration of renal function in those with severe bilateral renovascular disease (in whom the production of angiotensin II is playing a major role in maintaining renal perfusion by causing efferent arteriolar constriction at the glomerulus). They also cause mild dry cough in a number of patients, especially if prescribed at high doses, due to their effect on bradykinin. These are several ACE

69. These are several ACE inhibitors available. The drugs include enalapril (10–20mg daily), captopril (50–150mg daily) Ramipril (2.5– 10 mg daily), lisinopril (10–20 mg daily) and trandolapril (1– 4 mg daily).

70. Angiotensin II receptor antagonists This group of agents selectively block the receptors for angiotensin II. They share many of the actions of ACE inhibitors but, since they do not have any effect on bradykinin, do not cause a cough. They are currently used for patients who cannot tolerate ACE inhibitors because of persistent cough. Angioneurotic oedema and renal dysfunction are encountered less with these drugs than with ACE inhibitors. The agents include losartan (50–100 mg daily), candesartan (up to 32 mg daily), valsartan (80–160mg daily), irbesartan (75– 300 mg daily) and telmisartan (20–80 mg/daily).

71. Calcium-channel blockers These agents effectively reduce blood pressure by causing arteriolar dilatation, and some also reduce the force of cardiac contraction. Like the beta-blockers, they are especially useful in patients with concomitant ischaemic heart disease. The major side-effects are particularly seen with the

72. short-acting agents and include headache, sweating, swelling of the ankles, palpitations and flushing. Many of these side-effects can be lessened by the co-administration of a beta- locker. The short-acting agents, such as nifedipine (10–20 mg three times daily) are being replaced by once daily agents that are very well tolerated and include amlodipine (5–10 mg daily), felodipine (5–20 mg daily) and long-acting nifedipine (20–90 mg daily).

73. Alpha-blockers These agents cause post synaptic α1-receptor blockade with resulting vasodilatation and blood pressure reduction. Earlier short-acting agents caused serious first-dose hypotension, but the newer longer-acting agents are far better tolerated. These include doxazosin (1–4mg daily). Labetalol is an agent that has combined alpha- and beta-blocking properties, but is not commonly used, except in pregnancy-induced hypertension.

74. Renin inhibitors Aliskerin is the first orally active renin inhibitor which directly inhibits plasma renin activity: It reduces the negative feedback by which angiotensin II inhibits renin release. It has been used in combination with ACE inhibitors and angiotensin receptor blockers with a significant reduction in blood pressure. Side-effects are few but hypokalaemia occurs.

75. Other vasodilators These include hydralazine (up to 100 mg daily) and minoxidil (up to 50 mg daily). Both are extremely potent vasodilators that are reserved for patients resistant to other forms of treatment. Hydralazine can be associated with tachycardia, fluid retention and a systemic lupus erythematosus-like syndrome. Minoxidil can cause severe oedema , excessive hair growth and coarse facial features. If these agents are used, it is usually in combination with a beta-blocker.

76. Centrally acting drugs Reserpine is used in a low dose of 0.05 mg/day, which provides almost all its antihypertensive action with fewer side effects than higher doses. It has a slow onset of action (measured in weeks). Methyldopa is still widely used despite central and potentially serious hepatic and blood side-effects. It acts on central α2-receptors, usually without slowing the heart. Clonidine and moxonidine provide all the benefits of methyldopa with none of the rare (but serious) autoimmune reactions.

77. Management of severe or malignant hypertension Patients with severe hypertension (diastolic pressure > 140 mmHg), malignant hypertension (grades 3 or 4 retinopathy), hypertensive encephalopathy or with severe hypertensive complications, such as cardiac failure, should be admitted to hospital for immediate initiation of treatment. However, it is unwise to reduce the blood pressure too rapidly since this may lead to cerebral, renal, retinal or myocardial infarction, and the blood pressure response to therapy must be carefully monitored, preferably in a high dependency unit.

78. In most cases, the aim is to reduce the diastolic blood pressure to 100–110 mmHg over 24–48 hours. This is usually achieved with oral medication, e.g. atenolol or amlodipine. The blood pressure can then be normalized over the next 2–3 days.

79. When rapid control of blood pressure is required (e.g. in an aortic dissection), the agent of choice is intravenous sodium nitroprusside. Alternatively, an infusion of labetalol can be used. The infusion dosage must be titrated against the blood pressure response. Fenoldopam , a selective peripheral dopamine receptor agonist, is as effective as nitroprusside.

80. Prognosis The prognosis from hypertension depends on a number of features: ■ level of blood pressure ■ presence of target-organ changes (retinal, renal, cardiac or vascular) ■ coexisting risk factors for cardiovascular disease, such as hyperlipidaemia , diabetes, smoking, obesity, male sex ■ age at presentation. Several studies have confirmed that the treatment of hypertension, even mild hypertension, will reduce the risk not only of stroke but of coronary artery disease as well.

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