Dr. Hasan Fahmawi, MRCP(UK), FRCP(Edin) Consultant Internal Medicine HYPERTENSION Dr. Hasan Fahmawi, MRCP(UK), FRCP(Edin) Consultant Internal Medicine

DEFINITION Hypertension is chronic elevation of blood pressure above normal levels. Normal levels are associated with lowest mortality and morbidity. Readings Systolic Diastolic Optimal 120 80 Normal 130 85 High normal 130-139 85-89 Grade I(mild) 140-159 90-99 Grade II(moderate) 160-179 100-110 Grade III(severe) +180 +110 Isolated systolic hypertension . Grade I 140-159 90 Grade II +160 90 Pseudo-hypertension Sclerotic arteries giving high readings.

CONFIRMING HIGH BP To avoid treating normotensive persons, white coat hypertension and masked hypertension. NICE GUIDELINES Home 24 hrs BP monitoring: Two times every hr.during waking hrs for 14 hrs.from 08-22 Morning and evening measurements for 07 days, discard the first 02 days and take the median of the rest, two readings every time with one minute apart.Cheque pulse for AF,radiofemoral delay and compare both hands before measurement.

MORBIDITY Hypertension is the most modifiable risk factor for coronary heart disease(first cause of death), stroke(third cause), congestive cardiac failure, ESRD and peripheral vascular disease. Pathogenesis-in large arteries more than 4mm in diameter, the internal elastic lamina is thickened, smooth muscle is hypertrophied and fibrous tissue is deposited. The vessel wall become more tortuous and less compliant. In smaller arteries less than 1mm, hyaline arteriosclerosis occurs in the wall, the lumen narrows and aneurysms may develope. These changes often aggravate hypertension by increasing peripheral vascular resistance and reducing renal blood flow, thus activating the renin-angiotensin aldosterone axis.

Incidence 30% of adult Americans are hypertensive. Polygenic aetiology.Most common in African Americans and Japanese.

Sphygmomanometers Intra-arterial measurements. Mercury, not used any more due to mercury toxicity Aerated. Digital.

Risk Factors Age, gender, weight, physical activity, smoking, family history, serum cholesterol, diabetes mellitus, and pre-existing cardiovascular disease. Illicit drugs, cocaine, amphetamine, Qat, and cyclosporine. Clinical features-discovered due to routine check-up, or due to complications, some times underlying cause leads us to the diagnosis, e.g. radio-femoral delay n coarctation of the aorta, palpable kidney in polycystic kidney, abdominal bruit in renal artery stenosis, and the characteristic facies and habitus of Cushing disease.

Examination Vital signs, BMI, CVS (MI, AF, HF., LVH, increased A2, 4th Heart sound), AD, Pulmonary Oedema. Auscultation of major arteries for bruit. Funduscopic examination for retinal changes. Neurological examination and carotid bruit. Abdominal examination. Lower limb examination for oedema and pulses. Look for endocrine cause as hypo-or hyperthyroidism, Cushing’s syndrome, Acromegaly, Hirsutism for congenital adrenal hyperplasia, Muscle weakness for primary adrenal hyperplasia.

INVESTIGATIONS Renal- urine analysis for albumin, blood urea, and creatinine. Electrolytes- Na, K, Ca. TFT Metabolic- FBS, Lipid profile. CBC, ECG, CXR. Lipid profile.

Investigations in resistant cases Refractory hypertension Patients with drug resistance, 4 or more drugs used to control BP particularly in young age group, farther investigations should be done. Hyperaldosteronism, plasma rennin/aldosterone ratio. Low plasma rennin high aldosterone. Low K. Renal artery stenosis, catheter based angiography. CT Angiography, MRI Angiography. Flash back pulmonary oedema, recurrent attacks of pulmonary oedema and high BP caused by renal artery stenosis.

Pheochromocytoma, 24 hrs urinary fractionated metanephrin and catecholamine or in the serum. MRI, CT, Metaiodobenzylguinidine scanning. Coarctation of aorta, CT or MRI.

Hypertensive emergencies, high BP with end organ damage, as hypertensive encephalopathy, acute pulmonary oedema, microangiopathic haemolytic anaemia, progressive retinopathy(arteriolar spasm, haemorrhage, exudates, papilloedema), deteriorating of renal function with proteinuria. BP must be controlled in ICU or HDU by Intravenous drugs down to 160/100-90 mmHg, because cerebral autoregulation of cerebral blood flow is shifted to higher levels of arterial BP and rapid lowering of BP to below lower limits of autoregulation may precipitate cerebral ischaemia or infarction or occipital blindness as consequence of reduced cerebral blood flow, renal and coronary blood flow might be reduced as well. The initial goal of therapy is to reduce mean arterial pressure 25% less or to 160/100-90 mmHg in 2hrs,this might be accomplished by IV therapy of nitroprusside, or labetolol, nitroglycerine NGT, or nicardipine. Hypertensive urgencies, is malignant hypertension without catastrophic events no end organ damage, a symptomatic, it is advised to reduce BP over longer periods by frequent dosing of oral medications and IV Lasix.

Accelerated hypertension Malignant hypertension Rare condition which can complicate hypertension of any aetiology. It is characterised by accelerated CV damage with necrosis in the walls of small arteries and arterioles (fibrinoid necrosis) and by intravascular thrombosis. The diagnosis is based on evidence of high PB and rapidly progressive end organ damage, such as retinopathy (grade 3 or 4), renal damage (especially proteinuria) and or hypertensive encephalopathy. LVF may occur, and if this is untreated, death occur within months.

Treatment of Hypertension Stop any medications which cause high BP, e.g. NSAID, steroids, oestrogen, sympathomimetic Stop any illicit drugs, cocaine and excessive alcohol consumption. Stop cabonexolone. Life style modification, low salt diet , wt. reduction, exercise, low dietary animal fat, stop smoking, take fresh vegetables and fruits. Treat vitamin D deficiency.

Medications A, C, D. ACE inhibitors for those younger than 55 years or ARBS Calcium Channel Blockers for those older than 55 years, if they fail to tolerate or has heart failure go to D Diuretics in old age.

Resistant Hypertension If BP is not controlled use combination therapy A+C or A+C+D. In cardiac arrhythmias, (AF) Heart failure or ischaemic heart disease B-Blockers can be used. In aortic dissection B-Blockers IV if needed. Pheochromocytoma alpha blocker 10-14 days before operation, Phenoxybenzamine is the preferred drug. BP is monitored twice daily in seated and standing position. Hypertension in diabetes mellitus normal below 135/85, if 24hrs proteinuria is over 1gm 125/75. In renal disease hypertension is a cause and consequence, and proper control of BP will delay it’s progression, best test for evaluation is renal biopsy to see degree of fibrosis. In acute myocardial infarction BP should be dropped to below 180-160/100-90 to give thrombolytic therapy.  

ASPIRIN Powerful means of reducing CV risk but may cause bleeding, particularly intracerebral haemorrhage, in a small number of patients the benefits are thought to outweigh the risk in hypertensive patients aged 50 or over who have well controlled BP and either target organ damage, DM or 10 year coronary heart disease risk of equal or over 15%.