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TREATMENT OF SEVERE HYPERTENSION IN LOW RESOURCE SETTING Brian Rayner, Division of Hypertension, University of Cape Town Cardiovascular Mortality Risk Doubles with Each 20/10 mmHg Increment in Systolic/Diastolic Blood Pressure* CV mortality risk 8 8X risk 6 4 4X risk 2 0 1X risk 2X risk 115/75 135/85 155/95 175/105 Systolic BP/Diastolic BP (mmHg) *Individuals aged 40–69 years Lewington et al. Lancet 2002;360:1903-1913. TABLE 3 Definitions and classification of office blood pressure levels (mmHg) Copyright © 2013 Journal of Hypertension. Published by Lippincott Williams & Wilkins. Mancia, GiuseppeJournal of Hypertension. 31(7):1281-1357, July 2013. DEFINITIONS • Asymptomatic severe • Hypertensive urgency* • Hypertensive emergency* • * BP usually > 220/120 • * Frequent in young black men without obvious risk factors Definitions • Urgency – Severe hypertension with symptoms • Emergency (impending or progressive OD) – – – – – – – hypertensive encephalopathy cerebral infarction intracranial haemorrhage acute pulmonary oedema aortic dissection renal failure eclampsia Epidemiology • The syndrome of hypertensive emergency was first described by Volhard and Fahr in 1914 • In 1939 the1-year mortality of 79% and a median survival of 10.5 months • Approximately 1% of patients with hypertension will develop a hypertensive crises at some point during their lives. 7% before BP treatment • Parallels the distribution of essential hypertension in the community, being much higher among African-Americans and the elderly; however, men are affected two times more frequently than are women • Most previously been diagnosed as hypertensive and many have been prescribed antihypertensive therapy with inadequate blood pressure control • Illicit drug use has also been reported to be a major risk factor for the development of hypertensive emergency CAUSES • Most in Africans is primary hypertension • Risks are related to the severity of the underlying hypertension • Mechanical stress on the vessel wall appears to be critical in its pathogenesis • Vicious cycle of further vascular injury, tissue ischemia, and release of vasoconstrictor substances especially from the kidney • Volume depletion that results from pressure natriuresis further simulates the release of vasoconstrictor substances from the kidney • Activation of the RAAS has been strongly implicated in the initiation and perpetuation of the vascular injury • Vasopressin, endothelin and catecholamines are also implicated Also eye and brain Causes • • • Severe HT DM Stiff arteries KEY ASSESSMENTS • Adherence to medication • Symptoms – headache, chest pain, SOB • Consider secondary causes e.g. pulses, bruits, symptoms of phaeo • JVP, basal crackles • Fundi • Oliguria • Urine – blood and/or protein – settles with treatment FUNDI INVESTIGATIONS • ECG – LVH plus RCs • CXR – heart size, ULVD, pulmonary oedema, dissection • K+ - often low due to secondary hyperaldosteronism (primary aldo seldom causes hypertensive emergency) • Creatinine – often elevated and continues to rise • FBC – Hb due to micro-angiopathic haemolytic anaemia, ↑LDH R in AvL > 11 Cornel – (S in V3 + R in aVL + 6 in females) x QRS duration > 2440 >35 – Sokolow-Lyon) Harbinger of death ASYMPTOMATIC SEVERE • No symptoms, no impending or progressive TOD • Start any 2 of first line drugs in combination – ACE or ARB – CCB – Thiazide or thiazide like diuretic • Review within 1 week and escalate as needed URGENCY/EMERGENCY – KEY ISSUES • Loss or marked shift of autoregulation in eye, kidney, brain • Excessive lowering of BP can lead to stroke, visual loss and worsening kidney failure • ICU admission • Intra-arterial monitoring • Recommended 25% lowering in first few hours with intravenous therapy - labetalol, Na nitroprusside (avoid if AKI), or nitroglycerin (preferred if ischaemia) by titration • Furosemide if pulmonary oedema, possibly acute dialysis • Thereafter institution of long term oral treatment once stabilised LOW RESOURCE CENTRE • Often treated in the emergency unit or general ward • Intensive monitoring not feasible • Oral treatment often only option • Potential for excessive drops in BP that can’t be detected early or easily reversed easily SAHS 2014 ACE INHIBITORS • Hypertensive emergencies are often association with volume contraction • Marked activation of RAAS • Hence propensity to cause profound drops in BP • Preferably used once patient is more stable Nifedipine Dosing Clinical features Loading dose Maintenance BP > 130 mmHg 20mg PO or SL 10 every 30 min until target BP BP 115-130 10mg PO or SL 5-10 mg BP < 115 5-10 mg PO or SL 5mg Elderly, CAD, prior CVA, volume depletion, anti HPT drugs 5mg PO or SL 5mg Nifedipine Advantages • Rapid consistent BP lowering • Admission to hospital not always required • Reflex tachycardia common, but angina and MI uncommon • Improvement in CCF • Numerous dosage forms • Side effects minor and frequent Disadvantages • • • • Potential for hypotension and stroke Worsening of renal function Possible cerebral oedema (theoretical) Negligible buccal absorbtion Effect of Nifedipine Formulation on Concentration Time Profiles: Hypertensive Patients 200 Nifedipine Capsule (20mg) plasma conc (ng/ml) 150 100 Nifedipine Retard (20mg) 50 Nifedipine GITS (60mg) 0 0 4 8 12 Time (h) 16 20 24 Meredith & Elliott 2004 Effect of Nifedipine Formulation on Heart Rate Responses – Placebo-Corrected : Hypertensive Patients 50 Nifedipine Capsule (20mg) Heart Rate (beats/min) 40 30 20 Nifedipine Retard (20mg) 10 0 Nifedipine GITS (60mg) -10 0 4 8 12 Time (h) 16 20 24 Meredith & Elliott 2004 Effect of Nifedipine Formulation on Systolic BP Responses – Placebo-Corrected : Hypertensive Patients 5 Nifedipine Capsule (20mg) Systolic BP (mmHg) 0 -5 Nifedipine Retard (20mg) -10 -15 Nifedipine GITS (60mg) -20 -25 -30 0 4 8 12 Time (h) 16 20 24 Meredith & Elliott 2004 • Nifedipine not been approved by the FDAQ for labelling for treatment of hypertensive emergencies or of any other form of hypertension because of lack of outcome data • A review of the literature revealed reports of serious adverse effects such as cerebrovascular ischemia, stroke, numerous instances of severe hypotension, acute myocardial infarction, conduction disturbances, fetal distress, and death • Sublingual absorption of nifedipine has been found to be poor; most of the drug is absorbed by the intestinal mucosa • Given the seriousness of the reported adverse events and the lack of any clinical documentation attesting to a benefit, the use of nifedipine capsules for hypertensive emergencies and pseudoemergencies should be abandoned. APPROACH • History, examination • Basic tests, ECG, Na, K, creatinine, Dipsticks, CXR • Best to admit to ward or clinic area where patient can be monitored • Half hourly pulse and BP • Labetalol 20mg IVI repeated at 10 min intervals up to maximum of 80mg • or Start single oral drug MEDICATION • Furosemide if CCF or pulmonary oedema • Start nifedipine GITs 30 mg stat, do not chew or crush • Monitor BP, urine output, and neurological status • If poor response, take another 30mg • Continue to monitor ½ hourly BP • If BP drops > 25% consider giving fluids, elevate foot of bed especially if patient shows clinical deterioration Following Day • Check elecs and renal function • Monitor vital signs and clinical status • 25% lowering achieved continue nifedipine 30-60 mg • Not achieved – add second drug (diuretic/beta blocker) • After 48 hours aim to achieve BP closer to target • Consider ACE inhibitor • Monitor as out patient CONCLUSIONS • Treatment of severe hypertension is not based on RCTs and is largely observational • Treatment in low resource setting is even less well documented • A practical approach is given based largely on my personal perspective