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HYPERTENSION (HYPERTENSIVE EMERGENCIES (CLINICAL FEATURES (SYSTEMIC…
HYPERTENSION
HYPERTENSIVE EMERGENCIES
TYPICALLY >180 SYST AND >110 DIAST causing end organ compromise, typically encephalopathy, renal failure, myocardial ischaemia and retinopathy. The presence
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Accelerated HTN is where there is a recent elevation in baseline BP that is not assoc with papilloedema (there may be other retinal changes)
Malignant HTN requires the presence of papilloedema. Important complications conclude MI and intracranial haemorrhage.
AETIOLOGY
majority occur in pts with primary/essential HTN that has been undiagnosed or inadequately managed. up to 1% of those with essential HTN will suffer a hypertensive emergency
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CLINICAL FEATURES
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EXAMINATION FINDINGS
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retinal changes (haemorrhages, papilloedema)
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FIRST LINE
Blood tests: FBC, U&Es, creatinine, TFTs
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CXR: to exclude aortic dissection and complications of MI or HTN itself: both HTN and an MI may cause for eg LV dysfunction and HF
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SECOND LINE
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24hr urinary free cortisol excretion measurement (twice) and/or the overnight 1mg dexamethosone suppression test if suspected Cushing's syndrome
urine/plasma metanephrine: if suspected phaeochromocytoma (triad of headache, palpitations and HTN)
coarctation of the aorta - BP measurement of upper and lower limbs (typically higher in upper and low in lower); echo can establish presence and severity; MRI/CT can localise and grade and assess presence of collaterals
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PATHOPHYSIOLOGY
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BP regulation in HTN pts
an inc in BP = inc urine production and Na excretion to reduce intravasc vol and return atrial press to normal
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BARORECEPTORS ARE NOT INVOLVED in regulation of chronic HTN as they constantly reset themselves usually after 24-48hrs of high bp
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SECONDARY HTN
RENAL CAUSES
Parenchymal damage to the kidney causes: reduced Na and water excretion; increased intravascular volume and cardiac output
stenosis of the renal arteries due to atherosclerosis or fibromuscular dysplasia causes: dec renal perfusion, inc renin prod, inc ang II and aldosterone levels, vasoconc, inc Na and water retention
MECHANICAL CAUSES
Coarctation of aorta: obstruct BF to kidneys, stimulate RAAS; inc bp flow in area adjacent to aortic narrowing, lead to accelerated atherosclerosis and stiffening of aorta. Baroreceptor response to raised arterial pressure is lost
ENDOCRINE CAUSES
Conn's syndrome - secrete excess mineralocorticoids (primary aldosteronism) - inc reabsorption of Na at distal convoluted tubule and collecting duct. Inc K+ excretion in the urine
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Phaeochromocytoma: secrete catecholamine - excess of this causes vasoconstriction and tachycardia (sympathetic activation)
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MANAGEMENT
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initiating treatment
treatment threshold:
pts <80 yrs with stage 1 HTN who have target organ damage, CV or renal disease or diabetes
pts with stage 2 HTN, regardless of age
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GUIDELINES
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STEP 3
Triple combo - ACEi/ARB, CCB and thiazide-like diuretic
STEP 1
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55/AfroCarrib = CCB. add thiazide-like diuretic if develop SE (periph oedema) or evidence of HF or high risk of failure
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CLINICAL FEATURES
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SYMPTOMS
excess catecholamines (phaeochromocytoma): headaches, paroxysmal seats, palpitation
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step 2
ABPM (24hrs) - 2 readings per hour between waking hours (0800 - 2200), avg of a minimum of 14 readings required for diagnosis of HTN
alternative HBPM - lasts 4 days, BP measured twice a day, each entry should be the avg of 2 readings, taken at least 1 minute apart with the pt sitting down
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WHITE COAT HTN
TREATMENT TARGET FOR <80 = <135/85, >80 = <145/85
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50% OF HTN PTS UNTREATED BP WILL DIE FROM CAD OR HF
1/3 WILL HAVE STROKE
10-15% WILL DIE FROM RENAL FAILURE AND ITS SEQUELAE