hypertension Flashcards
definition of HTN
Defined as systolic BP >140mmHg and/or diastolic BP>85mmHg measured on three separate occasions.
definition of malignant HTN
BP >=200/130mmHg.
aetiology of HTN
primary - essential/idiopathic HTN - commonest >90% cases
secondary
- renal - renal artery stenosis, chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney disease, chronic renal failure, polyarteritis nodosa, systemic sclerosis, atheroma, fibromuscular dysplasia
- endo - dm, hyperthyroidism, cushings syndrome, conn’s, hyperparathyroidism, phaeochromocytoma, congenital adrenal hyperplasia, acromegaly
- CVS - aortic coarctation, raised intravascular volume
- drugs - Sympathomimetics, corticosteroids, oral contraceptive pill, MAOI, cocaine, amphetamines
- preg - pre-eclampsia
- liquorice
pathology of HTN
fibrotic intimal thickening of arteries, reduplication of elastic lamina and smooth muscle hypertrophy
arteriolar wall layers replaced by pink hyaline material with luminal narrowing
white coat and masked HTN
white coat hypertension - elevated clinic pressure, normal ABPM. dont treat, but increased risk of developing HTN in future and CVD
masked hypertension is the opposite
malignant or accelarated phase HTN
A rapid rise in BP leading to vascular damage (pathological hallmark is fibrinoid necrosis).
- severe hypertension (eg systolic >200, diastolic>130mmHg) + bilateral retinal haemorrhages and exudates; papilloedema may or may not be present.
- Symptoms are common, eg headache ± visual disturbance.
- It requires urgent treatment, and may also precipitate acute kidney injury, heart failure, or encephalopathy, which are hypertensive emergencies.
- Untreated, 90% die in 1yr; treated, 70% survive 5yrs.
- It is more common in younger and in black subjects.
- Look hard for any underlying cause.
epidemiology of HTN
Very common.
10–20% of adults in the Western world.
sx of HTN
asymptomatic
symptoms of complications
symptoms of cause
sx of accelarated HTN
scotomas - visual field loss
blurred vision
headache
seizures
nausea
vom
acute HF
signs of HTN
Measure on two to three different occasions before diagnosing hyper-tension and record lowest reading.
loud 2nd heart sound
4th heart sound
examine for causes:
- radiofemoral delay, weak femoral pulse (aortic coarction)
- renal artery bruit (renal artery stenosis)
- palpable kidney
- cushings
end organ damage - fundoscopy for retinopathy, LVH, proteinuria - indicates severity = worse prognosis
Keith–Wagner classification of retinopathy
(I) ‘silver wiring’;
(II) as above, plus arteriovenous nipping;
(III) as above, plus flame haemorrhages and cotton wool exudates;
(IV) as above, plus papilloedema.
Ix for HTN
- blood - UE, glucose, lipids, ca
- urine dipstick - blood and protein
- ECG
- echo - LVH, past MI
- Ambulatory BP monitoring (BP measured throughout the day)
- fasting glucose
- cholesterol
- Renal ultrasound/arteriography (renal artery stenosis);
- 24h urinary meta-adrenaline
- urinary free cortisol
- renin
- aldosterone
- MR aorta - coarctation
*
ECG for HTN
LVH: deep S wave in V1–2, tall R wave in V5–6,inverted T waves in I, aVL, V5–6, left-axis deviation)
ischaemia.
why do ambulatory BP monitoring
Excludes ‘white coat’ hypertension,
monitoring of treatment response,
assesses preservation of nocturnal dip.
Mx approach for HTN
assessment and modification of CVS risk factors
treat underlying causes
conservative
- stop smoking
- lose weight
- reduce alcohol
- reduce dietry Na
- increase exercise
investigate for secondary causes - young patients, malignant hypertension or poor response to treatment
Reduce blood pressure slowly; rapid reduction can be fatal, especially in the context of an acute stroke.
medical
target BP
140/80 non-dm
130/80 dm without proteinuria
125/75 dm with proteinuria
150/90 if >80yrs
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Mx of acute malignant HTN
IV b-blocker, labetolol or hydralazine sodium nitroprus-side.
Avoid very rapid lowering which can cause cerebral infarction. bed rest.
Oral therapy unless encephalopathy or CCF
approach to encaphalopathy in HTN
headache, focal CNS signs, seizures, coma
aim to reduce BP to 110 diastolic over 4hrs
admit
arterial line
Either IV labetalol (eg 50mg IV over 1min, repeated every 5min, max 200mg) or sodium nitroprusside infusion (0.5mcg/kg/min IVI titrated up to 8mcg/kg/min, eg 50mg in 1L glucose 5%; expect to give 100–200mL/h for a few hours only, to avoid cyanide risk).
medical Mx of HTN
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complications of HTN
HF
CAD and MI
CVA
PVD
emboli
retinopathy
renal failure
hypertensive encephalopathy
posterior reversible encephalopathy syndrome
malignany hypertension
premature death
50% of all vascular deaths
Px of HTN
good if BP controlled
Uncontrolled hypertension linked with increased mortality (6x stroke risk and 3x cardiac death risk).
Treatment reduces incidence of renal damage, stroke and heart failure.
when to treat HTN
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persistent HTN
High blood pressure at repeated clinical encounters
stage 1 HTN
clinic: 140/90 - 159/99
ABPM or HBPM 135/85 - 149/94
stage 2 HTN
clinic - 160/100 - 180/120
ABPM or HBPM >150/95
stage 3 HTN
clinic - >180/120