Hypertension Flashcards
what is hypertension
high blood pressure above 140/90 in clinic or 135/85 not in clinic
causes of hypertension
essential/primary
or
secondary:
R - renal disease; could be renal artery stenosis
O - obesity
P- pre-eclampsia
E - endocrine (conn’s syndrome which is hyperaldosteronism)
what is hypertension a major risk factor for?
stroke IHD heart failure CKD cognitive decline premature death
for every 2mm rise in BP, risk increases by 10%
how do you measure BP NICE guidance
measure BP in both arms, if difference in readings between both is 15mmHg and then take the highest
if pulse irregularity: measure manually
if BP in clinic is 140/90 or higher, take second then third and then lowest
if BP is between 140/90 and 180/120, offer ambulatory BP monitoring to confirm the diagnosis of HT
what is ABPM and HBPM
ambulatory - reflects patients BP, constantly measures it over 24 horus
HPMB - allows patients to measure their own BP, 2 consecutive measures, twice daily, for 4-7 days and discard measurements
what are the stages of HT
stage 1: 135/85 to 149/94
stage 2: 150/95 to 179/119
stage 3: >180/120 (can result in hypertensive emergency aka malignant hypertension)
what is hypertensive urgency
systolic >180 mmHg or diastolic >110
what are the symptoms of HU
headache
SOB
nose bleed
severe anxiety
management of HU
oral anti-hypertensives
treat as outpatient
no target organ damage
what is hypertensive emergency
malignant hypertension
- high BP leads to target organ damage
- systolic >180, or diastolic >120
what are the symptoms of hypertensive emergency
chest pain SOB back pain numbness and weakness vision change difficulty
can have severe, permanent effects on brain, heart and kidneys
how do you manage hypertensive emergency
IV nitroglycerine on admission
then IV and oral hypertensive drugs:
- peripheral vasodilators
- adrenergic inhibitors - eg labetalol
reduce 25% of BP over first few hours, then slowly over the next 24-48 hours to normal:
rapid drop should be avoided bc may precipitate cerebral or cardiac ischaemia
what investigations would you do for end organ damage
bloods:
- u&Es, GFR: renal function
- HbA1c
- lipid profile
- urine albumin:creatinine ratio - for proteinuria and dispstick for microscopic haematuria to assess for kidney damage
ECG for cardiac abnormalities
what is eye damage in hypertension
hypertensive retinopathy
grade 1: arteriosclerosis with moderatue vascular wall changes, to more severe hyperplasia
grade 2: AV nipping; predisposes to branch retinal vein occlusion (painless temporary vision loss)
grade 3: flame haemorrhages and cotton wool spots
grade 4: papilledema (optic disc oedema and yellow, hard exudates
end organ damage - brain
hypertensive cerebrovascular disease
end organ damage - heart
left ventricular hypertrophy, IHD with or without heart failure
- concentric hypertrophy or LV muscles, eventually decreasing stroke volume
- cardiomegaly
- dilated LV - displaced apex beat
- hypertrophied LV - tapping, powerful, apex beat
end organ damage - kidney
hypertensive nephropathy
-decreased blood flow to the kidneys from arterioral vasoconstriction = renin release = resulting in worsening hypertension via angiotensin 2 and aldosterone
-damaged glomeruli and decreased eGFR
what is the qrisk score
an algorithm for predicting CV risk estimates the risk of a person developing CVD over the next 10 years
NICE
what are the lifestyle factors involved in hypertension
healthy diet salt - reduce dietary sodium intake coffee - discourage excess smoking alcohol intake - reduce if in excess regular exercise
what is first line treatment for hypertension
ACE-I or ARB’s: if patients have diabetes or if they are <55 or if they are not african caribbean
CCB: if >55, or black african or caribbean any age
what is the second line treatment
ACE-I or ARB’s
+
CCB or thiazide-like diuretic
if black, >55 etc, then CCB + ACE-I or ARB or thiazide
what is the third line treatment
ACE-I or ABR + CCB + thiazide
what is step 4 in hypertension treatment
confirm resistant hypotension, give spironolactone if blood potassium level is <4.5 or alpha-blocker or beta-blocker if potassium >4.5
what is pheochromocytoma
tumour of adrenal gland tissue
- paroxysmal elevations in BP
- triad of headache, palpitations and sweating
what is primary aldosteronism
adrenal gland produces too much aldosterone which is responsible for balancing potassium levels
unexplained hypokalaemia with urinary potassium wasting; however, more than one-half of patients are normokalemic
what is cushing’s syndrome
high levels of cortisol
cushingoid faces, central obesity, proximal muscle weaknes
may have a history of gcc use
this increase in gcc increases Na+ and H20 retention
what is sleep apnoea syndrome
primarily seen in obese men who snore loudly while asleep
breathing starts and stop, leading to lower amounts of oxygen inhaled and hence heart pumps harder which increases BP
what is coarctation of the aorta
congenital disease when aorta is unusually narrow
hypertension in arms wth diminshed or delayed femoral pulses and low or unobtainable BP in the legs
left brachial pulse is diminished and equal to the femoral pulse if origin of left subclavian artery is distal to coarctation
what is primary hyperparathyroidism
elevated serum calcium
what is the short term control of BP
short term: CNS response, baroreceptors and chemoreceptors
what do the baroreceptors do
- activated by stretch
- carotid and aortic body
important in maintaining postural BP
what are chemoreceptors
sensitive to low O2, high CO2 and acidosis
2 carotid bodies and 1-3 aortic bodies
reduction in blood flow causes metabolic stimulation excitatory effect on vasomotor centre
long term control: RAAS
liver releases angiotensin
forms angiotensin 1 (by renin from the JGA) = angiotensin 2 by ACE from lungs and endothelium
what does angiotensin 2 do
increases:
- sympathetic activity of ANS
- Na, Cl reabsorption and k, H+ excretion and H20 retention
- aldosterone secretion from adrenal gland, which does the same
- ADH secretion from the posterior pituitary gland, which increases H20 resoprtion
- systemic arteriolar vasoconstriction
what is JGA
juxtoglomerular apparatus
-macula densa: sense changes in NaCl delivery to the distal convuluted tubule and causes renin release and reduction of afferent arteriole resistance, increasing glomerular filtration
- juxtaglomerular cells
- mesangial cells
basic summary: pathophys of hypertension
- reduction in blood flow
- kidneys release renin
- leading to two pathways
first: aldosterone = increase in sodium and water reabsorption = increase blood volume = increases CO = increase in BP and reduction in blood flow
second: angiotensin = ang 1 –> ang 2 –> vasoconstriction –>PR –> increase in BP
in certain conditions you avoid ACE-I, why?
bc blocks ACE so no vasoconstricition of efferent arterioles which means less glomeruli filtration rate
what receptor does adrenaline work on and what is its clinical use
works on beta > alpha
anaphylactic shock, cardiogenic shock, cardiac arrest
what receptor does noradrenaline work on and what is its clinical use
B1 and alpha 1 more than the others
severe hypotension and septic sock
what receptor does dopamine work on and what is its clinical use
B1 = B2 > alpha 1
acute heart failure, cardiogenic shock
what receptor does dobutamine work on and what is its clinical use
b1>b2>a1
acute heart failure
cardiogenic shock
refractory heart failure
how is the BP controlled by the ANS
sympathetic vasomotor nerve fibres leave cord through T and L spinal nerves to form sympathetic chain
sympathetic nerves innervate viscera eg heart and bowels
spinal innervate vasculature
vagus nerve - PNS
what does the vasomotor centre consist of
- vasoconstrictor area - origin of excitatory preganglionic vasoconstrictor neurones (pass to sympathetic chain)
- vasodilator area - internal inhibition of vasoconstrictor area
- sensory area - input from vagus and glossopharyngeal nerves modulate vasoconstrictor / dilator area activity
how does the SNS raise arterial pressure
SNS release NA from nerve terminals
acts on the alpha-adrenergic receptors of the vascular smooth muscle
all arterioles remain in state of partial constriction in homeostasis
heart is directly stimulated
things not innervated: capillaries, pre-capillary sphincters)
