Blood pressure Flashcards
what is stage 1 hypertension
clinical BP = 140/90 with ABMP or HBPM average BP = 135/85
what is stage 2 hypertension
clinic BP = 160/100 with ABMP or HBPM average BP = 150/95
what is stage 3 hypertension
clinic systolic > 180
clinic diastolic >110
if clinic BP is 140/90 or higher what should be done next
take a second measurement
offer ABMP to confirm diagnosis
offer HBPM is ABMP can’t be tolerated
how is HBPM measured
two consecutive measurements are taken at least 1 min apart with the person seated
BP is recorded twice a day, ideally morning and night for minimum 4 days, ideally 7
what is stage 3 hypertension also known as
severe hypertension
what should be done if a patient has suspected severe hypertension
start anti-hypertensives immediately while waiting for results of ABPM/HBPM
what should be done while awaiting confirmation of hypertension
investigations of target organ damage (e.g LV hypertrophy, CKD, hypertensive retinopathy)
formal assessment of cardiovascular risk
what is the first line treatment for a patient under 55 who is white
ACEI
what can ACEI be substituted for if it isn’t tolerated
ARB
what is the most common side effect for ACEI
dry cough
give examples of ACEIs
lisinopril, ramipril
ends “-pril”
give examples of ARBs
losartan, valsartan
ends “-sartan”
what is the side effect of ARBS
increase in blood potassium
what is the first line treatment for a black patient
Ca+ channel blocker
what is the first line of treatment for a patient >55
Ca+ channel blocker
what is the side effect of Ca+ channel blocker
swollen feet/ankles
give examples of Ca+ channel blocker
amlodipine, diltiazem, verapamil
what is the 2nd line of treatment
Ca+ channel blocker and ACEI/ARB
what is the 3rd line of treatment
Ca+ channel blocker and ACEI/ARB and thiazide-diuretic
what is the 4th line of treatment
refer to expert
add alpha or beta blocker
what type of hypertension would require a 4th step
resistant hypertension
give examples of thiazide diuretics
hydrochlorthiazide
indapamide
chlorthalidone
what are the common side effects of thiazide diuretics
GOUT, INCREASED URINATION, low sodium
what are the common side effects of alpha blockers
low BP
dizziness
give examples of alpha blockers
prazocin
doxazocin
what are common side effects of beta blockers
fatigue
depression
give examples of beta blockers
metoprolol
atenolol
ends “-olol”
what is essential hypertension
hypertension of unknown cause
what is secondary hypertension
hypertension resulting from a specific and potentially treatable cause
what is used to confirm white coat hypertension
AMBP
what non-pharmalogical interventions are recommended for hypertension
BMI<25 low fat and Na diet limit alcohol intake increase fruit, veg, and oily fish stop smoking
what is the mechanism of action of ACEI
inhibits the conversion of angiotensin 1 to angiotensin 2
what is the mechanism of action of ARB
blocks the effects of angiotensin 2 at the AT1 receptor
how can MAP be calculated
diastolic + 1/3 (systolic - diastolic)
[(2 x diastolic) + systolic]/3
what is a normal MAP
70-105
what is a normal systolic
<140
what is a normal diastolic
<90
what is pulse pressure
difference between systolic and diastolic BP
what are the main resistance vessels
arterioles
where are baroreceptors located
carotid bifurcation and the aortic arch
what are baroreceptors important for
moment-to-moment BP regulation
what is the baroreceptor reflex to DECREASED BP
decreased baroreceptor firing which:
decreases vagal activity and increases sympathetic activity + constrictor tone
this causes: increased HR, SV and vasoconstriction
what is the baroreceptor reflex to INCREASED BP
increased baroreceptor firing which:
increases vagal activity and decreased sympathetic activity + contractor tone
this causes: decreased HR, SV, and vasodilation
what are the 3 hormone pathways which control BP
RAAS
ADH (vasopressin)
NP
briefly describe the RAAS pathway
renin is released and causes angiotensinogen to be converted to angiotensin 1. this is then converted to angiotensin 2 by ACE. angiotensin 2 stimulates release of aldosterone.
what is the rate limiting step in the RAAS pathway
renin secretion
where is renin released from (RAAS pathway)
the kidney
what is the role of renin (RAAS pathway)
converts angiotensinogen to angiotensin 1
where is angiotensinogen produced (RAAS pathway)
the liver
where is angiotensin 1 formed (RAAS pathway)
the blood
where is ACE produced (RAAS pathway)
pulmonary vascular endothelium (lungs)
what is the role of ACE (RAAS pathway)
converts angiotensin 1 to angiotensin 2
what does angiotensin 2 do (RAAS pathway)
stimulates aldosterone release
vasoconstriction
increases thirst
increased ADH release
where is aldosterone produced
adrenal cortex
what does aldosterone do (RAAS pathway)
increases BP
increased plasma volume
increased Na and H20 reabsorption in kidneys
what does NP (natriuretic peptide) do
causes excretion of salt and water via the kidneys = decreases blood volume and BP
what are the 2 types of NPs, where are the located
atrial NP = stored in atrial muscle cells
brain-type NP = synthesised by heart ventricles, brain, and other organs
what systems acts as a counter-regulatory system for RAAS, how?
NP, decreases renin release
where is ADH synthesised and stored
synthesised = hypothalamus stored = pituitary gland
what does ADH do
increases reabsorption of water (increases plasma volume + BP)
causes vasoconstriction
