Session 3 Hypertension and Heart Failure Flashcards
calculation for MAP
MAP = CO x TPR
calculation for CO
CO = SV x HR
If your blood pressure decreases, how does the body respond to try and increase it back to the norm?
- Increased sympathetic activity which leads to 3 things:
1. activation of b1 adrenoceptors on the HEART = increased cardiac output
2. activation of a1 adrenoceptors on smooth muscle = increased venous return and increased peripheral resistance (due to vasoconstriction of smooth muscle)
3. activation of b1 adrenoceptors on kidney = increased renin
Decreased BP will also lead to decreased RBF and decreased GFR. Decreases lead to an increase in renin which increases the amount of angiotensin II = increased peripheral resistance and increased aldosterone = increased sodium and water retention to increase circulating blood volume
formula for resistance to flow?
= 8nL / pie x r4
r4 = radius of vessel which is the main determinant of flow!
outline the proposed pathophysiology of hypertension
elevated blood pressure leads to vascular changes which include remodelling and thickening plus hypertrophy
elevated BP leads to increased vasoactive substances (angiotensin II)
vascular remodelling can occur as a direct result of local salt sensitivity
hyperinsulinemia and hyperglycaemia can lead to endothelial dysfunction and ROS which decreases NO - this leads to permanent and maintained medial hypertrophy of vasculature (which will increase TPR and decrease compliance)
why is hypertension difficult to treat?
often presents asymptomatically so problems with adherence to treatment are common
define hypertension
= an elevation in BP that is associated with an increase in risk of some harm
= significantly high to cause end organ damage
= elevated BP that treated will do more good than harm
what BP is classed as hypertension?
140/90 mmHg (if under 80 years old inc. type 2 diabetes)
150/90 mmHg > 80 years old
135/85 mmHg type I diabetes
what is the most common ‘type’ of hypertension?
essential / primary / idiopathic = 90% of cases
i.e. don’t know how it occurs
Hypertension staging: 'desired' = stage 1 hypertension = stage 2 hypertension = stage 3 (severe) hypertension =
ABPM or HBPM
'desired' = 120/80 stage 1 hypertension = 140/90 stage 2 hypertension = 160/100 stage 3 (severe) hypertension = 180 systolic OR 120 diastolic
ABPM or HBPM
stage 1 = 135/85
stage 2 = 150/95
what BP is classes as ‘prehypertension’?
> 120/80 to <140/90
if someone presents as being prehypertensive, what can we do to reduce CVD risk?
promotion of regular exercise
modified diet/ balanced diet
reduction in stress and increased relaxation
limited or reduced alcohol intake
discourage excessive caffeine consumption
smoking cessation
reduction in dietary sodium
How do ACE inhibitors work?
inhibit circulating and tissue ACE (angiotensin converting enzyme) which converts angiotensin I to angiotensin II
therefore reduces angiotensin II which results in:
- vasodilation = leads to decreased peripheral vascular resistance which leads to a decreased afterload
- decreased aldosterone release = increased salt and water excretion which decreases circulating blood volume
- reduced ADH release = increased water excretion which decreases circulating blood volume
- reduced cell growth and proliferation of SM cells
What are two names of ACE inhibitor drugs?
lisinoPRIL
ramiPRIL
Problems with ACE inhibitors?
bradykinin is also a substrate for ACE so the use of ACE inhibitors therefore potentiates bradykinin
can lead to vasodilation via NOS/NO and PGI2
What are the side effects of ACE inhibitors?
hypotension
dry cough (associated with bradykinin)
hyperkalaemia (due to low aldosterone which leads to increased K+)
renal failure (especially renal artery stenosis where constriction of efferent arteriole is needed!)
angioedema (bradykinin is more common in black population)
What are the warnings/contraindications of ACE inhibitors?
these are the same for ARBs
renal artery stenosis acute kidney disease pregnancy breastfeeding chronic kidney disease (caution only)
what are the important interactions of ACE inhibitors?
these are the same for ARBs
drugs that increase K+
NSAIDs
other antihypertensive agents
What are 2 names of Angiotensin-II receptor blockers (ARBs)?
ARBs are also known as angiotensin II blockers, or AT1 receptor blockers
CandeSARTAN
loSARTAN
How do ARB’s work?
block angiotensin II from binding to AT1 and AT2 receptors
there is no effect on bradykinin so they are less effective in low-renin hypertensives (but decreased dry cough and decreased angioedema)
they directly target AT1 receptors so are more effective at inhibiting Angiotensin II mediated vasoconstriction
(as opposed to ACEi as angiotensin II is also produced from angiotensin I independently of ACE via chymases)
L-type calcium channels
what do they allow?
type of channel?
expressed where?
- allow inward Ca2+ flux into cells
- voltage gated calcium channels
- expressed throughout body - including vascular smooth muscle cells and cardiac myocytes plus SA and AV node
What do calcium channel blockers target?
target calcium initiated smooth muscle contraction in hypertension
how many classes of CBB are there? where do they act?
3 - all acting on different sites on alpha1 subunit of VOCC -
