Drugs for Arrhythmias & CVS Flashcards
What happens if you completely block receptors of the heart with propranolol and atropine?
Nothing much. Heart beats on its own.
T/F the autonomic system controls the beating of the heart itself.
false. only the rate.
SA node depolarizes spontaneously with what ion? What’s the membrane potential?
Ca2+ at ~60mV - +20mV
What happens at phase 3 of SA node spontaneous depolarization?
K+ out
How does the parasympathetic slow down the SA node?
via ACh –>muscarinic (M2) receptors –>GPCR decrease cAMP = open K+ channels which slows down pre potential threshold.
how does sympathetic acceleration of SA node happen?
NA –>B1 adrenoreceptors –>GPCR –>increase cAMP, open Ca2+ channels which increases slope of pre potential threshold
What’s a risk of accelerating the SA node?
can trigger dysrhythmias
resting membrane of ventricular action potential?
-90mV
ventricular action potential depolarization involves which ion?
Na+ in
4 Symptoms of dysrhythmias:
SOB, faiting, fatigue, chest pain
3 mechanisms of dysrhythmias:
- altered formation (Nodes)
- altered conduction (extra beats, or conduction block)
- triggered activity (excess sympathetic
What is conduction block?
ventricles adopt their own slower pace than the nodes
4 classes of antidysrhythmics
- Na+ (mild, mod, strong) (1a, 1b, 1c)
- B-adrenoceptor antagonist (SA node)
- K+ blocker, delay phase 3
- Ca2+ blocker (great for SA AV nodes
Na+ blockers reduce slope 0 and peak of SA/AV nodes. T/F?
False. it’s of the ventricular action potential.
What’s quinidine? does two things to the action potential graph:
moderate Na+ channel blocker
- prolong repol
- increase effective refractory period
what’s ERP
effective refractory period
what’s flecainide? how does it effect ERP?
strong Na+ channel blocker no effect on ERP
what’s lignocaine?does two things to the action potential graph:
mild Na+ channel blocker
- shorten repol
- decrease ERP
What else does lignocaine do? why is it dangerous as a dysrhythmic?
local anesthetic. small therapeutic window
2 ways how B-adrenoreceptor antagonists work?
- inhibit sympathetic
2. stabilising purkinje fibres
K+ channel inhibitors do what to the graph?
prolong the phase 3
Long term use of Amiodarone?
pulmonary fibrosis
What is Amiodarone
K+ channel inhibitor antidysrhythmic
Ca2+ blockers do what 2 things?
slow conduction, increase refractory
What’s verapamil?
Ca2+ channel blocker for SA/AV nodes
BP must be what to be called hypertension?
> 140/90 mmHg
1 treatment for hypertension?
lifestyle mods
- no smoking
- diet
- weight
- stress
2 ways body controls BP:
neuronal, hormonal
Sympathetic alpha-1 adrenoreceptors do what?
constrict vessels
Sympathetic beta-1 adrenoreceptors do what?
increase heart rate
5 classes of antihypertensive drugs:
ABCDO
- angiotensin
- Beta adrenoreceptor
- calcium channel blockers
- diuretic
- other
Renin converts what to what?
Angiotensinogen to angiotensin 1
‘prils’
ACE inhibitors block ang1 to II
Contraindicated for ‘prils’ and ‘sartans’
- Preg
- bilat renal stenosis
- angioneurotic oedema
Blocking Ang 1 to 2 does what 4 things:
reduces
- vascular tone
- aldosterone production
- cardiac hypertrophy
- preent bradykinin breakdown
Candesartan and Losartan, which is long and which is short acting
Losartan = short, reversible Candesartan = long irreversible
‘sartans’ targets what?
angiotension 1 receptors
‘olols’ target what?
B-adrenoreceptors
Beta blocker does what two things to cardiac output?
reduce rate and contractility
Do beta blockers affect renin release?
Yep. Reduces it.
How do you get CNS effects with B-adrenoceptor antagonists?
cause it’s lipid soluble
B-adrenoceptor antagonists contraindicated in:
Diabetes, asthma, AV block
What’s diltiazem?
Ca2+ blocker, not as strong as verapamil
What are the dihydropyridines?
Ca2+ blockers, Felodipine, Nifedipine both vascular, careful with tachyarrhythmias
Thiazide Diuretics do what?
decrease Na and Cl in renal tubes, so more water is excreted, less fluid = less BP and blood volume
