SVT Case Drugs

Question 1

Adenosine

Answer 1

Adenosine receptor agonist

MOA-
•Adenosine binds to A1 receptor on the surface membrane of the SA node cell which activates an inhibitory G protein
•Alpha subunit of the G protein breaks off and binds to adenylate cyclase and therefore inactivates it
•This inhibits cyclic AMP and therefore pka synthesis
•This decreases the influx of calcium ions into the cell and causes potassium efflux out of the cell
•This causes the SA node cell membrane to hyperpolarise
•The end result is to slow this nodal conduction
•Therefore , the dysrhythmic affect of adenosine is to delay the AP in the SA node
•Adenosine decreases heart rate at the SA node and reduces conduction velocity at the AV node

●Effects:
○Antiarrhythmic
○Relaxation of vascular smooth muscle
●Side Effects:
○Flushing
○Chest pain
○Difficulty breathing
○Light-headedness

Question 2

Propranolol

Answer 2

β-Adrenergic Antagonist (Beta-blocker)

MOA-
- Propranolol is a non-selective beta (acts on beta 1 in heart and beta 2 in lungs) adrenergic receptor blocker that acts by blocking beta 1 receptors on cardiac myocyte cells
- This inhibits the enzyme adenylate cyclase which means cyclic AMP cannot be synthesised.
- This inhibits the protein kinase A activity(PKA increases heart rate)
- Decrease in calcium influx through calcium channels
- Decrease in sympathetic effect on the myocardial cell = decrease in heart rate and contractility

●Effects:
○Prevention of migraines.
○Treat hypertension, MI etc.

●Side Effects:
○Bradycardia
○Hypotension
○Fatigue
○Dizziness
○Nightmares

Question 3

B-blockers

Answer 3

Beta blockers (beta-adrenergic blocking agents) are medications that reduce blood pressure. Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause the heart to beat more slowly and with less force, which lowers blood pressure. Beta blockers also help widen veins and arteries to improve blood flow.

Mechanism in cardiac muscle cells:

-Reduces adrenaline binding to B1 adrenoreceptors (G protein coupled receptors)
-Decreases intracellular levels of calcium as less influx through calcium channels (adenylate cyclase inhibited, less cAMP, inhibits pka)
-Reduced calcium binding to troponin
-Reduced actin-myosin cross-bridges form
-Reduced cardiac myocyte contraction
-Negative inotropy (decrease in contractility)

Mechanism in pacemaker cells:

-Block binding of adrenaline to B1 receptors
-Reducing rate of calcium influx
-Increases time taken to generate an action potential
-SA node= negative chronotropy, AV node= negative dromotropy

Non-selective- block B1 and 2 receptors
Cardioselective- target mainly B1 but target B2 at high doses