Human aspects of cardiovascular and renal pharmacology: Dysrhythmias Flashcards Preview

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Flashcards in Human aspects of cardiovascular and renal pharmacology: Dysrhythmias Deck (21):
1

Quinidine

VW class IA

2

Procainamide

VW class IA

3

Lidocaine

VW class IB
Local anaesthetic

4

Flecainide

VW class IC
Pro-dysrhythmic

5

Propranolol

D and L- propranolol have Class I actions
L-propranolol is a β-blocker (class II)

6

Atenolol

β1 antagonist (Class II actions)

7

Amiodarone

VW Class III
Inhibits both inward (Na and Ca) and outward (K) currents- AP duration would be shortened if inhibitory action was greater on inward than outward current, and vice versa.
Inhibition of inwards Na+ and Ca2+ currents show use-dependence (greater in tissues stimulated at higher frequencies), & also depends on voltage at which channels become de-inactivated (greater inhibition in tissues with less negative resting membrane potentials)
-> suppression of excitability & conductivity in both I[Na] and I[Ca] dependent cardiac tissues.
Various outward K+ channels also inhibited, but exactly which depends on [ ] of amiodarone present.

8

Verapamil

VW class IV

9

Nifedipine

Ca2+ channel blocker
Not effective as an antidysrhythmic
May be useful in myocardial salvage by decreasing Ca++ loading of damaged tissue.
Vasodilator effects reduce myocardial oxygen demand.

10

Adenosine

Antidysrhythmic, does not fit in VW classification
Acts on A1 receptors in AV node -> reduces cAMP levels via Gi.
Results in activation of I[K-ACh] current -> hyperpolarization of cardiac pacemaker & conductive tissue.
Used for certain supraventricular tachycardias, short half-life can have some advantages under these circumstances.

11

Cardiac glycosides

Antidysrhythmic, does not fit in VW classification
Increase vagal activity through an action in the CNS
Leads to inhibition at the AV node (slowing AV conduction)
Also affects arterial refractory period

12

Myocardial salvage

Ca2+ channel blockers e.g nifedepine may be useful by decreasing Ca++ loading of damaged tissue.
Beta-blockers will also decrease Ca2+ influx.

13

VW Class I

Block voltage gated Na+ channels- useful for suppression of inappropriate APs in cells that depend on VGNaC to generate the AP.
Subdivided into IA, IB, IC on basis of kinetics of association & dissociation with the channel, and effect on AP duration.

14

VW Class IA

Increased action potential duration
Intermediate rate of association/ dissociation
Affinity for open (activated) state > inactivated. Thus AP duration has no effect on drug action.
Show use-dependence at normal resting potentials
Work against atrial & ventricular dysrhythmias, but not commonly used.

15

VW Class IB

Decreased action potential duration
V fast association & dissociation
Affinity for inactivated > activated states. Thus influenced by length of AP.
Rate of dissociation during diastole decreases if MP is depolarised. As membrane repolarises & drug dissociates, effect removed.
Due to kinetics, most effective:
- at high rates of firing
- when diastolic (i.e resting membrane potential) is depolarised
- in parts of the heart where AP is longest.

16

VW class IC

No effect on action potential
Very slow association & dissociation -> thus good at suppressing ectopic heart beats (but also suppress everything else)
Pro-dysrhythmic. Only used in v unusual circumstances.
e.g flecainide

17

VW class II

Sympathetic (β1) antagonists
Decrease effects of catecholamines on the heart: negative chronotopic & inotropic.
Used in dysrhythmias when tissue abnormality leads to increased excitability: e.g MI, in which myocardium can become sensitised to catecholamines.

18

VW class III

Prolong the action potential and thus also the refractory period
Mechanism unclear- probably work by inhibiting K+ currents that result in repolarization.
May also prolong inactivation of Na+ channels- lengthening the AP, & helping to prevent re-entry & circus dysrhythmias.

19

VW class IV

Ca2+ channel blockers- reduce Ca2+ entry.
Selective for the myocardium.
Not normally used when cardiac function is severely compromised (after serious MI/ in cardiogenic shock)- as excessive amounts can inhibit contraction.

20

Sotalol

β-blocker
Also has class III actions.

21

Myocardium may become sensitized to catecholamines

Causes:
- after MI
- some drugs, e.g cardiac glycosides, volatile anaesthetics e.g halothane, chloroform.
Catecholamines can then produce enough inward current to produce APs & resultant ectopic foci.