Drugs Affecting Cardiac Rate And Force

Front 1

tachyarrhythmia

Back 1

includes atrial fibrillation, supraventricular tachycardia, ventricular tachycardia and ventricular fibrillation. Increase in HR

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bradyarrhythmias

Back 2

include heart block and asystolic arrest, which decrease HR. Opposite of tachyarrhythmia

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ecotopic focus

Back 3

when one region of myocardium depolarises spontaneously and is not linked with other electrical signals coming from other structures

Front 4

delayed after depolarisation

Back 4

phenomenon which occurs at phase III of the cardiac AP, and can lead to spontaneous activity due to calcium overload

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Vaughan-Williams systems of classification

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groups anti-arrhythmic drugs based on their electrophysiological effects.

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Different classes of Vaughan-Williams system

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Class I: Drugs that block voltage-sensitive sodium channels

Class II: B-adrenoceptor antagonists

Class III: drugs that prolong the cardiac action potential/K+ channel blockers

Class IV: calcium channel antagonists

Front 7

Class I drugs mechanisms and examples

Back 7

bind to alpha subunit of sodium channels to prevent Na+ entry.
Affect phase 0.
Some drugs such as lignocaine, flecainide and other local anaesthetics display use-dependent block.
Use-dependent block allows class I drugs to block high-frequency tachyarrhythmias without preventing normal beat frequency

Front 8

subunits of Class I drugs

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a, b and c.
Based on affinity/disassociation of the drug from the Na+ channel.

Note: anti-arrhythmic drugs affects RMP of cardiomyocytes can therefore increase the risk of arrhythmia

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Class II drugs mechanisms and examples

Back 9

Prevents Beta 1 adrenoreceptors from increasing HR.
Affects various phases.
As B-adrenoreceptor antagonists have anti-sympathetic effects (depress SA and AV node activity/conduction).
Propanolol is a non-selective beta adrenergic antagonist.
atenolol and metoprolol are B1-selective antagonists

Front 10

Why is atenolol and metoprolol better used following a myocardial infarction

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prevents non-selective B-antagonists binding to B2 receptors in the bronchi causing spasm, among other things like cold extremities, bradycardia and hypotension

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Class III drugs mechanisms and examples

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Prolong the plateau phase of the cardiac AP.
Believed to block the potassium channels in repolarization.
Affects phase III
Drugs include amiodarone and sotalol

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Class IV drugs mechanisms and examples

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Antagonists of voltage-sensitive L-type calcium channels, which shorten the plateau phase of the cardiac AP. Can also reduce AP generation in auto rhythmic cells and lowers the Ca2+ concentration in the cytosol of contractile cells, reducing the force of contractions as well.
Affects the plateau phase II
Drugs include verapamil and diltiazem

Front 13

Adenosine

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produced from ATP/ADP.
Acts at cardiac A1 adenosine receptors that are coupled to Gi.
Results in opening of K+ channels and hyperpolarization.
Short-lived and administration prevents tachycardia

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Dobutamine

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B1 agonists, which are positive inotropes, which increase contractile force

Front 15

Phosphodiesterase (PDE) and PDE inhibitors

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degrades cAMP and cGMP with different mechanisms for each.
PDE inhibitors such as Milrinone stop the degredation of cAMP and increased intracellular calcium concentration and prolonged contraction.

Front 16

Digoxin

Back 16

A cardiac glycosides have a steroid moiety. It acts on sodium/potassium ATPase on the extracellular binding site and inhibits the pump, changing the RMP by increasing intracellular sodium concentration. It also reduces the gradient and therefore the activity of the 3 sodium/ 1 calcium exchanger, allowing increased intracellular calcium, having a positive ionotropic effect and increasing the force of contraction. Calcium is then taken up into the SR.