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Flashcards in Cardiology Deck (26):

What are the two effects of local anaesthetics?

Anaesthetic properties on sensory nerves and antidysrhythmics due to action on cardiac Na channels.


What are the 5 types of anaesthetic application?

Surface, infiltration, intrathecal, nerve block and epidural.



Blocker of neuronal VG Na channels. Mutations in Glu387 of S6 of domain I leads to loss of TTX binding.



Blocks VG Na channels. Acts on intracellular portion to prevent inactivation and to move the membrane potential to more negative potential so channels open more readily.


Alpha-scorpion toxin

Blocks VG Na channels. Acts from outside of the Na channel to inhibit inactivation. In combination with batrachotoxin leads to near permanent opening.


Benzocaine and lidocaine

Local anaesthetics. Must be uncharged to cross the membrane and become charged in the cell, gaining access to the intracellular portion of the VG Na channel. Can act in uncharged (hydrophobic) form as it crosses the cell membrane. Exhibit use dependence - the more the channel is open, the more likely it is to be blocked.


What do local anaesthetics mainly do?

Prolong/enhance inactivation of the channel. The S6 region of domain IV confers anaesthetic selectivity.



L-type Ca channel antagonists. General consensus is that they bind to pore-lining region of domain IV. Binding is enhanced by depolarisation of the cell membrane, suggesting binding to the inactivated channel. Do not show use dependence.



Dihydropyridine - L-type Ca channel antagonist.


BAY K 8644

Dihydropyridine - L-type Ca channel agonist.


What effect do catecholamines have on the heart?

Stimulate beta-2 receptors. L-type Ca channels are phosphorylated by PKA - activated. Ryanodine receptors sensitised - positive ionotropic effect. Current at which If is activated shifts to a more positive potential so more frequent contractions - positive chronotropic effect. Various delayed rectifier K+ channels producing depolarisation are enhanced - positive chronotropic effect.


What effect does ACh have on the heart?

M2 receptors localised in nodal tissue. Gi coupled so decrease in cAMP. Negative chronotropic effect due to decreased Ca currents but little effect on ionotropic effect as receptors localised to nodal tissue. Negative chronotropic effect due to If current activation shift to more negative potentials. I(K-ACh) also activated - hyperpolarise cell so more difficult to elicit APs.


Why is the SAN the dominant pacemaker in the heart?

It has a higher frequency discharge than other pacemaker tissues (70 min-1). Stimulates other pacemaker cells to fire before their If current elicits an action potential.


What is an ectopic pacemaker?

A pacemaker at a site other than the SAN.


How is the heartbeat well organised?

3D branching arrangement of conduction fibres. Collision of fibres that extinguish each other. Channels become refractory preventing re-excitation at an inappropriate time.


What can disrupt the electrical properties of the heart?

SAN not functioning properly so ectopic foci develop. Damage to the myocardium.


What is the difference between a myocardial infarction and angina pectoris and the damage caused?

Myocardial infarction - part of the myocardium becomes hypoxic and loses function. Replaced by connective, non-conductive tissue. Angina pectoris - part of the myocardium becomes ischaemic and cannot operate efficiently but the tissue is still conductive.


What do class IA antidysrthymics do?

Block VG Na channels. Intermediate association/dissociation rate. Increased affinity for the open state - exhibit use dependence. Increase AP duration - but AP length has no effect on the action. E.g. Quinidine.


What do class IB antidysrthymics do?

Block VG Na channels. Fast association/dissocation. Greater affinity for inactivated states than activated states. Influenced by the length of the AP. Most effective in tissues with high firing rates, RMP at which the membrane is depolarised and in parts of the heart where the AP is the longest. E.g. lidocaine


What do class IC antidysrythmics do?

Block VG Na channels. Slow association/dissocation rates. Good at suppressing entropic beats but also good at suppressing everything. Pro-dysrhythmic. e.g. flecainide


What do Class II antidysrthymics do?

Beta-1 antagonists. Decrease the effect of catecholamines onto the heart. Negative chronotropic and negative ionotropic effects. Can be used in myocardial infarction where myocardium can become sensitised to catecholamines. E.g, atenolol


What do class III antidysrhythmics do?

Ca channel blockers e.g. amiodarone. Mechanism unclear. Prolong AP and refractory period. Shown to effect both outward and inward currents.


What do class IV antidyrhythmics do?

Ca-channel antagonists. E.g. verapamil. Must not be given excessively as would inhibit the contraction due to Ca importance in excitation-contraction coupling.


How is nifedipine helpful in myocardial salvage?

Nifedipine blocks L-type Ca channels, reducing Ca loading into the cell which can lead to cell death. Also has vasodilator effects, decreasing the oxygen demand of the tissue.



Anti-Dysrhythmic - binds to A1 receptors which are Gi coupled. Decreases cAMP and activates I (K-ACh) hyper polarising cardiac pacemaker and conductive tissue. Used in supra ventricular tachycardia.


Cardiac glycosides

Anti-dysrythmic - increase vagal activity by action in the CNS. Inhibition at the AV node. Also affects the AP refractory period.