Session 9

Question 0

What are the causes of arrhythmias?

Answer 0

Ectopic pacemaker activity e.g. latent pacemaker region activated due to ischaemia
After depolarisations - abnormal depol following an AP
Re-entry loop - conduction delay, accessory pathway

Question 1

What is an arrhythmia?

Answer 1

Abnormality of heart rate and rhythm e.g. bradycardia, atrial flutter, atrial fibrillation,, tachycardia (ventricular/supraventricular),ventricular fibrillation - emergency

Question 2

What effect does increase [Ca2+]i have?

Answer 2

Delay after depolarisation. Early after-depolarisation can lead to oscillations –> more likely to happen if AP is prolonged. Longer AP = longer QT.

Question 3

What is the re-entrant mechanism for generating arrhythmias?

Answer 3

Incomplete conduction damage (unidirectional block). Excitation can take a long route to spread the wrong way through the damaged area, setting up a circus of excitation.

Question 4

What are the four types of drugs that can be used to treat cardiac issues?

Answer 4

Na+ channel blockers
Antagonists of beta-adrenoreceptors
K+ channel blockers
Ca2+ channel blockers

Question 5

Give an example of a Na+ channel blocker

Answer 5

Lidocarine (local anaesthetic). Only block Na+ channels in open or inactive state. Dissociates rapidly in time for next AP. Won’t block uptake of Na+. By blocking Na+ channels, lidocarine prevents automatic firing of depolarised ventricular tissue.

Question 6

Give an example of beta adrenoreceptor antagonists

Answer 6

Atenolol (beta blockers). Block sympathetic activity by acting at beta1-adrenoreceptors in heart (decreases the slope of the pacemaker potential). Used following MIs. Can slow conduction in AVN.

Question 7

Give an example of a K+ channel blocker

Answer 7

Amiodarone. Prolongs AP by blocking K+ channels, thus lengthening the absolute refractory period.

Question 8

Give an example of a Ca2+ channel blocker

Answer 8

Verapamil. Decreases the slope of the pacemaker potential, decreases AVN conduction, decreases force of contraction (negative inotropy).

Question 9

What types of drugs are used in heart failure?

Answer 9

Positive inotropes increase cardiac output e.g. cardiac glycosides and beta-adrenergic antagonists

Question 10

Give an example of a cardiac glycoside

Answer 10

Digoxin (prototype) –> extracted from leaves of foxglove. Blocks Na+/K+ ATPase pumps. Ca2+ is extruded via Na+-Ca2+ exchanger. Due to blockage of the Na+/K+ ATPase pump there is an increase in [Na+], causing decreased activity of Na+-Ca2+ exchanger = increased [Ca2+] therefore increased force of contraction

Question 11

Give an example of a beta adrenoreceptor agonist

Answer 11

Dobutamine. Acts on beta 1 receptors. Uses: cardiogenic shock, acute but reversible heart failure

Question 12

What do ACE inhibitors do?

Give an example

Answer 12

Inhibit angiotensin converting enzyme. Angiotensin II is no longer produced therefore less Na+ and H2O is taken up by the kidneys. It is also a powerful vasoconstrictor (increases peripheral resistance). Decreases vasomotor tone, decreasing BP.
Ramparil

Question 13

What causes angina?

Answer 13

Oxygen supply to the heart is not sufficient leading to ischaemia of the tissue.

Question 14

How do you treat angina?

Answer 14

Decrease the workload of the heart by giving Ca2+ antagonists, beta-adrenoceptor blockers and organic nitrates.

Question 15

What do organic nitrates do?

Answer 15

React with thiols (-SH groups) in vascular SM, causing a release of NO2-. This is then reduced to NO which is a powerful vasodilator. NO activates guanylate cyclase which increases the levels of cGMP which lowers [Ca2+]i leading to relaxation of vascular SM cells.

Question 16

What is the primary action of organic nitrates?

Answer 16

On the venous system –> venodilation. This allows for a decreased pre-load and a decrease in the work load of the heart.

Question 17

What is the secondary action of organic nitrates?

Answer 17

Action on collateral arteries.