Session 9 - Drugs and the CVS

Question 1

What are the causes of arrythmias?

Answer 1

• Ectopic pacemaker activity
• Afterdepolarisations
• Re-entry loop

Question 2

What are the causes of arrythmias?

Answer 2

• Ectopic pacemaker activity
• Afterdepolarisations
• Re-entry loop

Question 3

What are the causes of arrythmias?

Answer 3

• Ectopic pacemaker activity
• Afterdepolarisations
• Re-entry loop

Question 4

What might cause ectopic pacemaker activity

Answer 4

Damaged area of myocardium becomes depolarised and spontaneously active
Latent pacemaker region activated due to ischaemia

Question 5

Explain why delayed after-depolarisations and early after-depolarisations occur

Answer 5

Delayed after- depolarisations are more likely to occur if there is high intracellular Ca+
Early after-depolarisations are more likely to occur if the AP are prolonged, the longer the AP the longer the QT. Can set up oscillations

Question 6

What is meant by a re-entry loop. What can several small re-entry loops in the atria lead to

Answer 6

A block in the conduction of the myocardium prevents conduction in the correct direction and therefore excitation spreads in the wrong direction
Can lead to atrial fibrillation

Question 7

What do Class 1 anti-arrythmic drugs do and give an example

Answer 7

Drugs that block voltage-sensitive sodium channels. Only when open or inactive state, therefore dissociates rapidly in time for next AP…. use-dependent block
e.g. Lidocaine

Question 8

Why does lidocaine automatically block damaged myocardium

Answer 8

As the damaged myocardium has more inactive and open sodium channels (use-dependent)

Question 9

What do class 2 anti-arrythmic drugs do and give an example

Answer 9

Beta adrenoreceptor antagonists (beta blockers)
Act at beta 1 receptors in the heart and block sympathetic action –> decrease in slope of pacemaker potential
Can slow the conduction at the AV node and therefore prevent supra ventricular tachycardias
e.g. propranolol, atenolol

Question 10

What do class 3 anti-arrythimic drugs do and give an example

Answer 10

Block K+ channels therefore prolong the AP –> lengthening of the absolute refractory period
e.g. amiodarone

Question 11

Why are class 3 anti-arrythmic drugs not used?

Answer 11

As they can become pro-arrythmic

Question 12

What can amiodarone be used to treat

Answer 12

Tachycardia associated with Wolff-Parkinson-White syndrome (re-entry loop due to an extra conduction pathway)

Question 13

What do class 4 anti-arrythmic drugs do and give an example

Answer 13

Block Ca2+ channels therefore decrease the slope of the pacemaker action potential, decrease AV nodal conduction and decrease the force of contraction
Also some peripheral and coronary vascodilation
e.g. verapamil

Question 14

What drugs act in the periphery at Ca+ channels

Answer 14

Dihydropyridine Ca2+ channel blockers act on vascular smooth muscle –> vasodilation

Question 15

What drugs act in the periphery at Ca+ channels

Answer 15

Dihydropyridine Ca2+ channel blockers act on vascular smooth muscle –> vasodilation

Question 16

How does Adenosine work

Answer 16

Produced endogenously but can be given pharmacologically

Acts on A1 receptors at the AV node to enhance K+ conductance and therefore hyperpolarise the cell

Question 17

What is heart failure?

Answer 17

Chronic failure of the heart to provide sufficient output to meet the body’s requirements

Question 18

What are the features of heart failure

Answer 18

• Reduced force of contraction
• Reduced CO
• Reduced tissue perfusion
• Oedema

Question 19

Explain why oedema forms in heart failure

Answer 19

As there is increased venous pressure and therefore there is increased pressure in the right ventricle so the hydrostatic pressure in the lungs is increased –> fluid leaves the capillaries

Question 20

Name the different classes of drugs that can be used to treat heart failure

Answer 20

• Cardiac glycosides
• Beta agonists
• ACE-inhibitors

Question 21

What is the mechanism of action of cardiac glycosides and give an example of one

Answer 21

Na+/K+ATPase blockers. This causes the NCX in the cell to become less effective as lost Na+ gradient as there is a rise in intracellular Na+ conc. Increase in intracellular Ca2+ therefore there is more stored in the SR –> increased force of contraction
Also increase vagal activity, slow AV conduction
e.g. Digoxin

Question 22

What do beta agonists do

Answer 22

Increase the myocardial contractility by acting on Beta 1 receptors
Used in cardiogenic shock
e.g. dobutamine

Question 23

Explain how ACE-inhibitors decrease the workload of the heart

Answer 23

Inhibit the action of angiotensin converting enzyme therefore prevent the formation of active angiotensin II from the inactive angiotensin I
Angiotensin II acts on the kidneys to increase Na+ and H20 reabsorption –> increase BP and blood volume
Angiotensin also is a vasoconstrictor
Therefore ACE-inhibitors reduce the after load and the preload

Question 24

Name another type of drug that decreases blood volume

Answer 24

Diuretics

Question 25

What is the primary action of organic nitrates

Answer 25

Venodilation –> decrease preload

Question 26

What is the secondary action of organic nitrates

Answer 26

Dilation of collateral arteries

Question 27

Give an example of an organic nitrate

Answer 27

Glyceryl trinitrate and isosorbide dinitrate

Question 28

What conditions carry increase risk of thrombus formation

Answer 28

Atrial fibrillation
Acute MI
Mechanical prosthetic heart valves

Question 29

Name 2 anticoagulants and their actions

Answer 29

Heparin - inhibits thrombin

Warfarin - antagonises vitamin K

Question 30

Name an antiplatelet drug

Answer 30

Aspirin

Question 31

Name 5 types of drugs that can be used to treat hypertension in theory

Answer 31

• Diuretics
• ACE-inhibitors
• Beta-blockers
• Ca2+ blockers on vascular smooth muscle
• Alpha 1 antagonists