CVS Session 9- Drugs And The CVS Flashcards Preview

SOPHIE'S ESA 2 > CVS Session 9- Drugs And The CVS > Flashcards

Flashcards in CVS Session 9- Drugs And The CVS Deck (34)
0

What is an arrhythmia and why do they arise?

Abnormalities of the heart rate or rhythm.
They arise due to disturbances in impulse generation and/or conduction.

1

What are the three causes of cardiac arrhythmias?

-ectopic pacemaker activity
-after depolarisations
-Re-entry loop

2

What is ectopic pacemaker activity?

When a damaged area of myocardium becomes depolarised and spontaneously active, latent pacemaker regions are activated due to Ischaemia and dominate over the SA node.

3

What is an after depolarisation?

An abnormal depolarisation following an action potential.

4

What is a re-entry loop caused by?

Conduction problems or accessory pathways

5

What is bradycardia defined as?

Heart rate < 60bpm

6

What is tachycardia defined as?

Heart rate>100bpm

7

What is atrial flutter?

A disturbance in the rhythm of the atria.

8

When may atrial fibrillation or flutter occur?

As a result of conditions which may put extra pressure/ stretch on the atria.

9

What is a major consequence of atrial fibrillation?

Thrombus formation

10

When is a delayed afterdepolarisation most likely to occur?

When the intracellular calcium concentration is high.

11

When is early afterdepolarisation most likely to occur?

When the action potential is prolonged.

12

What does early afterdepolarisation lead to? (2)

Oscillations
A longer QT wave.

13

What is the result of a unidirectional block?

A re-entry loop that means the excitation goes the wrong way through the damaged area-> circus of excitation.

14

What are the 4 classes on anti-arrhythmic drug?

1. Voltage gated sodium channel blockers
2. Beta adrenoreceptor antagonists (beta blockers)
3. Potassium channel blockers
4. Calcium channel blockers

15

What do voltage gated sodium channel blockers do?

They block sodium channels in the open or inactive state.

16

What do beta blockers do?

Block sympathetic activity- beta 1 adrenoreceptors in the heart and therefore decrease pacemaker potential slope and lower heart rate and AV conduction.

17

When are beta blockers used and why?

Following an MI.
Because they reduce sympathetic activity and therefore can prevent ventricular arrhythmias that often arise due to increased sympathetic activity.

18

What do potassium channel blockers do?

Prolong the action potential and therefore the absolute refractory period. This should prevent premature APs.
ACTUALLY PROARRHYTHMIC!

19

What is the exception potassium channel blocker?

Amiodarone

20

What do calcium channel blockers do? (3)

Decrease the SAN pacemaker action potential slope,
AV node conduction
and force of contraction.

21

What is adenosine and what does it do?

An anti-arrhythmic drug that doesn't fall into one of the classes.
It acts on alpha 1 adrenoreceptors at the AVN and enhance potassium conductance.
Momentarily stops the heart so it can reset into a normal rhythm.

22

What are inotropic drugs?

Drugs that affect the force of contraction of the heart.

23

Define heart failure

A chronic failure of the heart to provide sufficient output to meet the body's requirements.

24

What are 4 features of heart failure?

-decreased force of contraction
-decreased cardiac output
-decreased tissue perfusion
-oedema.

25

How is oedema caused in heart failure?

The heart has to work harder, therefore pressure rises inside the heart and in veins supplying the heart. This causes capillary pressure to rise such that fluid is forced out and causes oedema.

26

What two classes of treatment are used in heart failure and what are the two types within each class?

-positive inotropes - cardiac glycosides, beta adrenoreceptor agonists
-work loading reducing drugs - ACE inhibitors, beta adrenoreceptor antagonists

27

How do cardiac glycosides increase the force of contraction?

They inhibit sodium potassium pump and therefore cause a rise in intracellular sodium.
This inhibits the activity of the sodium calcium exchanger and therefore causes calcium levels to rise intracellularly.
This is stored in SR. More is available per AP therefore increased force of contraction.

28

How do ACE inhibitors reduce the workload of the heart?

They inhibit the action of angiotensin converting enzyme therefore prevent the conversion of angiotensin one to two.
As angiotensin 2 normally vasoconstricts and increases sodium and water reabsorption- both of these are opposed; lowering bp and blood volume, therefore reducing pre and after load.

29

By does atrial fibrillation have a risk of thrombus formation?

Because it increases stasis of blood.

30

What is angina?

Insufficient oxygen supply/ Ischaemia of the heart that leads to chest pain upon exertion.

31

What do organic nitrates do in the treatment of angina?

Release nitric oxide which is a powerful vasodilator.
This activates guanylate cyclase which converts GTP to cGMP, which causes intracellular calcium levels to fall. -> relaxation of smooth muscle.

32

What is the primary action of organic nitrates?

Venodilation

33

What is the secondary action of organic nitrates?

Dilate collateral arteries

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