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Pharmacology Yr2 > Drugs to treat arrhythmia and congestive heart failure > Flashcards

Drugs to treat arrhythmia and congestive heart failure Flashcards

1
Q

What are some characteristics of HF?

A 
Progressive cardiac dysfunction
Raised CVP
Tiredness
Breathlessness
Oedema
Sudden cardiac death
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2
Q

What are some physiological compensation methods for heart failure?

A

Heart failure = decreased CO.

Decreased CO means increased TPR to increase BP, as BP = CO x TPR. Increase TPR by increased sympathetic tone to arterioles.

Also increase activation of the renin angiotensin aldosterone system in order to raise blood pressure and filling pressures.

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3
Q

How does increased RAP (right atrial pressure) lead to dilatation of the heart?

A

Increased filling pressure means increased volume in the right atrium.

Would mean that there is a increased CO due to length tension relationship in myocardium of ventricle however due to weak heart, cant pump all blood out so some is left in the ventricle.

Ventricle fills up again and puts more stress on the heart walls and they dilate further which leads to even less contraction strength and more blood in the ventricle at the end of systole.

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4
Q

What are some causes of heart failure

A

Volume overload - valve regurgitation

Pressure overload - Systemic hypertension

Loss of muscle (post MI, chronic ischaemia)

Restricted filling (pericardial disease)

Chronic heart failure

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5
Q

What drugs are usually used in order to improve symptoms of heart failure?

A

Diuretics
ACE inhibitors or ATI antagnists
Digoxin

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6
Q

What drugs are usually used in order to improve survival of heart failure?

A

ACE inhibitor or ATI inhibitor
B blockers
Spironolactone

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7
Q

Name two ACE inhibitors?

A

Captopril

Enalapril

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8
Q

What is the function of ACE inhibitors?

A

Inhibit production of AIi

Inhibit aldosterone production

Vasodilation

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9
Q

What are ACE inhibitors useful for?

A

Controlling K+ loss

Hypertension

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10
Q

What are some side effects of ACE inhibitors?

A

hyperkaleamia

Hypotension

Cough (inhibition of bradykinin breakdown).

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11
Q

What is an example of an ATII receptor blocker?

A

Losartan

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12
Q

Why use ATII over ACE inhibitor?

A

No cough , better tolerated.

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13
Q

What are some side effects ofATII inhibitors?

A

birth defects

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14
Q

Give an example of a loop agent

A

Furosemide

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15
Q

Where do loop agents act in the nephron?

A

Act at thick ascending limb of loop of henle Na/K/2CL transporter.

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16
Q

What are the side effects of furosemide?

A

Hypokaleamia
Hypovolaemia
Hypomagnesia
Ototoxicity

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17
Q

How much of filtered NA+ are furosemide responsible for?

A

30%

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18
Q

Where do thiazides act

A

distal convoluted tubule Na/Cl transporter

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19
Q

What is another effect that thiazides have?

A

Vasodilators of smooth muscle.

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20
Q

What are some side effects of thiazides?

A

K loss, hypotension

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21
Q

Where does Spironolactone act

A

Convoluted tubule

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22
Q

What is the method of action of spironolactone

A

It is an aldosterone antagonist.

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23
Q

What is spironlactone useful for

A

Controlling K+ loss

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24
Q

What are some potential side effects of spironolactone?

A

hyperkalaemia.

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25
Q

What are the actions of cardiotonic steroids

A

F orce increae

E xcitability increase

A a-v conduction decrease

R rate decrease

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26
Q

Name two cardiotonic steroids

A

Digitoxin, Digoxin

27
Q

What are the properties of digitoxin

A

Long duration

Slow onset - half life 5-7 days

High affinity for serum proteins with strong binding

28
Q

What are the properties of Digoxin

A

Rapid onset

Low oral activity

Low affinity for serum proteins

29
Q

What is the mechanism of action of cardiotonic steroids?

A

Cardiotonic steroids inhibit the Na/k atpase

Increasing intracellular Na+

Meaning more Activity for the Na+/Ca2+ antiporter

Increasing intracellular Ca2+

Increasing Ca2+ released from sarcoplasmic reticulum

Increased contraction strength.

30
Q

What are side effects of cardiotonic steroids

A

Arrhythmias

Gastrointestinal

Narrow theraputic range. - risk of toxicity

31
Q

What is the use of digitalis?

A

To treat heart failure in old sedentary patients.

32
Q

How can nitrates be used to treat congestive heart failure?

A

GTN (glycerol trinitrate ) spray can be administered to release NO which is a vaso dilator.

It therefore reduces the amount of preload and afterload

33
Q

How can GTN be administered?

A

Sublingual or injection

34
Q

When is GTN spray mostly used in heart failure?

A

Acute HF collapse due to tolerance

35
Q

What are some side effects of nitrates?

A

Headache

Dizziness

36
Q

Give an example of a sympathomimetic inotrope

A

Milrinone, Dopamine (IV)

37
Q

When are sympathomimetic ionotropes usually used for HF?

A

Reversible heart failure

38
Q

What does the first class of antiarrhythmatic drugs target?

A

Na channel blockade

Reduce phase 0 slope & AP peak

39
Q

What does the second class of antiarrhythmatic drugs target?

A

B-blockers

Block sympathetic drive, reduce rate, conduction & excitability

40
Q

What does the third class of antiarrythmatic drugs target?

A

K+ channel blockers

Delay repolarisation

41
Q

What does the fourth class of antiarryhthmatic drugs target?

A

Ca 2+ blockers

Reduce rate & conduction

42
Q

Give an example of a class 1a antiarrythmatic drug?

A

Quinidine

43
Q

What is the mechanism of action of Quinidine

A

Prolong AP durating and reduce upstroke

Decrease sodium entry into cell

44
Q

What is quinidine used for?

A

Ventricular arrhythmias

45
Q

What is an example of a class 1b antiarrhythmatic drug?

A

Lignocaine

Lidocaine

46
Q

What is the mechanism of action of lignocaine?

A

Decrease AP duration and reduce upstroke

Prolong refractory period by binding to inactivated Na+ channels so they cant be opened again.

Decrease Na+ influx

47
Q

What is lignocaine used for

A

Treatment during and immediately after myocardial infarction.

48
Q

What is an example of a class 1c anti arrythmatic drug

A

Flecainide

49
Q

What is the mechanism of action of flecainide?

A

No change in APD.

Blocks sodium entry

Supress Automaticity

Increases refractory period

50
Q

Give an example of a class II anti arythmatic drug

A

atenolol

51
Q

How does atenolol work to treat anti arrhythmias

A

B blocker

Reduces the effect of sympathetic drive

Lengthens action potential duration

Prolong refractory period

Decrease conduction + excitability + rate

52
Q

When is atenolol used?

A

superventricular tachycardia

53
Q

Give an example of a class III anti arrhythmic drug?

A

amiodarone

54
Q

How does amiodarone work?

A

K+ channel blocker

Prolong APD

Prolong ERP

55
Q

What is amiodarone used to treat?

A

V tachycardia

Atrial fibrillation

56
Q

Give an example of a Ca2+ channel blockers which is used to treat arrhythmias

A

Diltiazem

57
Q

How does Dilitiazem work?

A

Selectivity for cardiac muscle (verapamil & diltiazem)

Block AV node ( good for supraventricular trachyarrythmia)

58
Q

What are the uses of dilitiazem?

A

Supraventricular tachycardia

Reduce ventricular rate in patients with atrial fibrillation.

59
Q

Give an example of a class V anti arrythmatic drug?

A

Dixogin

60
Q

How does Digoxin work to treat arrythmias?

A

Decreases A-V conduction

Decreases ventricular contraction rate.

61
Q

What is digoxin mainly used for?

A

Supraventricular tachyarrhythmias

62
Q

What drug can be used to turn atrial flutter to atrial fibrillation?

A

Digoxin

  • As decreases A-V conduction and rate of heart.

Need to be careful to control clotting via the use of warfarin/heparin.

63
Q

What is the role of magnesium in the control of arrhythmias?

A

Decreases calcium entry into the sarcolemma, therefore less calcium released from sarcoplasmic reticulum.

Regulates metabolic processes in intracellular space by binding to ATP

Valuable in ventricular arrythmias in ischeamic cells especially if there is hypomegnesemia.

Pharmacology Yr2 (11 decks)

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