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Cardiovascular System > Arrhythmia: therapies Drugs for irregular heart rhythms, and anticoagulation > Flashcards

Arrhythmia: therapies Drugs for irregular heart rhythms, and anticoagulation Flashcards

1
Q

What is an arrhythmia

A

Deviation from the normal rhythm of the heart

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2
Q

Types of arrhythmias

A

Sinus
Tachycardia
Bradycardias

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3
Q

Tachycardias

A 
Supraventricular (atrial fibillation and SVT (junctional)
Ventricular arrhythmia (Tachycardia and fibrillation)
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4
Q

Resting Membrane Potential

A
  • During RMP the inside of the cell is a net negative charge relative to the outside
  • Dependent on the sodium-potassium ATPase pump (requires energy)
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5
Q

Action Potential (3)

A
  1. Na+ enters the cell causing depolarisation once the threshold hits -40 mV
  2. Ca++ enters the cell, initiation of contraction
  3. K+ exits the cell causing repolarisation
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6
Q

Vaughan-Williams Classification antiarrhythmics

A

Class I- V

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7
Q

Class IA electrophysiological property

A

(moderate) sodium-channel blockade, thus reducing amplitude of AP and conduction velocity

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8
Q

Class IA examples (3)

A

Quinidine
Procainamide
Dispyramide

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9
Q

Class IB electrophysiological property

A

(Weak) sodium-channel blockades, thus reducing amptitude of AP and conduction velocity

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10
Q

Class IB drugs examples (3)

A

Lidocaine
Mexeletine
Tocainide

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11
Q

Class IC electrophysiological properties

A

(strong) sodium-channel blockade thus reducing amplitude of AP and conduction velocity

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12
Q

Class IC drug examples

A

Flecainide

Propafenone

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13
Q

Class II electrophysiological properties

A

B-Adrenergic receptor antagonism

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14
Q

Class II examples

A

Atenolol

Bisoprolol

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15
Q

Class III electrophysiological peoperties

A

Prolong refractoriness (slow K flow out of cells)

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16
Q

Class III drug examples

A

Amiodorane
Bretylium
Sotalol

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17
Q

Class IV electrophysiological properties

A

Calcium channel blockade

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18
Q

Class IV drug examples

A

Diltiazem

Verapamil

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19
Q

Class V drug

A

Other

Digoxin

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20
Q

Class I drug most commonly used

A

Fleicanide

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21
Q

Action of Class II (2)

A

Prolongs phase 4 depolarisation (slows SA discharge and AV conduction and reduces excitability in non-nodal cardiac tissues)
Shortens phase 2- negative effect on contractility

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22
Q

First line for atrial fibrillation

A

Class II drugs

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23
Q

Class III drugs are used for

A

dysrhythmias that are difficult to treat

• Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter- resistant to other drugs

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24
Q

Use of Amiodarone

A

VT and supraventricular tachycardia

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25
Q

Drug interactions of Amidodarone

26
Q

Side effects of Amiodarine (5)

A 
Thyroid (hypo or hyper)
Pulmonary fibrosis
Slate grey pigmentation
Corneal deposits
LFT abnormalities
27
Q

Class IV (4)

A
  • Calcium channel blockers- bind to Lcard- type voltage gated Ca++ channels
  • Depress phase 4 depolarisation in SA and AV nodes
  • Slow the HR (decrease automaticity and slows AV conduction)
  • Shortens phase 2 plateau phase (reduce contractility)
28
Q

Digoxin (class 5) properties

A

have properties of several classes and are not present in a particular class

29
Q

Action of Digoxin (5)

A
  • Cardiac glycoside
  • Inhibits the sodium-potassium ATPase pump
  • Increases vagal tone- slows SA/AV node conduction
  • Complex effect on the cardiac action potential- reduces the refractory period in the myocardium
  • Increases Ca++ intracellular- positive inotropic effect
30
Q

Indications for Digoxin (2)

A

Atrial dysrhythmias

Heart failure

31
Q

Digoxin Toxicity (6)

A
  • Nausea and vomiting
  • Xanthopia- objects appear yellow
  • Bradycardia
  • Tachycardia
  • Arrhythmias: VT and VF
  • Reverse tick appearance of ST segment in lateral leads
32
Q

Digoxin Toxicity Treatment (3)

A

Stop digoxin
Give Digibind
More serious is potassium levels are low

33
Q

Action of Adenosine

A

Slows/blocks conduction through AV node

34
Q

Use of Adenosine

A

Used to convert paroxysmal supraventricular tachycardia to sinus rythm

35
Q

Features of Adenosine (4)

A

Very short half life
Only administered as fast IV push
May cause asystole for a few seconds
Minimal side effects

36
Q

All antiarrhythmics can cause___

A

arrhythmias

37
Q

Indications for anticoagulation

A

Atrial fibrillation- risk of stroke and pulmonary embolism
Metallic heart valves
DVT/PE

38
Q

Thrombosis in AF is caused when what 3 things are compromised

A

Stasis
Abnormal blood
Abnormal vessels

39
Q

Characteristics of the ideal anti-coagulant (6)

A
  • Oral
  • No need for monitoring
  • No interaction with food or drugs
  • Given once or twice a day/fixed dose irrespective of body weight/age
  • As effective as warfarin
  • Safer than warfarin
40
Q

Oral anticoagulants and their function (3)

A
  • Warfarin- Vitamin K reductase antagonist- prevents the production if active clotting factors
  • Dabigatran- Direct Thrombin Inhibitor
  • Rivaroxaban, Apixaban, Edoxaban- Direct Xa inhibitors
41
Q

Production of Clotting factors (5)

A
  1. Vitamin K epoxide reductase
  2. Reduced vitamin K
  3. Vitamin K epoxide
  4. Clotting factor precursors
  5. Complete clotting factors (II, VII, IX and X)
42
Q

INR

A

Prothrombin Time
Time it takes for blood to clot
International normalised ratio

43
Q

Normal INR

44
Q

Therapeutic INR is normally

45
Q

Adverse effects of Warfarin (6)

A 
•	Bleeding (dose related)
•	Interaction with multiple drugs
•	Pregnancy
	Teratogenic (chondrodysplasia)
	Retroplacental bleeding and foetal intracerebral bleeding
	Avoid in first and third trimester
46
Q

What enzyme metabolises Warfarin and what are the consequences of this (4)

A

Cytochrome P450
Interacts with drugs such as macrolide AB
Antifungals
Antiepileptic drugs

47
Q

Drugs that increase warfarin activity (5)

A 
Aspirin
Sulfonamides
Cimetidine
Erythromycin
Antibiotics (oral)
48
Q

How does Aspirin

Sulfonamides increase warfarin activity

A

Decrease binding of warfarin to albumin

49
Q

How does Cimetidine

Erythromycin increase warfarin activity

A

Inhibit degradation of warfarin

50
Q

How does Antibiotics (oral) increase warfarin activity

A

Decrease synthesis of clotting factors

51
Q

Drugs that promote bleeding (2)

A

Aspirin

Heparin

52
Q

How does aspirin promote bleeding

A

Inhibition of platelets

53
Q

How does Heparin promote bleeding

A

Inhibition of clotting factors

54
Q

Drugs that decrease Warfarin activity (4)

A

Barbiturates
Phenytoin
Vitamin K
Cholestyramine

55
Q

How does Barbiturates and Phenytoin decrease warfarin activyt

A

Induction od metabolising enzyme cytochrome P450

56
Q

How does Vitamin K decrease warfarin activity

A

Promote clotting factor synthesis

57
Q

How does Cholestyramine decrease warfarin activity

A

Reduces absorption

58
Q

Inhibitors of Cytochrome P450 (8) (increases effect of warfarin)

A
  • Omeprazole
  • Disulfiram
  • Erythromycin
  • Valproate
  • Isoniazid
  • Ciprofloxacin and Cimetidine
  • Ethanol (acutely)
  • Sulphonamides
59
Q

Inducers of Cytochrome P450 (reduced effect of Warfarin)

A
  • Alcohol (chronic use)
  • Barbiturates
  • Carbamazepine
  • Phenytoin
  • Rifampicin
  • Sulphonylureas
60
Q

Monitoring warfarin therapy (4)

A
  • Regular INR
  • Watch if therapy altered
  • Patient education
  • Alcohol intake

Cardiovascular System (42 decks)

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