Arrthymia: therapies, Drugs for irregular heart rhythms Flashcards Preview

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Flashcards in Arrthymia: therapies, Drugs for irregular heart rhythms Deck (32)
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1
Q

What is an arrhythmia?

A
  • A deviation from the “normal” rhythm of the heart.
  • (Sinus arrhythmia)
  • Tachycardias: supraventricular arrhythmia, Ventricular arrhythmia
  • (Bradycardias(Heart block))
2
Q

Features of the resting membrane potential

A
  • Inside the cell is a net negative charge relative to the outside:
  • Due to uneven distribution of ions across the cell membrane.
  • Dependant on the sodium-potassium ATPase pump (needs energy)
3
Q

Vaughan-Williams classification drugs of antiarrhythmics

A
  • IA: Quinidine, Procainamide, Dispyramide
  • IB: Lidocaine, mexiletine, tocainide
  • IC: Flecainide, propafenone
  • II: Atenolol
  • III: Amidarone, bretylium, sotalol
  • IV: Diltiazem, verapamil
  • V: Digoxin
4
Q

Vaughan-Williams class I features

A
  • Membrane-stabilising agents: decrease the amplitude (size of action potential)
  • Reduces velocity of conduction/excitability
  • Act on “Fast” sodium channel responsible for phase 0: present in “Non-nodal” cells
  • Divided into Ia, Ib and Ic agents.
  • Show use dependence (i.e. More effective at higher HR)
5
Q

What is the agent mainly used in class I antiarrhythmics?

A

Flecainide

  • Strong Na+ channel blockade
  • prolongs ERP (effective refractory period)
6
Q

Vaughan-Williams class II features

A

Beta blockers: atenolol, bisoprolol, propanolol

  • Acts via Beta1 receptors to block sympathetic stimulation of the heart: prolongs phase 4 depolarisation, shortens phase 2
  • Now first line for atrial fibrillation (Bisoprolol)
7
Q

Vaughan-Williams class III features

A

Amiodarone, bretylium, sotalol

  • Increase action potential duration
  • Prolong repolarisation in phase 3
  • Prolongs ERP
  • Used for dysrhythmias that are difficult to treat
  • Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter: resistant to other drugs
  • Sustained ventricular tachycardia
8
Q

Features of Amidarone

A
  • Used for VT (ventricular tachycardia) and occasionally in supraventricular tachycardia
  • Many interactions with other drugs: particularly digoxin
  • Because of tissue effects has striking side effect profile: thyroid, pulmonary fibrosis, Slate-grey pigmentation, corneal deposits, LFT abnormalities
9
Q

Vaughan-Williams class IV features

A

Verapamil, Diltiazem

  • Calcium channel blockers: bind to Lcard type voltage gated Ca channels
  • Depress phase 4 depolarisation in SA and AV nodes: slows the heart rate
  • Shorten phase 2 plateau phase (reduce contractility)
  • Show use dependence
  • Used for paroxysmal supraventricular tachycardia; rate control for atrial fibrillation and flutter.
10
Q

Vaughan-Williams class V features

A

Other antiarrhythmics

  • Digoxin, adenosine
  • Have properties of several classes and are not placed into one particular class.
11
Q

Features of Digoxin

A
  • Cardiac glycoside
  • Inhibits the sodium-potassium ATPase pump
  • Increases vagal tone through: slows SA/AV node conduction
  • Complex effect on the cardiac action potential: reduces the refractory period in myocardium
  • Increases Ca2+ concentration intracellular: positive inotropic effect
12
Q

What are indications for Digoxin?

A

Atrial dysrhythmias

  • AF
  • Atrial flutter
  • (SVT)

Heart failure

13
Q

Features of Digoxin toxicity

A
  • Nausea and vomiting
  • Xanthopsia!
  • Bradycardia
  • Tachycardia
  • Arrhythmias: VT and VF
14
Q

Signs of digoxin toxicity

A
  • ‘Reverse tick’ appearance of ST segment in lateral leads
  • Confusion
  • Irregular pulse
15
Q

What is Digoxin toxicity treatment?

A
  • Stop digoxin: but long half life
  • If levels very high and risk of significant arrhythmia: give Digiband
  • Digoxin toxicity is more serious if potassium levels are low
16
Q

What is Digiband?

A
  • Digoxin immune antibody
  • Binds with digoxin, forming complex molecules
  • Excreted in urine
17
Q

Features of Adenosine

A
  • Slows/blocks conduction through the AV node
  • Used to convert paroxysmal supraventricular tachycardia to sinus rhythm
  • Very short half-life
  • Only administered as fast IV push
  • May cause asystole for a few seconds
  • Other side effects minimal
18
Q

What are side effects of antiarrhythmias?

A
  • ALL antiarrhythmias can cause arrhythmias.
  • Learn about one drug from each of the VW classifications (including betablocker, verapamil)
  • Learn about digoxin and amiodarone
19
Q

What are indications for anticoagulation?

A
  • Atrial fibrillation: risk of stroke, peripheral emboli

- Thrombus in AF

20
Q

Cardiovascular indications for anticoagulation

A
  • Metallic heart valves

- DVT/PE: treatment, prophylaxis

21
Q

What are characteristics of the “ideal” anticoagulant?

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
22
Q

Examples of oral anticoagulants

A
  • Warfarin: vitamin K antagonist
  • Dabigatran: direct thrombin inhibitor
  • Rivaroxaban, Apixaban, Edoxaban- direct Xa inhibitors
23
Q

Know about inhibition of factors II, VII, IX and X

A

On powerpoint

24
Q

Monitoring warfarin therapy: What is normal INR (international normalised ratio)?

A
  • Normal INR is 1

- Therapeutic INR is normally 2.5 - 4.0 depending on the clinical indication.

25
Q

Adverse effects of warfarin therapy

A
  • Bleeding (dose related)
  • Interaction with multiple other drugs
  • Pregnancy: teratogenic (chondrodysplasia), Retroplacental bleeding and foetal intracerebral bleeding
  • Avoid in first and third trimesters
26
Q

What are drugs that increase warfarin activity?

A
  • Aspirin, Sulfonamides: decrease binding to albumin
  • Cimetidine, Erythromycin: inhibit degradation
  • Antibiotics (oral): decrease synthesis of clotting factors
27
Q

Drug interaction with warfarin: drugs that promote bleeding

A
  • Aspirin: inhibition of platelets

- Heparin antimetabolites: inhibition of clotting factors

28
Q

Drug interaction with warfarin: drugs that decrease warfarin activity

A
  • Barbiturates, Phenytoin: induction of metabolising enzymes (cytochrome P450)
  • Vitamin K : promote clotting factor synthesis
  • Cholestyramine: reduced absorption
29
Q

How is warfarin metabolised?

A

It is metabolised by Cytochrome P450 pathway.

  • So it interacts with drugs such as macrolide antibiotics, antfungals, anti-epileptic drugs
30
Q

Inhibitors of Cytochrome p450

A
  • Omeprazole
  • Disulfiram
  • Erythromycin
  • Valproate
  • Isoniazid
  • Ciprofloxacin and Cimetidine
  • Ethanol (acutely)
  • Sulphonamides
31
Q

Inducers of cytochrome p450

A
  • Alcohol (chronic use)
  • Barbiturates
  • Carbamazepine
  • Phenytoin
  • Rifampicin
  • Sulphonylureas
32
Q

Monitoring warfarin therapy methods

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