CPT1: Dysrhythmias 2 Flashcards
1
Q
What is the basis of how anti-arrhythmic drugs work?
A
They act by altering ion fluxes within excitable tissues in the myocardium
2
Q
What are the 3 main ion channels of importance?
A
Na+, Ca2+, K+
3
Q
What are anti-arrhthmic drugs classed upon
A
Their ability to either directly or indirectly block the movement of ions across the membrane of excitable cardiac tissue
- 4 major classes depending on their electophysiological mechanisms of action. Have effects on different phases of action potentials
May be classed clinically into those which act primarily on:
- Supraventricular arrhythmias (e.g. verapamil)
- Both Supraventricular and Ventricular (e.g. disopyramide)
- Ventricular arrhythmias (e.g. Lignocaine)
4
Q
Describe conduction through purkinje/ Ventricular myocytes
A
- Phase 0: Depolarization. Influx of Na+ ions through fast acting voltage Na+ channels
- Phase 1: Rapid repolarization. Outflow of K+ ions (triggered by change in polarity)
- Phase 2: Plateau as influx of K+ is electrically balanced with influx of Ca2+ through slowly inactivatin L-type Ca2+ channels which proceeds contractio
- Phase 3: Repolarisation: Eflux of K+ and reduced influx of Ca+ caused by activation of Na+/K+ ATPase
- Phase 4: Membrane potenital restored. Prepotential Na+ influx
5
Q
Describe conduction through the SA node
A
- Phase 4: Prepostpotenital. Unstable resting membrane potential - climbs back towards threshold. This is due to alteration in K+ outflow current in relation to background current
- Phase 0: Slow upstroke. No functional Na channels therefore depolarisation due to slowly activating Ca2+ channels and Ca2+ influx
- Phase 3: Repolarisation. Opening of K+ channels and eflux of K+
6
Q
Complete the table
A
7
Q
Describe Class I
A
- Block Na+ Channels
- Class I is split into 3 subgroups: IA, IB, IC
- Subgroups dependent on effect on repolarisation (Phase 4) and potency towards blocking sodium channels (phase 0)
8
Q
Describe Class A and give an example of a drug
A
- High potency for blocking Na+ channels (Prolong QT interval) and usually prolong repolarisation (QRS) interval through blockage of K+ Channels
- Quinidine
9
Q
Describe IB class and give an example
A
- IB drugs = lowest potency as Na+ blockers, produce little if any change in action potential duration (no effect on QRS interval) in normal tissue, and shorten repolarization (decrease QT interval)
- lignocaine
10
Q
Describe Class C drugs and give an example
A
- IC = most potent Na+ blocking agents (prolong QRS interval), and have little effect on repolarization (no effect on QT interval)
- flecainide
11
Q
Describe class II and its uses
A
- B-Blockers
- Act directly or indirectly on electrophysiological parameters by blocking B-adrenergic receptors (slow sinus rhythm, prolong PR interval, no effect on QRS interval or QT interval)
- Used for arrhythmia origining from sympathetic output/ circulating catecholamines
- Valuable in SA/AV node arrhythmias induced by stress/ anxiety/ exercise
12
Q
Describe Class III and an example of a drug
A
- Prolong AP
- drugs prolong repolarization (increase refractoriness) by blocking outward potassium conductance (prolong QT interval), with typically little effect on the rate of depolarization (no effect on QRS interval)•E.g. Amiodarone But can also cause Na+ channel blockade
13
Q
Describe Class IV and examples
A
- Calcium Channel blockers
- drugs are relatively selective AV nodal L-type calcium-channel blockers (slow sinus rhythm, prolong PR interval, no effect on QRS interval)
- •E.g. verapamil, diltiazem
14
Q
What are examples of drugs which do and dont follow this classification system
A
•NB Some drugs (e.g. nifedipine) have no place in this classification, while others have properties in more than one class (e.g. Amiodarone)
15
Q
- What is the most common arrhymia?
- What increases risk?
- If left untreated it could result in>?
A
- Atrial Fibrillation
- More common with increasing age
- Stroke, dementia, Heart failure
16
Q
What are common symptoms with atrial fibrillation
A
- Palpatations
- light Headedness
- Fatigue
- Fainting
- Shortness of breath
- Chest discomfort
17
Q
What is the goal of treatment of atrial fibrillation?
A
To restore the hearts normal rhythm
If this is not possible, to slow the irregulat heart rate, alleivate symptoms and prevent complications
18
Q
What can aterial fibrillation be classed into?
A
- Paroxysmal (discrete self terminatinf episodes)
- Persistant (Prolonged episodes that can be terminated by electrical or chemical cardioversion)
- Permanent
19
Q
A number of drugs are available to restore the normal heart rhythm. What do you need to be careful off?
A
drugs are effective but may have significant side effects, so they will need to be monitored for tolerability.
20
Q
What classes of drugs are typically reserved for AF?
A
I, II, III
21
Q
- What are examples of IC drugs used to treat AF?
- Dosage regime?
- Side effects?
- Drugs used for?
A
- Flecainide and Propafenone
- Flecainide - twice daily. Propafenone - up to 3x daily
- Heart faliure, unstable cardiac rhythms, excessive slowing of HR
- Drugs, while effective, typically reserved for young people with AF and no structural heart disease
22
Q
Class II drugs can be used (B-blockers) for AF. Answer the following questions:
- What do they do?
- Patient group?
- Contraindications?
- Drug examples
A
- Used to slow heart rate
- Best in active patients with bettwe exercise capacity
- Avoid use in patients with ashtma, emphysema or with a slow heart rate
- Includes Atenolol, bisprolol, metoprolol
23
Q
Class III drugs can be used to treat AF:
- Mechanism
- Examples of drugs
- Dosaage regime
- Side effects
A
- BLock K+ channel in cardiac cells
- Satalol and Amiodarone. Satalol can also be used as a B-blocker and slows heart rate, but at higher doses is used to stablilse heart rhytm
- Taken twice or three times daily
- Low BP and slow HR
24
Q
Class IV drugs can be used:
- Examples
- Caution for use in which patient group
- Side effects
- X should not be used with?
A
- Verapamil and Diltiazem
- Those with Heart failure
- Flushing, headache, swollen ankle, low BP
- Verapamil and B-blockers
25
1. What risk is high with AF?
2. Causation?
3. What is commonly given?
4. When may this not be the case?
5. How is risk reduced?
1. AF associated with high incidence of stroke.
2. Related to thrombus formation in disorganised blood flow in the atrium.
3. NEARLY all patients given anticoagulants (warfarin) or if contraindicated aspirin.
4. Exceptions = young patients with “lone AF”, risk of stroke is low and high risk of bleeding on warfarin.
5. Warfarin reduces stroke rate by 2/3rds
6. Aspirin reduces stroke risk by 1/5th
26
What are alternatives to warfarin and Aspirin?
* Dabigatran (thrombin inhibitor) has a similar effect in reducing stroke due to blood clots in AF but a lower risk of bleeding complications.
* Rivaroxaban (an inhibitor of activated factor X (factor Xa)): been shown to be at least as effective at reducing the risk of stroke in AF patients as warfarin
27
What types of AV block is there?
1. First degree
2. Second Degree
3. Third Degree
28
What is first degree block?
The PR interval is defined as the inital deflection of the P wave from baseline to the begining of the QRS complex
P wave normally takes 0.12 - 0.20 seconds
In first degree heart block the PR interval on the ECG is prolonged and is \>0.2s
29
What are the main causs of first degree heart block?
The following are the most common causes of first-degree heart block:
* Intrinsic AV nodal disease
* Enhanced vagal tone
* Acute MI,
* Electrolyte disturbances
* Drugs e.g CCB, BB, cardiac glycosides
30
What does treatment of first degree block involve?
* •No specific therapy is required.
* •However, patients with concomitant MI should receive appropriate therapy.
* •First-degree heart block does not require hospital admission unless the patient has an associated MI.
* •Identify and correct electrolyte abnormalities.
* •Withhold any offending medications
31
What happens in 2nd degree heart block?
•Second-degree heart block or second-degree atrioventricular (AV) block refers to a disorder of the cardiac conduction system in which some P waves fail to conduct to the ventricle and to generate a QRS complex.
32
What types of 2nd degree heart block is there?
Mobitz 1 and Mobitz 2
33
Describe Mobitz 1
•Mobitz I AV block, or Wenckebach block: prolongation of the PR interval causing progressive R-R interval shortening until a P wave fails to conduct to the ventricle.
–Mobitz I block can be caused by acute MI, states of vagal stimulation or enhanced vagal tone, or toxicity relating to digitalis, beta-blockers, or calcium channel blockers.
34
Describe Mobitz II
•Mobitz II AV block is characterized by sudden unexpected blocked P waves without variation or prolongation of the PR interval.
–Mobitz II block most commonly is caused by acute MI.
35
Describe treatment aims for block II
•The goal: improve conduction via AV node.
Anticholinergic -- Drug therapy in second-degree heart block is aimed at vagolysis; atropine is the only currently available agent.
NB. This is effective only if the site of block is the AV node.
•For patients with infranodal second-degree heart block, atropine generally is ineffective
36
What is 3rd degree block?
•Third-degree heart block, also referred to as third-degree atrioventricular (AV) block or complete heart block, is a disorder of the cardiac conduction system with complete absence of AV conduction. No P waves conduct to the ventricle, and AV dissociation is complete.
37
What are consequences in patients with 3rd degree block
•Patients with complete heart block frequently are haemodynamically unstable. This may lead to cardiovascular collapse, syncope, and death.
38
What is treatment for 3rd degree block?
* •Drug therapy in third-degree heart block is aimed at vagolysis, with atropine being the only currently available agent. Catecholamines have only a limited role.
* • Atropine: Enhances sinus node automaticity and blocks effects of acetylcholine at AV node, thereby decreasing refractory time and speeding conduction through AV node.
* •Insufficient doses may cause paradoxical effects, further slowing heart rate!!
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