Lecture 4: Treatment of cardiac rhythm disturbances Flashcards
What are the common causes of tachycardias?
- Automacity / triggered activity
- Re-entrant mechanisms
What are the common causes of bradycardias?
SAN/AVN conduction disorders
How can arrhythmias be characterised?
- Simply-> Complex
- Bening -> Malignant
- Structural -> Functional
What are the treatment options for arrhythmias?
- Not curative
- Must consider SE/Drug interactions
- Drugs or Devices or Intervention interface
What are the sources of bradycardias?
- Physiological
- Sinus node
- AV node
- Neural mediated
What are the sources of tachycardias?
- Atrial
- Junctional (SVT)
- Ventricular
-> Scar
-> ‘normal’ hearts
What are the cardiac devices that can be used for rhythm disturbances?
1) Single or dual chamber pacing or ICD
2) Rate support:
- AV synchrony
- VV synchrony
3) Other:
- Vasovagal syncope device
- Monitors
Is ectopy a concern? how can it be treated?
- Common, benign
- Assess and can Tx with;
-> Beta blocker
-> Ablation
What are the common treatments of rhythm disturbances?
- Assess
- Re-assurance
- Drug therapy
- Withdraw of drug Rx
- Manage underlying conditions
- Device
- Ablation
What do anti-arrhythmic drugs do?
- Ectopic suppression
- Alters conduction
- Alters autonomic tone
What is the vaughn williams classification?
Class One: Na channel agents (Predom blocking, 1a,1b,1c)
Class Two: Beta blockers i.e metoprolol, propranolol
Class Three: K channel blockers i.e amiodarone
Class Four: Slow Ca channel blockers i.e verapamil, nifidipine
Describe the class 1a,1b,1c effects:
1a: Reduce Vmax, prolong AP. [Onset/Offset rapid]
1b: No vmax effect, shortens AP. [Onset,offset fast]
1c: Reduce Vmax, slow conduction. [Onset/offset slow]
What drugs to the vaughn williams classification miss?
- Adenosine
- Digoxin
How do anti-arrhythmic drugs work at a physiological level?
Anti-arrhythmia
- Cell membrane, ANS, vagal tone
Cell membrane activity effects:
- Conduction velocity, length of refractory period, automacity of the SA or AV node.
What are the effects of altered vagal tone?
Increased vagal tone:
- Dec HR, SA automacity, slower conduction through AVN
Decreased vagal tone:
- Inc. HR, SA automacity, increased conduction V through AVN
Describe how class 1a Na channel blockers work:
-> Slower depolarisation
-> Prolongs refractoriness
-> Reduces conduction velocity
-> Widens QRS interval
** Consider that it may enhance AVN conduction thus might also need rate lowering drugs
What things should you always consider when thinking of arrhythmia treatment?
- AP duration
- Refractoriness
- Conduction velocity
What do class 1B Na channel blockers do?
- Decrease duration of AP
- Shortens refractory period
What do 1C Na channel blockers do?
- Decrease conduction velocity of AP
- Little or no effect on refractory period
How do class 2 beta blockers work to stop arrhthmias?
- Decreases SNS tone, slows conduction velocity
What are the possible side effects of beta blockers? when are they useful?
- Bradycardia (Chronic Tx might require pacing)
- Fatigue (Start low go slow)
- Cardioselective B1 or non-cardioselective = differing S/E
- C/I in asthmatics
- Good for atrial or ventricular arrhythmia
What are the effects of class three K channel blockers?
- Increases duration of AP
- Increases duration of refractory period
Also effects Na and Ca channels
What are the considerations for K channel blockers?
-> Toxicity (Cumulative)
-> Can impact defib thresholds
-> May slow but not stop VT
-> Atrial or ventricular arrhythmias also…
How do class four Ca channel blockers act?
- Mainly affects SA and AV nodes
- Not pro-arrhythmic
- Rate-altering
How does digoxin treat arrhythmogenesis?
- Increased PSN activity
- Slows atrial rate and AV conduction
How does adenosine treat arrhythmogenesis?
- AV node block
- Typically IV admin
What are the mechanisms of arrhythmogenesis?
- Prolonged repolarisations
- Development of EADs -> Torsades
- Re-entry pathways
- Structural abnormalities i.e HF
- Afib is regularly irregular…
What is AV node re-entrant tachycardia?
- Ectopic beat in ventricles can conduct back through AVN to atria
- Structural abnormalities elsewhere can also allow loop formation (ante vs orthodromic tachycardia)
How does VT occur?
- Re-entrant or automatic trigger around scar tissue
- VT invades rest of ventricle
What causes the broad complex characteristics?
- Cell-cell activation, not conduction system
- Atria continue to activate and contract normally
How do you manage VT/VF?
- Resus if emergency
- Treat underlying pathology: Ischeamia, bradycardia, structured disease, metabolic or drug cause
- Anti-arrhythmias
-> Class one [+ICD back up]
-> Class 2+3 - Device ICD or Pacemaker
- Ablation
Whats the considerations when using amiodorone (K channel blocker)?
- Drug interactions ie warfarin, digoxin
- Many SE: Myalgias, insomnia, prolonged prothrombin time.
- Toxicity: Liver, renal failure, pulmonary fibrosis, corneal deposits
