Arrhythmias Flashcards
How does the heart work?
- Sinoatrial node fires electrical impulse (Sets normal pace of heart rhythm)
- Atrial depolarisation (Impulse travels through atria, contracts + empty blood into ventricles)
- AV node funnels impulse (Slows or blocks impulse too closely spaced giving time for blood to fill ventricles)
- Ventricular depolarisation (Impulse travels through ventricles + Contracts - pump blood to lungs + body)
- Atrial repolarisation (Atria recharge + refill w blood)
- Ventricular repolarisation (Ventricles recharge + refill w blood)
What are the types of arrhythmias?
Supraventricular:
- AF
- Atrial flutter
- Paroxysmal SV tachycardia
Ventricular:
- Ventricular tachycardia + fibrillation
- Torsade de pointes
What are the symptoms of AF?
- Palpitations
- Dyspnoea
- Dizzy
- Tired
What are the types of AF?
- Paroxysmal: episodes last <7 days
Usually stops w/in 48h - Persistent: episodes last >7 days
- Permanent: present all the time
What is the treatment for AF?
First line: Rate control:
- Beta-blocker (not sotalol)
- Rate limiting CCB (diltiazem, verapamil)
- Digoxin (sedentary patient + non-paroxysmal)
What is the treatment for AF if rate control is ineffective?
Offer dual therapy (AVOID beta-blocker + verapamil)
What is the treatment for AF in reduced LVEF?
Beta-blocker + digoxin
- Avoid CCB: may worsen condition
- BBlockers red sympathomimetic activity
What are the exeptions for rate control as first line for AF?
- New onset
<48h rate or rhythm >48h rate - HF (avoid diltiazem + verapamil)
- Reversible cause
- Atrial flutter suitable for ablation
What is used for rhythm control in AF?
Anti-arrhythmic drugs:
- Amiodarone
- Flecainide
- Propafenone (avoid in IHD (angina))
- Standard beta-blocker (1st line post-cardioversion)
What is used for stroke prevention?
Calculated using CHADsVASc
2+ (high risk): Offer warfarin or DOAC (non valvular)
What is the treatment for paroxysmal supraventricular tachycardia?
Reflex vagal nerve stimulation (parasympathetic NS activated)
- Face in ice cold water
- Valsalva manoeuvre - motion used when straining on defecation
If ineffective: IV adenosine, verapamil
Recurrent episodes: catheter ablation OR anti-arrhythmic drugs
What is the treatment for ventricular arrhythmias?
Pulseless or fibrillation: CPR + defibrillator
Maintenance: high risk of cardiac arrest:
- Cardioverter defibrillator implant OR
- Anti-arrhythmic drug
Haemodynamic instability: Direct current
- Stable + sustained: IV anti-arrhythmic drug
- Non-sustained: beta blocker
What is tosade de pointes caused by?
- Drugs that prolong QT prolongation
- Hypokalaemia
- Bradycardia (severe)
What are the symptoms of torsade de pointes?
- Syncope
- Seizures
- Palpitations
- Dyspnoea
What is the treatment for torsade de pointes?
IV magnesium sulphate
What is in Class I of the vaughn william classification?
Na+ channel blockers
- Flecainide (avoid in structural/IHD + CI in asthma)
What is in Class II of the vaughn william classification?
Betablockers
What is in Class III of the vaughn william classification?
K+ channel blockers
- Amiodarone
- Sotalol
- Dronedarone (hepatotoxicity and HF side effects)
What is in Class IV of the vaughn william classification?
Rate limiting Ca2+ channel blockers
- Diltiazem
- Verapamil
Which anti-arrhythmic drug is CI in asthma/COPD?
Adenosine + flecainide
What is the MOA of amiodarone?
Blocks K+ channels that repolarise heart during phase 3 of cardiac action potential
What is the indication of amiodarone?
- Arrhythmias
- CPR: revive pts w pulseless ventricular tachycardia/fibrillation
What is the oral loading dose of amiodarone?
- 200mg TDS - 1 week, BD - 1 week,
- OD maintenance
What are the side effects of amiodarone?
Corneal micro-deposits - crystals form in outer layer of eye causing glares + halos
Optic neuropathy
Grey skin
Phototoxicity
- broad spec SPF sunscreen for several months after stopping
Pulmonary toxicity
Thyroid dysfunction
Hepatotoxicity
- Monitoring: LFTs. Stop if 3x AST + ALT
Peripheral neuropathy - pins + needles. Numbness
QT prolongation
What is the MHRA alert for amiodarone?
Serious side effects may persist for a month/longer after stopping (long HL). Regular reviews. Monitor: LFT + TFT. CT scan if pulmonary toxicity suspected
What are the interactions of amiodarone?
- Enzyme inhibitors → inc amiodarone levels, risk of toxicity
- Amiodarone is an enzyme inhibitor → inhibits metabolism of other drugs (Digoxin - half dose of digoxin)
- Beta-blockers, digoxin → bradycardia
- Rate limiting CCB → cardio depression
- Statins → rhabdomyolysis (Simvastatin: max dose 20mg)
- QT prolongation - Drugs that cause hypokalaemia inc risk of torsade de pointes
- Isoniazid, metronidazole, nitrofurantoin, phenytoin, vinca alkaloid → peripheral neuropathy
What is the MOA of digoxin?
- Derived from fox glove plant
- Inc force of contraction by inhibiting Na+/K+ ATPase in myocardium
- Dec HR + SA node automaticity + AV node conductivity
What is the indication of digoxin?
- Sedentary patients with non paroxysmal atrial fibrillation
- Heart failure
What is the therapeutic index of digoxin and when should you monitor digoxin levels?
0.8 - 2MCG/L
- Samples taken 6 hours after dose
- If stable: no regular monitoring unless: Suspected toxicity OR RI (digoxin renally cleared)
What is the dose for digoxin?
Determined by RI + lower in elderly
Loading - rapid treatment in AF to restore sinus rhythm
Maintenance: OD
- Non-paroxysmal AF in sedentary patients: 125 - 240mcg
- Worsening or severe HF: 62.5 - 125mcg
- Switching from IV to oral: inc dose by 20% - 33% to maintain same digoxin levels
What are the signs of digoxin toxicity?
- Acute: N+V, diarrhoea, abdominal pain
- Chronic: yellow halos, confusion, delirium, arrhythmias
What increases the risk of digoxin toxicity?
Hypokalaemia: acts on same site as K on Na/K ATPase pumps, when potassium levels are low digoxin combined more easily inc effect
- Co-prescribe: potassium sparing diuretic
Renal impairment
Hypomagnesia
Hypercalcaemia
What are the interactions of digoxin?
- Hypokalaemia → predisposes digoxin toxicity
- Dose adjustment: 1/2 digoxin dose: amiodarone, quinine, dronedarone
- Inducers → RED digoxin levels = therapeutic failure
- ACEi/ARB, NSAIDs → RED renal excretion = toxicity
- Beta-blockers, rate limiting CCB → bradycardia
- Hypercalaemia (Vit D + calcium supplement) → predispose to digoxin toxicity
