Cardiovascular

• Arrhythmias


  Changes in rate or rhythm
• Impulse generation and conduction


  1. Impulses arise in SAN (pacemaker)

  2. Conducted across both atria to the AV node

  3. Down the bundle of His into the purkinje fibres
• Atria and ventricles


  • Atria contract before ventricles to ensure optimal filling
• Arrhythmias


  Changes to impulse generation or impulse conduction
• Ventricular fibrillation


  Ventricles cease to beat properly and quiver (LIFE THREATENING)
• Atrial fibrillation


  Most common arrhythmia - atria beat irregularly, chaotic signals generated from sources other than the SAN, leading the atria to 'quiver' instead of contracting
• Atria do not contract regularly


  Blood doesn't empty efficiently into ventricles, pools in the atria creating clots which can travel to the brain leading to stroke
• All patients with atrial fibrillation should undergo assessment of stroke risk
• Causes of atrial fibrillation


  • Cardiac causes (hypertension, valvular heart disease, heart failure, ischaemic heart disease)
  • Respiratory causes (chest infection, lung cancer)
  • Systemic causes (excessive alcohol, hyperthyroidism, electrolyte depletion, infection, diabetes)
• Management for acute atrial fibrillation


  1. Rate control or rhythm control

  2. If onset within 48 hours - urgent electrical cardioversion if haemodynamically unstable

  3. If onset within 48 hours without instability - rate or rhythm control

  4. If onset >48 hours or uncertain - rate control preferred

  5. If rate control - beta blocker or verapamil (if LVEF >=40%)

  6. Consider pharmacological or electrical cardioversion for rhythm control
• Management for non-acute atrial fibrillation


  1. Offer rate control as first-line except in certain cases

  2. Offer beta-blocker or rate-limiting calcium-channel blocker for rate control

  3. Consider digoxin monotherapy if other options ruled out

  4. Combination therapy if single drug fails

  5. Consider rhythm control if symptoms not controlled
• Cardioversion


  1. Electrical cardioversion - sending electrical signals to restore sinus rhythm

  2. Pharmacological cardioversion - anti-arrhythmic drugs like flecainide or amiodarone
• If AF duration >48 hours, cardioversion should not be attempted until patient has been anticoagulated for 3 weeks
• Paroxysmal atrial fibrillation


  Episodes of AF that stop within 7 days, usually within 48 hours, without treatment
• 'Pill-in-the-pocket' strategy


  Taking antiarrhythmic drugs only when an episode starts, for those with infrequent paroxysms and few symptoms
• Dronedarone may be considered as a second-line treatment option for persistent or paroxysmal AF
• Beta-blockers licensed for atrial fibrillation


  • Atenolol, acebutolol, metoprolol, nadolol, oxprenolol, propranolol
• Anti-arrhythmic drug classification


  Class I - Na+ channel blockers, Class II - Beta-blockers, Class III - K+ channel blockers, Class IV - Rate limiting CCBs
• Class I anti-arrhythmic drugs


  • Disopyramide (1A), Lidocaine (1B), Flecainide/Propafenone (1C)
• Amiodarone should be considered 4 weeks before and 12 months after cardioversion to increase effectiveness and maintain sinus rhythm
• Dronedarone has hepatotoxic and heart failure side-effects
• Digoxin


  Used in sedentary patients with non-paroxysmal AF and in patients with associated CHF
• Adenosine


  Contraindicated in COPD/asthma
• Stroke prevention in AF

  1. Assess stroke risk using CHA2DS2-VASc score

  2. Offer anticoagulation with DOAC if score >=2, considering bleeding risk

  3. Consider anticoagulation with DOAC if male with score of 1, considering bleeding risk

  4. Do not offer anticoagulation if very low stroke risk (score 0 for men, 1 for women)

  5. Assess bleeding risk using ORBIT score
• Atrial flutter


  Atria beat regularly but faster than usual and more often than the ventricles
• Management of atrial flutter


  1. Control ventricular rate or restore sinus rhythm

  2. Ventricular rate controlled by beta blocker, diltiazem, or verapamil

  3. Digoxin can be added if rate control inadequate

  4. Conversion to sinus rhythm - electrical or pharmacological cardioversion, or catheter ablation
• If atrial flutter duration is unknown or >48 hours, cardioversion should not be attempted until patient has been fully anticoagulated for 3 weeks
• Anti-arrhythmic drugs have limited role in atrial flutter as their use is not always successful
• Paroxysmal supraventricular tachycardia


  Extra electrical pathway in the heart causes a rapid heartbeat by a short-circuit
• Management of paroxysmal supraventricular tachycardia


  1. Terminate spontaneously with vagal nerve stimulation (Valsalva manoeuvre, cold water immersion)

  2. IV adenosine if above doesn't work (contraindicated in COPD/asthma)

  3. IV verapamil as last resort
• Ventricular rate controlled by


  Beta blocker, diltiazem, or verapamil
• Digoxin


  Can be added if rate control remains inadequate
• Conversion to sinus rhythm


  Electrical or pharmacological cardioversion or catheter ablation
• If the duration is unknown or lasted for over 48 hours, cardioversion shouldn't be attempted until the patient has been fully anticoagulated for at least 3 weeks
• Oral anticoagulation should be given after cardioversion and continued for at least 4 weeks
• Limited role for anti-arrhythmic drugs as their use is not always successful
• Patients should be assessed for their risk of stroke and the need for thromboprophylaxis
• Paroxysmal supraventricular tachycardia can terminate


  Spontaneously reflex vagal nerve stimulation e.g., with the Valsalva manoeuvre by immersing face in cold water
• I/V adenosine


  Used if the above doesn't work (c/i in COPD / asthma)
• I/V verapamil


  Used as last line