by sasha darwazeh fy1 arrhythmias. types of arrhythmias site of abnormality: ● supraventricular...
TRANSCRIPT
By Sasha Darwazeh FY1
Arrhythmias
Types of arrhythmias
Site of abnormality:
●Supraventricular●Ventricular
Abnormalities of heart rate:
●Tachyarrhythmias●Bradyarrhythmias
Tachyarrhythmias
Supraventricular Tachycardias:
Atrial Fibrillation0.4% of population2.4-4% >60 year olds, 4% >80 years olds.
50% of paroxysmal & 15-20% of chronic AF are idiopathic.2º AF caused by dilatation, ↑ muscle mass, inflammation, infiltration & fibrosis.
Generally associated with LA hypertrophy.Ineffective contractions = blood stasis in atria → thrombus formation.If from LA, can cause CVA; in RA can cause PE's.
3 types of AF:Acute AF - associated with systemic disease, precipated by electrolyte disturbance or hypoxia, resolves with treatment of underlying pathologyParoxysmal AF - recurrent episodes of AF lasting <48 hours which can progress to:Chronic AF - aka permanent AF.
Risk factorsHTNHeart diseaseLung diseaseBinge drinkingHyperthyroidismCarbon monoxide poisoning
Clinical FeaturesEarly signs vague - fatigue & dyspnoea.Chronic phase- Irregular pulse (some impulses from atrial walls reach the ventricle, throwing it out of sinus rhythm).Force of contraction irregularDeteriorates with exerciseAbsent 'a' waves in JVPThromboembolic events - CVA & PE.
InvestigationsECG
Chronic AF- ECG
Paroxsysmal- 24h ECG.
Bloods
FBC
U+Es
TFTs
Imaging
CXR
Echo - size of LA, LV function.Transoesophageal echo for assessment of thrombus formation .
Management
Aim: return to SR.If not possible, control ventricular rate & thromboembolism risk
ConservativeAvoid alcohol & caffeine.Correct underlying pathologies - electrolyte disturbance, hypoxia.
MedicalAcute onset:If haemodynamicaly unstable → emergency cardioversion if life-threatening. IV amiodarone if not.
Paroxysmal - treat only if symptomatic:Beta-blockers 1st-line BISOPROLOLClass Ic antiarrhythmics 2nd-line FLECAINIDE or SOTALOL
ChronicRate-control<65; symptomatic; presenting 1st time; lone AF; or congestive heart failure.Digoxin + rate-limiting calcium-channel blocker i.e verapamil/diltiazem or digoxin + beta blocker.If fails pacemaker + ablation.
Rhythm-control>65; coronary heart disease; contraindications to antiarrhythmics or elctrical cardioversion; no congestive heart failure.1st line chemical cardioversion- amiodarone.2nd-line: flecainide/sotalol, amiodarone in structural heart disease.
Thromboprophylaxis- CHADS-VASc.Warfarin - ↓ incidence of stroke by 70%. INR 2-3.
SurgeryPercutaneous radiofrequency ablation: catheter up femoral vein to heart with radiological guidance. Ablate abnormal tissue.
Never use verapamil & beta blocker together as can cause heart block & asystole
Popular question in pharm exams!
Atrial flutterAtrial contraction rate >250-300 bpm.
Re-entrant circuit of excitation- it goes straight back into the atria instead of impulses only travelling to ventricles.Causes: IHD, hyperthyroidism, cardiomyopathy & rheumatic heart, idiopathic.
Clinical Features:PalpitationsChest painSOB
O/E:Regular, fast pulse'A' waves in JVP exceeds pulse rateCarotid compression may slow rateSigns of heart failure
InvestigationsECG:3:1 block (3 atrial contractions: 1 ventricular contraction) → saw-tooth2:1 block, P waves difficult to see.Carotid sinus pressure can uncouple atria & ventricles, revealing P waves.Consider in patients with a regular rate of 150 bpm.
Blood:U+EsTFTs
Imaging:Echo
ManagementDrugs- antiarrhythmics:Class Ia - DisopyramideClass Ic - Flecanide, PropafenoneClass III - Sotalol
DC CardioversionPacing
Re entry SVT'sCaused by 2nd connection between atria & ventricles, in addition to normal conduction system.
2 types:●AVRNT (Atrio-Ventricular Node Re-entry Tachycardia) - 2nd connection closely related to AV node.●AVRT (Atrio-Ventricular Re-entry Tachycardia) - 2nd connection not related to AV node.
Clinical Features:
Palpitations
Syncope/presyncope
Chest pain & polyuria (release of ANP due to ↑ atrial pressures from contraction of atria against closed AV valve.)
Symptoms often associated with exertion
Investigation:ECGRate 130-250. Narrow QRS complexP waves are inverted & one P wave per QRS complex.- masked by QRS complex (AVNRT)- or occur halfway between complexes (AVRT)
ManagementVagal - carotid sinus massage, valsalva manoeuvre, apply ice to faceDrugs- adenosine/verapamil.(Or flecanide, sotalol)Electrical - pacing & cardioversionAblation - burn away extra conduction pathway.
WPW aka pre-excitation syndrome
Abnormal accessory pathway between atrium & ventricle.Rare → 0.1-0.3% of the population. Males> females, young peoplePredisposition to sudden death.
Clinical Features:Mostly asymptomatic. Occasionally, palpitations/sudden death, general cardiac symptoms (SoB, dizziness or syncope)
InvestigationsECG: Delta wavePR interval <0.12s
ManagementAblation 1st line in symptomaticsIf unstable - cardioversionAmiodarone/procainamide
Ventricular Tachyarrhythmias
Ventricular FibrillationVentricular muscle fibres contract randomly causing complete failure of ventricular function.
Occurs in those with pre-existing disease i.e CHD.
Risk Factors:CAD & MIVT which often precedes to VFAntiarrhythmic drug adminsitrationHypoxiaIschaemiaAFRapid rates in pre-excitation syndromes (e.g. WPW)Shock during cardioversionElectric shockPacing to terminate VT
Clinical FeaturesMI → Chest pain, fatigue, palpitations
InvestigationsECG: VF and If survive look for evidence of MI, WPW etc.
Bloods●Cardiac enzymes: troponin-T 12 hours after onset of symptoms●U+Es: metabolic acidosis, hypokalaemia, hyperkalaemia, hypocalcaemia, hypomagnasaemia●Drug levels of any antiarrhythmic, particularly digoxin●Toxicology: cocaine can induce vasospasm●TSH: hyperthyroidism
CXR: signs of left heart failure, pulmonary hypertension
Echo: check for structural deficienciesAngiography
Management of VFShockable rhythmCheck for response
Check for pulse/ breathing for up to 10 seconds2222
Head tilt/chin liftGet help
Chest compressions 30:2Attach monitorAssess rhythm
Stand back & shockContinue compressions for 2 mins
Adrenaline IV every 2-3 mins
VTBroad-complex tachycardia (QRS >120ms/3 small squares).
Risk Factors:
Structural heart disease/CHD
Electrolyte disturbances: hypokalaemia, hypocalcaemia & hyponatraemia
Clinical Features:
Features of ischaemic heart disease or haemodynamic compromise. Chest pain, palpitations, dyspnoea, dizziness, syncope & symptoms of heart failure.
Investigations
ECG
Bloods: U+Es: particularly calcium, potassium & magnesium.
Levels of therapeutic drugs like digoxin
Trop T for MI
CXR -? heart failure
Management of VT●Pulseless VT: treat using ALS
●Unstable VT: synchronised cardioversion- can result in VF! Amiodarone 1st -line for haemodynamically unstable VT. Treat electrolyte disturbances.
●Stable VT: treat with IV lidocaine & cardioversion if lidocaine ineffective
●Refractory VT: amiodarone.
●Torsades de pointes (polymorphic VT) -●Acute(acquired) – Stop QT prolonging drugs ?examples●IV magnesium, then beta 1-adrenergic agonist (isoprenaline), temporary pacing●Long-term - beta-blockers (congenital), pacing
Bradycardias
Heart Block1st degree heart block - PR interval > 0.2s; no dropped QRS complex
2nd -degree heart blockType 1 (Mobitz I/Wenkebach) - PR interval ↑ with each beat until you get a dropped QRS complexType 2 (Mobitz II) - intermittent failure of P waves to conduct, not preceded by P wave elongation2:1 & 3:1 type - regularly dropped QRS complexes with a 2:1 or 3:1 ratio3rd -degree heart block (complete heart block) - P waves never conduct & are unrelated on ECG
Causes: usually CAD, inferior or anterior wall MI.
Management1st degree - no treatment2nd degree – pacemaker if consciousness is affected.3rd -degree – pacemaker
Atropine can be used if symptomatic
If patient has heart block, they need to avoid:●Anti-arrhythmics - amiodarone, flecainide.●Beta blockers - such as atenolol, bisoprolol, propanolol.●Calcium channel blockers - such as verapamil, diltiazem.
Bundle branch blockDelay of electrical conduction down either the left of right bundle branch.LBBB: aortic stenosis, dilated cardiomyopathy, MI, CAD.RBBB: atrial septal defect, PE, MI
ECG ChangesWiLLiaM & MaRRoWWide QRS complexes.
LBBB: there is a W shape in V1 and an M shape in V6.RBBB: there is an M shape in V1 and a W shape in V6
ManagementGenerally nothing but if bundle branch block is severe, needs pacemaker