by sasha darwazeh fy1 arrhythmias. types of arrhythmias site of abnormality: ● supraventricular...

Download By Sasha Darwazeh FY1 Arrhythmias. Types of arrhythmias Site of abnormality: ● Supraventricular ● Ventricular Abnormalities of heart rate: ● Tachyarrhythmias

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  • By Sasha Darwazeh FY1 Arrhythmias
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  • Types of arrhythmias Site of abnormality: Supraventricular Ventricular Abnormalities of heart rate: Tachyarrhythmias Bradyarrhythmias
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  • Tachyarrhythmias
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  • Supraventricular Tachycardias:
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  • Atrial Fibrillation 0.4% of population 2.4-4% >60 year olds, 4% >80 years olds. 50% of paroxysmal & 15-20% of chronic AF are idiopathic. 2 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 pathology Paroxysmal AF - recurrent episodes of AF lasting
  • Chronic Rate-control 65; coronary heart disease; contraindications to antiarrhythmics or elctrical cardioversion; no congestive heart failure. 1 st 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. Surgery Percutaneous radiofrequency ablation: catheter up femoral vein to heart with radiological guidance. Ablate abnormal tissue.
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  • Never use verapamil & beta blocker together as can cause heart block & asystole Popular question in pharm exams!
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  • Atrial flutter Atrial 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: Palpitations Chest pain SOB O/E: Regular, fast pulse 'A' waves in JVP exceeds pulse rate Carotid compression may slow rate Signs of heart failure
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  • Investigations ECG: 3:1 block (3 atrial contractions: 1 ventricular contraction) saw-tooth 2:1 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+Es TFTs Imaging: Echo Management Drugs- antiarrhythmics: Class Ia - Disopyramide Class Ic - Flecanide, Propafenone Class III - Sotalol DC Cardioversion Pacing
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  • Re entry SVT's Caused by 2 nd connection between atria & ventricles, in addition to normal conduction system. 2 types: AVRNT (Atrio-Ventricular Node Re-entry Tachycardia) - 2 nd connection closely related to AV node. AVRT (Atrio-Ventricular Re-entry Tachycardia) - 2 nd 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
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  • Investigation: ECG Rate 130-250. Narrow QRS complex P waves are inverted & one P wave per QRS complex. - masked by QRS complex (AVNRT) - or occur halfway between complexes (AVRT) Management Vagal - carotid sinus massage, valsalva manoeuvre, apply ice to face Drugs- adenosine/verapamil.(Or flecanide, sotalol) Electrical - pacing & cardioversion Ablation - burn away extra conduction pathway.
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  • WPW aka pre-excitation syndrome Abnormal accessory pathway between atrium & ventricle. Rare 0.1-0.3% of the population. Males> females, young people Predisposition to sudden death. Clinical Features: Mostly asymptomatic. Occasionally, palpitations/sudden death, general cardiac symptoms (SoB, dizziness or syncope) Investigations ECG: Delta wave PR interval
  • VT Broad-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
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  • Management of VT Pulseless VT: treat using ALS Unstable VT: synchronised cardioversion- can result in VF! Amiodarone 1 st -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
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  • Bradycardias
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  • Heart Block 1 st degree heart block - PR interval > 0.2s; no dropped QRS complex 2 nd -degree heart block Type 1 (Mobitz I/Wenkebach) - PR interval with each beat until you get a dropped QRS complex Type 2 (Mobitz II) - intermittent failure of P waves to conduct, not preceded by P wave elongation 2:1 & 3:1 type - regularly dropped QRS complexes with a 2:1 or 3:1 ratio 3 rd -degree heart block (complete heart block) - P waves never conduct & are unrelated on ECG Causes: usually CAD, inferior or anterior wall MI.
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  • Management 1 st degree - no treatment 2 nd degree pacemaker if consciousness is affected. 3 rd -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.
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  • Bundle branch block Delay 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 Changes WiLLiaM & MaRRoW Wide 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 Management Generally nothing but if bundle branch block is severe, needs pacemaker
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