Lecture 7.1 - Arrhythmias and ECG Changes PDF

Arrythmias: ◦Abnormal electrical activity in the heart ◦Abnormality in rate/rhythm/sequence of conduction/origin of conduction ◦Normal HR: 60-100bpm ◦Bradyarrythmias 100bpm Reasons for bradyarrythmias: ◦Decreased automaticity (initiate electrical activity by itself - heart d...

Arrythmias: ◦Abnormal electrical activity in the heart ◦Abnormality in rate/rhythm/sequence of conduction/origin of conduction ◦Normal HR: 60-100bpm ◦Bradyarrythmias 100bpm Reasons for bradyarrythmias: ◦Decreased automaticity (initiate electrical activity by itself - heart doesn't need help): ‣ Increased vagal tone (endurance athletes) - parasympathetic nervous system is overactivated ‣ Inferior wall MI - clot in right coronary artery can cause arrythmia ‣ Drugs that slow down conduction velocity (adenosine, beta blockers, calcium channel blockers, digoxin) ‣ Slow metabolic activity (hypothyroidism, hypothermia) ‣ Electrolyte imbalance - hyperkalaemia slows down conduction velocity, (K+, Mg2+ and Ca2+ can all decrease automaticity) ‣ High intracranial pressure (Cushing's triad) - low high rate and hypertension ‣ Lyme carditis - bacterial infection that induces bradycardia Bradyarrythmias: Classification and ECG changes: ◦Sinus bradycardia: ‣ After every p-wave there is QRS ‣ Slower HR but normal PR interval ◦AV nodal conduction delays ‣ First degree heart block Prolonged PR interval (> 5 small boxes) ‣ Second degree heart block Mobitz I (Wenckeback) ◦Progressive prolongation of PR interval ◦Dropped QRS complex Mobitz II ◦PR interval is fixed ◦Sudden drop of QRS complex ‣ Third degree heart block Inconsistent PR interval Dropping QRS complex and wide QRS Complete dissociation between atria and ventricles (different atrial and ventricular rates) Tachyarrythmias >100bpm: ◦Supraventricular tachycardia (SVT)/atrial tachycardia: ‣ Sinus tachycardia (SA node firing too fast) ‣ Focal atrial tachycardia (FAT) (one ectopic area in atria firing abnormally) ‣ Atrial fibrillation (AF) ‣ Atrial flutter - near the tricuspid valve ‣ AVNRT (AV nodal re-entrant tachycardia) - re-entering of a current  ‣ AVRT ◦Ventricular tachycardia (VT): ‣ Monomorphic VT - whole ECG strip shoes waves having the same amplitude ‣ Polymorphic VT ‣ Polymorphic VT with prolonged QT interval (Torsades Depointes - fatal) ‣ Ventricular fibrillation (VF) - fatal Reasons for tachyarrythmias: ◦Increased automaticity: ‣ Increased sympathetic tone - response to hypotension ‣ Sympathomimetic drugs (drugs like cocaine that mimic) ‣ Increased metabolic activity (fever, hyperthyroidism) ◦Triggered activity (irritable area (MI, ischaemic tissue etc) within ventricular or atrial myocardium) ‣ Due to early after depolarisations (EADs) -> electrolyte imbalance (caused by hypokalaemia) Polymorphic VT with prolonged QT interval - lethal (Torsades Depointes) ‣ Due to delayed after depolarisation (DADs) -> ischaemia FAT, MAT, VT ◦Re-entrant circuit: ‣ AVNRT, AVRT ‣ Atrial flutter (recurrent current in the atria at one point), atrial fibrillation (multiple re-entering circuits) ‣ Wolff-Parkinson-White syndrome - congenital Additional pathways in heart is known as accessory pathways Ventricles receiving current from any part of the heart other than the AV is a problem due to missing AV nodal delay ‣ VT (recurrent circuit in ventricle), VF (multiple recurrent circuitd in ventricles) Tachyarrythmias - ECG variations: ◦Narrow QRS (regular rhythm) ‣ Sinus tachycardia ‣ FAT ‣ AVRT, AVNRT ‣ Atrial flutter ◦Narrow QRS (irregular rhythm) ‣ Atrial fibrillation ‣ Atrial flutter with variable block ‣ MAT ◦Wide QRS (regular rhythm) - ventricular depolarisation ‣ VT (monomorphic) ‣ Bundle branch blocks ◦Wide QRS (irregular rhythm) ‣ VT (polymorphic) ‣ VF  Narrow QRS (regular rhythm): ◦Sinus tachycardia ‣ No waves missing ‣ All waves upright in respective leads ◦Focal atrial tachycardia: p-waves inverted in lead II, upright in aVR -> excess activity in a single point; signal goes away from positive electrode ◦AVRT, AVNRT: p-waves hidden within QRS or retrograde p-waves (p-wave comes at the tail of QRS) -> atria and ventricles depolarise at the same time ◦Atrial flutter: saw-tooth p-waves (II, III, avF), constant ratio ◦Regular rhythm can usually be corrected with fluids to increase blood volume. If not, drugs can be administered (ABCD drugs), which slow down the heart rate (AV conduction). Cardioversion can be used as a last resort to shock the heart back into its rhythm. Long-term correction includes defibrillation. Narrow QRS (irregular rhythm): ◦Atrial fibrillation (fibrillation waves in V1) ◦Atrial flutter with variable conduction (saw-toothed waves in II/III/avF/V1) with conduction ratios ranging from 2:1 to 4:1 ◦Multi-focal atrial tachycardia (3 or more morphologically different p-waves in the same lead) Wide QRS (regular rhythm): ◦Wide QRS (regular rhythm) ‣ VT (monomorphic) ‣ Right bundle branch block (RBBB) RSR' pattern in V1-3 (M-shaped wave), inverted T waves Wide, slurred S waves (V5-6) ‣ Left bundle branch block (LBBB) Dominant S wave in V1 Broad, notched (M shaped) R wave Wide QRS (irregular rhythm): ◦Wide QRS (irregular rhythm) ‣ VT (polymorphic) Normal QT interval Prolonged QT interval (>500 ms) ‣ VF ECG changes in hyper and hypokalaemia:  ECG changes in myocardial infarction: ECG evolution during acute STEMI