Ventricular Arrhythmias

1. Ventricular Arrhythmias

2. Bundle Branch Block • Conduction blockage in left or right Purkinje bundle • ECG – wider QRS complex (>.12s) • Shape dependent on left or right • Right – Late activation of right ventricle • Broad S waves in leads 1 and V6 • Tall late R wave in lead V1 • rsR pattern in V1 • Left – Late activation of left ventricle • Broad QS waves in lead V1 • Broad notched R wave in leads 1 and V6 • Abnormal Q waves

3. Bundle Branch Block – Clinical Features and Causes • Usually assymptomatic • RBBB • Wide splitting of S2 – physiological • Alone, RBBB does not alter electrical axis of heart • Causes – Congenital heart diseases, pulmonary disease, myocardial disease • LBBB • Reverse splitting of S2 • Complete LBBB associated with extensive left ventricular disease • Causes – left ventricular outflow obstruction, CAD

4. Premature Ventricular Complexes Caused by AP initiated and propagated away from ectopic focus in ventricle → early ventricular depolarisation and contraction Followed by a missed beat (compensatory pause) ECG patterns variable – depends on site of origin Volume of blood ejected by PVC – less then normal Volume of blood ejected following pause – greater

5. Premature Ventricular Complexes • Can occur in patterns • Bigeminy – every 2nd • Trigeminy – every 3rd • Multifocal – arising from different sites

6. PVC – Clinical Features Healthy people Excessive caffeine Anaemia Anxiety Organic heart disease Medications Metabolic abnormalities – incl hypoxia, hypokalemia, acidosis, alkalosis, hypomagnesium Only treat if symptomatic – using beta blockers

7. Ventricular Tachycardia 3 or more PVCs in a row Wide abnormal QRS complex with an LBBB pattern May occur for short periods or sustained run (>30s) HR – 120-250 beats/min Causes – MI, PVC landing on a T wave, cardiac drug toxicity, electrolyte imbalance Tendency to transition into ventricular fibrillation

9. Sustained Ventricular Tachycardia • Results in haemodynamic compromise • Clinical signs and symptoms • Dizziness • Syncope • Hypotension • Cardiac arrest • Intermittent cannon ‘a’ wave in JVP • Variable intensity of S1 • BUT may be well tolerated in some patients

10. VT - Treatment • Emergency • Sustained polymorphic VT – defibrilate – following ALS algorithm • If not haemodynamically compromised ie. BP and CO maintained – use IV therapy with amiodarone • First line drug treatment is lignocaine infusion – chemical cardioversion • If medical therapy is unsuccesful DC cardioversion is necessary • Long term • VT patients w/ structural heart disease – ICD implantation • Those with history of VT -prevention with anti arrhythmic drugs • Catheter ablative therapy (pt with structural heart disease) – cure rate of 80%

11. Long QT Syndrome • ECG where ventricular repolarisation (QT interval) is greatly prolonged (>440ms) • Congenital Long QT – 8 different genetic mutations • Defects in cardiac ion channels responsible for repolarisation • Enhanced Na or Ca inward • Inhibit K outward • Genotype influences prognosis and determines treatment • Triggers – vary but include exercise, emotional stress, sleep, certain drug exposures (egsalatol – changes channel function) • Treatment – varies but may include B blockers (but contraindicated in some types) • ICD if life threatening arrhythmia , pt with syncope , male with LGT3, if QT greater then 500ms

12. Ventricular Fibrillation • Rapid and irregular ventricular activation with no mechanical effort • Usually provoked by ventricular ectopic beat • ECG • Shapeless rapid oscillations, no organised complexes

13. VF • Signs and symptoms • Pulseless • Becomes rapidly unconscious • Cardiac arrest • Rarely reverses spontaneously • Treatment – BLS and ALS • Defibrillation is only effective treatment • If related to MI (within 2 days) prophylactic therapy not rqd • If not related to MI – long term risk of recurrent cardiac arrest and sudden deat • First line therapy is ICD