Cardiac arrhythmias. The arrhythmia. The arrhythmia. The arrhythmia. The arrhythmia. Surgical Meeting. Cardiorespiratory focus. Carlos F.

Transcription

1 Surgical Meeting Cardiorespiratory focus Cardiac arrhythmias Carlos F. Agudelo Carlos F. Agudelo VFU Brno VFU Brno Importance -Decrease in cardiac output: hypotension a decreased tissue and coronary perfusion -Sign of extra-cardiac disease (trauma, inflammation, cancer) -Sudden death -Breed: - Signalement WHWT, Springer Spaniel, Boxer, Doberman, etc. -Colour - History Exercise intolerance Dyspnoea Palpitations Fanting episodes Long term cardiac disease (drugs) Trauma Inflammation Cancer (therapy) - Clinical Hypotension Pale MM Irregular heart beats Pulse deficit Sudden death Ventricular arrhythmia -Cardiomyopathy Supraventricular arrhythmia -Enlargement of the atria Diagnosis -Myocarditis / endocarditis -Myocarditis / endocarditis -Myocardial hypoxia -Ongoing heart disease -Congenital heart disease -Ischemic foci in the atria -Digitalis intoxication -Electrolytic abnormalities -Drugs (digitalis, anesthetics) -Abnormal AV pathways ECG Holter event recorders -Hypothermia -Systemic disease -Systemic disease 1

2 Diagnosis Atropine SC, IM, IV: mg/kg Classification according to 1-Rhythm 2-Origin and transmission 3-Time interval 4-Frequency 5-Aetiology -Bradyarrhythmia vs. tachyarrhythmia b) Sinus block - arrest a) Sinus bradycardia - PQRST- -trained individuals -Increase vagal stimulation c) Atrioventricular (AV) block 1 st degree AV block 2 nd degree AV block M2 2 nd degree AV block M1 3 rd degree AV block 2

3 Tachycardia a) Sinus tachycardia b) Atrial tachycardia c) Ventricular tachycardia Origin and transmission a) Supraventricular Atrial premature complexes Origin and transmission b) Nodal junctional escape complexes Nodal complex Atrial fibrillation Nodal rytmus Origin and transmission c) Ventricular Ventricular tachycardia -Premature Time interval Slow vent. tachycardia (accelerated idioventricular rhythm) Idioventricular rhythm -Escape (after pauses) 3

4 Frequency pathology -Isolated - Physiologic = sinus arrhythmia -Paroxismal -Persistent pathology pathology b) Primary disease = DCM -ARVD pathology c) Secondary trauma / abdominal disease / hypoxic situations / neoplasia / drugs -Not only heart disease -Based on the history, clinical findings (auscultation, pulse palpation), blood pressure, laboratory findings, and others -Each antiarrhythmic drug has also pro-arryhthmic effects 4

5 Supraventricular arrhythmias -Physiologic or compensatory be aware Supraventricular arrhythmias: APC, SVT, AF -Acute onset of congestive heart failure -Vagal manoeuvre or thump -Goal at home: dogs beats/min; cats 200 beats/min. -Some cases of pre-clinical DCM: β-blockers? Cardioversion? -Pharmacological intervention Supraventricular arrhythmias acute management -Diltiazem 0.25 mg/kg IV bolus over 2 minutes. Repeat bolus at 15 minute intervals until conversion (max. dose of 0.75 mg/kg). -Verapamil 0.05 mg/kg slow IV bolus. Repeat boluses up to a total dose of 0.15 mg/kg. -Esmolol (incremental doses of 0.05 to 0.1 mg/kg q 5 min up to a maximum dose of 0.5 mg/kg). AF chronic therapy - Digoxin Dogs: 0,005-0,01mg/kg PO. SID-BID (dogs >20kg: 0,22 mg/m 2 ). Maximal dose in Dobermans is 0.25 mg BID. - Digoxin Cats to mg/kg SID PO. ¼ tablet mg ( mg/cat) PO in a 2-3 kg = ¼ q48h; 4-5 kg = ¼ SID; 6 kg or > = ¼ BID. Levels are measured after 1 week of therapy (0.5-2 ng/ml). Watch out digoxin toxicity (about 15% of cases) and renal disease (decrease dose by 30-50%). PLUS - Diltiazem: dogs: mg/kg PO, BID-TID, cats mg/cat PO SID, BID - ß-blockers (atenolol or metoprolol) AF chronic therapy -Cases with normal thoracic radiographs and echocardiogram = conversion back to sinus rhythm. Quinidine: 6-11 mg/kg IM, PO, QID. PLUS Diltiazem or sotalol may convert atrial fibrillation to sinus rhythm in some dogs. Amiodarone? Isolated VPCs. -Treat? Dogs: No, however be aware of breed predisposition Cats: Further investigate 5

6 Ventricular trigeminy duplets and triplets. Treat? +/- Yes: clinical signs or recent or known cardiac disease (predisposition) No: without findings and normal heart frequency. Further investigation Monomorphic slow ventricular tachycardia (<180 beats/min) ventricular bigeminity. Treat? Yes: digoxin, clinical signs or recent or known cardiac disease (predisposition) Polymorphic ventricular tachycardia. Treat? Yes -Several locations. Be aware of worsening at any moment Ventricular tachycardia (heart frequence higher than 200 beats/min) Yes -Risk for sudden death Persistent ventricular tachycardia Yes -General myocardial dysfunction -Sudden death -Secondary pathology Ventricular tachycardia -Lidocain: bolus 2,2 mg/kg slow IV. Max. 4 applications (total 8,8 mg/kg). Continue CRI (40-75[100] μg/kg/min) -If ineffective = combination of different antiarrhythmic drugs 6

7 Ventricular tachycardia If ineffective β-blockers Esmolol: Bolus μg/kg IV up to 500 μg/kg. Continue CRI μg/kg/min (Tilley et al 2010). Amiodarone: Bolus 3-5 mg/kg IV. Continue CRI μg/kg/min (Ware et al 2011). *Ventricular tachycardia chronic oral therapy Metoprolol: 0,2-0,5 mg/kg BID Amiodarone: 8 to 15 mg/kg BID for 7 days, then 5 to 10 mg/kg BID Sotalol: 1-3,5 mg/kg PO, BID. Atenolol: mg/kg BID alone or in combination with mexiletinem (5-8 mg/kg BID-TID). Ventricular Fibrillation -Immediate electrical defibrillation -Drug therapy alone (virtually ineffective) *Intravenous amiodarone (3-5 mg/kg) and magnesium ( meq/kg) *Low doses of epinephrine Bradyarrhyhtmia. Low probability of pacemaker implantation -sinus bradycardia, -sinus arrest or block -1st degree and some cases of 2nd AV blocks Bradyarrhyhtmia. High probability of pacemaker implantation -Advanced 2nd AV block -3rd AV block -Sick sinus syndrome Bradyarrhyhtmia -Negative = (no reaction) = pacemaker implantation -Positive or limited pacemaker implantation -primary problem Salbutamol: 0,05 mg/kg PO, BID Aminophillyn: 5-10 mg/kg PO, TID-QID (extended release) 7

8 Questions? 8