docArrythmias presentation by Prof Celia Marr
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Arrythmias presentation by Prof Celia Marr
Cardiac dysrhythmias in horses Celia M Marr [email protected] Control of heart rate at rest • Equine resting heart rate is low: 25 - 42 bpm • Horses have very little or no sympathetic tone at rest • Parasympathetic tone is high • The vagus innervates both the sinoatrial and the atrioventricular nodes • The horse can reduce its heart rate by delaying conduction at the atrioventricular node 3 © cmarr 2013 SECOND DEGREE ATRIOVENTRICULAR BLOCK • • • First: • closure of the atrioventricular valves • opening of the semilunar valves Second: • closure of the semilunar valves • opening of the atrioventricular valves Fourth: • atrial systole Le-lub-dub 4 Le-lub-dub © cmarr 2013 Le Le-lub-dub ECG Interpretation 5 SECOND DEGREE ATRIOVENTRICULAR BLOCK P QRST P QRST P P P P Sinus rhythm restored during exercise © cmarr, 2013 6 QRST P QRST Pathogenesis of atrial fibrillation RE-ENTRY Requires an area of Unidirectional block UNIFORM REFRACTORY PERIODS CRITICAL ATRIAL MASS © cmarr, 2013 VARIABLE REFRACTORY PERIODS Pathogenesis of atrial fibrillation Normal heart: high vagal tone maintains low heart rate Intermittent conduction through atrioventricular node Irregular R-R interval with f waves © cmarr, 2013 8 Significant underlying heart disease: increased sympathetic tone: high ventricular rate Pathogenesis of atrial fibrillation CRITICAL ATRIAL MASS VARIABLE REFRACTORY PERIODS • High vagal tone • normal horses • Myocardial pathology • Electrolyte disturbances disease • Normal horses • Atrial enlargement • Mitral or tricuspid regurgitation • Congenital heart disease 9 © cmarr 2013 ATRIAL FIBRILLATION: PRESENTING SIGNS • Atria contribution to ventricular filling = 15% • With no other cardiac disease, AF will only cause exercise intolerance if in vigorous exercise • Racehorses, Eventers, some hunters • Can be an incidental finding • Breeding stock, hacks, some show jumpers 10 © cmarr 2013 ATRIAL FIBRILLATION • Exercise intolerance/poor performance • Reluctance to participate in exercise • Irregularly-irregular cardiac rhythm • intermittent long pauses interspersed with rapid runs • no fourth heart sound • loud third heart sound • Variable pulse quality • Variable intensity of heart sounds • Exercise-induced pulmonary haemorrhage 11 © cmarr 2013 PAROXYSMAL ATRIAL FIBRILLATION Ohmura H et al, JAVMA, 2003, 223, 84-88 • gastrointestinal disease (ventricular arrhythmias more common) • exercise-induced • minimum frequency = 0.03% (no. of episodes/no.of starts) minimum prevalence = 0.29%(no. of horses with AF/no. of horses) • prevalence in slow/non-finishing horses = 1.39% • recurrence rate = 6.1% (10 year study, 115 horses, 108 single episode, 6 two episodes, 1 three episodes • 92% resolved spontaneously within 24 hours without treatment, • 12 2 with 15-20g QS at 24 hours, 2 spontaneously within 48 hours, 4 with 15-20g QS within 48-120 hours © cmarr 2013 Sustained Atrial Fibrillation Diagnostic Approach Goal • identify and characterise any underlying cardiac disease • clinical exam • echocardiography • clinical pathology 13 © cmarr 2013 • Atrial fibrillation is an effect and not a cause of congestive heart failure 14 © cmarr 2013 Clinical Findings that might indicate underlying heart disease: • tachycardia • heart rate > 50 bpm • cardiac murmurs • particularly murmurs of AV regurgitation • venous distension and pulsation • peripheral oedema 15 © cmarr 2013 CLINICAL DECISION-MAKING Incidental Finding Athlete with exercise intolerance Heart failure Cardioversion Palliative furosemide digoxin ACE inhibitors No treatment 16 © cmarr 2013 Quinidine • Class 1A sodium channel blocker • Prolongs the effective refractory period • Decreases myocardial conduction velocity & prolongs QRS and QT intervals • • • • 17 Vagolytic Alpha-adrenergic antagonist Proarrhythmic Gastrointestinal ulceration © cmarr 2013 18 © cmarr 2013 Quinidine Sulphate 6 4 2 0 0 2 4 6 8 10 12 14 16 18 20 22 • Administer by nasogastric tube until either normal sinus rhythm restored or serious side-effects occur © cmarr 2013 Extra-cardiac side effects • • • • • • • respiratory stridor penile protrusion neurological deficits flatulence diarrhoea colic tend to be seen in horses that require prolonged treatment • GI effects are the main cause of treatment failure 20 © cmarr 2013 Cardiovascular side-effects • hypotension • rapid supraventricular tachycardia • ventricular arrhythmias • both potentially fatal arrhythmias • independent of plasma concentrations • monitor the ECG continuously 21 © cmarr 2013 Hypotension ALPHA ADRENERGIC ANTAGONIST 22 • • keep the horse calm • iv fluids (or phenylephrine) may be necessary do not allow any form of exercise during treatment © cmarr 2013 Ventricular Arrhythmias PROARRHYTHMIC EFFECT • Magnesium sulphate • Propanolol • Lignocaine • NOT Procainamide (same class as quinidine) 23 © cmarr 2013 Atrial fibrillation: Pre-treatment Supraventricular tachycardia: ventricular rate around 200 Supraventricular tachycardia with variable conduction following digoxin Normal sinus rhythm 24 © cmarr 2013 RAPID SUPRAVENTRICULAR TACHYCARDIA VAGOLYTIC EFFECT • Emergency treatment required if ventricular rate > 120 /min and rising • • • 25 Digoxin Propanolol Diltiazem © cmarr 2013 Can we predict which horses will develop major problems during quinidine treatment? IN ADVANCE • Tachyarrhythmias • not really - appears to be an individual horse, idiosyncratic response • GI and other extra-cardiac side effects • prolonged treatment duration, usually horses with under-lying heart disease and/or longstanding AF 26 © cmarr 2013 Can we predict which horses will develop major problems during treatment? DURING TREATMENT • Prolonged QRS duration • Ventricular premature depolarisation • Long QT and ST segment changes 27 © cmarr 2013 How many horses develop major problems during quinidine treatment? • Depends on case type • dose and duration of treatment are influenced by AF duration and underlying heart disease • Variable population including older animals around 40% have side-effects • Young, racing STD/TBs have problems less commonly • Life threatening arrhythmias: 4 - 8% • Diarrhoea: 15 - 25 % 28 © cmarr 2013 Electrical Cardioversion RA RPA LA LPA Frye et al, 2002, J. Am Vet Med Assoc, 2002; 220: 1039-1045. McGurrin MK, Physick-Sheard PW, Kenney DG.J Vet Intern Med 2008;22:609-615. McGurrin MK, Physick-Sheard PW, Kenney DG, et al. J Vet Intern Med 2005;19:695-702. McGurrin MK, Physick-Sheard PW, Kenney DG, et al. J Vet Intern Med 2003;17:715-718. De Clercq D, van Loon G, Schauvliege S, et al. Vet J 2008;177:198-204. 29 © cmarr 2013 McGurrin, KJ, Physick-Sheard, PW, Kenney, DG (2005) How to perform transvenous electrical cardioversion in horses with atrial fibrillation J. Vet. Cardiol. 7, 109-119 RPA LPA 30 © cmarr 2013 31 © cmarr 2013 Side-effects: fatal arrhythmias • Ventricular fibrillation • Third degree AV block 32 © cmarr 2013 Atrial Fibrillation and poor performance Onset within last 48 hours Monitor 33 Onset >48 hours, < 3 - 4 months normal echocardiogram Quinidine sulphate © cmarr 2013 Uncertain or prolonged duration, mild heart disease Quinidine failure 1. DC conversion, 2. alternative anti-dysrhythmics Long-term Prognosis Depends on • degree of underlying cardiac disease • duration prior to treatment • less than 3 months • recurrence rate 15% • greater than three months • recurrence rate 60% • higher prevalence of side-effects associated with prolonged duration of treatment 34 © cmarr 2013 Does sustained atrial fibrillation cause collapse or death during exercise? 35 • Typically, horses with sustained atrial fibrillation do NOT collapse • Sudden onset (paroxysmal) AF can be associated with collapse or severe distress • Some horses with sustained AF have exerciseinduced ventricular tachycardia or inappropriately high ventricular rates • Some horses will have EIPH at relatively low intensity exercise © cmarr 2013 ORIGIN OF PREMATURE DEPOLARISATIONS Base-apex lead Sinus: bifid P negative QRS Supraventricular: premature abnormal P with normal QRS-T Ventricular No P premature abnormal QRS-T © cmarr, 2013 36 PATHOGENESIS OF TACHYARRHYTHMIAS Primary Myocardial disease • Viral • • Bacterial • Toxic • • Nutritional • • Neoplasia • Idiopathic Parasitic Cardiomyopathy Secondary to other factors • Hypoxia • Endotoxaemia • Electrolyte disturbances • Acid-base disturbances • Catecholamine-induced • Vagally-induced Immune-mediated © cmarr 2013 • Hypocalcaemia, hypomagnesaemia, hypokalaemia and metabolic acidosis © cmarr 2013 Clinical management of tachydysrhythmias • High index of suspicion required • Judge arrhythmias by the company they keep • Aim treatment at underlying cause • Reserve specific anti-arrhythmic therapy for life-saving situations 39 © cmarr 2013 Summary • Many normal horses have bradydysrhythmias at rest that are of no clinical significance • Atrial fibrillation is the most important clinically significant arrhythmia • Atrial fibrillation requires treatment if it is affecting the horse's role as a performance animal • Other tachydysrhythmias are seen occasionally, usually secondary to physiological/pathophysiological states associated with exercise or systemic illness 40 © cmarr 2013 DVD includes 70 cases contributed by 17 authors 42 © cmarr 2013 If you buy this book also buy a stethoscope speaker pad: www.blaufuss.org
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Atrial Fibrillation (AF) is the most common type of arrhythmia that causes an irregular and often fast heart rhythm. Over the past two decades, an increasing prevalence of atrial fibrillation cases is seen across the globe.
