Arrhythmias Flashcards
Findings of ORCA study for Afib
prospective study of rate control treatment in dogs with AF with various aetiology.
Use of holter HR to assess if rate control (<125bpm) was assoc with outcome.
Achieving a mean HR ≤125 bpm was associated with a 74% reduction in the risk of death.
After adjusting for CHD and NT-proBNP, risk of death increased by 35.5% for every 10 bpm increase in mean HRHolter
Similar earlier retrospective study reported Mean HR based on holter recording at home was independently assoc with all cause mortality
Both higher CRP and larger left atrial dimensions significantly increased the odds of not achieving rate control
Left atrial size (LA : Ao) at time of enrollment was strongly associated with ability of a dog to achieve a meanHRHolter ≤125 bpm
For each 0.1 unit increase in LA : Ao ratio, the odds of not-achieving a meanHRHolter ≤125 bpm increased by 31%. Similar to earlier study that reported larger left atrial size as an independent risk factor for sudden cardiac death.
In ORCA, presence of CHF most likely contributed to cardiac-related death in dogs with AF, as suggested by univariate analysis. However, CHF was not an independent risk factor for mortality in final exploratory Cox proportional hazards multivari-able mode
The relationship of primary (lone) AF and survival could not be analysed because none of the dogs in the primary AF group died during the study
Treatment for SVT
SVT - suppress ectopic pacemaker firing
Ca channel blockers (as SA node dependent on this for depol) - eg diltiazem or verapamil in acute setting
B blockers - removes SNS input. if no evidence of heart failure with compensatory input from SNS keeping dog alive
Chronic - diltiazem + digoxin
Treatment of Afib
Slow conduction to maximise CO
- maximise diastolic potential with digoxin and diltiazem
Can add B blocker in if above are ineffective and no signs of CHF
Also trial vagal manoeuvre
Causes of Vent arrhythmia
DDX: structural heart disease (DCM, HCM, congenital)
Heart failure
Trauma
Inflammation (endo/myo-carditis)
Myocardial ischaemia/infarction
Systemic dz: splenic, hypoxia (anaemia, resp); hypoK; hypoMg, acidosis); autonomic imbalance;
systemic inflammation; abdominal organ dz
ARVC - Boxer
DCM - Doberman
Inherited - GSD
Treatment of VPC, VTac
Lignocaine in acute setting (targets diseased myocardial cells)
Mixelitine is oral form of this
Chronic - sotalol for polymorphic
Mixelitine
Causes of AV block
Tissue around SA node fails to conduct the depol to atria and ventricles
1st = degenerative or inflammatory disease of conduction tissue. Also 2ry to digoxin, B blockers, Ca channel blockers, hyperK, high vagal tone)
2nd = type I most likely increased vagal tone.
Type II more likely caused by disease of AV node. More P waves blocked the more severe it is and may cause clinical signs of reduced exercise tolerance
Hereditary in some Pugs, hyperthyroidism.
3rd = usually unknown. Possible degenerative disease
Cause of BBB
an intraventricular conduction defect may result from a delay or block in one or more of the conduction pathways below the Bundle of His. The delay in the process of depolarization results in a change in the configuration of the QRS complex, lengthening the duration of the QRS complex beyond its normal limits.
Often rate dependent: When the heart rate increases to a certain rate, the cardiac electrical impulse finds the bundle branch refractory to stimulation and so conduction, and when it slows the cells have time to repolarize fully, allowing conduction to occur at slower heart rates.
Causes of SSS and potential ECG findings, Tx options, breeds
May be assoc with MMVD
Fibrosis of SA node with partial involvement of other conductive tissues (idiopathic)
Breeds: Min Schanuzer, WHWT; Cocker Spaniel, Doberman, Boxer
Complex disturbance of conductive tissue defects in sinus activity causing sinus bradycardia and disturbances in ventricular excitability (tachycardia)
Paroxysyms of sinus/SV tachycardia may be interspersed with periods of bradycardia/asystole.
ECG:
slow irregular atrial rate (severe sinus bradycardia);
long asystole with no escape beats;
impaired AV conduction (2nd or 3rd degree);
slow and irregular ventricular escape beats;
paroxysyms of SVT alternating with severe sinus bradycardia
Tx:
- If respond to vagolytic (atropine) then can treat with anticholinergic meds (theophylline, aminophylline, isoproterenol) and reponse to medical management is thought to be good.
- Pacemaker if not responsive
SSS Prognosis
JVetCardiol 2016 retrospective case review
Those with SND were less likely to nmeed Tx
SSS often needed treatment to reduce syncope.
Medical amanagement and pacemaker therapy had good response and generally good outcome with only 32% dying from cardiac related disease (most were progression to CHF).
Causes of arrhythmia in cats
96% of cats in one study of 106 cats with ventricular arrhythmias had a cardiomyopathy
Treatment is challenging: unproven benefit, palliative nature, medication intolerance
AV block in 21 cats caused by structural disease in 11/18 that had echo
AFib - most often underlying structural heart disease
MOA, indications, examples of type Ia anti-arrhythmic
Quinidine
Procainamide
Disopyramide
Block Na channel depress phase 0 depolarisation (slow conduction) in working myocardium/His tissue
Prolong repolarisation (like class III)
Decreases excitability, contractility and slows conduction velocity
Also depresses automacity conduction
Refractory ventricular arrhythmias and SVT
Macro-re-entry syndromes
Procainamide may be used when unable to differentiate AFib and SVT from VT.
MOA, indications, examples of type Ib anti-arrhythmic
Lignocaine
Mixelitine
Tocainide
Phenytoin
Block Na channel depresses phase 0 depolarisation in abnormal tissue (affinity for binding with inactivated sodium channels thereby selectively acting on diseased or ischaemic tissue).
Shorten repolarisation in diseased tissue - greater homogeneity of refractory periods. Prolongs refractoriness in ischaemic cardiac cells - greater effect on abnormal cells (can help hyperpolarize damaged cells which have more positive membrane potentials
Little effect on normal myocardium, SA or AV nodes
Ventricular arrhythmia
(converting vagally mediated AFib)
May reduce VPC frequency in ARVC - unknown if clinically significant
Little effect on supraventricular tachycardia and not recommended where chronic cardiac disease is cause of arrhythmia
MOA, indications, examples of type II anti-arrhythmic
Atenolol > propranolol > esmolol (short acting IV)
Anti-adrenergic drugs - mainly B-AdrR blockers (inhibits catecholamine induced increase in cAMP which causes: myocardial work, pacemaker activation and Ca-channel stimulation).
Reduce myocardial O2 demand
Decrease sinus rate and slow AV conduction
Inhibit generation of ectopy and slow AV node conduction
Slow ventricular rate in atrial tachycardia (especially AF where type IV and digoxin have failed and not in CHF)
SVT of AV node - slow SNS input (provided not in HF)
Some VTs
MOA, indications, examples of type III anti-arrhythmic
Prolong repolarisation in all areas of heart via inhibition of repolarising K channel currents
This slows impulse conduction (or blocks it), Reduces the myocardiums ability to generate a new action potential before repolarizing
Increases threshold for AFib and VF conduction
Many of the drugs in this class also exhibit properties of other anti arrhythmogenic classe
Sotalol (also class II effects)
Induces systolic and diastolic hypotension and considered to have 30% beta blocking potency compared to propranolol
Amiodarone (traits of all classes)
Ventricular arrhythmia
SVT including those involving AV node and AF conversion
Sotalol - Protective against pro arrhythmia and life threatening ventricular arrhythmias
Amiodarone -Used in dogs with LV systolic dysfunction helps rate control and can convert Afib to sinus
Not well described benefits in dogs, not been tested in cats
MOA, indications, examples of type IV anti-arrhythmic
Selectively inhibit slow inward calcium current channels during the AP - inhibit slow (L) Ca-channels resulting in decreased rate of depolarisation of nodal cells (dose-dependent slowing of both SA and AV nodes)
Diltiazem - Benzothiazepine Ca channel blockers. Improves diastolic function through negative inotropic and chronotropic effects → improved relaxation (lusiotropic)
Dilation of coronary arteries improves O2 delivery
Verapamil - used for acute termination of Supraventricular tachycardias (IV)
As most effects are on nodal tissue (as they rely on Ca for automated firing), used primarily for supraventricular arrhythmias
Slow ventricular conduction rate in SVT - can be given IV in acute setting to try and convert.
Interrupt reentry, slow sinus rate and AV conduction for Afib or SVT
Feline SVT (negative inotropic effects not problematic)
