Cardiac Dysrrhythmias

• generates rhythmical regular action potentials (flow of ions across cell membranes)
• conducts action potentials through myocardium in organized, synchronized manner for effective pumping
• Made up of specialized muscle cells including intercalated discs to work as one organ called a syncitia

groups of cells working as one organ.  Atria and ventricles are separate syncitia

microscopic identifier of heart muscle, connects individual cells into syncytia

• SA depolarizes
• Rapidly passes to AV node through internodal pathways
• depolarization spreads more slowly across atria.  Conduction slows after AV node
• depolarization moves rapidly through ventricular conduction system to apex of heart
• Depolarization spreads upward from apex through ventricles.

• Graphic recording of electrical currents generated by heart as measured on the surface of the body by vectors (mean vector), which are measured by both magnitude and direction
• Voltage changes are recorded as wave forms
• Major wave forms are P, Q, R, S, T

first, atrial depolarization.  Positive

• Q negative, R positive, S negative.
• Ventricular depolarization
• Should be upright and narrow (otherwise there is a problem with the ventricles)
• Width of wave reflects width of tissue impulse went through.  Wide QRS means travelling through muscle, not conduction tissue

positive, last, ventricular repolarization

• Lead II
• Right lateral
• White negative on right forelimb
• black on left forelimb
• Green on right hindlimb
• Red positive on left hindlimb

• Tells which way the ECG wave will point.  In depolarization, toward + lead on left hind limb is positive
• in repolarization, toward - lead on right front limb is positive

Time for impulse to pass from SA to ventricles

summation of ventricular depolarization to repolarization (systole)

distole

early atrial repolarization

• early ventricular repolarization
• See deviations in hypoxia

50mm/sec

• small: 0.02 seconds (3000 in a minute)
• large: 0.1 seconds (5x5 small boxes, 600 in a minute)
• Count small and/or large boxes between R and R.  Divide 3000 or 600 by that number.

• any deviation from normal cardiac rate or rhythm
• deviation from normal site of origin of impulse, usually SA node
• deviation from normal sequence of activation of atria and ventricles
• Inefficient pumping causes decrease in CO

• Brachiocephalics (high vagal tone)
• hyperthyroid (high sympathetic tone)
• HBC, up to 72 hours (traumatic myocarditis), or other trauma
• Heart disease
• hypoxemia
• anesthesia
• catecholamines
• digoxin
• inhalant anesthetics
• electrolyte imbalance

• an abnormality in impulse generation, changing automaticity of heart cells
• or an abnormality in impulse conduction

• the ability to spontaneously initiate a depolarization, triggering an action potential
• All fibers of cardiac conduction system can do this

• Only SA node exhibits automaticity
• SA node has the most automaticity so beats fastest.  If another set of cells depolarizes faster, ectopic focus.

• a group of cells in the heart that depolarizes faster than the SA node, demonstrating automaticity (causing impulse generation from an abnormal area)
• cells in cardiac conduction system other than SA node exhibit enhanced automaticity and act as pacemaker.

• SA nodal cells discharge action potentials abnormally fast due to increased automaticity
• Still a P for every QRS and waves look normal, but coming faster.  
• Could be cause by increased sympathetic like hyperthyroid.  Figure out underlying cause.  Give Atenolol (B blocker) to treat

• Give B blockers.  
• nonselective: propranolol (not for asthmatics)
• cardio-selective: esmolol (short-acting, IV), atenolol (PO, longer)

• Give Muscarinic antagonist (anticholinergic) like atropine or glycopyrrolate
• give B1 adrenergic agonist like isoproterenol

• SA node discharges action potentials abnormally slow.  
• SA node still pacemaker, waves look normal, but long spaces in between.
• Usually treat when HR reaches 60 but varies with size and species.
• If asymptomatic don't have to treat, but if consistent likely needs a pacemaker

• not constant rhythm, related to changes in respiration
• Speeds up on inspiration, slows down on expiration
• Don't usually treat, often asymptomatic
• common in dogs, rarer in cats possibly due to stress

AV node and His-Purkinje system have automaticity but rarely show it (not as much as SA node)

cells in cardiac conduction system other than SA node exhibit enhanced automaticity and act as pacemaker (ectopic focus/foci)

• ischemia, hypoxia
• excessive sympathetic drive like catecholamine release
• Drugs like B agonists, catecholamines, caffeine, nicotine
• heart disease including HW, endocarditis (inflammation of leaflets), pericarditis

inflammation of valve leaflets

• can occur when ectopic focus initiates a contraction before contraction should occur.
• Supraventricular premature contraction (SVPC) (when ectopic in atria)
• Ventricular premature contraction (VPC) when in ventricles

• Premature P wave which looks different than normal sinus P wave.  Premature QRS with a normal configuration.  
• Can be seen in older dogs
• P often on previous T
• treat with digoxin unless cardiac decompensation
• B blocker only if cardiac function is okay

visible, normal P waves, premature QRS that is wide and bizarre, not associate with P wave.

• Flutter/wavy line where the p wave should be.
• "Delirium cordis", old term.  A fib sounds like a drum roll.  
• No ordinary electric activity in atria.  Usually tachyarrhythmia.  
• Treat with digoxin.  Common in Newfies.

• multiform ectopic focus
• more than 16 VPC/minute
• runs of 2 or more consecutively
• R on T, when the R of QRS falls of preceding T animal is about to have a problem
• Treat with lidocaine.  Na-blocker stops action potential.  Bolus, then CRI

• P is normal, QRS can bury it.  Somewhere in ventricles showing atomaticity.  
• Unifocal or uniform if always look the same.  If not, multifocal

When ventricular premature contraction always looks the same, and is likely caused by one group of cells in the ventricles depolarizing.

When ventricular premature contraction is morphologically different, caused by multiple sets of ectopic foci.  Treat.

Na-blocker used in all ventricular dysrrhythmia  Bolus, then CRI

• can change depending on which ventricle is beating
• Right ventrical has ectopic focus, QRS wave is negative
• left ventrical has ectopic focus, QRS wave is positive.  
• Multiple foci cause both.

uneven, not connected to P waves, heading towards v-fib.  Treat if there are no normal beats or if multi-foci.

Just zig zag on ECG.  Treat with CPR or can defibrillate

CPR and defibrillation right away, just a wavy unpredictable line on ECG

• No motion from atria, no P wave.  Bradycardia
• Abnormality in impulse initiation
• Treat with atropine, glycopyrrolate, isoproterenol or a pacemaker
• Caused by hyperkalemia usually (Addison's, DKA, blocked cat)
• Treat by lowering K, saline, insulin and dextrose, etc.

• automaticity occurring above AV node
• Include paroxysmal supraventricular tachycardia, sinus pause and sinus arrest

• tachycardia generated by AV or above (ectopic focus)
• Paroxysmal due to abrupt start and end of tachycardia
• Hard to tell from sinus tachycardia, vagal manuver to tell.
• Treat with B locker or digoxin

short period of time where sinus isn't working, flat line.

To help tell if sinus or supraventricular tachycardia, press on eyes (increnase IOP pressure) or massage carotid.  Response varies, but use drugs to enhance (Morphine or Edrophonium)

• Heart is flat line for 2x as long as the normal R-R.  
• Often present with fainting.

• Result for disturbance in normal sequence of impulse propagation through cardiac conductions system.  
• Two major abnormalities: heart (AV) block or reentry (reentrant arrhythmias)

• Impulse not normally conducted from atria to ventricles. 
• Caused by: Ischemia of AV node or His/Perkinje system, heart disease, excessive vagal tone
• drugs with negative chromotropic effect.
• Can be caused by wrong atropine dose or any B blocker, also by aging.

Impulse doesn't die after stimulating heart, just keeps going around heart, reexciting anything that has left hyperpolarization phase.

• Prolonged P-R interval, from 0.16 sec to 0.38 sec, ie.  
• Don't usually treat if asymptomatic.

• Intermittant failure or disturbance of AV valve.  Ventricular rhythm slower than atrial, has 2 types.  
• Mobitz type I: progressive prolonging of P-R until one gets blocked and has no associated QRS
• Mobitz type II: fixed relationship between number of P and number of QRS (like 1:3, not 1:1)
• Often caused by excess vagal tone, get the atropine or glycopyrrolate.
• Seen the most with anesthesia

• complete heart block.  
• P waves are steady, QRS are wider than usual and there is no correlation between them.  
• Mobitz type II often becomes type III.  
• Caused by aortic stenosis, ventrical septical deflect, digoxin toxicity, infiltrative neoplasia, endocarditis, pericarditis, hyperkalemia, idiopathic scarring of heart.

Mobitz type II often becomes type III.  Caused by aortic stenosis, ventrical septical deflect, digoxin toxicity, infiltrative neoplasia, endocarditis, pericarditis, hyperkalemia, idiopathic scarring of heart.

• Present with sycope (fainting). 
• Drugs are useless, need a pacemaker.
• Try isoproterenol or Epi, but unlikely
• DO NOT use B blocker, Lidocaine (will stop heart).  Can't treat because it's keeping animal alive

fainting

progressive prolonging of P-R until one gets blocked and has no associated QRS in secondary heart block

fixed relationship between number of P and number of QRS (like 1:3, not 1:1) in secondary heart block.

• AV block = impulse conduction, need + dromotrope
• AV block due to excessive vagal tone needs cholinergic antagonist (atropine)
• Refractory life-threatening AV block needs catecholamine (isoproterenol) or B1 agonist

• When there is a unidirectional block in the conduction of the heart, the impulse keeps going retrograde and re-stimulates any cells that are out of refractory state.
• ECG is repetitive spikes, never rests
• Can happen up to 36 hours after ischemic event or 72 hours after trauma

• Period between action potentials--long (150-500ms)
• 1st contraction is almost over before 2nd action potential can begin, allows relaxation for diastolic filling.

• V tach (ventricular tachycardia) first, no rest or normal wave/complex, just steady spikes that all look similar.
• Use lidocaine, quickly leads to ventricular fibrillation (coarse or fine), then to a-fib.

• coarse or fine.  Coarse, reach for defibrillator, fine reach for lidocaine.  
• DO CPR, there is no CO, too chaotic to function

• repetitive similar waves, never stop or rest, wide and bizarre QRS from ectopic beat.  
• Can take 36 hours to start after ischemia, 72 hours after trauma

• Singh Vaugn classification based on mechanism, most common.  
• 5 classes, 1 has a, b and c.

• Na channel blockers
• depress myocardial excitability, prolong refractory period, decrease automaticity, increase conduction times
• Used in atrial and ventricular arrhythmias
• Quinidine - ventricular arrhythmias and v tach (lido better), afib (digoxin better)
• Procainamide - PCV (best after lido), v tach, some forms of a tach
• Disopyramide

• Class 1A antiarrhythmic drug
• Historical, rarely used now
• Used for ventricular arrhythmias and v tach (now lidocaine)
• Used for a fib (now digoxin)

• Class 1A antiarrhythmic
• Used for PVC if lidocaine unavailable (most common use)
• also used in v tach or some forms of a tach

• stabilize myocardial cell membranes by blocking influx of Na (channel blockers)
• Decrease automaticity, ectopic foci
• Used in ventricular arrhythmias
• Lidocaine, used esp in PVC and v tach
• Phenytoin, Mexilatine, Tocanide

• antiarrhythmic Class 1B
• Used in ventricular arrhythmias, esp PVC and V tach

• Only used in humans
• Flecainide, Propafenone, Moricizine
• Na channel blockers

• B blockers, both nonselective and cardioselective
• Upregulate adrenergic receptors to improve cardiac efficiency.  Good for CHF when sympathetic tone wears out receptors
• used in atrial or ventricular arrhythmias
• Propanolol, nonselective, HCM, Hyperthyroid
• Atenolol, cardioselective, SVT, PVC, hypertension, cardiomyopathy, HCM
• Esmolol-short acting IV cardioselective
• Timolol, Metoprolol, Bisprolol

• Ca Channel blockers.  Decrease automaticity
• Diltiazem for SVT, used to be HCM in cats
• Amlodipine for hypertension
• Verapamil

• Class II antiarrhythmic
• nonselective B blocker IV
• Used in HCM, hyperthyroid

• Class II antiarrhythmic
• cardioselective B blocker
• used in SVT, PVC, hypertension and HCM

• Class II antiarrhythmic
• B blocker, cardio selective
• short acting, IV

• Class IV antiarrhythmic
• Ca channel blocker
• Hypertension

• Class IV antiarrhythmic
• Ca channel blocker/anti-automaticity
• used in SVT, occasional HCM
• Prevents recurrance of paroxysmal supraventricular tachycardia

• Potassium channel blockers
• Sotalol - PO B blocker too
• PCV in dogs that need to go home (PO), would be on IV lidocaine otherwise

• Class III antiarrhythmic
• Oral beta blocker and potassium channel inhibitor
• Used in PVC in dogs that need to go home (can't use IV lidocaine), v tach and a fib

• Class V antiarrhythmic drug
• Used in supraventricular arrhythmias esp heart failure with a fib, NOT in ventricular fibrillation

• Class II antiarrhythmic
• B blocker
• Used in CHF, controversial

• - R from right ventricle
• + R from left ventricle

• No P waves, normal otherwise
• primary cause is hyperkalemia (addison's, DKA, blocked cat)
• decrease K+, give NaCl, insulin with dextrose