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)
impulse initiation abnormalities
cells in cardiac conduction system other than SA node exhibit enhanced automaticity and act as pacemaker (ectopic focus/foci)
Causes of enhanced automaticity in cardiac cells
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
premature contractions/ectopic beats
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
Atrial ectopic beat
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
ventricular ectopic beat
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.
when to treat Ventricular Premature Contraction (VPC) (4) and with what
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
Ventricular premature contraction
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
VPCs, negative or positive
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.
accelerated idioventricular rhythm
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
coarse ventricular fibrillation
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
Paroxysmal supraventricular tachycardia
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.
Abnormalities in impulse conduction
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.
First degree AV block
Prolonged P-R interval, from 0.16 sec to 0.38 sec, ie.
Don't usually treat if asymptomatic.
Second degree AVblock.
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
third degree AV block
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.
causes of third degree AV block
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.
treatment/signalment of third degree AV
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
Mobitz type I
progressive prolonging of P-R until one gets blocked and has no associated QRS in secondary heart block
Mobitz type II
fixed relationship between number of P and number of QRS (like 1:3, not 1:1) in secondary heart block.
Pharmacological therapy of AV 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
Cardiac refractory period
Period between action potentials--long (150-500ms)
1st contraction is almost over before 2nd action potential can begin, allows relaxation for diastolic filling.
Ventricular reentry arrhythmias
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.
ventricular fibrillation and types/treatments
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
Antiarrhythmic drug classification
Singh Vaugn classification based on mechanism, most common.