Cardiac Dysrhythmias Flashcards
normal ECG (lead II) in dogs
P followed by QRS
- stable, unchanging PQ interval
- positive P wave
- net positive, narrow QRS
- positive or negative T wave that does not change
normal ECG in horses (base-apex lead)
P followed by QRS
- stable, unchanging PQ interval
- M shaped, biphasic P wave
- net negative, narrow QRS
- positive or negative T wave that does not change
normal sinus rhythm
NSR; regular rhythm initiated by the sinus node, conducted normally, and normal rate for the species
sinus bradycardia
lower than normal rate
rest is the same as NSR
sinus tachycardia
higher than normal rate
rest is the same as NSR
sinus arrhythmia
regularly irregular
rate increases and decreases at regular/predictable intervals
respiratory sinus arrhythmia: normal in dogs; increases HR on inspiration, decreases HR on expiration
supraventricular
originating from the upper chambers (atria)
junctional
originating from the atrioventricular junction (around AV node)
ventricular
originating from the lower chambers (ventricles)
what is ECG not sensitive for detecting
heart failure/disease resulting in dysfunction
what is paper speed used to measure
- heart rate
- complex/interval duration
standard paper speeds and corresponding values
25 mm/s: small box is equal to 0.04 seconds
50 mm/s: small box is equal to 0.02 seconds
what does a faster or slower paper speed correlate to
faster paper speed = widens complexes (stretches out X axis)
slower paper speed = narrows complexes (squishes in X axis)
do you use a faster or slower paper speed in cats
faster
allows better visualization of complexes due to fast HR
what is calibration used to measure
complex size
standard complex sizes
10 mm/mV: small box = 0.1 mV
20 mm/mv: small box = 0,05 mV
what causes artifact on ECG
poor electrode contact
shivering
purring
electrical interference
respiratory motion
reversed leads
limb movement
do artifacts disrupt the underlying rhythm
NO - should still have underlying rhythm
QRS complexes always followed by T wave
what does the P wave correspond to and how does it look on ECG
atrial depolarization
SA: small, rounded, positive
LA: M shaped/biphasic
what does the PQ interval correspond to
conduction through the slow AV node; includes depolarization of atria and specialized conduction system
should NOT vary between beats
what does the QRS complex correspond to
ventricular depolarization
should be NARROW
SA: negative Q, positive R, negative S
LA: negative QRS
what does the T wave correspond to
ventricular repolarization
J point
end of the R or S wave (if S is present)
starting point of the ST interval
ST segment
isoelectric line - no current should be flowing
should be at the same level as the TP interval
TP interval
isoelectric line
does not change polarization
what is ST depression
when the ST segment is below (more negative) than the TP interval
what is ST elevation
when the ST segment is above (more positive) than the TP interval
what does the QT interval correspond to
ventricular depolarization + repolarization
slow HR= longer QT interval
what is the risk of prolonged QT interval
increased risk of premature depolarizations leading to ventricular fibrillations
mean electrical axis
average vector of depolarization
sum of all electrical activity during ventricular depolarization
depends on origin of AP, size of ventricles, speed of electrical conduction
what is the normal QRS MEA in dogs
left caudal
most positive leads are lead II and aVF
what is the normal QRS MEA in cats
left and right caudal
most positive leads are leads II, III, and aVF
p mitrale
wide P wave
caused by LEFT atrial enlargement (takes longer for depolarization to occur
p pulmonale
tall P wave
caused by RIGHT atrial enlargement (amplifies depolarization)
what causes abnormal P wave morphology
non-SA node, supraventricular generated AP (atrial escape beats)
negative P wave
what causes unrelated P waves
random P waves not associated with QRS complex
caused by miscommunication between atria and ventricles (AV block w/ ventricular escape)
what causes absent P waves
- failure of SA or other nodes to depolarize
- ectopic/normal P waves are hiding in the preceding complex
- SA node usurped by abnormal rhythm (atrial fibrillation, flutter, ventricular tachycardia)
what causes an abnormal PQ interval
miscommunication between atrium and ventricle (AV block, ventricular tachycardia)
what does a tall QRS complex mean
left ventricular enlargement
NORMAL MEA - direction is normal but depolarization is strong (concentric or eccentric hypertrophy)
what does a wide QRS complex mean
abnormal ventricular depolarization or conduction
(ventricular ectopy, ventricular premature complexes, ventricular escape rhythm, bundle branch block)
where does sinus rhythm originate from
SA node
where does atrial escape beats originate from
atrium but non SA node
where does junctional escape beats originate from
atrioventricular junction
where does a L sided ventricular premature complex (VPC) originate from
left ventricle (negative QRS)
where does a R sided VPC originate from
right ventricle (positive QRS)
what does an overly narrow QRS complex mean
supraventricular origin of AP
what are the steps of evaluating cardiac rhythm
- heart rate
- sinus rhythm, yes or no?
- ID arrhythmias and conduction abnormalities
bradyarrhythmia
slow HR that is not initiated by SA node
tachyarrhythmia
fast HR that is not initiated by SA node
how to calculate HR at 25 mm/s paper speed
count the number of beats in 30 big boxes
30 big boxes = 6 seconds
10 x # beats = # of beats per minute
how to calculate HR at 50 mm/s paper speed
count the number of beats in 30 big boxes
30 big boxes = 3 seconds
20 x # beats = # beats per minute
how to measure instantaneous heart rate
count the number of big boxes between the R-R interval
25 mm/s: 300 / # of big boxes between R-R interval
50 mm/s: 600 / # of big boxes between R-R interval
how to evaluate if there is sinus rhythm
- are there p waves?
- are the p waves associated with QRS?
- is the p wave MEA normal?
- if the rate is variable - does it behave like sinus rhythm (gradually increase/decrease)?
- look for respiratory sinus arrhythmia (dogs; wandering pacemaker)
wandering pacemaker
change in P wave height within one reading caused by change in ANS tone
variable ANS innervation –> rate and location of SA node discharge changes
respiratory sinus arrhythmia: inspiration
vagal tone predominates –> slows HR, moves SA discharge apically
respiratory sinus arrhythmia: expiration
vagal tone decreases –> increases HR –> moves SA discharge back to SA node
regularly irregular rhythm
changes in rhythm occurs at regular intervals
can be NORMAL (dogs - respiratory sinus arrhythmia)
can be ABNORMAL (complete AV block with ventricular escape OR supra-ventricular tachycardia)
irregularly irregular rhythm
changes in rhythm are patternless/chaotic
always abnormal (ex. atrial fibrillation, ventricular tachycardia)
premature complexes
early depolarizations, can be ventricular or atrial in orign
ventricular premature complexes (VPCs)
sinus rhythm followed by a ventricular depolarization
bigeminy
normal beat followed by abnormal beat
can be ventricular or atrial
atrial premature complexes (APCs)
sinus rhythm with early atrial depolarizations (supra ventricular)
P waves are hidden in the preceding QRS because the atrium depolarizes too early
examples of QRS without a P wave
sinus arrest
atrial standstill
atrial fibrillation
ventricular tachycardia
atrial premature complexes
sinus arrest
SA node fails, causing a period of arrest (isoelectric line) before a non-SA node takes over and slowly spontaneously generates an AP (junctional escape beat)
atrial standstill
atrial muscle dysfunction causing complete lack of atrial depolarization (no P wave)
atrial fibrillation
SA node is being usurped by an ectopic rhythm
causes “jiggling baseline” from small fibrillary waves
no p wave, highly variable R-R interval
ventricular tachycardia
SA node is still firing and atrium is still contracting, but ventricle is driven by ectopic focus
alternates from sinus to arrhythmia and back
AV block
disruption in the communication between the atria and ventricles
caused by increased vagal tone (AV node disease, drugs, athletic dogs)
1st degree AV block
prolongation/delay of PQ interval
2nd degree (type I) AV block
PROGRESSIVE delay of PQ interval until non-conducted P wave
normal sinus rhythm followed by a P without a QRS
can be benign (calm horses at rest)
2nd degree (type II) AV block
PQ interval is normal up until the non-conducted P wave (NO progressive delay of PQ interval)
NOT benign - caused by conduction system disease
low grade 2nd degree type II AV block
one non-conducted P wave at a time (2:1 AV conduction)
high grade 2nd degree type II AV block
> 1 non-conducted P wave at a time (>3:1 AV conduction)
3rd degree AV block
complete dissociation of atria and ventricles; no conduction across AV node occurs
bundle of his/purkinje have to take over conduction of ventricles (bradyarrhythmia) BUT SA node is still firing at its own pace
causes 2 independent pacemakers to be firing
right axis deviation
MEA deviates to right cranial or right caudal
caused by: right ventricular enlargement or right bundle branch block
right ventricular enlargement
MEA becomes right and caudal with NARROW QRS
negative lead I
net positive aVF
narrow QRS
ex. pulmonary stenosis
right bundle branch block
MEA becomes right and caudal with WIDE QRS
delayed conduction though R bundle branch leading to slow depolarization of RV
what causes a wide QRS complex
QRS takes longer than normal:
ventricular: VPC or ventricular escape (most wide complexes)
SA/supraventricular: atrial fibrillation, junctional escape beats, bundle branch block
left bundle branch block
normal MEA (left caudal) with wide R wave in lead II
left axis deviation
MEA deviates to left cranial (not caudal bc that is normal)
caused by L anterior fascicular block
L anterior fascicular block
delayed conduction through anterior fascicle of left bundle branch
common in CATS only due to concentric left ventricular hypertrophy
causes positive lead I, negative aVF
what causes arrhythmias (in general)
disorders of impulse formation
OR
disorders of impulse conduction
OR
both (most often)
paroxysmal
arrhythmias that last <30 seconds
sustained
arrhythmias that last >30 seconds
