ECGs & Arrhythmias Flashcards
what is the resting membrane potential of cardiomyocytes
-90 mV
steps of cardiac action potential
SA node sends impulse –> Na+ entry –> cardiomyocyte depolarization –> Ca influx –> cardiac muscle contraction –> K+ efflux out –> repolarization –> cardiac muscle relaxation
what is the path of electrical activity in the heart
- SA node
- internodal conduction tracts –> R atrium –> L atrium
- AV node
- bundle of his
- purkinje fibers
- cardiomyocytes
SA node
sinoatrial node
FASTEST pacemaker
located in the RA wall
spreads current RAPIDLY to through the internodal tracts to reach the AV node
superior exit from atrium
high in atrial wall
common exit taken by the current with high sympathetic tone (tall P wave)
inferior exit in atrium
low in atrial wall
common exit taken by the current with high parasympathetic tone (shorter P wave)
wandering pacemaker
variable P wave height due to variable exit pathways based on autonomic input
AV node
atrioventricular node
SLOW pacemaker
located in the septum between RA/RV near the center of the heart
gatekeeper - the ONLY conduction pathway between the atria and the ventricles
current spreads slowly through the AV node to allow for atrial depolarization and contraction to finish before sending signal to the ventricles
bundle of his
conducts current RAPIDLY to the ventricles via the L and R bundle branches
allows for coordinated contraction across the ventricles
purkinje fibers
penetrating fibers that conduct signal through the ventricles to the myocytes
once current reaches myocytes –> cell to cell signaling occurs
how is an ECG generated
heart is activated by a depolarizing current that moves as a boundary between resting and activated tissues
electrical field gets generated onto the body surface –> detected by ECG surface electrodes
TP interval
time in between depolarizations
time during which the SA node initiates conduction PRIOR to the P wave
(not strong enough to be detected on ECG)
P wave
atrial depolarization
SA node –> R atrium –> L atrium
- slight delay between R and L atrial depolarization
PQ interval
conduction from SA node –> AV node –> bundle of his
represents the time required to travel through the AV node
QRS wave
ventricular depolarization
3 vectors in species with category A conduction
ST interval
early ventricular repolarization
duration of ventricular contraction - Ca coming into cells but no electrical activity
T wave
ventricular repolarization
QT interval
entire time for ventricular depolarization and repolarization
what leads are bipolar
leads I, II, III
what leads are unipolar
aVR
aVL
aVF
what is the correct positioning for the animal when taking an ECG
right lateral recumbency
can be standing or sternal if only looking at rate and rhythm
what are indications for running an ECG
- clinical signs - weakness, collapse, syncope
- auscultation - abnormal heart rate or rhythm
- diagnosis of heart disease or a systemic disease that causes arrhythmias
- monitoring of critically ill patients/anesthesia
what are the steps to evaluating an ECG
- heart rate
- heart rhythm
- P wave for every QRS
- QRS for every P wave
- complex morphology
how to calculate average HR if paper speed is 25 mm/s
number of beats per 30 big boxes x 10
how to calculate average HR if the paper speed is 50 mm/s
number of beats per 30 big boxes x 20
how to calculate instantaneous HR if the paper speed is 25 mm/s
1500 / number of small boxes in the R-R interval
how to calculate instantaneous HR if the paper speed is 50 mm/s
3000 / number of small boxes in the R-R interval
what are the supraventricular rhythms
APCs
atrial fibrillation
supraventricular tachycardia
what are the ventricular arrhythmias
VPCs
ventricular tachycardia
ventricular escape beats
ventricular fibrillation
what are the conduction disturbance arrhythmias
AV blocks
bundle branch blocks
what causes sinus arrhythmia
high resting vagal tone
normal in dogs
abnormal for cats in the clinic (normal at home)
faster during inspiration
slower during expiration
sick sinus syndrome (SSS)
sinus node dysfunction causing sinus arrest AND clinical signs of collapse/syncope
(must have both clinical signs and ECG findings)
sinus arrest
period of >2 seconds or >2 P-P intervals without sinus node function
often followed by a ventricular escape beat
supraventricular arrhythmias
irregular heartbeats that originate above the ventricles
atrial premature complexes (APCs)
abnormal early depolarization of the atria that gets normally conducted to the ventricles
- NARROW QRS that comes before the next sinus beat is expected
- can often hide the T wave of the previous beat
supraventricular tachycardia
tachycardia caused by rapid signaling from above the ventricles
- tachycardia
(dogs > 160-180; cats > 260) - regular rhythm
- P waves are present but can be difficult to find due to tachycardia
atrial fibrillation
areas of the atria continuously depolarizing/repolarizing and bombarding the AV node over and over again
AV node can help slow down rhythm but patient is still tachycardic
- irregular R-R interval
- NO P waves
- tachycardia
- variable R amplitude
- narrow QRS complex
- irregular rhythm
- undulating baseline
ventricular arrhythmias
abnormal heart rhythms that occur due to irregular ventricular beats
complexes are WIDE and BIZARRE looking
do not have a P wave initiating the complex
ventricular premature complexes (VPCs)
ventricles depolarize before the atria (comes in early)
- wide QRS coming in where a sinus beat should be
ventricular escape beat
SA node fails to fire so the slow AV node takes over (comes in late)
bradycardia
- dogs: 40-60
- cats: 100-140
- wide QRS complexes coming in after a prolonged TP interval
accelerated idioventricular rhythm
rhythm in which ventricular ectopic beats exceed the rate of SA node firing (take over)
dogs: 60-160 bpm
cats: within 10% of sinus
ventricular fibrillation
disorganized ventricular rhythm due to random depolarization of areas of the ventricles
unable to have a coordinated contraction
- short, wide QRS complexes
- disorganized, varying heights
ventricular tachycardia
rapid heart rate generated from the ventricles
- wide QRS complexes
- regular rhythm
- lack of P wave association
- tachycardia
(dogs < 160; cats > 220)
can be paraoxysmal, sustained, monomorphic, or polymorphic
hyperkalemia (sinoventricular rhythm)
high potassium –> increases resting membrane potential –> harder to depolarize the atria before the ventricles
impulse is still generated in the SA node, but it reaches the AV node and ventricles before the atria can depolarize
- tall, tented T wave
- NO P waves
- bradycardia
- wide QRS
AV block
delayed or absent conduction through the AV node
- long PQ interval
- P waves without QRS
first degree AV block
prolonged PQ interval but ALL P waves are conducted
caused by high vagal tone
tx with atropine
second degree AV block
some P waves are conducted, some are not
low grade: roughly every other P wave is conducted
high grade: more than every other P wave is blocked
second degree mobitz type I AV block
PQ interval gradually prolongs until one P wave is blocked
caused by high vagal tone
tx with atropine
(normal in horses)
second degree mobitz type II AV block
consistent PQ interval but P waves are randomly blocked
caused secondary to heart disease
NOT responsive to atropine
third degree AV block
no P waves are conducted
QRS is entirely dissociated from P waves
- no consistent PQ interval
- SA node consistently fires at its own rhythm
- AV node fires junctional escape beats randomly throughout
caused by AV node disease
tx with pacemaker
P pulmonale
tall P wave
cause: RA enlargement
P mitrale
wide P wave
cause: LA enlargement
tall R wave
LV enlargement
R cranial deviation
RV enlargement
