ECG & arrhythmias Flashcards
Bipolar limb leads
I: LA + RA -
II: LL + RA -
III: LL + LA -
all in frontal plane
Unipolar limb leads
aVR: RA + LA & LL -
aVL: LA + RA & LL -
aVF: LL + RA & LA -
all in frontal plane
Precordial/chest leads
6 chest leads in horizontal plane
anterior –> posterior
V1-6
Rate on ECG
300/# big squares btw each QRS complex
P waves
reflect atrial pacemaker
also note P to QRS relationship
PR interval
normal = 0.12 - 0.2 s (3-5 small squares)
from beginning of P to beginning of anything that represents QRS
QRS complex
normal = 0.12 s (3 small squares)
“delta” wave - gradual incline in QR segment –> WPW
Sinus bradycardia
Rate < 60
Sinus tachycardia
Rate > 100
max 180-200 (except babies)
First degree heart block
long PR interval
1:1 P:QRS
ischemia, fibrosis of AV node
2nd degree heart block: Morbitz type I/Wencheback
PR interval increases with each beat, then missing QRS
misses QRS regularly
2nd degree heart block: Morbitz type II
No pattern in missing QRS complexes
PR interval constant
most likely develop into type III block
Third degree heart block
complete dissociation of P and QRS atrial rate faster than ventricular rate usually QRS are wide, rarely it can be low SA node --> atrial pacemaker ectopic --> ventricular pacemaker
Atrial flutter
atrial rate 300
ventricular rate 150, 100, or 75 depending on block
rhythm is regularly irregular
atrial rate > rate at which AV node can conduct (Refractory period)
“saw-tooth” p waves
common block patterns are 2:1 (AV node blocks every 2nd atrial impulse) or 3:1
ectopic atrial pacemaker
Atrial fibrillation
rhythm is irregularly irregular
no p waves, but background noise present
high amount of uncoordinated electrical activity in atria –> quivering
multiple ectopic atrial sites acting as pacemaker
can lead to embolism
Supraventricular tachycardia
Any narrow tachycardia with narrow QRS and P waves are not obvious
Orthodromic AVRT
anterograde impulse via AV node
retrograde via accessory pathway
Antidromic AVRT
anterograde impulse via accessory pathway
retrograde via AV node
Ventricular tachycardia
100-250 bpm P waves absent wide QRS ventricular ectopic pacemaker can easily cause cardiac arrest
Ventricular fibrillation
Uncoordinated activity only Multiple ventricular ectopic pacemakers No ventricular contractions One example of cardiac arrest code blue & defibrillate!
Asystole
has been in pulseless rhythm for a while
sustained hypoxia to heart and brain
Automatic cause of bradycardia
increase parasympathetic drive
decrease slope of phase 4 (vagus + cholinergic stimulation of SA node –> reduce probability that pacemaker channels are open)
increase threshold value
RMP more negative
if SA node is slow enough, an escape rhythm can take over - ectopic pacemaker (slower rate)
Automatic cause of tachycardia
Decrease parasympathetic drive
Increase slope of phase 4 (B1 stimulation)
Threshold value more negative
RMP more positive
ectopic beat formation along the conduction pathway faster than the SA node may also produce tachycardia –> overstimulation of sympathetic drive
Injury to membranes
Re-entry circuits
Faster conducting, slower refractory alpha
Slower conducting, faster refractory beta
Early after-depolarization
During plateau of phase 2 or phase 3 (repol)
most Na channels inactivated but become abnormally activated, self-propagating action potential
torsades de pointes
Late after-depolarizations
after repolarization is complete
high intracellular calcium / excessive catecholamine stimulation
Conduction block
causes: ischemia, fibrosis, inflammation, drugs
secondary to refractoriness of cells: functional block
damage: fixed block
escape rhythm = third degree heart block
Tx of bradycardia
Invasive: pacemaker
Sinus node: symptomatic - pacemaker; asymptomatic - no treatment
AV node: 1st degree block: no treatment; type 2: pacemaker
3rd degree: pacemaker
Catheter ablation
FR energy delivered to myocardial tissue, disrupts arrhythmia substrate
Cardioverter/defibrillator implantation
cardioversion: sync shock with QRS complex; good for SVTs or organized ventricular tachycardias
Vagal maneuvers:
valsalva, carotid sinus massage, diving reflex
Valsalva maneuver
increase in intrathoracic pressure = increase in aortic pressure (transient baroreceptor response)
decrease in CO, no stimulation of baroreceptor response –> v/c
release of pressure at the end of the maneuver –> return CO, but SVR still high
baroceptor detects increased pressure –> reduce HR
Preload
the volume (load) filling the ventricle prior to contraction; equivalent to end-diastolic volume.
When preload is increased, according to the Frank-Starling Law, there will be a compensatory increase in SV to accommodate it.
Afterload
wall stress experienced by the ventricle as it contracts to produce a pressure necessary to open the aortic valve and eject blood into the systemic circulation
