ECG Flashcards
normal PR interval length
0.12-0.2 s
normal sinus rhythm pattern
upright p wave
each p wave followed by a QRS
each QRS preceded by a P wave
PR interval length = 0.12-0.2 s
how much time is denoted by 5 little horizontal squares
0.2 s
how much voltage is denoted by 5 little vertical squares
0.5 mV
in what order do you assess aspects of a rhythm strip
rate rhythm P wave PR interval QRS complex
what 4 questions do you ask yourself about P waves
present?
same shape and size?
how many P waves per QRS?
what is the relationship between P waves and the QRS?
what do P waves of the same P wave type indicate
1 atrial pacemaker
what do P waves of different types on the same strip indicate?
more than 1 atrial pacemaker
if there are no P waves, is there a PR interval?
NO
what two questions do you ask yourself about PR intervals
short or long?
constant or changing?
what is the normal length of the QRS complex?
0.12 s (3 small squares)
what does a wide (>0.12 s) QRS indicate
LBBB
RBBB
ventricular pacemaker
what does a narrow (
indicates pacemaker and conduction along His-Purkinje pathway (likely SA node pace)–> NORMAL
what is a delta wave
a gradual incline in the QR segment
what condition exhibits a delta wave in the ECG
wolff-parkinson-white syndrome
congential accessory pathway and episodes of tachyarrhythmia
sinus bradycardia on ECG
only abnormality is rate
sinus tachycardia on ECG
only abnormality is rate is >100
normal P waves, QRS complex, and PR interval
SA node is pacemaker and is just firing at a higher rate
what is the max sinus rate
180-200 bpm (except in babies)
what is indicated when HR exceeds 180-200 on ECG?
anything above this rate, the sinus node is not involved
common during exercise, fear and pain
other causes: volume depletion increased metabolic demand impaired cardiac filling decreased afterload
1st degree AV block on ECG
“1st degree heart block”
wife = P wave husband = QRS
Wife waits at home for husband, and he comes home late every night, but he makes it home every night and he comes home at the same (late) time every night
due to slow conduction at the AV node
- long PR interval
- each P wave is associated with a QRS
- SA node = pacemaker
can coexist with other abnormalities (i.e sinus brady)
what can cause 1st degree heart block
ischemia or fibrosis of AV node
2nd degree AV block Type I
“2nd degree heart block Type I”
“Wenchebach” or “Morbitz”
wife = p wave husband = QRS
QRS comes home later and later every night until one night he doesnt come home at all
- irregular rhythm with pattern–> regularly missing QRS complexes
- more P waves than QRS complexes
- PR interval increases with each heart beat until it is so long that the signal doesnt reach the ventricles and the depolarization is “blocked” at the AV node
- SA node is the pacemaker
2nd degree AV block Type II
“2nd degree heart block Type II”
wife= p wave husband = QRS wave
QRS sometimes comes home and sometimes doesn’t–> when he does come home, its always at the same time
- irregularly irregular (NO pattern) rhythm–> randomly missing QRS complexes
- more P waves than QRS complexes
- PR interval = constant (when a QRS is present)
- SA node = pacemaker
- more likely to develop into Type III heart block
3rd degree AV block
“complete heart block”
wife = p wave
husband =QRS
P wave no longer waits on QRS. P wave and her husband are on completely different schedules and they are not associated at all. They are completely independent of each other and live totally separate lives
- atrial rate = faster than ventricular rate
- P waves are no longer associated with QRS complexes–> they are not conducted to the ventricles, they may become buried in the QRS
- there are more P waves than QRS complexes
- PR intervals are random
- QRS complexes are usually wide (rarely are narrow)
- SA node + ectopic side are the pacemakers (SA for atria, ectopic for ventricles)
Atrial flutter on ECG
- type of tachycardia?
- pacemaker?
- atrial rate?
- ventricular rate?
- rhythm
- why are there two different rhythms atria/ventricle?
- characteristic waves on ECG
- common block patterns
- supraventricular tachy
- ECTOPIC atrial site = pacemaker–> too fast for sinus node, which maxes at 180-200 bpm
- 300 bpm
- 150, 100 or 75 usually, depending on the block pattern
- rhythm usually is regularly irregular, but can be irregularly irregular if the AV block is variable (AV block is usually regular)
- atrial rate exceeds the rate at which the AV node can conduct and therefore there is a physiological block at the AV node due to the inherent REFRACTORY PERIOD
- SAW TOOTH P WAVES = characteristic of atrial flutter
- 2:1 (AV node blocks every 2nd atrial impulse) or 3:1
atrial fibrillation on ECG
- type of tachycardia?
- pacemaker?
- are there P waves?
- rhythm?
- what is the relationship between atrial and ventricular rhythm?
- what is a risk of atrial fibrillation?
- supreventricular
- multiple ectopic atrial sites act as pacemaker
- no p waves–> background noise is present due to the high amount of uncoordinated electrical activity in the atria from the multiple ectopic pacemakers–> this results in quivering
- irregularly irregular
- the electrical activity is uncoordinated in the atria–> the AV node conducts this activity when it can and as fast as it can
- increases danger of blood clots forming–> can lead to embolism
what is a supraventricular tachycardia?
any narrow tachycardia where QRS complexes are narrow and P waves are not obvious/affected
tachycardic rhythm that originates from ABOVE the bundle of His
i.e sinus tachycardia, atrial tachycardia, atrial flutter, atrial fibrillation, multifocal atrial tachycardia (MAT) which has 3 or more P wave morphologies, junctional tachycardia, and re-entry tachycardia
ventricular tachycardia on ECG
- rate?
- are there P waves?
- what does the QRS complex look like?
- pacemaker?
- what is the danger with this rhythm?
- between 100-250 bpm
- p waves are absent (just QRS complexes over and over)
- QRS complex is wide
- sustained VENTRICULAR ECTOPIC pacemaker
- can easily cause cardiac arrest–> call code blue immediately
**bottom line: wide QRS and fast rate–> looks like just big up and down waves over and over
ventricular fibrillation on ECG
- pacemakers?
- are there ventricular contractions?
- what is this an example of? (i.e in what condition/state might you see this rhythm?)
- what do you do when you see this rhythm on a strip
- MULTIPLE ECTOPIC VENTRICULAR sites= pacemakers
- NO ventricular contractions–> no cardiac output, no BP, no pulse
- one example of cardiac arrest
- call a code blue and use a defibrillator
- *uncoordinated electrical activity only
- high amount of uncoordinated electrical activity in the ventricles which results in quivering
- just random ups and downs all over the place
describe the usual progression of “electrical failing” of the heart that can lead to asystole
brady or narrow complex tachy–> ventricular tachycardia–> ventricular fibrillation–> agonal –> asystole
asystole = flat line; no electrical activity in the heart, patient has been in a pulseless rhythm for quite some time; hypoxic damage to the heart and brain from which recovery is not possible
what is the most common cause of supreventricular tachycardias
AVNRTs–> AV nodal re-entrant tachycardias
what is an AVNRT
when there is a re-entry tachycardia where the re-entry pathways is localized to the AV node
2 pathways–>
Alpha = normal conducting and normal refractory
Beta = slow conducting and fast refractory
the re-entry circuit is triggered by a premature atrial impulse that sends impulses into this circuit
what is a sinus nodal re-entry tachycardia
same as AVNRT but localized in the SA node
what is the second most common cause of supreventricular tachycardias
AV re-entrant tachycardias (not localized to AV node)
what is an AVRT
occurs in the presence of ACCESSORY PATHWAYS/bypass tracts which are errant strands of myocardium that bridge the mitral or tricuspid valves
these bypass tracts mean that the bundle of His is now no longer the only way for impulses to get from the atria to the ventricles
the impulses usually travel anterograde down the AV node and retrograde via the accessory pathway from ventricles to atria (orthrodromic AVRT)–most common
if it travels anterograde down the accessory pathway, this results in pre-excitation of the ventricles and thus a delta wave as seen in WPW–excitation then travels retrograde through AV node (antidromic AVRT)
what 4 things cause abnormal heart rhythms/rates
- problems with or alterations to the hearts automaticity
- re-entry circuits (causing tachy)
- after-depolarizations (causing tachy)
- conduction block (usually causing brady)
what mechanisms can the body use to induce bradycardia
- increase parasympathetic drive
- decrease the phase 4 slope, by using the vagus nerve and cholinergic stimulation of the SA node to decrease the probability that pacemaker channels are open
- increase the threshold value (i.e the probability of open Ca2+ channels in phase 0 decreases)
- make the “resting membrane potential” more negative which increases the probability that K+ channels are open at rest
what can happen if SA node pacemaker cells are slowed enough
Escape rhythm
meaning other conducting tissues like the AV node or the His-Purkinje system can take over the pacemaker role except at the slower than normal rate compared to normal SA function
by what mechanisms can the body induce tachycardia
- decrease parasympathetic drive
- increase the phase 4 slope through Beta 1 adrenergic stimulation of the AV node to increase the probability that the pacemaker channels are open
- make the threshold lower (more negative) to increase the probability that voltage sensitive channels are capable of opening in phase 0
- make “RMP” more positive
- can also be caused by ectopic beat formation along the conduction pathway faster than can be produced by the SA node–> happens with overstimulation of the SNS, in hypoxia, ischemia or with electrolyte disturbances or drug toxicities
- injury to membranes causing them to become leavy and thus atrial or ventricular cells to become partially depolarized causing ectopic beats
name a condition that is characterized by early after-depolarizations
torsades de pointes
some Na+ channels become abnormally activated in plateau or phase 3 of depolarization leading to self-propagating AP
