dysrhythmias Flashcards
rapid dysrhythmia with HR of 150-250
rate so fast that it overrides SA node
P wave lost in preceding T wave- making it hard to determine where the impulse originates
supraventricular tachycardia
arises from above the ventricles but can’t tell if it’s from the atria or junction
SA node transiently stops firing and 3+ beats are dropped
sinus arrest
complete heart block
3rd degree AV heart block
dysrhythmia with a rhythm of 40 to 100 bpm (___ the inherent rate of the ventricles)
wide and bizarre QRS
T wave in the opposite direction of the R wave
absent P wave (hidden in the QRS)
accelerated idioventricular rhythm
(exceeds the inherent rate of the ventricles)
PVCs that all look the same
unifocal
complete block of conduction at or below the AV node, the impulses do not reach the ventricles
3rd degree AV heart block
sinus tachycardia is HR b/w
100 to 160
early ectopic beats that interrupt the normal rhythm
originate from an irritable focus in the ventricular conduction system or myocardium
retrugrade impulse inhibits the firing of a normally fired SA node impulse; SA node timing unaffected
PVC
PR intervals that are longer than 0.20 secs and constant
everything else pretty normal
1st degree AV heart block
SA node transiently stop firing and 1-2 beats are dropped
sinus pause
normal sinus rhythm for 4 y/o
75 to 115
periods of brady, tachy, prolonged pauses, or alternating brady and tachycardia that cause cardiac insufficiency and hypoperfusion
usually happens in elderly due to degenerative SA node
sinus node dysfunction
aka
sick sinus syndrome
PVCs that look different from each other
multifocal
these are more concerning b/c it means the ventricles are irritable and that the early beats are arising from more than one location
what makes it impossible to differentiate b/w mobitz 1 and mobitz 2
what is this called
if every other P wave is conducted
b/c you cannot assess for progressive prolongation or fixation
called a 2:1 AV block
which heart blocks are emergent
2nd degree AV block, type 2
and
3rd degree AV heart block (life threatening)
(3 or more) P waves that change appearance (absent/ inverted/ abnormal) because pacemaker site shifts b/w SA node and or AV junction
wandering atrial pacemaker
INTERMITTENT block at the level of the bundle of His or bundle branches
this results in atrial impulses NOT ALWAYS being conducted to the ventricles
2nd degree AV block, type 2
sustained VT
peristant PVCs for more than 30 seconds
run VT
aka
burst VT
aka salvo VT
a brief episode of 3 or more PVCs in a row
wide ( > 0.12 secs) bizarre QRS complexes
T wave in the opposite direction of the R wave
no P wave
ventricular dysrhythmia
varient of polymorphic ventricular tachycardia
associated wprolonged QT interval
drug induced or from electrolyte abnormalities
torsades de pointes
“twisting of points”
common rhythm after a cardiac arrest
junctional tachycardia
PVCs that occur on or near a previous T wave are called ____ and may precipitate ___
PVCs that occur on or near a previous T wave are called R-on-T PVCs and may precipitate ventricular tachycardia/ fibrillation
difference b/w PAC with aberrant ventricular conduction and PVC
PAC does not have a compensatory pause
wenckebach
2nd degree AV heart block, type 1
noncompensatory pause is associate with
PACs
VT w/ each QRS looking the same
monomorphic
atrial dysrhythmias are thought to be caused by what 3 mechanisms
- disorders of impulse formation
- automaticity
- triggered activity
- disorder of impulse conduction
- reentry
tx for pt with torsades de pointe in cardiac arrest
defibrillation
tx for pt with torsades de pointe, NOT in cardiac arrest
magnesium sulfate
don’t let them brady down
(FYI- Mag mediates K influx during phase 4 of the action potential, during hypomagnesemia, K influx is partially inhibited… this causes delayed ventricular depolarization)
PR interval is prolonged and the same duration for every beat
intermittently a P wave occurs and is not follwed by a QRS complex
2nd degree AV block, type 2
dysrhythmia that arises from the ventricles with 100 to 250 bpm
wide ( >0.12 secs) and bizarre QRS
T wave in the opposite direction of the R wave
absent P wave (hidden in the QRS)
present when there are 3+ PVCs in a row
ventricular tachycardia
upright and round P waves seem to march right through the QRS complexes
immeasurable PR intervals
3rd degree AV heart block
early ectopic beats that originate outside the SA node and produce an irregular rhythm
followed by a noncompensatory pause
PAC
w/ atrial Flutter, what determines the ventricular rate
the number of impulses conducted through the AV node
(ex: 3:1 conduction ratio)
dysrhythmia with HR of 120-150 that arises from atria
P waves that change morphology
rhythm is irregular due to multiple foci
multifocal atrial tachycardia
a partial delay or complete interruption in the conduction b/w the atria and ventricles that disrupts ventricular filling
heart block
patterned irregularity
HR increases during inspiration and decreases during expiration
occurs naturally in: athletes, kids, geris
also occurs in: inferior wall MI, CVD, digitalis, morphine, intracranial pressure
sinus dysrhythmia
sinus bradycardia is HR below ___, pts are less tolerant and symptomatic at rates below ___
sinus bradycardia is HR below 60, pts are less tolerant and symptomatic at rates below 45
two PVCs in a row are called ___ and indicate ___
two PVCs in a row are called a couplet and indicate extremely irritable ventricles
flat line
asystole
sawtooth atrial waveforms
atrial Flutter (F wave)
no association b/w P waves and QRS complexes
3rd degree AV heart block
normal sinus rhythm for 6 + y/o
60 - 100
difference b/w multifocal atrial tachycardia and wandering atrial pacemaker
MAT is a faster rate
- normal atrial rate
- ventricular pacemaker is an escaped rhythm
- if from the AV junction, rate is 40-60
- if from the ventricles, rate is 20-40 and the QRS will be wide
- the atrial and ventricular rhythms are not related to one another
3rd degree AV heart block
fast ectopic rhythm that arises from the bundle of his
100 to 180 bpm
P wave can be inverted, buried in QRS, can come before QRS, or can come after QRS
normal QRS
junctional tachycardia
where do atrial dysrhythmias originate
atrial tissue
or
internodal pathways
most common cause of prehospital cardiac arrest in adults
V-fib
chaotic firing of multiple sites in the ventricles- 300 to 500 unsynchronized impulses per minute)
QRS is a wavy chaotic line
full cardiac arrest, unresponsive, pulseless
Ventricular Fibrillation
(mycoardium is quivering but not contracting and there is no perfusion)
why is the SA node timing unaffected in PVCs
b/c the pause is compensated
intermittent block at the level of the AV node
2nd degree AV heart block, type 1
dysrhythmia w/ HR of 20-40 bpm
wide and bizarre QRS
T wave in the opposite direction of the R wave
absent P wave (hidden in the QRS)
idioventricular rhythm
organized electrical rhythm on the ECG monitor but the pt is pulseless and apneic
pulseless electrical activity
(PEA)
a consistent delay of conduction at the level of the AV node
1st degree heart block
not a true block
what can notching in a T wave be
hidden P waves,
like in 3rd degree AV heart block
mobitz 2
2nd degree AV block, type 2
difference b/w multifocal atrial tachycardia and a-fib
in MAT, P waves are discernible
short bursts of rapid dysrhythmia with HR of 150-250 that arises from atria
rate so fast that it overrides SA node
paroxysmal atrial tachycardia (PAT)
irregular pattern with no discernible P waves and instead there is a chaotic baseline of weird waves respresenting atrial activity
HR greater than 350
atrial fibrillation (f waves)
irregular rhythm due to early beat
short PR interval
P wave can be inverted, buried in QRS, can come before QRS, or can come after QRS
normal QRS
premature junctional complex (PJC)
rapid dysrhythmia with HR of 150-250 that arises from atria
rate so fast that it overrides SA node
atrial tachycardia
P waves that differ in appearance from normal sinus P waves (P’ waves)
abnormal (short or long) PR interval
normal (and narrow) QRS
atrial dysrhythmias
what can happen w/ a-fib
stroke
loss of atrial kick and decreased CO causes blood to stagnate in atrial chambers causing clots to form
rapid depolarization re-entry circut in the atria at a rate of 250-350
atrial Flutter (F wave)
impulse arises from AV junction
rate is b/w 40 and 60 bpm
P wave can be inverted, buried in QRS, can come before QRS, or can come after QRS
normal QRS
junctional escape rhythm
what is the regularity in a 2nd degree AV block, type 2
regular or irregular
depends on the conduction ratio; if the conduction ratio is the constant then it will be regular
not a true heart block and of little or no clinical significance b/c impulses are conducted to the ventricles
1st degree AV heart block
VT w/ varying morphology of QRS’s
polymorphic VT
aka
torsades to pointes
mobitz 1
2nd degree AV heart block, type 1
PR interval progressively increases until a QRS is dropped, then the next PR interval is shorter
this means not all P waves are follwed by a QRS complex
patterned irregularity
2nd degree AV block type 1
normal sinus rhythm for 2 y/o
85 to 125
normal sinus rhythm for newborn
110 to 150
impulse arises from AV junction at 60 to 100 bpm
P wave can be inverted, buried in QRS, can come before QRS, or can come after QRS
normal QRS
accelerated junctional rhythm
early ectopic beats that originate outside the SA node and produce an irregular rhythm
followed by a noncompensatory pause
wide QRS complexes
PAC with aberrant ventricular conduction
can affect ventricular filling time and diminish the strength of the atrial contraction
which causes decreased CO and decreased perfusion
atrial dysrhythmias
can occur w/ or w/out pulses
pt may or may not be stable
ventricular tachycardia
what is a PVC that falls in between 2 normal complexes and doesn’t disturb the normal cycle
there will be no compensatory pause because the SA node was not inhibited by retrograde PVC conduction
more common w/ brady
interpolated PVCs
