dysrhythmias Flashcards by Rebecca Lea

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

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SA node transiently stops firing and 3+ beats are dropped

sinus arrest

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complete heart block

3rd degree AV heart block

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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)

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PVCs that all look the same

unifocal

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complete block of conduction at or below the AV node, the impulses do not reach the ventricles

3rd degree AV heart block

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sinus tachycardia is HR b/w

100 to 160

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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

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PR intervals that are longer than 0.20 secs and constant

everything else pretty normal

1st degree AV heart block

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SA node transiently stop firing and 1-2 beats are dropped

sinus pause

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normal sinus rhythm for 4 y/o

75 to 115

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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

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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

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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

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which heart blocks are emergent

2nd degree AV block, type 2

and

3rd degree AV heart block (life threatening)

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(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

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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

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sustained VT

peristant PVCs for more than 30 seconds

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run VT

aka

burst VT

aka salvo VT

a brief episode of 3 or more PVCs in a row

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wide ( > 0.12 secs) bizarre QRS complexes

T wave in the opposite direction of the R wave

no P wave

ventricular dysrhythmia

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varient of polymorphic ventricular tachycardia

associated wprolonged QT interval

drug induced or from electrolyte abnormalities

torsades de pointes

“twisting of points”

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common rhythm after a cardiac arrest

junctional tachycardia

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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

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difference b/w PAC with aberrant ventricular conduction and PVC

PAC does not have a compensatory pause

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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

dysrhythmias Flashcards

(78 cards)