Clinical-Atrial Arrhythmias- Brandecker Flashcards
What is an arrhythmia?
Any rhythm that is NOT normal sinus rhythm
Lead II should have what type of P wave?
upright
For many rapid arrhythmias to occur, 2 major factors have to be present:
A trigger that initiates the arrhythmia
▸ premature beat that can be atrial, junctional, ventricular
▸ A substrate that allows the arrhythmia mechanism to continue
▸ infarction, structural abnormality, ischemic tissue, scar, fibrosis, electrolyte abnormalities
What are premature atrial complexes (PAC) or premature atrial beats (PAB)?
Originate in the atrium outside of the SA node
P wave may have a different morphology or P-R interval
QRS usually the same
Can occur in healthy hearts
How do we know that this extra beat is originating above the AV node?
Because the QRS complex looks the same
Note: this beat has a QRS that looks different and so we know it started in the ventricle
Describe what is happening with this PAC?
Followed by a slight pause, SA node reset after the premature beat
What is meant by narrow complex tachycardias (NCTs)?
QRS duration will be less than 120 ms with a rate that is greater than 100
What is another name for narrow complex tachycardias?
supraventricular tachycardias (SVTs)
What is sinus tachycardia?
normal P and QRS with rate faster than 100
What are paroxysmal supraventricular tachycardias (PSVTs)?
They have an abrupt onset
-can have regular beat (60 bpm) and a premature beat occurs (along with structural abnormality) jumps up to passed 100.
What 3 types of paroxysmal supraventricular tachychardias are there?
▸ Supraventricular arrhythmias refer to any arrhythmias arising from above the level of the Bundle of .
His
Note: Should have a normal QRS duration and shape that does not change from baseline
Why did this PAC not conduct down to the AV node to promote QRS?
▸ The PAC arrives at the AV node when it is still refractory
▸ May cause a slight irregularity of the heartbeat since the SA node is reset
Which paroxysmal supraventricular tachycardia (PSVT) results from reentry in the AV node area with 2 (pathological) functional conduction channels with different electrical properties (dual pathways)?
ATRIAL VENTRICULAR NODAL REENTRY TACHYCARDIA-AVNRT
Describe the 2 possible pathological pathways of atrial ventricular nodal reentry tachycardia (AVNRT)?
▸ One pathway has fast conduction speed and slow refractory period
▸ Other pathway has slow conduction and rapid refractory period
Note: will see narrow complex tachycardia w/o P wave or retrograde P wave or burried P wave in QRS complex
No P wave in this tracing
Circular movement of 2 channels of AVNRT through AV node at a rapid rate causing rapid ventricular rates, 140-bpm
220 bpm
Note: ▸ P wave not seen, buried in the QRS complex or retrograde
Concerning AVNRT
●A premature atrial beat (or less commonly, a premature junctional or ventricular beat with retrograde conduction) arrives at the AV node when the fast pathway is in its refractory period. Thus, antegrade conduction down the fast pathway is blocked/passes through.
blocked
Concerning AVNRT (dual pathway pathology)
●If the premature beat arrives in a specific time window (ie, a “critically timed” premature beat), the slow pathway, with a shorter refractory period than the fast pathway, is available/not available for conduction to the ventricle.
●The premature beat conducts via the slow pathway, through the final common pathway, to the bundle of His. As a result, the PR interval of the premature beat will be shorter/longer than those of normal beats conducted through the fast pathway.
●If the fast pathway has recovered its excitability by the time the slow pathway impulse reaches the distal junction of the two pathways, the impulse can/cannot conduct retrograde up the fast pathway. The circuit may then become repetitive with antegrade conduction back down the slow pathway and retrograde conduction up the fast pathway resulting in a sustained/unsustained tachycardia.
available
longer
can
sustained
Describe the AVNRT:
Examples of retrograde P waves disguised as other waves
How is AVNRT different from AVRT?
AVNRT deals with pathology in the AV node itself while AVRT deals with the AV node and atrioventricular bypass tract, accessory pathway, Bundle of Kent
The AV node is not the source of pathology in AVRT but is still involved in the tachycardia
AVRT can be initiated by a PAC as well as .
PVC
Wolff-Parkinson-White Syndrome is and example of which type of narrow complex tachycardia?
atrioventricular re-entry tachycardia (AVRT)
WPW is one of the causes of AVRT
What are the characteristics of ECG of Wolff-Parkinson-White Syndrome?
Delta wave due to the accessory pathway (Bundle of Kent) not pausing as the AV nodal pathway normally does.
Describe the PR interval and QRS complex of Wolff-Parkinson-White syndrome?
PR interval is shortened, frequently < 0.12 seconds
QRS is widened but this is not because of a bundle branch block but the appearance of the Delta wave, early conduction of the ventricle
waves relatively slow conduction through the ventricular muscle at the bypass tract (conduction through myocytes which are slower than along the bundles)
Delta
Why do Delta waves have relatively slow conduction through the ventricular muscle?
the bypass tract causes conduction through myocytes which are slower than along the bundles.
What does it mean if the signal is orthodromic?
Signal goes down AV node and up the bypass tract
▸ Narrow complex QRS (< 0.12 sec)
(treat with adenosine of B blocker)
It is difficult to tell the difference between an AVNRT and an AVRT with signalling
orhtodromic
What is meant if the signalling is antidromic in AVRT?
▸ Signal goes down bypass tract and up the AV node
Describe how antidromic AVRT shows up on ECG:
▸ Wide complex QRS can be mistaken for ventricular tachycardia
▸ Treat as Vtach, don’t use AV node blocker
▸ Use Procainamide (if it’s wide, use procainamide)
Why is this diagram probable orhtodromic AVRT?
The findings are that of a reentrant type PSVT. Note the inverted P waves in leads II, III, and F; with upright P waves in aVR, consistent with retrograde activation of the atria from region in or near the AV node. Somewhat atypically for AVNRT, the P waves are located in the ST segment proper, not hidden in the QRS or just after the QRS. However, most likely this is still an AV nodal reentrant tachycardia variant with somewhat slow conduction in the retrograde (“fast pathway”) limb. AV reentrant tachycardia (AVRT) involving a concealed bypass tract in the septal area is possible. The clinical setting (single event in middleaged woman) favors AVNRT. The ECG, by itself, could represent either mechanism. Adenosine response (which blocks the reentrant circuit in the AV node) does not distinguish between response to AVNRT or AVRT. Definitive answer would likely call for EP study, not indicated by the present clinical scenario, but would be consideration for recurrent, symptomatic episodes. Compare with other examples of PSVT on the site.
What type of QRS complex is this an example of?
Wide (QRS) complex (antidromic-going backwards through the AV node)
It was determined WPW
-avoid adenosine, AV nodal blockers, use procainamide
What is the overall treatment goal for PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA?
Treatment revolves around increasing refractory period of the AV node (if narrow QRS)
Vagal maneuvers or carotid massage increase parasympathetic tone
▸ Medications
▸ Adenosine—blocks AV Node
▸ Calcium channel or beta blockers, increase refractory period
▸ If unstable cardioversion
What non-drug treatment can be used to treat PSVT and help diagnose some atrial arrhythmias which involves stimulating the vagus nerve (parasympathetics) which inhibits firing of the SA node and slows or blocks AV node conduction?
Carotid Sinus Massage
Can be used to convert PSVT back to sinus rhythm
Which PSVT is being described:
Usually due to single ectopic focus
▸ Atrial rate 110-250 if 1:1 conduction, atrial rate equals ventricular rate
▸ P wave morphology is abnormal when compared with P waves originating from the SA node (maybe upside down)
▸ If rate is fast, p waves may not be visualized
Atrial tachycardia
Very hard to diagnose
What is the difference between P and P’? And why does the P wave change on V1 when patient goes into atrial tachycardia?
P’ signifies a premature beat
P waves only seen in V1, the p waves vary because it is initiated from an ectopic beat and not SA node
How would you describe an AFIB beat and/or ECG?
completely disorganized
Difference between atrial tachycardia and AFIB?
atrial tachycardia has on ectopic foci firing while AFIB has several ectopic foci
Describe AFIB?
Most common arrhythmia
▸ Irregularly irregular tachydysrhythmia
▸ Disorganized atrial electrical activity caused by many ectopic atrial foci firing very fast
▸ Ventricular rate typically 100-160 (when atrial ectopic foci hit the AV node when not refractory)
Describe what is happening with the ventricles in AFIB and what is the ventricular rate?
Ventricular rate depends on the AV node’s ability to conduct the impulses it is bombarded with
▸ AV node blocks most of the impulses
▸ A fib with rapid ventricular response, ventricular rate >100
What are the differences in rate between atrial flutter and AFIB?
Rate in atrial flutter is around 300. Atrial fibrillation rates exceed 300 and there is no organized activity.
How do we decide the risk benefit to use anticoagulatives for AFIB pts?
CHADs score
How does atrial flutter differ from AFIB?
rapid regular atrial rate around 300bpm
ventricles around 150bpm and this rate is regular or irregular
classic sawtooth (flutter waves) appearance (2, 3, aVF, and V1)
Atrial flutter with variable AV block
Note the different patterns and sawtooth appearance
V1 is a good place to look for flutter waves
When the rate is faster/slower in atrial flutter, its easier to see the classic sawtooth waves.
slower
What medication can be used if unsure about rhythm and want to check for flutter waves?
Adenosine will block the AV node (it is not a treatment for atrial flutter but will reveal it)
Describe this atrial flutter?
Atrial Flutter with Variable Block
Inverted flutter waves in II, III + aVF with atrial rate ~ 300 bpm Positive flutter waves in V1 resembling P waves
The degree of AV block varies from 2:1 to 4:1
Is this AFIB or atrial flutter?
AFIB, rhythm all over the place
AFIB or atrial flutter?
flutter, it’s a bit more organized
When to deliver cardioversion shock?
R wave called synchronized cardioversion in supraventricular tachycardias
How to differentiate Multifocal atrial tachycardia?
▸ P waves have multiple different morphologies (at least 3) and irregular rhythm (differing R to R intervals)
-multi foci are firing, hence, the different P wave morpholigies
Note: arrows point to varying P waves
Brandecker flow chart
Follow the questions for this case
▸ Is the rhythm fast or slow? fast, 150
▸ Is the rhythm regular or irregular? regular
▸ Is the QRS wide or narrow? narrow
▸ If it is narrow, are P waves present? no
▸ Is the patient hemodynamically stable or unstable? stable
treat with adenosine, vagal, or carotid massage, B blocker, Ca2+ blocker (verapamil)
The ECG shows a very regular, narrow complex tachycardia (NCT) with a ventricular rate of about 150/min. The NCT rules out antidromic conduction with a concealed bypass tract, which should produce a wide-complex tachycardia. If you look carefully, especially at a magnified high resolution presentation of this ECG, you will see subtle positive/negative deflections near the terminal part of the QRS in leads aVR/II, consistent with retrograde P waves from AV nodal reentry. These waves are sometimes called pseudo-R and pseudo-S waves, respectively. The low voltage QRS complexes were likely due to obesity. The substrate for AVNRT relates to so-called “dual-pathways” in the AV node that allow for the initiation and maintenance of a reentrant type rhythm. Typically AVNRT is initiated by an atrial premature complex. The retrograde P waves during the tachycardia may be seen just after the QRS, as in this case, or may be “hidden” in the QRS if the atria and ventricles are stimulated simultaneously. Rarely, the retrograde P waves with AVNRT will precede the QRS.
EKG interpretation: irregular rhythm with occasional sinus beats, a short run of atrial flutter, and atrial fibrillation, rate approximately 120, normal axis positive 30°, early R wave progression, no ST elevation or depression, no abnormal T-wave inversion
Treatment rate control, consider beta-blocker or calcium channel blocker or digoxin. Anticoagulation with warfarin, apixaban or one of the other novel agents. Obtain a TSH (thyroid stimulating hormone) level to evaluate for possibility of hyperthyroidism contributing to atrial fibrillation. Also consider other potential underlying causes. Order echocardiogram.
EKG interpretation: atrial fibrillation, variable-rate 100 – 150, normal axis, no QS elevation or depression, no abnormal T-wave inversions, no information from lead V2, QRS duration 80 ms
