Clinical-Atrial Arrhythmias- Brandecker

Question 1

What is an arrhythmia?

Answer 1

Any rhythm that is NOT normal sinus rhythm

Question 2

Lead II should have what type of P wave?

Answer 2

upright

Question 3

For many rapid arrhythmias to occur, 2 major factors have to be present:

Answer 3

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

Question 4

What are premature atrial complexes (PAC) or premature atrial beats (PAB)?

Answer 4

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

Question 5

How do we know that this extra beat is originating above the AV node?

Answer 5

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

Question 6

Describe what is happening with this PAC?

Answer 6

Followed by a slight pause, SA node reset after the premature beat

Question 7

What is meant by narrow complex tachycardias (NCTs)?

Answer 7

QRS duration will be less than 120 ms with a rate that is greater than 100

Question 8

What is another name for narrow complex tachycardias?

Answer 8

supraventricular tachycardias (SVTs)

Question 9

What is sinus tachycardia?

Answer 9

normal P and QRS with rate faster than 100

Question 10

What are paroxysmal supraventricular tachycardias (PSVTs)?

Answer 10

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.

Question 11

What 3 types of paroxysmal supraventricular tachychardias are there?

Answer 11

Question 12

▸ Supraventricular arrhythmias refer to any arrhythmias arising from above the level of the Bundle of .

Answer 12

His

Note: Should have a normal QRS duration and shape that does not change from baseline

Question 13

Why did this PAC not conduct down to the AV node to promote QRS?

Answer 13

▸ 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

Question 14

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)?

Answer 14

ATRIAL VENTRICULAR NODAL REENTRY TACHYCARDIA-AVNRT

Question 15

Describe the 2 possible pathological pathways of atrial ventricular nodal reentry tachycardia (AVNRT)?

Answer 15

▸ 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

Question 16

Circular movement of 2 channels of AVNRT through AV node at a rapid rate causing rapid ventricular rates, 140-bpm

Answer 16

220 bpm

Note: ▸ P wave not seen, buried in the QRS complex or retrograde

Question 17

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.

Answer 17

blocked

Question 18

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.

Answer 18

available

longer

can

sustained

Question 19

Describe the AVNRT:

Answer 19

Question 20

Examples of retrograde P waves disguised as other waves

Answer 20

Question 21

How is AVNRT different from AVRT?

Answer 21

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

Question 22

AVRT can be initiated by a PAC as well as .

Answer 22

PVC

Question 23

Wolff-Parkinson-White Syndrome is and example of which type of narrow complex tachycardia?

Answer 23

atrioventricular re-entry tachycardia (AVRT)

WPW is one of the causes of AVRT

Question 24

What are the characteristics of ECG of Wolff-Parkinson-White Syndrome?

Answer 24

Delta wave due to the accessory pathway (Bundle of Kent) not pausing as the AV nodal pathway normally does.

Question 25

Describe the PR interval and QRS complex of Wolff-Parkinson-White syndrome?

Answer 25

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

Question 26

waves relatively slow conduction through the ventricular muscle at the bypass tract (conduction through myocytes which are slower than along the bundles)

Answer 26

Delta

Question 27

Why do Delta waves have relatively slow conduction through the ventricular muscle?

Answer 27

the bypass tract causes conduction through myocytes which are slower than along the bundles.

Question 28

What does it mean if the signal is orthodromic?

Answer 28

Signal goes down AV node and up the bypass tract ▸ Narrow complex QRS (\< 0.12 sec) (treat with adenosine of B blocker)

Question 29

It is difficult to tell the difference between an AVNRT and an AVRT with signalling

Answer 29

orhtodromic

Question 30

What is meant if the signalling is antidromic in AVRT?

Answer 30

▸ Signal goes down bypass tract and up the AV node

Question 31

Describe how antidromic AVRT shows up on ECG:

Answer 31

▸ 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)

Question 32

Why is this diagram probable orhtodromic AVRT?

Answer 32

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.

Question 33

What type of QRS complex is this an example of?

Answer 33

Wide (QRS) complex (antidromic-going backwards through the AV node) It was determined WPW -avoid adenosine, AV nodal blockers, use procainamide

Question 34

What is the overall treatment goal for PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA?

Answer 34

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

Question 35

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?

Answer 35

**Carotid Sinus Massage** Can be used to convert PSVT back to sinus rhythm

Question 36

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

Answer 36

**Atrial tachycardia** Very hard to diagnose

Question 37

What is the difference between P and P'? And why does the P wave change on V1 when patient goes into atrial tachycardia?

Answer 37

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

Question 38

Why are atrial tachycardia, AVNRT, and AVRT all grouped into paroxysmal supra ventricular tachycardia (PSVT)?

Answer 38

All abrupt and Atrial tachycardia looks very similar to AVNRT and AVRT

Question 39

What is the most common arrhythmia?

Answer 39

atrial fibrillation (AFIB)

Question 40

How would you describe an AFIB beat and/or ECG?

Answer 40

completely disorganized

Question 41

Difference between atrial tachycardia and AFIB?

Answer 41

atrial tachycardia has on ectopic foci firing while AFIB has several ectopic foci

Question 42

Describe AFIB?

Answer 42

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)

Question 43

Describe AFIB ECG?

Answer 43

no P waves, chaotic fibrillation waves on ECG “f waves”, causing a rapid arterial rate up to 400-600/min

Question 44

Describe what is happening with the ventricles in AFIB and what is the ventricular rate?

Answer 44

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

Question 45

What is a major cause of AFIB?

Answer 45

Hyperthyroidism-enhances sympathetic effects -check TSH levels

Question 46

Describe valvular dz as it concerns AFIB?

Answer 46

Valvular heart disease causing atrial enlargement from mitral stenosis - atria so large it won't hold a normal rhythm -common to get an echo on AFIB pts. to look for valvular heart dz.

Question 47

Why is it common to get an echo with pts. with AFIB?

Answer 47

look for valvular heart dz

Question 48

What else can you do, other than an echo, with suspicion of valvular dz?

Answer 48

listen for a murmur (stenosis)

Question 49

What medications can stimulate the sympathetic nervous system and cause AFIB?

Answer 49

cocaine or other medications that stimulate SNS (cocaine, theophyline, amphetamines, caffeine)

Question 50

List other causes of AFIB other than hyperthyroidism, valve dz, and stimulants:

Answer 50

▸ Pulmonary embolism ▸ Ischemic heart disease ▸ Hypertension (chronic HTN tends to dilate atria) ▸ Alcohol — holiday heart ▸ Hypothermia

Question 51

What are the differences in rate between atrial flutter and AFIB?

Answer 51

Rate in atrial flutter is around 300. Atrial fibrillation rates exceed 300 and there is no organized activity.

Question 52

What are some related complications from AFIB?

Answer 52

▸Rate related cardiomyopathy and heart failure due to prolonged high HR Atrial thrombus due to stagnant blood with formation which can lead to emboli

Question 53

What are some anticoagulation medications to use for possible stagnant blood (mural thrombi) due to AFIB?

Answer 53

warfarin, apixaban, dabigatran

Question 54

How do we decide the risk benefit to use anticoagulatives for AFIB pts?

Answer 54

CHADs score

Question 55

What are the 4 classifications of AFIB ?

Answer 55

1. Paroxysmal (less than 7 days, terminates spontaneously) 2. Persistent (7 days +, or less than 7 days with med/electic cardioversion) 3. Long-standing persistent (1 yr +) 4. Permanent (1 yr +, not to pursure restoration)

Question 56

What is the treatment for AFIB or atrial flutter if **stable** for rate control? (depends on hemodynamic stability)

Answer 56

1. slow down ventricular rate (Beta blockers, calcium channel blockers or digoxin) by increasing AV refractory period

Question 57

Which should you control first? Rate or rhythm?

Answer 57

rate should be controled first (less than 100) to allow for perfusion and then rhythm.

Question 58

What causes atrial flutter?

Answer 58

ectopic focus in the atria

Question 59

How does atrial flutter differ from AFIB?

Answer 59

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)

Question 60

Atrial flutter with variable AV block Note the different patterns and sawtooth appearance

Answer 60

V1 is a good place to look for flutter waves

Question 61

When the rate is **faster/slower** in atrial flutter, its easier to see the classic sawtooth waves.

Answer 61

slower

Question 62

What medication can be used if unsure about rhythm and want to check for flutter waves?

Answer 62

**Adenosine** will block the AV node (it is not a treatment for atrial flutter but will reveal it)

Question 63

Describe this atrial flutter?

Answer 63

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

Question 64

Is this AFIB or atrial flutter?

Answer 64

AFIB, rhythm all over the place

Question 65

AFIB or atrial flutter?

Answer 65

flutter, it's a bit more organized

Question 66

What non-medication method can be used to diagnose some atrial arrhythmias such as atrial flutter?

Answer 66

Carotid sinus massage ▸ Slowing of the ventricular rate and allows for easier identification of flutter or fibrillatory waves

Question 67

Which nerve is stimulated with the carotid sinus massage and what does it do?

Answer 67

Stimulates the vagus nerve which inhibits firing of the SA node and slows AV node conduction

Question 68

What is the treatment for atrial flutter?

Answer 68

First, slow down the ventricular rate by increasing the refractory period of the AV node (calcium channel blockers or digoxin) (same treatment for afib and a flutter) consider an anticoagulant as well

Question 69

Why would you want to consider treating with an anticoagulant with afib and a flutter?

Answer 69

stagnant blood causing emboli

Question 70

How do you treat patients who are stable vs unstable (hypotensive, cardiogenic shcock, acute heart failure, BP not perfusing, ischemic chest pain) with arrhythmias?

Answer 70

cardioversion (shock)

Question 71

What is the criteria to deliver cardioversion shock for an unstable patient?

Answer 71

Hypotensive systolic BP \<90\* mm Hg, cardiogenic shock, acute heart failure Altered mental status Ischemic chest pain low blood pressure (not perfusing, normally systolic less than 90)

Question 72

When to deliver cardioversion shock?

Answer 72

R wave called synchronized cardioversion in supraventricular tachycardias

Question 73

What can happen if cardioversion delivered at T wave instead of R wave (as recommended)?

Answer 73

Energy delivered during T wave can result in conversion to ventricular arrhythmia

Question 74

When to treat with synchronized cardioversion and defribillation?

Answer 74

synchronized cardioversion - supraventricular tachycardias defribillation - venticular fibrillation and v tach w/o a pulse

Question 75

What is cardiac ablation used for?

Answer 75

Map out abnormal areas of electrical activity and then eliminate these areas Can be used to treat supraventricular tachycardias (PSVTs, A flutter, Afib)

Question 76

What type of arrhythmia to worry about with severe chronic lung disease?

Answer 76

Multifocal atrial tachycardia.

Question 77

Which medication do you want to use cautiously with Multifocal atrial tachycardia patients?

Answer 77

Beta Blockers ( because of lung issues)

Question 78

How to differentiate Multifocal atrial tachycardia?

Answer 78

▸ 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

Question 79

Brandecker flow chart

Answer 79

Question 80

How is sinus tach different from other supraventricular tachycardias?

Answer 80

This is usually a physiologic response to some **other** pathology (septic or hypovolemic shock) in order to maintain CO.

Question 81

Run down of how to treat afib or a flutter?

Answer 81

**rate control** to control tachycardia so that the rate is less than 110. Use **beta-blocker,** calcium channel blocker, digoxin **Adenosine** will **not control the rate because it has short half-life** (good to diagnose a flutter), effective for 30 seconds or less rhythm control- **antiarrhythmic’s** can be used to try to maintain normal sinus rhythm with patients with history of atrial fibrillation – **amiodarone, sotalol, flecanide** Remember anticoagulation for patients with recurrent atrial fibrillation- **warfarin, apaxiban, dibigatran, rivaroxaban**

Question 82

5 questions to ask for treatment of Arrhythmia?

Answer 82

▸ Is the rhythm fast or slow? ▸ Is the rhythm regular or irregular? ▸ Is the QRS wide or narrow? ▸ If it is narrow, are P waves present? ▸ Is the patient hemodynamically stable or unstable?

Question 83

Follow the questions for this case

Answer 83

▸ 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)**

Question 84

Answer 84

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.

Question 85

Answer 85

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.**

Question 86

Answer 86

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