Clinical-Atrial Arrhythmias- Brandecker Flashcards Preview

ICOM-Cardio > Clinical-Atrial Arrhythmias- Brandecker > Flashcards

Flashcards in Clinical-Atrial Arrhythmias- Brandecker Deck (86)
Loading flashcards...
1
Q

What is an arrhythmia?

A

Any rhythm that is NOT normal sinus rhythm

2
Q

Lead II should have what type of P wave?

A

upright

3
Q

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

A

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

4
Q

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

A

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

5
Q

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

A

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

6
Q

Describe what is happening with this PAC?

A

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

7
Q

What is meant by narrow complex tachycardias (NCTs)?

A

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

8
Q

What is another name for narrow complex tachycardias?

A

supraventricular tachycardias (SVTs)

9
Q

What is sinus tachycardia?

A

normal P and QRS with rate faster than 100

10
Q

What are paroxysmal supraventricular tachycardias (PSVTs)?

A

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.

11
Q

What 3 types of paroxysmal supraventricular tachychardias are there?

A
12
Q

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

A

His

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

13
Q

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

A

▸ 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

14
Q

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)?

A

ATRIAL VENTRICULAR NODAL REENTRY TACHYCARDIA-AVNRT

15
Q

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

A

▸ 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

16
Q

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

A

220 bpm

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

17
Q

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.

A

blocked

18
Q

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.

A

available

longer

can

sustained

19
Q

Describe the AVNRT:

A
20
Q

Examples of retrograde P waves disguised as other waves

A
21
Q

How is AVNRT different from AVRT?

A

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

22
Q

AVRT can be initiated by a PAC as well as .

A

PVC

23
Q

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

A

atrioventricular re-entry tachycardia (AVRT)

WPW is one of the causes of AVRT

24
Q

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

A

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

25
Q

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

A

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

26
Q

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

A

Delta

27
Q

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

A

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

28
Q

What does it mean if the signal is orthodromic?

A

Signal goes down AV node and up the bypass tract

▸ Narrow complex QRS (< 0.12 sec)

(treat with adenosine of B blocker)

29
Q

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

A

orhtodromic

30
Q

What is meant if the signalling is antidromic in AVRT?

A

▸ Signal goes down bypass tract and up the AV node

31
Q

Describe how antidromic AVRT shows up on ECG:

A

▸ 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)

32
Q

Why is this diagram probable orhtodromic AVRT?

A

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.

33
Q

What type of QRS complex is this an example of?

A

Wide (QRS) complex (antidromic-going backwards through the AV node)

It was determined WPW

-avoid adenosine, AV nodal blockers, use procainamide

34
Q

What is the overall treatment goal for PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA?

A

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

35
Q

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?

A

Carotid Sinus Massage

Can be used to convert PSVT back to sinus rhythm

36
Q

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

A

Atrial tachycardia

Very hard to diagnose

37
Q

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

A

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

38
Q

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

A

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

39
Q

What is the most common arrhythmia?

A

atrial fibrillation (AFIB)

40
Q

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

A

completely disorganized

41
Q

Difference between atrial tachycardia and AFIB?

A

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

42
Q

Describe AFIB?

A

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)

43
Q

Describe AFIB ECG?

A

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

44
Q

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

A

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

45
Q

What is a major cause of AFIB?

A

Hyperthyroidism-enhances sympathetic effects

-check TSH levels

46
Q

Describe valvular dz as it concerns AFIB?

A

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.

47
Q

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

A

look for valvular heart dz

48
Q

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

A

listen for a murmur (stenosis)

49
Q

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

A

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

50
Q

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

A

▸ Pulmonary embolism

▸ Ischemic heart disease

▸ Hypertension (chronic HTN tends to dilate atria)

▸ Alcohol — holiday heart

▸ Hypothermia

51
Q

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

A

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

52
Q

What are some related complications from AFIB?

A

▸Rate related cardiomyopathy and heart failure due to prolonged high HR

Atrial thrombus due to stagnant blood with formation which can lead to emboli

53
Q

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

A

warfarin, apixaban, dabigatran

54
Q

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

A

CHADs score

55
Q

What are the 4 classifications of AFIB ?

A
  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)
56
Q

What is the treatment for AFIB or atrial flutter if stable for rate control?

(depends on hemodynamic stability)

A
  1. slow down ventricular rate (Beta blockers, calcium channel blockers or digoxin) by increasing AV refractory period
57
Q

Which should you control first? Rate or rhythm?

A

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

58
Q

What causes atrial flutter?

A

ectopic focus in the atria

59
Q

How does atrial flutter differ from AFIB?

A

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)

60
Q

Atrial flutter with variable AV block

Note the different patterns and sawtooth appearance

A

V1 is a good place to look for flutter waves

61
Q

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

A

slower

62
Q

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

A

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

63
Q

Describe this atrial flutter?

A

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

64
Q

Is this AFIB or atrial flutter?

A

AFIB, rhythm all over the place

65
Q

AFIB or atrial flutter?

A

flutter, it’s a bit more organized

66
Q

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

A

Carotid sinus massage

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

67
Q

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

A

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

68
Q

What is the treatment for atrial flutter?

A

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

69
Q

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

A

stagnant blood causing emboli

70
Q

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

A

cardioversion (shock)

71
Q

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

A

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)

72
Q

When to deliver cardioversion shock?

A

R wave called synchronized cardioversion in supraventricular tachycardias

73
Q

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

A

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

74
Q

When to treat with synchronized cardioversion and defribillation?

A

synchronized cardioversion - supraventricular tachycardias

defribillation - venticular fibrillation and v tach w/o a pulse

75
Q

What is cardiac ablation used for?

A

Map out abnormal areas of electrical activity and then eliminate these areas

Can be used to treat supraventricular tachycardias

(PSVTs, A flutter, Afib)

76
Q

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

A

Multifocal atrial tachycardia.

77
Q

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

A

Beta Blockers ( because of lung issues)

78
Q

How to differentiate Multifocal atrial tachycardia?

A

▸ 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

79
Q

Brandecker flow chart

A
80
Q

How is sinus tach different from other supraventricular tachycardias?

A

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

81
Q

Run down of how to treat afib or a flutter?

A

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

82
Q

5 questions to ask for treatment of Arrhythmia?

A

▸ 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?

83
Q

Follow the questions for this case

A

▸ 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)

84
Q
A

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.

85
Q
A

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.

86
Q
A

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