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Circulation Part 2 > Arrhythmias- Lecture > Flashcards

Arrhythmias- Lecture Flashcards

1
Q

Tachyarrhythmias with wide QRS

A

Tachyarrhythmias with wide QRS:
* Ventricular tachycardia
* SVTs with bundle-branch block

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1
Q

_ is a tachyarrhythmia without a QRS complex

A

Ventricular fibrillation is a tachyarrhythmia without a QRS complex

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2
Q

Four types of tachyarrhythmias with narrow QRS

A
  1. Atrial fibrillation
  2. Multifocal atrial tachycardia
  3. Atrioventricular node reentrant tachycardia
  4. Atrial flutter
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3
Q

The most common mechanism of tachyarrhythmia is _

A

The most common mechanism of tachyarrhythmia is reentry

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4
Q

The two types of abnormal impulse formations that lead to tachyarrhythmias are _ and _

A

The two types of abnormal impulse formations that lead to tachyarrhythmias are increased automaticity and trigger activity

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5
Q

The mechanism of triggered activity that can lead to tachyarrhythmias involves _

A

The mechanism of triggered activity that can lead to tachyarrhythmias involves a prior beat causing an abnormal subsequent beat

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6
Q

Explain the mechanism of reentry

A
  1. Some individuals are born with two pathways through the AV node, for example
  2. One pathway will be fast and one pathway is slow; when both are transmitting signals the heart will beat normally
  3. When the fast pathway is blocked (like an early beat leaves the fast pathway in a refractory period) then the pathway only goes down the slow route
  4. If the signal down the slow route, reaches the connection point when the fast pathway is ready again, then it can transmit the signal up
  5. We end up with a re-entry circuit
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7
Q

Wide QRS is a result of _

A

Wide QRS is a result of not traveling through the normal conduction system
* Either via aberrency (bundle block)
* Or signal originates in an abnormal starting place

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8
Q

Tachycardias with narrow QRS and regular rhythm

A
  1. Sinus tachycardia
  2. Atrial flutter
  3. Paroxysmal SVT
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9
Q

Tachycardias with wide QRS and regular rhythm

A
  1. Ventricular tachycardia
  2. Abberency or accessory pathway
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10
Q

Tachycardias with narrow QRS and irregular rhythm

A
  1. Atrial fibrillation
  2. Atrial flutter with variable block
  3. APBs
  4. Multifocal atrial tachycardia
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11
Q

Tachycardias with wide QRS and irregular rhythm

A
  1. Ventricular premature beat
  2. Polymorphic VT (Torsades)
  3. Ventricular fibrillation
  4. Other irregular rhythm tachycardias + aberrency or accessory pathway
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12
Q

If you see narrow QRS with an irregular rhythm, the most common cause will be _

A

If you see narrow QRS with an irregular rhythm, the most common cause will be atrial fibrillation

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13
Q

What normally triggers atrial fibrillation?

A

Atrial fibrillation is triggered by abnormal automaticity or triggered activity in pulmonary venous mucle sleeves

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14
Q

Atrial fibrillation is maintained via _ mechanism

A

Atrial fibrillation is maintained via multiple functional reentrant circuits primarily in the left atrium

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15
Q

The hot spot for automaticity that can result in atrial fibrillation is around the _

A

The hot spot for automaticity that can result in atrial fibrillation is around the pulmonary veins

The pulmonary veins are very autoarrythmic

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16
Q

Some of the manifestations of atrial fibrillation include _ and the consequences include _

A

Some of the manifestations of atrial fibrillation include persistent palpitations, SOB, syncope and the consequences include heart failure, stroke
* Note: the atria experience rapid activity of 350-600 beats per minute but not all of those signals are transmitted; HR up to 175

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17
Q

The reason that atrial fibrillation can lead to stroke is due to the tendency for stagnant blood and clotting, particularly in the _

A

The reason that atrial fibrillation can lead to stroke is due to the tendency for stagnant blood and clotting, particularly in the left atrial apendage

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18
Q

To avoid stroke, we often start atrial fibrillation patients on _

A

To avoid stroke, we often start atrial fibrillation patients on anticoagulants
* Warfarin
* NOACs- rivaroxaban, apixaban

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19
Q

The idea behind administering antiarrhythmics for atrial fibrillation is to _

A

The idea behind administering antiarrhythmics for atrial fibrillation is to increase the refractoriness of the AV node
* Heart rate control
* Rhythm control

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20
Q

Treatment options for atrial fibrillation

A
  1. Beta blockers
  2. Non-dihydropyridine CCBs
  3. Class I antiarrhythmics
  4. Class III antiarrhythmics
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21
Q

The presence of a delta wave is suggestive of _

A

The presence of a delta wave is suggestive of Wolf-Parkinson-White (WPW)
* The delta wave is a pre-excited ventricle

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22
Q

The cause of WPW delta waves is _

A

The cause of WPW delta waves is presence of a bypass pathway
* We have an accessory pathway which sets up reentry circuits

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23
Q
A

WPW

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24
Q

What has happened to the WPW patient?

A

Patient is now in AVRT (a reentry pattern not through the AV node) this was triggered by WPW

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25
Q

AVRT and AVNRT are tachycardias that involve the AV node; therefore we must administer _ to interrrupt the AV nodal transmission

A

AVRT and AVNRT are tachycardias that involve the AV node; therefore we must administer adenosine to interrrupt the AV nodal transmission
* The adenosine will block the activity through the AV node
* However, adenosine does not prevent it from happening again
* We can also use vagal maneuvers like valsalva, carotid sinus massage, cold water
* Beta blockers, CCBs can also slow conduction through the AV node

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26
Q
A

V tach

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27
Q

Ventricular tachycardia can be caused by two different mechanisms: _ or _

A

Ventricular tachycardia can be caused by two different mechanisms: reentry or triggered arrhythmia
* Reentry is often the cause for patients with previous heart disease because scar tissue leads to a unidirectional block
* Triggered arrhythmia (delayed after depolarizations) is ofte the cause in patients without structural heart disease

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28
Q

Symptoms of ventricular tachycardia

A
  • Paroxysmal (sudden) or persistent palpitations
  • Shortness of breath
  • Pre-syncope or syncope
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29
Q

V tach is dangerous because it can lead to _ or _

A

V tach is dangerous because it can lead to heart failure or sudden death

30
Q

Stable patients in V tach can be treated with _

A

Stable patients in V tach can be treated with antiarrhythmic drugs (amiodarone, lidocaine, procainamide)

31
Q

Unstable V tach patients should be treated with _

A

Unstable V tach patients should be treated with cardioversion or defibrillation

32
Q

Cardioversion is (synchonized/ asynchronized)

A

Cardioversion is synchronized

Defibrillation on the other hand is asynchronous

33
Q

Cardioversion works by _

A

Cardioversion works by depolarizing bulk myocytes simultanously –> this resets the electrical rhythm of the heart
* This should always be used over defibrillation unless we have polymorphic VT or ventricular fibrillation

34
Q

For patients with recurrent life-threatening V tach, we can give them _

A

For patients with recurrent life-threatening V tach, we can give them automatic implantable cardioverter-defibrillators

35
Q

Polymorphic ventricular tachycardia is also known as _

A

Polymorphic ventricular tachycardia is also known as torsades de pointes

36
Q

The risk of having prolonged QT intervals is development of _

A

The risk of having prolonged QT intervals is development of torsades de pointes

37
Q

Some patients are predisposed to torsades or prolonged QT due to _ ; others acquire the condition from _

A

Some patients are predisposed to torsades or prolonged QT due to congenital channelopathy ; others acquire the condition from electrolyte abnormality or medications

38
Q

Electrolyte abnormalities including _ have the risk of causing torsades

A

Electrolyte abnormalities including low K or Mg have the risk of causing torsades

39
Q

Medications that can cause prolonged QT include:

A

The 5 A’s
* Antiarrhythmics
* Antibiotics
* Antipsychotics
* Antidepressants
* Antiemetics

40
Q

Two mechanisms for bradyarrhythmias are _ and _

A

Two mechanisms for bradyarrhythmias are reduced automaticity and conduction block
* Destinguished by narrow or wide QRS

41
Q

Junctional escape rhythm is a condition in which _

A

Junctional escape rhythm is a condition in which SA node dysfunction leads AV nodal cells to act as subsidiary pacemaker –> bradycardia

42
Q

The AV nodal cells set a slower pace than the SA node due to _

A

The AV nodal cells set a slower pace than the SA node due to slower phase 4 depolorization

43
Q

What causes junctional escape rhythm?

A

Junctional escape rhythm may be caused by:
* Sick sinus syndrome
* Electrolyte abnormalities
* Medications
* Enhanced vagal tone
* Ischemia

44
Q

We can identify junctional escape rhythm on an ECG by _

A

We can identify junctional escape rhythm on an ECG by the lack of P waves

45
Q

_ is when every P wave leads to a QRS complex but with a long PR interval

A

1st degree AV block is when every P wave leads to a QRS complex but with a long PR interval
* PR interval is longer than normal but consistant
* Normal PR is 120-200 ms
* 3-5 small boxes (normal)

46
Q

_ is regular P waves but some P waves lead to QRS and other have dropped beats

A

2nd degree heart block is regular P waves but some P waves lead to QRS and other have dropped beats

47
Q

Mobitz type I is _

A

Mobitz type I is when PR prolongs on subsequent beats and then drops a QRS
* “Longer longer longer drop, wenkebach”

48
Q

Mobitz type II is _

A

Mobitz type II is when the PR interval is fixed and we drop QRS

49
Q

3rd degree heart block is _

A

3rd degree heart block is dissociated P and QRS waves

50
Q

Causes of 1st degree heart block:

A
  • High vagal tone
  • Degenerative disease
  • Medications
  • Ischemia
51
Q

In Mobitz Type I, the block is in the _

A

In Mobitz Type I, the block is in the AV node

52
Q

In Mobitz type II, the block is in the _

A

In Mobitz type II, the block is within the bundle of His or bundle branches

53
Q

Mobitz (type I/ type II) is more serious

A

Mobitz type II is more serious
* May progress to third degree heart block
* Mobitz type I can be normal in young athletes and is usually asymtomatic

54
Q

Interventions like atropine and exercise are effective at improving Mobitz (type I/ type II)

A

Interventions like atropine and exercise are effective at improving Mobitz type I
* Meanwhile carotid massage (increase in vagal tone) worsens mobitz type I
* Mobitz type II is unaffected by all

55
Q
A

Third degree heart block

56
Q

_ can provide short term improvement for AV block but _ is usually needed by Mobitz II and 3rd degree

A

Beta-agonists can provide short term improvement for AV block but pacemaker is usually needed by Mobitz II and 3rd degree
* These two conditions are located distal to the AV node, so are minimally responsive to beta-agonists or anticholergic agents

57
Q
A

RBBB

58
Q

RBBB can be indicative of:

A

RBBB can be indicative of:
* ASD
* pulmonary hypertension
* valvular lesions
* degeneration of conduction system
* chronic CAD
* PE

59
Q

Re-entry circuit in the right atrium with a 2:1 conduction rhythm (atria beating faster than ventricles) describes _

A

Re-entry circuit in the right atrium with a 2:1 conduction rhythm (atria beating faster than ventricles) describes atrial flutter

60
Q

Three classic structures associated with atrial flutter include the _ , the _ , and the _

A

Three classic structures associated with atrial flutter include the tricuspid valve, the fossa ovalis, and the inferior vena cava

61
Q

The classic ECG finding that distinguishes atrial flutter is _

A

The classic ECG finding that distinguishes atrial flutter is sawtooth appearance of P waves

62
Q

The classic ventricular rate in atrial flutter is _

A

The classic ventricular rate in atrial flutter is 150 bpm
* If you see a heart rate that is 150 think about atrial flutter

63
Q

Sick sinus syndrome is distinguished on ECG by _

A

Sick sinus syndrome is distinguished on ECG by delayed P waves followed by dropped P waves

64
Q

An irregularly irregular tachycardia with no discernible P waves is likely to represent _

A

An irregularly irregular tachycardia with no discernible P waves is likely to represent atrial fibrillation

65
Q

Wide complex polymorphic tachycardia is typical of _

A

Wide complex polymorphic tachycardia is typical of torsades de pointes

66
Q

Wide complex tachycardia with short PR interval and delta waves is typical of _

A

Wide complex tachycardia with short PR interval and delta waves is typical of Wolff-Parkinson-White syndrome

67
Q

Regular narrow QRS complex tachycardia with P waves burried in QRS represents _

A

Regular narrow QRS complex tachycardia with P waves burried in QRS represents atrioventricular nodal re-entrant tachycardia

68
Q

The most common form of supraventricular tachycardia (SVT) is _

A

The most common form of supraventricular tachycardia (SVT) is atrioventricular nodal re-entrant tachycardia (AVNRT)

69
Q

Wolff-Parkinson-White syndrome is a cardiac conduction disorder that involves aberrant conduction through an ectopic circuit called the _

A

Wolff-Parkinson-White syndrome is a cardiac conduction disorder that involves aberrant conduction through an ectopic circuit called the bundle of Kent
* It typically causes AVRT

70
Q

The most typical presentation of Atrioventricular nodal re-entrant tachycardia is _

A

The most typical presentation of Atrioventricular nodal re-entrant tachycardia is young patient with no significant PMH presenting with palpitations

71
Q

What electrocardiographic findings are most consistent with Wolff-Parkinson-White syndrome in sinus rhythm?

A

Wide QRS, short PR interval, delta waves

72
Q

Which medications are associated with torsades?

A

antiArrhythmics (quinidine)
antiBiotics (macrolides)
antipsyChotics (haloperidol)
antiDepressants (tricyclic antidepressants - methadone)
antiEmetics/Electrolytes (ondansetron/hypomagnesemia, hypokalemia, hypocalcemia)
antiFungals (azoles)

Circulation Part 2 (15 decks)

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