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PHAR 253 > Atrial Arrhythmia > Flashcards

Atrial Arrhythmia Flashcards

1
Q

What are the two main types of atrial arrhythmias?

A
  1. Atrial fibrilation
  2. Atrial flutter
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2
Q

What are some characteristics associated with atrial fibrillation?

A

Electrical impulses triggered from multiple locations in atria

Electrical activity is chaotic rather than organized

Atrial walls, quiver rather than contract

EF is reduced due to loss of atrial kick (significant for patients with medium and reduced EF)

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3
Q

What are some characteristics of atrial flutter?

A

Electrical activities in atria is coordinated

Atria do contract but at a very rapid rate (250-350 contractions per minute, only 1/2 get across to the AV node)

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4
Q

Which of the two atrial arrhythmias is most common?

A

Atrial fibrillation is more common compared to atrial flutter

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5
Q

Is atrial fibrillation on its own life-threatening?

A

No, but it is associated with significant impairment of life and increases of stroke and LVH (due to loss of atrial kick)

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6
Q

What is atrial kick?

A

This phenomenon relies on the Frank-Starling Laws. In Afib, the atria no longer pump an extra amount of blood into the ventricles during diastole. This results in less stretching of the ventricles, which in turn causes less forceful ejection of blood during systole

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7
Q

What happens to the ECG reading of a patient with atrial fibrillation?

A

Each cycle of ECG waves lasts a different duration

They are the same duration in healthy patients

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8
Q

How common is atrial fibrillation?

A

Fairly rare in in patients under 60 (0.4%)

2-5% in those over the age of 60 (more than 6% in patients over the age of 80)

10-30% of heart failure patients have atrial fibrillation

More common in men

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9
Q

What is the main mechanism by which atrial fibrillation can pose risk for significant impairments in functional capacity?

A

Clots can form in the atria in atrial fibrilation and pieces of these clots can cause thromboemolic events

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10
Q

What are some symptoms of atrial fibrillation?

A

May have all or some of the following symptoms:
- Fatigue
- Palpitations
- Chest pain
- Dyspnea
- Dizziness

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11
Q

What is the etiology of atrial fibrillation?

A

Caused by ectopic foci that generate electrical impulses (multiple smaller pacemakers instead of one strong SA node)

This erratic generation of electrical impulses causes an irregular ventricular rhythm

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12
Q

What does the AV node do to signals from the SA node?

A

It is a damper to the signals. It slows down the frequency of impulses in healthy and atrial fibrillation patients

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13
Q

What are the main classifications of atrial fibrillation?

A

Valvular

Non-valvular

Lone atrial fibrillation

Paroxysmal

Persistant

Longstanding persistent

Permanent

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14
Q

What are some causes of atrial fibrillation?

A

Significant disease/damage/repair to heart valves

Often use warfarin for treatment

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15
Q

What are some characteristics of Lone atrial fibrillation?

A

Absence of clinical or ECG findings:
- Other CVD (including HTN)
- Related pulmonary disease
- Cardiac abnormalities (enlargement of the left atrium)
- Age under 60

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16
Q

What are some charcteristics of a paroxysmal atrial fibrillation?

A

This is atrial fibrillation that lasts longer than 30 sec and self-terminates within 7 days

Patient is usually not in atrial fibrillation

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17
Q

What are some characteristics associated with persistent atrial fibrillation?

A

Continuous atrial fibrillation lasting longer than 7 days, but less than 1 year

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18
Q

What are the differences between persistent and longstanding persistent atrial fibrillation?

A

Continuous atrial fibrillation equal or greater than 1 year despite rhythm control management

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19
Q

What are the characteristics of permanent atrial fibrillation?

A

It is continuous atrial fibrillation for which a therapeutic deision has been made not to pursue sinus rhythm restoration (rate control alone)

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20
Q

How should HCPs investigate potential atrial fibrillation?

A
  1. Get history of similar episodes (get info about duration, frequency, and nature of episodes)
  2. Determine potential risk factors or triggers (alcohol, physical exertion)
  3. Identify any potential reversible causes (acute infection, drug-related) or AF secondary to another disease (acute cardiac pathology)
  4. Review family and medical history
  5. Examine patient vitals and perform physical exam
  6. Perform the following:
    a. 12-lead electrocardiogram
    b. ECG
    c. Laboratory investigations
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21
Q

What are the goals of therapy for atrial fibrillation?

A
  • Prevent stroke or systemic thromoembolism
  • CV risk reduction
  • Improve symptoms, functional capacity and QoL
  • Prevent complications (LV dysfuntion and falls)

The above measures should improve survival, and reduce healthcare utilization

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22
Q

What is the purpose of determining a stroke risk stratification score?

A
  • Estimate risk of stroke in patients with atrial fibrilation
  • Used to determine degree of antithrombotic therapy required based on an individuals patient’s risk of developing stroke
  • Estimate bleeding risk
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23
Q

What is CHADS2?

A

It is a score that helps determine risk of atrial fibrilation

The following variables help generate risk assessment:

  1. Recent CHF
  2. Hypertension
  3. Age over 75
  4. Diabetes
  5. History of Stroke
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24
Q

What is the risk reduction of warfarin in stroke?

A

Compared to placebo, warfarin reduces the risk of stroke by 66%

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25
Q

What is the benefit of DOACs in stroke vs. Warfarin?

A

10% fewer mortality over all vs. warfarin

20% more reduction in stokes

50% reduction in bleeding in the head

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26
Q

What populations see the greatest improvement in thromboembolic event rates following anticoagulant use?

A

Older patients (especially after the age of 85)

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27
Q

What are some obesity adjusted anticoagulant therapy choices?

A

Use any DOAC under BMI of 40

Use apixaban & edoxaban with caution in patients with BMI between 40 to 49

Only use warfarin in patients with BMI over 50 (usually refer to cardiologist)

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28
Q

What are some renal function adjusted doses for Dabigatran?

A

CrCl over 50mL/min (use 150mg BID)

CrCl between 30-49mL/min (Consider 110mg BID)

CrCl under 29mL/min (No RCT Data)

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29
Q

What are some renal function adjusted doses for Rivaroxaban?

A

CrCl over 50mL/min (use 20mg daily)

CrCl between 30-49mL/min (15mg daily)

CrCl under 29mL/min (No RCT Data)

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30
Q

What are some renal function adjusted doses for Apixaban?

A

CrCl over 50mL/min (use 5mg BID)

CrCl between 30-49mL/min :
- Use 5mg in patients under 80, weigh more than 60kg, and SCr under 133mmol/L
- Use 2.5mg if one of the above do not apply

CrCl under 29mL/min (No RCT Data)

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31
Q

What are some renal function adjusted doses for Edoxaban?

A

CrCl over 50mL/min (use 60mg daily)

CrCl between 30-49mL/min (30mg daily)

CrCl under 29mL/min (No RCT Data)

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32
Q

What is an antidote for dabigatran?

A

Idarucizumab (draws free dabigatran from the body)

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33
Q

What are some contraindications for DOAC therapy?

A
  • Patients with mechanical heart valves
  • 3A4 and P-gp drug interactions
  • Pregnancy and lactations
  • Use caution in very underweight or obese
  • In combination with DAPT (drop ASA if using DOAC with Clopidrigrel following a MI)
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34
Q

How is anticoagulant therapy monitored?

A
  • Adherance
  • Frequency of adverse effects
  • Signs and symptoms of bleeding and bleeding risk factors
  • Regular SCr, CrCl, HgB
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35
Q

Is there a significant difference in CV outcomes for rate or rhythm control in arrhythmia?

A

No, there is no significant difference in CV outcomes between the two

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36
Q

What is the general goal for rate control in arrhythmia treatment?

A

Reduction in HR greater than 20% with control of symptoms

Target:
- resting HR under 100bpm

Use beta-blocker or non-DHP CCB as first line

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37
Q

Can cardioversion be attempted in atrial fibrillation patients immediately?

A

No, need to use anticoagulants for 3 weeks before attempting cardioversion (patient has been in atrial fibrillation for longer than 24-48 hours) OR perform imaging to determine if there is atrial clotting

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38
Q

What is the benefit of rhythm control in arrhythmia treatment?

A
  • Relief of symptoms such as palpitations
  • Improve CO and exercise tolerance
  • Prevention of tachycardia-induced myocardial remodelling and heart failure
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39
Q

What patient groups should be put on on rhythm control for arrhythmia?

A
  • Stable and healthy patients with recent-onset atrial fibrilation
  • Heart failure
  • Angina
  • Hypotension
40
Q

Is electrical cardioversion more effective compared to pharmacological cardioversion?

A

Yes, electrically-induced cardioversion is more effective

41
Q

Can digoxin be used to pharmalogically cardioconvert irregular sinus rhythm?

A

No, it is only used for rate control, not rhythm control

42
Q

Can beta-blockers be used to pharmalogically cardioconvert irregular sinus rhythm?

A

No, it is only used for rate control, not rhythm control

43
Q

Can CCBs be used to pharmalogically cardioconvert irregular sinus rhythm?

A

No, it is only used for rate control, not rhythm control

44
Q

What drugs are used to perform pharmalogical cardioconversion?

A

Procainamide IV
Flecainide IV and PO
Propafenone PO
Sodium Channel Blockers
amiodarone IV and PO

45
Q

What is the sequence of conduction events?

A

SA node –> AV node –> Bundle of His –> Bundle branches –> Purkinje fibers

46
Q

Why does the AV node delay conduction?

A

Allows for the filling of atria and ventricles

47
Q

What ion is responsible for initial depolarization in non-pacemaker cells?

A

Na+ influx causes rapid depolarization

48
Q

What ion is responsible for initial repolarization?

A

K+ efflux begins initial repolarization

49
Q

What ion causes initial repolarization to slow down?

A

Ca2+ influx balances the flow of K+, which effectively causes slower repolarization

50
Q

What ion causes full repolarization to occur?

A

K+ efflux continues, resulting in full repolarization

51
Q

What ion is involved in pacemaker cell depolarization?

A

Calcium gated channels open and cause an influx of Ca2+

52
Q

What are the two types of refractory periods?

A
  • Absolute Refractory Period
  • Relative Refractory Period
53
Q

What is the absolute refractory period?

A

This is the time following a depolarization event in which the cell cannot be re-excited

54
Q

What is the relative refractory period?

A

This is the time immediately after the absolute refractory period, when the cell can be re-excited but requires a higher voltage than the usual threshold

55
Q

Review slide 86 for ECG wave

A
56
Q

What event does the P-wave represent?

A

Atrial depolarization

57
Q

What event does the QRS complex represent?

A

Ventricular depolarization

58
Q

What event does the T wave represent?

A

Ventricular repolarization

59
Q

Why does atrial repolarization not have a separate wave on an ECG?

A

It is obscured within the large QRS complex (ventricular depolarization)

60
Q

What is automaticity?

A

It is the spontaneous impulse generation in latent pacemaker cells

Cells beyond the SA node are generating depolarization

ex. sinus tachycardia

61
Q

What is re-entrant arrhythmias?

A

It is the indefinite propagation of the impulse and continued activation of previously refractory cells (can result in impulses that move backwards)

62
Q

What are three requirements for re-entry arrhythmia?

A
  1. Two pathways for impulse conduction
  2. An area of unidirectional block (prolonged refractoriness)
  3. Slow conduction in the other pathway
63
Q

How do anti-arrythmia drugs work?

A

They work by blocking ion channels by binding to a site on the ion channel proteins (significant impact action potential, and by extention conduction of electricity in the heart)

64
Q

What are the main drug classes involved in antiarrhythmia drugs?

A

(Class Ia, Ib, Ic) are Na+ channel blockers

Class II are beta-blockers

Class III are K+ channel blockers

Class IV are CCBs

65
Q

What are the Class Ia antiarrhythmia drugs and what is their specific impact on the ECG?

A

Quinidine

Procainamide

They increase QRS and QT duration by blocking on Na+ channels

66
Q

What are the Class Ib antiarrhythmia drugs and what is their specific impact on ECG readings?

A

Lidocaine

Mexilitene

They reduce QT duration by shortening repolarization phase

67
Q

What are the Class Ic antiarrhythmia drugs and what is their specific impact on ECG readings?

A

Propafenone

Flecanide

They significantly increase QRS (more potent Na+ channel blockers than Class Ia). They do this by prolonging depolarization

68
Q

What is the benefit of beta-blockers in anti-arrhythmia therapy?

A

Anti-adrenergic action
- Slows down conduction velocity
- Longer refractoriness
- Reduced automaticity

69
Q

What are some examples of Class III anti-arrhythmia drugs?

A

Amiodarone, sotalol, dofetilide, dronedarone, ibutilide

K+ channel blockers (prolong refractory period)

70
Q

What antiarrhythmia drug is the most effective?

A

Amiodarone
- Na+ blockade
- Beta blockade
- K+ blockade
- Ca2+ channel blockade

Due to broad action, amiodarone also has lots of side effects

71
Q

What are some examples of Class IV anti-arrhythmia drugs?

A

Verapamil

Diltiazem

  • Slow conduction
  • Prolong refractoriness
  • Decrease automaticity of Ca2+ dependent cells in the SA and AV nodes
72
Q

What is the use of digoxin in anti-arrhythmia therapy?

A

Inhibitor of Na+/K+/ATPase

Increases vagal tone (reduced conduction velocity)

Increases AV node refractoriness

73
Q

What are the four classifications of arrhythmias?

A

Bradyarrhythmia

Tachyarrhythmia

Supraventricular (above the ventricles)

Ventricular (occurring within the ventricles)

74
Q

What are some characteristics of bradyarrhythmia?

A

Usually patients won’t have symptoms unless heart rate is dropping below 50bpm

Caused by a conduction delay or block in an area of the AV conduction system (due to myocarditis, b-blockers, CCBs, acute MI, congenital disease)

75
Q

What are the different degrees of AV block?

A
  • First degree (least prolonged PR interval)
  • Second degree
  • Third degree (most severe due to absense of AV conduction)
76
Q

What are some symptoms of bradyarrhythmia?

A

Symptoms include the following:
- Fatigue
- Lightheadedness
- Palpitations
- Syncope

77
Q

What is the treatment option for bradyarrhythmia?

A

Pacemaker

78
Q

What is sick sinus syndrome?

A

It is a type of bradyarrhythmia

  • Pauses or dropped beats due to SA node dysfunction
  • Usually caused by degenerate changes due to age
  • Leave it alone, unless symptomatic, then pacemakers
79
Q

What are some characteristics of supraventricular tachycardia?

A

Heart rates are greater than 100bpm

Usually caused by re-entry mechanisms

80
Q

What are some symptoms associated with supraventricular tachycardia?

A
  • Palpitations
  • Fatigue
  • Lightheadedness
  • Neck fullness
  • Chest pain
81
Q

What are some treatment options for supraventricular tachycardia (tachyarrhythmia)?

A

For narrow QRS complex:
- First line (vagal maneuvers)
- Second line (adenosine, IV beta-blocker, CCB)

82
Q

What are some classfications of supraventricular tachycardia (tachyarrhythmia)?

A
  • Atrial fibrilation/flutter
  • Multifocal Atrial Tachycardia (MAT)
  • AV Nodal Re-entrant Tachycardia (AVNRT)
  • AV re-entrant tachycardia (AVRT)
83
Q

What are some types of ventricular tachyarrhythmia?

A

Premature Ventricular Complexes (PVCs)
- benign, common

Ventricular tachycardia (VT)
- Potentially fatal. life-threatening

Ventricular fibrillation (VF)
- Fatal, medical emergency

84
Q

What are some characteristics associated with pre-mature ventricular complexes?

A

Often asymptomatic, can occur in healthy individuals

Usually don’t require any treatment (can use beta-blockers if patient is affected significantly)

85
Q

What are some characteristics of ventricular tachyarrhythmia?

A

Can be acutely caused by metabolic abnormality, ischemia, or drug toxicity, or can be chronic and recur in paroxysmal form

86
Q

What are some treatment options for ventricular tachyarrhythmias

A

Sustained VT, unstable patient
- direct current cardioversion

Stable patient:
- IV procainamide, amiodarone, lidocaine

87
Q

What is the most effective maintenance therapy to prevent VT recurrence?

A

Amiodarone is most effective as maintenance therapy to prevent VT recurrence

Sotalol is also a potential drug maintenance therapy

Ablation can be considered if medication therapy fails

88
Q

What is torsade de pointes?

A

Life threatening form of VT

Associated with long QT interval on ECG

Treatment: Magnesium sulfate 2g IV, DC cardioversion

89
Q

What is an implantable cardioverter defibrillator?

A

It is an option for secondary prevention of spontaneous coronary death secondary to life threatening ventricular arrhythmia

But beta-blockers are often used to prevent future ventricular arrhythmia

90
Q

What are some adverse effects associated with amiodarone use?

A

QT prolongation

Hyper/hypothyroidism

Blue-gray discolouration

Liver enzyme elevation

Optic neuropathy

91
Q

What are some events associated with the QT wave?

A

Ventriular depolarization and atrial repolarization

When it is prolonged, there is a delay in repolarization

Can lead to torsade de pointes

92
Q

What is the risk of QT prolongation with anti-arrhythmic medications?

A

Higher due to potassium channel blocking properties

Sotalol risk of torsade de pointes is 4% (Extremely high compared to other drugs like antibiotics)

93
Q

What is QTc?

A

It is corrected QT interval

This helps better determine if patients are at risk for QT prolongation.

Need to be worried if QTc exceeds 500ms

94
Q

What scale is used to assess risk for Torsade de Pointes?

A

Tisdale score helps dentify individual patient risk score

  • Age over 68
  • Female sex
  • Loop diuretic (hypokalemia)
  • QTc interval beyond 450ms
  • HFrEF
  • Many more
95
Q
A

PHAR 253 (10 decks)

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