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Cardio All My Notes > Arrhythmia > Flashcards

Arrhythmia Flashcards

1
Q

Explain the guide for interpreting an electrocardiogram (ECG) reading.
Answer: The guide for interpreting an ECG reading is as follows:

A
  • 0.04 s represents a small box on the ECG.
  • 5 small boxes make up 1 big box.
  • 5 small boxes multiplied by 0.04 s equals 0.20 s.
  • Therefore, 0.20 s represents 1 big box on the ECG.
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2
Q

What is supraventricular tachycardia?

A

Answer: refers to any arrhythmia occurring above the ventricles in the heart.

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3
Q

What are the two types of supraventricular tachycardia?

A

Answer:

Sinus tachycardia: SA node firing too fast.

Atrial tachycardia: Irritable atrial firing to the AV node before the SA node fires towards the AV node.

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4
Q

What are the different types of atrial tachycardia?
Answer:

A
  • Focal Atrial Tachycardia: One area firing consistently, ectopic focus.
  • Multifocal Atrial Tachycardia: Three areas firing.
    Atrial fibrillation: Faster than multifocal atrial tachycardia.
  • Atrial flutter: Near the tricuspid valve, creates a re-entry circuit.
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5
Q

What is paroxysmal SVT?

A

Answer:
refers to arrhythmias that include AVNRT (Atrioventricular nodal reentrant tachycardia) and AVRT (Atrioventricular reentrant tachycardia).

It may also involve focal atrial tachycardia.

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6
Q
  1. What causes ventricular tachycardia?
A

Answer: is caused by an irritable area in the ventricle that generates abnormal electrical activity.

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7
Q

What are the types of ventricular tachycardia?
Answer:

A
  • Monomorphic ventricular tachycardia: Most common type, involving one location of an irritable area that’s firing.
  • Polymorphic ventricular tachycardia: Involves multiple locations of irritable areas that are firing.
  • Normal QT-Interval
  • Prolonged QT-Interval (Torsades de Pointes): characterized by twisting of the points.
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8
Q

What is ventricular fibrillation?

A

Answer: Ventricular fibrillation is a condition where multiple ectopic foci within the ventricles are firing simultaneously, leading to chaotic and ineffective heart contractions.

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9
Q

What is the characteristic of ventricular fibrillation?

A

Answer: characterized by the presence of reentry circuits.

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10
Q

Which part of the nervous system innervates the heart and influences its automaticity?

A

Answer: The parasympathetic nervous system, specifically the vagus nerve (CN 10), innervates the heart and influences its automaticity.

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11
Q

What is the effect of increased sympathetic nervous system activity on automaticity?

A

Answer: increased automaticity in the heart.

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12
Q

What are the factors that can cause an increase in automaticity in tachyarrhythmias?

A

Answer:

  • sympathetic nervous system stimulation (T1-L2),
  • hypovolemia,
  • hypoxia,
  • sympathomimetic drugs,
  • pain/anxiety, and
  • increased metabolic activity.
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13
Q

What is triggered activity in tachyarrhythmias?

A

Answer:
the presence of an irritable area in the myocardium (atrium/ventricle) that initiates abnormal conduction,

  • starting from an ectopic area instead of the SA-AV node pathway.
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14
Q

What is the difference between early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs)?

A

Answer:

  • EADs occur when an irritable cell fires during or immediately after repolarization,
  • while DADs occur when an irritable cell fires right after the latter phase of repolarization.
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15
Q

What are some causes or etiologies associated with EADs and DADs?
Answer:

A
  • EADs: Electrolyte imbalances (hypokalemia, hypocalcemia, hypomagnesemia) and certain drugs (anti-arrhythmics, antibiotics, antipsychotics, antidepressants, antiemetics).
  • DADs: Underlying ischemia, underlying hypoxia, inflammation, stretched-out myocardium, and increased sympathetic tone.
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16
Q

What arrhythmias are associated with EADs and DADs?
Answer:

A
  • EADs: Polymorphic ventricular tachycardia with prolonged QT interval or Torsades de pointes.
  • DADs: Multifocal atrial tachycardia, focal atrial tachycardia, and monomorphic or polymorphic ventricular tachycardia with normal QT intervals.
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17
Q

What is a re-entry circuit in tachyarrhythmias?

A

Answer: A re-entry circuit refers to an abnormal conduction pathway that allows electrical impulses to circulate within the heart, leading to the perpetuation of tachyarrhythmias.

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18
Q

What is AVRT and what is the underlying abnormality associated with it?

A

Answer:

  • AVRT (Atrioventricular Reentrant Tachycardia) is a type of re-entry circuit that occurs due to the presence of an abnormal accessory pathway between the atria and ventricles.
  • This pathway is known as the bundle of Kent, and it is commonly seen in patients with Wolff-Parkinson-White (WPW) syndrome.
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19
Q

What are the two types of AVRT and how do they differ?

A

Answer:

  • Orthodromic AVRT: In this type, conduction starts at the AV node and proceeds down the normal pathway, but it doesn’t stop at the ventricles and continues to go up the atria via the bundle of Kent. This results in a narrow QRS complex on the ECG.
  • Antidromic AVRT: In this less common but more lethal type, conduction starts at the SA node and proceeds through the accessory pathway (bundle of Kent) to the ventricles, then back up to the atria. This produces a wide QRS complex on the ECG.
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20
Q

What is AVNRT and what are the possible causes of this condition?

A

Answer:
* AVNRT (Atrioventricular Nodal Reentrant Tachycardia) is another type of re-entry circuit that occurs within the AV node itself.

  • Possible causes of AVNRT include scarring in the AV node (e.g., due to myocardial infarction or heart surgery), idiopathic fibrosis (common in older individuals), and other factors leading to abnormal pathways within the AV node.
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21
Q

Describe the two pathways involved in AVNRT and their characteristics.
Answer:

A

Alpha pathway: This pathway within the AV node is responsible for slow conduction. During its downward pathway, the beta pathway repolarizes, and the alpha pathway joins with the beta pathway to form a cycle. The alpha pathway has a short refractory period, resulting in quicker repolarization.
Beta pathway: This pathway within the AV node is responsible for fast conduction toward the bundle of His, bundle branches, and ventricles. It circles around to go up to the beta pathway while the alpha pathway cancels it going down. The beta pathway has a long refractory period, leading to slower repolarization.

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22
Q

What arrhythmias are associated with abnormal re-entry circuits at the tricuspid valve?

A

Answer:
Atrial flutter and atrial fibrillation are arrhythmias associated with abnormal re-entry circuits at the tricuspid valve.

  • In atrial flutter, the re-entry circuit is located at the cavotricuspid isthmus,
  • while in atrial fibrillation, multiple irritable areas within the atria create their own circuits, leading to chaotic atrial activation.
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23
Q

What is the difference between ventricular tachycardia and ventricular fibrillation in terms of the re-entry circuit?

A

Answer:

  • In ventricular tachycardia, there is an irritable area in the ventricle that generates abnormal activity, resulting in a re-entry circuit involving a single area within the ventricle.
  • In ventricular fibrillation, there are multiple ectopic foci within the ventricles that are firing simultaneously, creating multiple re-entry circuits and leading to chaotic and ineffective ventricular contractions.
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24
Q

What are the causes of heart blocks?

A
  • Heart blocks are conduction blocks in the atrioventricular (AV) node, leading to a loss of electrical activity connection between the atria and ventricles.
  • Causes of heart blocks include inferior wall myocardial infarction, fibrotic AV node, hyperkalemia, certain medications (such as beta blockers, calcium channel blockers, and digoxin), infiltrative diseases (amyloidosis, sarcoidosis), and Lyme’s disease.
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25
Q

What is the pathophysiology behind decreased automaticity in bradyarrhythmias?

A
  • Decreased automaticity in bradyarrhythmias can result from increased parasympathetic nervous system (PSNS) or vagal tone.
  • Stimulation of the PSNS releases acetylcholine (ACh) to the SA node, leading to an increase in potassium (K+) and hyperpolarization.
  • This slows conduction to the AV node and subsequently decreases the heart rate (HR).
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26
Q

How does conduction block contribute to bradyarrhythmias?

A
  • Conduction block refers to the interruption of electrical conduction, particularly in the AV node.
  • It can shut down AV conduction and result in bradyarrhythmias. Causes of conduction block include inferior wall myocardial infarction, fibrotic AV node, hyperkalemia, certain medications, infiltrative diseases, and Lyme’s disease.
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27
Q

What is sick sinus syndrome (SSS) and its associated rhythm abnormalities?

A
  • Sick sinus syndrome (SSS) is a condition characterized by dysfunctional firing of the SA node.
  • It can result from fibrosis, myocardial scarring, or intrinsic problems of the SA node.
  • SSS leads to sinus bradycardia as the SA node fails to fire as fast as it should.
  • Compensatory mechanisms may lead to episodes of supraventricular tachycardia (SVT), including atrial flutter, atrial fibrillation, or premature atrial contractions.
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28
Q

What does the irregular presence of P-waves after QRS complexes indicate?

A

The irregular presence of P-waves after QRS complexes suggests a 2nd degree heart block, specifically Mobitz Type I (Wenckebach).

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29
Q

What pattern of P-wave presence and absence suggests Mobitz Type II in a 2nd degree heart block?

A

If P-waves are present and absent in a consistent pattern, it indicates a 2nd degree heart block, Mobitz Type II.

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30
Q

What is the 2:1 variant of Mobitz Type II 2nd degree heart block?

A

The 2:1 variant of Mobitz Type II 2nd degree heart block refers to a pattern where every other P-wave is conducted to the ventricles, resulting in a 2:1 ratio of P-waves to QRS complexes.

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31
Q

How can you identify a 3rd degree heart block on an EKG?

A

A 3rd degree heart block is characterized by the absence of P-waves and the presence of a wider QRS complex.

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32
Q

How can you determine the timing of the PR-interval in bradyarrhythmias?

A

By analyzing the EKG, you can assess the timing of the PR-interval, which is the interval between the P-wave and the QRS complex.

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33
Q

hat does a prolonged PR-interval indicate in bradyarrhythmias?

A

A prolonged PR-interval suggests a 1st degree heart block. It can also be progressively prolonged, accompanied by dropped QRS complexes, indicating Mobitz Type I 2nd degree heart block (Wenckebach).

34
Q

What does a normal PR-interval suggest in bradyarrhythmias?

A

A normal PR-interval is seen in Mobitz Type II 2nd degree heart block, as well as in the 2:1 variant of Mobitz Type II and 3rd degree heart block.

35
Q

Q: In which leads should the P-wave be upright and inverted in sinus tachycardia?

A

A: The P-wave should be upright in Lead II and inverted in Lead aVR in sinus tachycardia.

36
Q

: What is the typical response of sinus tachycardia to fluid administration, and why?

A

A:

  • Sinus tachycardia typically improves with fluid administration due to the underlying cause of hypovolemia.
  • The increased automaticity and sympathetic nervous system activity triggered by hypovolemia are usually responsible for the tachycardic response.
37
Q

Q: Name some underlying causes of sinus tachycardia and their respective treatments.

A

A:

  • fever, hypoxia, and hypovolemia.
  • Treatment approaches include administering Tylenol for fever, providing oxygen for hypoxia, and checking urine output.
  • In certain cases, drugs like Heparin or Tissue plasminogen activator may be used.
38
Q

Q: What distinguishes focal atrial tachycardia (FAT) from sinus rhythm?

A

A:

  • Focal atrial tachycardia (FAT) can be distinguished from sinus rhythm by the presence of visible P-waves with each QRS complex, an inverted P-wave in Lead II, and an upright P-wave in Lead aVR.
  • It is important to ensure that the observed inverted P-wave is not misplaced before diagnosing FAT.
39
Q

Q: What is the explanation behind an inverted P-wave in lead II in FAT?

A

A:

  • An inverted P-wave in lead II in focal atrial tachycardia (FAT) occurs when there is a focal area of firing in the left atrium that moves away from the usual direction (inferior, downwards) toward the positive electrode of Lead II.
  • This results in an upward deflection of the P-wave, causing it to be inverted.
40
Q

Q: Which maneuver can be used to increase vagal tone and slow down AV node conduction?

A

A: Vagal maneuvers, such as the Valsalva maneuver (like a pooping position) or the blow-into-a-plunger maneuver (increasing intrathoracic pressure), can be employed to increase vagal tone, which leads to the slowing down of AV node conduction.

41
Q

Q: What is the next line of drugs for treating FAT if adenosine doesn’t work?

A

A: the next line of drugs to consider are beta-blockers (BB) or calcium channel blockers (CCB).

  • However, contraindications should be taken into account before administering these medications.
42
Q

Q: When should electrical cardioversion be considered in the management of FAT?

A

A:

  • if the patient is unstable, exhibiting symptoms such as hypotension, altered mental status, chest pain, or pulmonary edema.
  • It is prioritized in such cases to restore a normal heart rhythm promptly.
43
Q

Q: What is the long-term treatment approach for FAT?

A

A:

  • The long-term treatment for FAT involves radiofrequency ablation of the abnormal tissue.
  • This procedure aims to burn the re-entry circuits responsible for generating abnormal electrical activities.
  • In the case of FAT, the circuit is typically located in ectopic foci within the atria.
44
Q

Q: How can atrial flutter (AFL) be identified on an ECG?

A

A: Atrial flutter (AFL) can be identified on an ECG by the presence of jacked-up sawtooth waves, known as flutter waves. These waves are typically visible in Leads II, III, and aVF, but checking Lead V1 is also recommended if they are not clearly seen.

45
Q

Q: What causes the characteristic sawtooth waves in AFL?

A

A:
The characteristic sawtooth waves in atrial flutter (AFL) are caused by re-entry circuits within the atria, specifically a counterclockwise pattern.

  • The sawtooth waves represent multiple atrial depolarizations for every QRS complex, maintaining a consistent 1:1 ratio throughout the ECG strip.
46
Q

Q: What are the key features to differentiate AVRT/AVNRT (SVT) from other rhythms on an ECG?

A

A:
AVRT/AVNRT (atrioventricular reentrant tachycardia) typically presents with hidden P waves within the QRS complexes and may sometimes show a retrograde P wave after the QRS in Leads II, III, and aVF.

  • The absence of visible P waves, flutter waves, or distinct T waves helps differentiate it from other rhythms.
47
Q

Q: How can atrial fibrillation (A. Fib) be identified on an ECG?

A

A:

  • Atrial fibrillation (A. Fib) is identified on an ECG by the presence of “squiggly lines” instead of visible P-waves every QRS complex.
  • These squiggly lines represent multiple ectopic foci and re-entry firing within the atria.
  • Lead V1 is the most visible lead to observe this pattern.
48
Q

Q: What is the characteristic rhythm pattern in atrial fibrillation (A. Fib)?

A

A: Atrial fibrillation (A. Fib) is characterized by irregularly irregular R-R intervals.

The intervals between consecutive R-waves on the ECG strip do not follow a consistent pattern.

49
Q

Q: What is the recommended approach for vagal maneuver in atrial fibrillation (A. Fib)?

A

A: Vagal maneuvers, such as the Valsalva maneuver or blowing into a plunger maneuver, can be attempted in atrial fibrillation (A. Fib) but are generally not effective in converting the rhythm back to normal sinus rhythm.

50
Q

Q: What are the next line of drugs used in the management of atrial fibrillation (A. Fib)?

A

A:
If vagal maneuvers are unsuccessful, the next line of drugs to consider for atrial fibrillation (A. Fib) are adenosine, beta-blockers (BB), or calcium channel blockers (CCB).

However, the effectiveness of these drugs can vary for different individuals.

51
Q

Q: When should electrical cardioversion be performed in the management of atrial fibrillation (A. Fib)?

A

A:

  • if the patient is unstable, presenting with symptoms such as hypotension, altered mental status, chest pain, or pulmonary edema.
  • It is prioritized to restore a normal heart rhythm promptly in such cases.
52
Q

Q: What is the long-term treatment approach for atrial fibrillation (A. Fib)?

A

A:

  • The long-term treatment for atrial fibrillation (A. Fib) involves radiofrequency ablation of the abnormal tissue.
  • This procedure aims to burn the re-entry circuits or multiple foci responsible for generating abnormal electrical activities.
  • Additionally, beta-blockers (BB) may also be needed for long-term management.
53
Q

Q: What is the CHAD-VASC score used for in relation to atrial fibrillation (A. Fib)?

A

A: The CHAD-VASC score is used to predict the risk of thromboembolism, specifically stroke, in individuals with atrial fibrillation (A. Fib).

A score of >2 indicates an increased need for anticoagulation therapy to reduce the risk of blood clots reaching the brain.

54
Q

Q: What are the characteristics of SVT with BBB on an ECG?

A

A:

  • SVT with BBB is identified by wide complex tachycardia on the ECG,
  • with a QRS duration less than 0.14 seconds,
  • no AV dissociation,
  • no extreme right axis deviation,
  • and no significant cardiovascular disease history in patients younger than 35 years old.
55
Q

Q: Why is it important to differentiate SVT with BBB from ventricular tachycardia?

A

A:
Differentiation is crucial because the treatment approaches differ.

Mistakenly treating ventricular tachycardia as SVT with BBB can worsen the condition or be life-threatening.

56
Q

Q: What is the drug of choice and long-term treatment for SVT with BBB?

A

A:
Adenosine is the preferred drug for SVT with BBB.

Long-term treatment involves radiofrequency ablation of the abnormal tissue causing the arrhythmia.

57
Q

Q: How should Antidromic AVRT be treated, and what is the recommended long-term treatment?

A

A:
* Antidromic AVRT can be treated as ventricular tachycardia with drugs like amiodarone or procainamide.

  • AV nodal blockers should be avoided. Long-term treatment involves radiofrequency ablation.
58
Q

Q: What are the characteristics and management of polymorphic ventricular tachycardia (PMVT)?

A

A: P
MVT is characterized by varying QRS complexes and irregular R-R intervals.
Management includes drugs like amiodarone or procainamide, synchronized cardioversion, and long-term radiofrequency ablation.

59
Q

Q: How should A. Fib with WPW syndrome be managed?
.

A

A: A. Fib with WPW syndrome is managed similarly to PMVT with a normal QT-interval using drugs like amiodarone or procainamide.

AV nodal blockers should be avoided, and long-term treatment involves radiofrequency ablation

60
Q

Q: How should A. Fib with BBB be managed?

A

A: A. Fib with BBB is managed with beta-blockers or calcium channel blockers as drugs or cardioversion.
Long-term treatment involves radiofrequency ablation.

61
Q

Q: What should be done in the case of ventricular fibrillation (V. Fib)?

A

A:
* Ventricular fibrillation is a life-threatening arrhythmia.

  • Immediate CPR, administration of epinephrine, and defibrillation are necessary to restore a normal heart rhythm.
62
Q

Q: What are the characteristics and management of 1st-degree heart block?

A

A: 1st-degree heart block is identified by a prolonged PR interval (>200 ms).

It is usually benign, and monitoring is recommended.

63
Q

Q: What are the characteristics and management of 2nd-degree heart block type I (Wenckebach)?

A

A:
progressive prolongation of the PR interval until a dropped QRS complex occurs.

If unstable, atropine or pacing may be necessary.

64
Q

Q: What should be done in cases of unstable 2nd-degree heart block type I?

A

A: Unstable cases of 2nd-degree heart block type I may require treatment with atropine, epinephrine, or pacing.

65
Q

Q: What are the causes and treatments for 2nd-degree heart block type II?

A

A:
2nd-degree heart block type II is characterized by intermittent dropped QRS complexes with a normal PR interval.
Causes vary, and treatment depends on the underlying cause.

66
Q

Q: What are the characteristics of 2nd-degree heart block type II, variant 2:1?

A

A:
2nd-degree heart block type II, variant 2:1, is characterized by a regular pattern of one dropped QRS complex for every two P waves.

67
Q

Q: What are the characteristics and management of 3rd-degree heart block?

A

A:
3rd-degree heart block is characterized by complete dissociation between P waves and QRS complexes.

  • The ventricular rate is usually slower than the atrial rate. Pacing is the definitive treatment.
68
Q

Q: Which class of anti-arrhythmic drugs acts by reducing the sodium channel current?

A

A: Class 1 drugs, such as lignocaine, quinidine, flecainide, and propafenone, act on phase 0 of the action potential.

69
Q

Q: Which class of anti-arrhythmic drugs acts as B-Adrenergic antagonists?

A

A: Class II drugs, like propranolol, act on phase 4 of the action potential.

70
Q

Q: Which class of anti-arrhythmic drugs prolongs the action potential?

A

A: Class III drugs, including amiodarone, sotalol, and dronedarone, act on phases 3 and block potassium channels.

71
Q

Q: Which class of anti-arrhythmic drugs acts as Ca channel antagonists?

A

A: Class IV drugs, like verapamil, act on phase 2 of the action potential.

72
Q

Q: What is the general principle of anti-arrhythmic drug therapy for classes I and IV?

A

A: Anti-arrhythmic drugs in classes I and IV are primarily used for rhythm control.

73
Q

Q: What is the general principle of anti-arrhythmic drug therapy for classes II and III?

A

A: Anti-arrhythmic drugs in classes II and III are primarily used for rate control.

74
Q

Q: What are the three main mechanisms that can enhance the automaticity of pacemaker cells?

A

A: The three main mechanisms are increased rate of phase 4 depolarization, negative shift in threshold potential, and positive shift in maximum diastolic potential.

75
Q

Q: When enhanced automaticity occurs in the SA node, what is the resulting condition called?

A

A: Sinus tachycardia, which is an increase in heart rate, can result from enhanced automaticity in the SA node.

76
Q

Q: What are some possible causes of sinus tachycardia?

A

A: Sinus tachycardia can be physiological, due to increased sympathetic tone during exercise, or pathophysiological, resulting from hypovolemia, ischemia, or electrolyte disturbances.

77
Q

Q: What is the mechanism of action of Class 1 anti-arrhythmic drugs?

A

A: Class 1 drugs reduce the sodium channel current (phase 0).

78
Q

Q: Name four examples of Class 1 anti-arrhythmic drugs.

A

A: Lignocaine, quinidine, flecainide, and propafenone.

79
Q

Q: Which phase of the action potential do Class II anti-arrhythmic drugs act on?

A

A: Class II drugs act on phase 4 of the action potential.

80
Q

Q: Provide an example of a Class II anti-arrhythmic drug.

A

A: Propranolol is a Class II anti-arrhythmic drug.

81
Q

Q: What is the primary effect of Class III anti-arrhythmic drugs?

A

A: Class III drugs prolong the action potential duration.

Cardio All My Notes (13 decks)

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