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Diagnostic Medicine > Tachycardia > Flashcards

Tachycardia Flashcards

1
Q

Identify the atrial tachyarrhythmias

A

PACs
SVT (WPW, AVNRT, Atrial Tachycardia)
Atrial Flutter
Atrial Fibrillation

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2
Q

Identify the ventricular tachyarrhythmias

A

PVCs
Ventricular Tachycardia
Torsades de Pointes
Ventricular Fibrillation

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3
Q

What happens in Premature Atrial Contraction (PAC)

A

Early atrial depolarizations

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4
Q

Premature atrial contraction (PAC)

A

P wave morphology may be different (comes from a different site)
May be nonconducted
If in a pattern: Bigeminal or Trigeminal.

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5
Q

Premature atrial contraction (PAC) treatment

A

Usually self limited and not symptomatic.

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6
Q

Sinus Tachycardia

A

In adults: HR>100 bpm but rarely over 200 ppm.

P wave always followed by a QRS in a 1:1 fashion.

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7
Q

Why does sinus tachycardia occur

A

a physiological response to stress or other stimuli.

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8
Q

Supraventricular Tachycardia (SVT)

A

Narrow QRS complex
HR at 140-240 bpm.
Abrupt onset and offset.
P wave is usually buried in the QRS but if you can see it, morphology is different.

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9
Q

What commonly causes Supraventricular Tachycardia (SVT)

A

An accessory pathway: Within the AV node=AV nodal reentry tachycardia 2/3 of patients, Outside the AV node/through the bundle of Kent=AV reentrant tachycardia 1/3 of patients.

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10
Q

Treatment for supra ventricular tachycardia (SVT)

A

Adenosine

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11
Q

What happens in an AV nodal reentry tachycardia?

A

A premature beat (PAC) arrives while the accessory pathway is still in refractory. It activates the AV node, slowly (cause its continuing to repolarize). Reaches the ventricle, the accessory pathway has recovered, transmits the signal retrograde to the atria. Then the atria reactivate the ventricle through the AV node.

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12
Q

What makes an accessory pathway named a concealed pathway?

A

If the patient has SVT via an accessory pathway but has a normal EKG.

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13
Q

What makes an accessory pathway named a Wolff Parkinson White?

A

If the patient has an SVT via an accessory pathway and has a delta wave on the resting/sinus EKG.

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14
Q

What is pre-excitation

A

If you see a delta wave on resting/sinus EKG.

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15
Q

Wolff Parkinson White

A

Narrow PR interval in sinus.

Accessory pathway leads to SVT.

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16
Q

What is the definition of Wolff Parkinson White?

A

Patient must have SVT symptoms and a delta wave on EKG.

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17
Q

What happens in WPW?

A

Pre-excitation of the ventricle in the location of the accessory pathway (delta wave), while also conduction through the AV node while in sinus rhythm. When tachycardia, the delta wave disappears.

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18
Q

What are the two pathways present in a dual AV nodal physiology?

A

Slow (slow conducting) pathway with a fast recovery time.

Fast (fast conduction) pathway with a slow recovery time.

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19
Q

What is the normal AV nodal physiology?

A

Only one pathway present: Fast conducting pathway with slow recovery time.

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20
Q

What happens in AV nodal reentry tachycardia?

A

Normal impulse conducted through the fast pathway.
PAC occurs, conducted through the slow pathway (fast is still in refractory).
When the conducted PAC reaches the end of the slow pathway, the fast pathway is recovered and transmits the signal retrograde to the atria, setting up look tachycardia.

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21
Q

Treatment for AVNRT

A

Adenosine

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22
Q

AVNRT

A

HR 180-220 bpm.
Regular.
When in tachycardia, cannot see P wave.
No delta waves.

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23
Q

Atrial tachycardia may be a precursor to what?

A

Atrial fibrillation, usually caused by atrial scarring, or drugs (digoxin).

24
Q

What is atrial tachycardia?

A

A tachycardia originating within the atria but outside of the sinus node. (rate is faster than the sinus rate, takes over as the main pacemaker of the heart).

25
Q

Atrial tachycardia

A

HR 140-220 bpm.
Rarely sustained for long periods of time.
P wave can be difficult to find, buried within the T wave.

26
Q

Does adenosine work on atrial tachycardia?

A

No. It is an AV node blocker and in atrial tachycardia, the impulse originates higher than the AV node.

27
Q

Treatment for atrial tachycardia

A

Cardioversion

May also require medication to suppress if symptomatic

28
Q

What happens in Multifocal atrial tachycardia?

A

Multiple ectopic foci in the atria firing, resulting in multiple P wave morphologies

29
Q

Multifocal Atrial Tachycardia

A

Multiple P wave morphologies.

HR 100-150s.

30
Q

What is the most common cause of multifocal atrial tachycardia?

A

COPD

31
Q

Thought of as a transitional arrhythmia from atrial tachycardia to

A

Atrial fibrillation

32
Q

Atrial fibrillation is best described as

A

irregularly irregular

33
Q

Atrial fibrillation

A

Ventricular rates usually fast (over 100) but can be slow or normal.
No organized atrial rhythm, no P waves. (firing at 300-400 ppm)

34
Q

Afib carries the risk of what?

A

CVA

Evaluate with CHADSVASC scoring system

35
Q

What is the most common chronic arrhythmia

A

Atrial fibrillation

36
Q

Treatment for Atrial Fibrillation

A

Rate control
Stroke prevention
Cardioversion
Antiarrhythmic medications

37
Q

Atrial Flutter

A

“Saw tooth pattern” in inferior leads of a 12 lead EKG (II, III, and aVF)
2:1 or 3:1 or 4:1 ventricular response.

38
Q

What happens in Atrial Flutter

A

There is a short re-entrant circuit within the RA that is conducting at 300 bpm. Ventricular response is usually regular 2:1 but can be 3:1 or 4:1 patterns, or variable.

39
Q

What is atypical atrial flutter?

A

A re-entrant circuit in the atria from any other location in the atria

40
Q

What is the risk of Atrial Flutter?

A

CVA

41
Q

Treatment for atrial flutter

A

anticoagulation, ablation and/or antiarrhythmics.

42
Q

Will Adenosine work on atrial flutter?

A

No but it is acceptable to give adenosine if you aren’t sure because it will decipher if it is AFIB/A flutter or something with the AV node.

43
Q

Premature Ventricular Contractions (PVCs)

A

Wide QRS beats usually without preceding P waves.

Bigeminal or trigeminal patterns.

44
Q

Treatment for premature ventricular contractions

A

Beta blockers or Ca channel blocker.

Ablation if symptomatic or if they are causing cardiomyopathy.

45
Q

Monomorphic is most likely due to

A

a re-entrant circuit within the ventricle, commonly caused by a myocardial scar.

46
Q

Polymorphic VT indicates

A

more electrically unstable/irritable ventricle.

47
Q

What is cardioversion

A

Distinct QRS complex. Shock in sync with the QRS complex. If shocking on the T wave, can cause VT.

48
Q

What is defibrillation

A

Asynchronously shocking. No rhythm to shock on.

49
Q

Wide complex tachycardia

A

Can also be aberrantly conducted SVT, when SVT occurs in the setting of conduction system disease or depending on the rate of the tachycardia, one bundle can block intermittently.

50
Q

Treatment of wide complex tachycardia

A

Treated as VT until proven otherwise.

If patient is hemodynamically unstable, treatment is always cardioversion regardless of cause.

51
Q

Who can diagnose a wide complex tachycardia?

A

Cardiology or an electrophysiologist.

52
Q

Torsades de Pointes

A

Form of polymorphic VT
Long QT intervals.
Twisting of QRS complex along the isoelectric baseline.

53
Q

Torsades de Pointes can also occur in what?

A

Complete heart block

54
Q

Treatment for Torsades de Pointes

A

Emergent defibrillation; leads to sudden cardiac death.

Magnesium also used to treat after cardioversion.

55
Q

What happens in ventricular fibrillation

A

No discernable ventricular activity. If you could could 200-300 ppm.
Patient is pulseless.

56
Q

Treatment for ventricular fibrillation

A

Emergent defibrillation as quick as possible. Next step is asystole.

57
Q

What are the indications for an implantable cardioverter defibrillator (ICD)

A

EF less than 35%

Previous cardiac arrest (VT/VF) in the absence of a reversible cause.

Diagnostic Medicine (4 decks)

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