Arrhythmias Flashcards

1
Q

What are the native pacemaker cells and where are they located in the heart?

A

SA node (junction of the RA and SVC) + AV node (RA septal wall anterior to the coronary sinus)

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2
Q

Describe how an action potential occurs for a cardiac pacemaker cell.

A

Phase 4: slow Na and Ca influx (via leak and L and T-type Ca channels) -> Phase 0: threshold voltage reached causing rapid Ca influx (via L-type Ca channel) while K permeability decreases -> Phase 3: Peak voltage reached, Ca channels close and permeability to K is restored (K efflux)

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3
Q

Describe how an action potential occurs for a myocyte (not a pacemaker cell).

A

Phase 0: Reaching threshold opens Na-channels (rapid Na influx) -> Phase 1: peak voltage reached, Na channels close and K permeability increases (K-efflux) -> Phase 2: Plateau phase (K+ efflux and Ca influx via slow Ca channels) -> Phase 3: rapid depolarization (from slow Ca channels closing leading to rapid K efflux)

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4
Q

How do myocytes propagate the action potential?

A

Via gap junctions between cells

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5
Q

What is the pathway for normal heart conduction?

A

SA node -> internodal pathway (anterior/middle/posterior) -> AV node -> left and right bundle branches -> His-Purkinje fibers

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6
Q

How does the electrical pathway go from the RA to the LA?

A

Via Bachmann’s Bundle

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7
Q

What portion of heart conduction has the fastest conduction?

A

The His-Purkinje system has 50x the amount of Na channels (compared to the AV node) and generates the fastest conduction velocities to allow for nearly simultaneous and organized ventricular contraction

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8
Q

What supplies the parasympathetic innervation to the heart?

A

The vagus nerve (CN X) via M2 muscarinic receptors (stimulated by acetylcholine)

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9
Q

What supplies the sympathetic innervation to the heart?

A

T1-T4 sympathetic chain via beta1 receptors (stimulated by catecholamines)

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10
Q

What is the most common dysrhythmia associated with acute MI?

A

Sinus tachycardia

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11
Q

What is the second most common dysrhythmia associated with acute MI?

A

PACs

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12
Q

Do you see a compensatory pause with PACs? PVCs?

A

You see it with PVCs but not with PACs

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13
Q

How does typical atrioventricular nodal reentry tachycardia work?

A

90-95% of AVNRTs; Forward conduction along slow pathway through the AV node followed by retrograde conduction along fast accessory pathway (causes a reentrant loop)

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14
Q

How does atypical AVNRT work?

A

5-10% of AVNRTs; forward conduction occurs down the fast pathway and retrograde conduction up the slow pathway (opposite of typical AVNRT)

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15
Q

How can you tell if it is AVNRT via ECG?

A

The rate is 160-180 bpm + most cases, the p wave is hidden in the QRS complex but sometimes you will have a pseudo-R in V1 or a pseudoS in V2 (retrograde depolarization)

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16
Q

What is the treatment for hemodynamically stable AVNRT? Unstable? Recurrent?

A

Stable: vagal maneuvers, adenosine, CCBs or beta blockers; Unstable: CDV; Recurrent: digoxin, CCBs, beta-blockers, or ablation

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17
Q

What is an atrioventricular reentrant tachycardia (AVRT)?

A

Reentrant loop that involves the AV node as one leg and an accessory pathway as the other leg

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18
Q

How is AVNRT different from AVRT?

A

AVRT has one leg of the loop that is outside of the AV node (while AVNRT is all within the node)

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19
Q

What are the ECG findings of antidromic AVRT?

A

Shortened PR interval + delta wave + QRS > 0.12 sec

20
Q

What is orthodromic AVRT?

A

AVRT where the antegrade limb from the atria to the ventricle is via the AV node and the retrograde limb is via an accessory bundle; 95% of AVRTs (most common form)

21
Q

What does the ECG look like for orthodromic AVRT?

A

QRS is normal (since antegrade limb is via the AV node) + p wave follows the QRS and is retrograde (inverse); rate is 150-250 bpm

22
Q

What is antidromic AVRT?

A

AVRT where the antegrade limb from the atria to the ventricle is via an accessory pathway and the retrograde limb is via the AV node; 5% of AVRTs

23
Q

What are the ECG findings of antidromic AVRT?

A

QRS > 0.12 sec (since antegrade is via accessory pathway) + p-wave before QRS + delta wave; rate is 150-250 bpm; sometimes confused for VT since QRS is wide

24
Q

What is Wolff-Parkinson-White (WPW) Syndrome?

A

An AVRT where the accessory pathway is via the Bundle of Kent

25
Q

What medication should you avoid in WPW syndrome?

A

AV-nodal blockers (adenosine, CCBs, beta blockers) as they will decrease conduction through the AV node and allow the accessory pathway to propagate signals leading to potential Vfib

26
Q

What is the treatment for orthodromic AVRT?

A

Adenosine, CCBs, beta blockers, vagal maneuvers, or ablation

27
Q

What is the treatment for antidromic AVRT?

A

Amiodarone, procainamide, propafenone, sotalol, flecainide, or ablation

28
Q

What is atrial flutter?

A

A large re-entrant circuit contained within the RA with variable passes through the AV node

29
Q

What is the normal rate of atrial flutter?

A

Usually organized at around 250-350 bpm with varying degrees of AV block (classically 2:1 leading to a rate of 150 bpm)

30
Q

What are common causes of atrial flutter?

A

Secondary to triggering events (i.e. pulmonary disease, MI, EtOH or s/p cardiac surgery or thryotoxicosis)

31
Q

What is the treatment for atrial flutter?

A

Vagal maneuvers, amiodarone, CCB, beta blockers, procainamine, synchronized CDV, or ablation

32
Q

What is multifocal atrial tachycardia?

A

Multiple ectopic atrial pacemakers, HR 100-180 bpm; usually triggered by underlying pulmonary exacerbation

33
Q

What are the ECG findings for multifocal atrial tachycardia?

A

> 3 p wave morphologies with variable PR intervals; HR 100-180 bpm

34
Q

What is the treatment for multifocal atrial tachycardia?

A

Treat underlying pulmonary condition or decompensation; MgSO4, CCBs, beta-blockers (but worry about bronchospasm)

35
Q

What is the difference between atrial fibrillation and atrial flutter?

A

Afib is when multiple areas in the atrium depolarize in an unorganized manner

36
Q

What are the sub-categories of atrial fibrillation?

A

Paroxysmal (2-7 days), persistent (>7 days), long-standing persistent (>12 months), permanent

37
Q

What is the definition of VT?

A

> 3 PVCs in succession with HR > 100 bpm; sustained = >30 sec and non-sustained = <30 sec

38
Q

What are the ECG findings for monomorphic VT?

A

QRS > 0.12 sec + AV dissocation (ventricular rhythm is faster than atrial rhythm so p wave is hidden in QRS) + same QRS morphology

39
Q

What is the treatment for monomorphic VT?

A

Acute stable: lidocaine, amio, procainamide; Acute unstable: synchronized CDV; Chronic: amio, beta-blocker, ICD placement

40
Q

What are examples of polymorphic VT?

A

Torsade de pointes, Brugada syndrome, Short QT syndrome, V fib

41
Q

What is torsades de pointes?

A

Polymorphic VT usually 2/2 prolonged QT syndrome devolving into VT due to QT prolonging agents

42
Q

What is the treatment for torsades?

A

Amio, magnesium, mixelitine

43
Q

What is Brugada syndrome?

A

A channelopathy condition where an ectopic beat can lead to polymorphic VT

44
Q

What is the triad of Brugada syndrome?

A

RBBB during sinus rhythm with ST elevations, VF and sudden death

45
Q

What is Short QT Syndrome?

A

Inherited channelopathy (loss of inward Ca current + gain of functional outward K current) -> increased risk of polymorphic VT; QTc < 360sec

46
Q

What is ventricular fibrillation?

A

Form of polymorphic VT with rapid, irregular ventricular arrhythmia + variable QRS cycle length and morphology

47
Q

What is the treatment of bradycardia if secondary to CCB or beta blocker toxicity?

A

Glucagon