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CV <3 > Lecture 21: Dysrhythmias Part 1 > Flashcards

Lecture 21: Dysrhythmias Part 1 Flashcards

1
Q

What is the underlying mechanism behind sinus arrhythmias?

A

Reflex changes in vagal influence on normal pacemaker, which disappears when holding your breath or increasing HR.

NON PATHOLOGIC

Inspiration = increased HR

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2
Q

At what point is sinus bradycardia considered severe and potentially an indication of sinus node pathology?

A

< 45 BPM

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3
Q

In what demographic is sinus bradycardia “normal”?

A

Athletes

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4
Q

What physiological conditions can result in sinus bradycardia?

A
  • OSA
  • Increased ICP (r/o neurologic symptoms)
  • Hypothyroidism
  • Inferior wall MI (RCA is the main supply to the sinus node)
  • Hypothermia

Cushing’s reflex = Widened pulse pressure, hypotension, irregular respirations => increasing ICP

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5
Q

What is sick sinus syndrome?

A
  • Recurrent supraventricular arrhythmias
  • Brady-tachy syndrome
  • Chronotropic incompetence

Different versions!

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6
Q

How do you treat sick sinus syndrome?

A

If symptomatic => Permanent pacemaker implant

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7
Q

What is the key management step in sinus bradycardia?

A

Seeing if they are symptomatic and if the symptoms are correlated with their bradycardia.

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8
Q

How do you calculate max HR?

A

220-Age

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9
Q

What are the MCC of sinus tachycardia?

A
  • Exercise
  • Anger/stress
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10
Q

At what point are P waves difficult to see on EKG in sinus tachycardia?

A

> 140 BPM

Superimposed on preceding T wave

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11
Q

If someone has structural HD but is presenting with tachycardia, what could occur physiologically?

A
  • Increased O2 consumption
  • Decreased Coronary blood flow
  • Decreased CO due to shortened ventricular filling time
  • Exacerbation of existing HD
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12
Q

What is inappropriate sinus tachycardia?

A

Exaggerated responses or increased resting HR during exercise.

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13
Q

In patients with symptomatic/inappropriate sinus tach, what is the first-line therapy?

A
  1. BBs
  2. non-DHP CCBs or ivabradine

Verapamil/Dilt

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14
Q

Where do mobitz type 1 and 2 differ in terms of physiology of conduction?

A
  1. Type 1 is characterized by abnormal conduction within the AV Node
  2. Type 2 is characterized by abnormal conduction within the bundle of His

Higher type = higher up

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15
Q

What is 1st deg AVB?

A

PR interval > 0.2s with all atrial impulses conducted

Just takes longer to go from the atrium to the ventricle

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16
Q

What is Mobitz Type 1 and Type 2 2nd deg AVB?

A
  1. Type 1 = Progressive lengthening of AV conduction time
  2. Type 2 = Intermittently nonconducted AV beats not preceded by lengthening of AV conduction time
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17
Q

What is 3rd deg AVB?

A
  • Complete heart block
  • Complete A-V dissociation

Atria and ventricles have 0 communication with each other.

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18
Q

What typically causes 1st deg and mobitz type 1?

A
  • Heightened vagal tone
  • Drugs (digitalis, CCBs, BBs)
  • Electrolyte abnormalities
  • Organic diseases (infilitrative processes that affect muscle)

could potentially be normal

19
Q

What typically causes Mobitz Type II or 3rd deg AVB?

A

Organic disease involving infranodal conduction

20
Q

How do people with 1st deg AVB typically present?

A

Asymptomatic.

21
Q

How do people with mobitz type 1 present?

A

Usually asymptomatic

Can be auscultated!

22
Q

What is the main symptom difference in Mobitz Type 2 and Type 1?

A

Type 2 has weakness also as a symptom

Can also be auscultated!

23
Q

What other cardiac condition may be seen in someone with complete heart block?

A

Heart failure

24
Q

How do we manage 1st deg AVB?

A

Just avoid medications that prolong PR interval or slow AV conduction

25
Q

How do we manage Mobitz type 1?

A
  • Avoid AV node slowing drugs
  • Treat identifiable causes
26
Q

How do we manage Type 2 and 3rd deg AVB?

A
  • Unstable needs PPM
  • Temporary pacing if due to a transient organic process
27
Q

What characterizes a PAC?

A
  • Different P-wave morphology
  • Ectopic focus in atria, that comes in early and may have a QRS following
  • Frequently occur in normal hearts
28
Q

What are the treatments for PACs?

A
  • None usually
  • BBs for significant
  • Class IC antiarrhythmics (Propafenone and flecainide)
29
Q

What are PVCs characterized by?

A
  • Wide QRS
  • Compensatory pause after
30
Q

What normal task can help suppress PVCs?

A

Exercise

31
Q

What is the first-line therapy for symptomatic PVCs?

A

BBs

32
Q

What is the alternative managment to BBs for symptomatic PVCs?

A
  • Class IC (propafenone, flecainide)
  • Class III
  • Catheter ablation for significant ectopic burdens
33
Q

Why does having a lot of PVCs not affect HR?

A
  1. PVCs are nonsignificant beats, in that they involve the squeezing of the ventricle WITHOUT blood moving.
  2. A person’s real HR therefore might be a lot lower
34
Q

What is the most common mechanism for PSVT?

A

Reentry tachycardia.

AVNRT

35
Q

What are the two types of reentry tachycardias?

A
  1. AVNRT (AV nodal re-entry tachycardia)
  2. AVRT (AV reciprocating/re-entry tachycardia via accessory pathway)

AVRT often is due to WPW

36
Q

What does PSVT typically look like?

A
  • Narrow complex QRS usually
  • 140+ BPM
  • Regular rhythm
37
Q

What are some mechanical things we can have the patient do to treat PSVT?

A
  • Valsalva
  • Stretching arms/legs
  • Head between knees
  • Cough, holding breath
  • Splashing cold water on face or ice
38
Q

What are the initial drugs for PSVT?

A
  1. Adenosine
  2. CCBs (Class IV)
  3. BBs (Class II)

All IV, ABC for SVT!

MUST KNOW adenosine is the #1 drug to treat SVT.

39
Q

What drug can treat antidromic PSVT and what does antidromic PSVT look like?

A

Procainamide is first-line for antidromic SVT, which is a WCT due to WPW

Antidromic SVT is an AVRT

However, it looks like VTach! Treat it as VTach until otherwise proven.

40
Q

When is cardioversion indicated for PSVT as first-line tx?

A

Hemodynamically unstable

100J start

Otherwise, you use adenosine.

41
Q

What is first-line therapy for recurrent, symptomatic PSVT?

A

Ablation

42
Q

What are the medications used for prevention/long-term management of PSVT?

A
  • BBs and CCBs as AV node blockers
  • Class IC antiarrhythmics or Class III (amiodarone or sotalol)
43
Q

What is the one exception to long-term management of PSVT?

A

AVRTs (accessory pathways) require usage of both Class IC/Class III and an AV nodal blocking drug.

Need to work on both pathways to prevent rapid ventricular rates.

AV nodal blockers do not affect refractory period of accessory pathway.
AVN blockers are BBs and non-DHP CCBs.

CV <3 (25 decks)

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