Lecture 21: Dysrhythmias Part 1

Question 1

What is the underlying mechanism behind sinus arrhythmias?

Answer 1

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

NON PATHOLOGIC

Inspiration = increased HR

Question 2

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

Answer 2

< 45 BPM

Question 3

In what demographic is sinus bradycardia “normal”?

Answer 3

Athletes

Question 4

What physiological conditions can result in sinus bradycardia?

Answer 4

• 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

Question 5

What is sick sinus syndrome?

Answer 5

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

Different versions!

Question 6

How do you treat sick sinus syndrome?

Answer 6

If symptomatic => Permanent pacemaker implant

Question 7

What is the key management step in sinus bradycardia?

Answer 7

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

Question 8

How do you calculate max HR?

Answer 8

220-Age

Question 9

What are the MCC of sinus tachycardia?

Answer 9

• Exercise
• Anger/stress

Question 10

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

Answer 10

> 140 BPM

Superimposed on preceding T wave

Question 11

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

Answer 11

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

Question 12

What is inappropriate sinus tachycardia?

Answer 12

Exaggerated responses or increased resting HR during exercise.

Question 13

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

Answer 13

1. BBs
2. non-DHP CCBs or ivabradine

Verapamil/Dilt

Question 14

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

Answer 14

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

Question 15

What is 1st deg AVB?

Answer 15

PR interval > 0.2s with all atrial impulses conducted

Just takes longer to go from the atrium to the ventricle

Question 16

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

Answer 16

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

Question 17

What is 3rd deg AVB?

Answer 17

• Complete heart block
• Complete A-V dissociation

Atria and ventricles have 0 communication with each other.

Question 18

What typically causes 1st deg and mobitz type 1?

Answer 18

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

could potentially be normal

Question 19

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

Answer 19

Organic disease involving infranodal conduction

Question 20

How do people with 1st deg AVB typically present?

Answer 20

Asymptomatic.

Question 21

How do people with mobitz type 1 present?

Answer 21

Usually asymptomatic

Can be auscultated!

Question 22

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

Answer 22

Type 2 has weakness also as a symptom

Can also be auscultated!

Question 23

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

Answer 23

Heart failure

Question 24

How do we manage 1st deg AVB?

Answer 24

Just avoid medications that prolong PR interval or slow AV conduction

Question 25

How do we manage Mobitz type 1?

Answer 25

* Avoid AV node slowing drugs * Treat identifiable causes

Question 26

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

Answer 26

* Unstable needs PPM * Temporary pacing if due to a transient organic process

Question 27

What characterizes a PAC?

Answer 27

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

Question 28

What are the treatments for PACs?

Answer 28

* None usually * BBs for significant * Class IC antiarrhythmics (Propafenone and flecainide)

Question 29

What are PVCs characterized by?

Answer 29

* Wide QRS * **Compensatory pause after**

Question 30

What normal task can help suppress PVCs?

Answer 30

Exercise

Question 31

What is the first-line therapy for **symptomatic PVCs**?

Answer 31

BBs

Question 32

What is the alternative managment to BBs for symptomatic PVCs?

Answer 32

* Class IC (propafenone, flecainide) * Class III * Catheter ablation for significant ectopic burdens

Question 33

Why does having a lot of PVCs not affect HR?

Answer 33

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

Question 34

What is the most common mechanism for PSVT?

Answer 34

Reentry tachycardia. | AVNRT

Question 35

What are the two types of reentry tachycardias?

Answer 35

1. AVNRT (AV nodal re-entry tachycardia) 2. AVRT (AV reciprocating/re-entry tachycardia via accessory pathway) ## Footnote AVRT often is due to WPW

Question 36

What does PSVT typically look like?

Answer 36

* Narrow complex QRS usually * 140+ BPM * **Regular rhythm**

Question 37

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

Answer 37

* Valsalva * Stretching arms/legs * Head between knees * Cough, holding breath * Splashing cold water on face or ice

Question 38

What are the initial drugs for PSVT?

Answer 38

1. **Adenosine** 2. CCBs (Class IV) 3. BBs (Class II) | All IV, ABC for SVT! ## Footnote MUST KNOW adenosine is the #1 drug to treat SVT.

Question 39

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

Answer 39

Procainamide is **first-line** for antidromic SVT, which is a **WCT due to WPW** | Antidromic SVT is an AVRT ## Footnote However, it looks like VTach! Treat it as VTach until otherwise proven.

Question 40

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

Answer 40

Hemodynamically **unstable** | 100J start ## Footnote Otherwise, you use adenosine.

Question 41

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

Answer 41

Ablation

Question 42

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

Answer 42

* BBs and CCBs as **AV node blockers** * Class IC antiarrhythmics or Class III (amiodarone or sotalol)

Question 43

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

Answer 43

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