Lecture 21: Dysrhythmias Part 1 Flashcards
What is the underlying mechanism behind sinus arrhythmias?
Reflex changes in vagal influence on normal pacemaker, which disappears when holding your breath or increasing HR.
NON PATHOLOGIC
Inspiration = increased HR
At what point is sinus bradycardia considered severe and potentially an indication of sinus node pathology?
< 45 BPM
In what demographic is sinus bradycardia “normal”?
Athletes
What physiological conditions can result in sinus bradycardia?
- 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
What is sick sinus syndrome?
- Recurrent supraventricular arrhythmias
- Brady-tachy syndrome
- Chronotropic incompetence
Different versions!
How do you treat sick sinus syndrome?
If symptomatic => Permanent pacemaker implant
What is the key management step in sinus bradycardia?
Seeing if they are symptomatic and if the symptoms are correlated with their bradycardia.
How do you calculate max HR?
220-Age
What are the MCC of sinus tachycardia?
- Exercise
- Anger/stress
At what point are P waves difficult to see on EKG in sinus tachycardia?
> 140 BPM
Superimposed on preceding T wave
If someone has structural HD but is presenting with tachycardia, what could occur physiologically?
- Increased O2 consumption
- Decreased Coronary blood flow
- Decreased CO due to shortened ventricular filling time
- Exacerbation of existing HD
What is inappropriate sinus tachycardia?
Exaggerated responses or increased resting HR during exercise.
In patients with symptomatic/inappropriate sinus tach, what is the first-line therapy?
- BBs
- non-DHP CCBs or ivabradine
Verapamil/Dilt
Where do mobitz type 1 and 2 differ in terms of physiology of conduction?
- Type 1 is characterized by abnormal conduction within the AV Node
- Type 2 is characterized by abnormal conduction within the bundle of His
Higher type = higher up
What is 1st deg AVB?
PR interval > 0.2s with all atrial impulses conducted
Just takes longer to go from the atrium to the ventricle
What is Mobitz Type 1 and Type 2 2nd deg AVB?
- Type 1 = Progressive lengthening of AV conduction time
- Type 2 = Intermittently nonconducted AV beats not preceded by lengthening of AV conduction time
What is 3rd deg AVB?
- Complete heart block
- Complete A-V dissociation
Atria and ventricles have 0 communication with each other.
What typically causes 1st deg and mobitz type 1?
- Heightened vagal tone
- Drugs (digitalis, CCBs, BBs)
- Electrolyte abnormalities
- Organic diseases (infilitrative processes that affect muscle)
could potentially be normal
What typically causes Mobitz Type II or 3rd deg AVB?
Organic disease involving infranodal conduction
How do people with 1st deg AVB typically present?
Asymptomatic.
How do people with mobitz type 1 present?
Usually asymptomatic
Can be auscultated!
What is the main symptom difference in Mobitz Type 2 and Type 1?
Type 2 has weakness also as a symptom
Can also be auscultated!
What other cardiac condition may be seen in someone with complete heart block?
Heart failure
How do we manage 1st deg AVB?
Just avoid medications that prolong PR interval or slow AV conduction
How do we manage Mobitz type 1?
- Avoid AV node slowing drugs
- Treat identifiable causes
How do we manage Type 2 and 3rd deg AVB?
- Unstable needs PPM
- Temporary pacing if due to a transient organic process
What characterizes a PAC?
- Different P-wave morphology
- Ectopic focus in atria, that comes in early and may have a QRS following
- Frequently occur in normal hearts
What are the treatments for PACs?
- None usually
- BBs for significant
- Class IC antiarrhythmics (Propafenone and flecainide)
What are PVCs characterized by?
- Wide QRS
- Compensatory pause after
What normal task can help suppress PVCs?
Exercise
What is the first-line therapy for symptomatic PVCs?
BBs
What is the alternative managment to BBs for symptomatic PVCs?
- Class IC (propafenone, flecainide)
- Class III
- Catheter ablation for significant ectopic burdens
Why does having a lot of PVCs not affect HR?
- PVCs are nonsignificant beats, in that they involve the squeezing of the ventricle WITHOUT blood moving.
- A person’s real HR therefore might be a lot lower
What is the most common mechanism for PSVT?
Reentry tachycardia.
AVNRT
What are the two types of reentry tachycardias?
- AVNRT (AV nodal re-entry tachycardia)
- AVRT (AV reciprocating/re-entry tachycardia via accessory pathway)
AVRT often is due to WPW
What does PSVT typically look like?
- Narrow complex QRS usually
- 140+ BPM
- Regular rhythm
What are some mechanical things we can have the patient do to treat PSVT?
- Valsalva
- Stretching arms/legs
- Head between knees
- Cough, holding breath
- Splashing cold water on face or ice
What are the initial drugs for PSVT?
- Adenosine
- CCBs (Class IV)
- BBs (Class II)
All IV, ABC for SVT!
MUST KNOW adenosine is the #1 drug to treat SVT.
What drug can treat antidromic PSVT and what does antidromic PSVT look like?
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.
When is cardioversion indicated for PSVT as first-line tx?
Hemodynamically unstable
100J start
Otherwise, you use adenosine.
What is first-line therapy for recurrent, symptomatic PSVT?
Ablation
What are the medications used for prevention/long-term management of PSVT?
- BBs and CCBs as AV node blockers
- Class IC antiarrhythmics or Class III (amiodarone or sotalol)
What is the one exception to long-term management of PSVT?
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.
