deck 1 Flashcards
Usual rate for aflutter?
240-340 bpm
Which ARDs can slow down flutter waves? (3)
- type Ia ARDs (quinidine)
- type 1c ARDs (flecainide)
- type III ARDs (dofetilide)
(NOTE: carotid massage and AVN blocking agents cannot slow down AFl waves)
Describe the EKG morphology of typical AFlutter (F) waves. (3)
F waves have the following properties:
- inferior lead pattern: inverted sawtooth W/OUT isoelectric baseline
- V1 pattern: small positive deflections WITH isolectric baseline
- characteristic cycle length: 175 -250 ms (240-340 bpm)
Atypical Aflutter wave (F’) characteristics? (2)
F’ wave characteristics:
- variable morphology: but usually positive inferiorally w/out isolectric baseline
- characteristic cycle length: same as for typical Aflutter waves (175-250 ms)
Usual conduction ratios for Aflutter?
even numbered ratios are more common (2:1 and 4:1)
Pt is found with WCT at rate of 280, an EP study shows:
- focus of arrhythmia around the tricuspid annulus
- re-entry mechanism
Explain the underlying rhythm.
underlying rhythm is Aflutter w/ 1:1 conduction & aberrent conduction
- Aflutter conducts 1:1 → refractory His-Purkinje system
- →infranodal conduction velocity slows
EKG shows LAD and R wave of 14 mm in aVL. What to look for next on tracing?
look for signs of LAFB:
- qR in lateral leads and rS in inferior leads
- poor R wave progression
* LAFB can masquerade as LVH → if LAD present always r/o LAFB before diagnosing LVH
Most common cause of bifascicular block (RBBB + LAFB)?
CAD (greater than 50% of cases)
Pt with acute AWMI has signs of new bifascicular block on EKG. You place a TVP and the intern wants to know why. What to tell her?
- 20% of acute AWMIs w/ new bifascicular block will progress to CHB
- TVP should be considered in all patients with AWSTEMI who develop BFB
Why do patients with acute AWMI often develop bifascicular block?
if AWMI involves occlusion of LAD proximal to septals, then get compromised RBB and LAF perfusion
- RBB and LAF have single blood supply from septal branches of LAD → pLAD occlusion causes BFB
- posterior fascicle has dual blood supply from Cx and LAD → need to occlude Lt main to get LPFB
What is the difference between a compensatory pause (CP) & a NON-compensatory pause (NCP)?
- NCP: PP’ < 2PP (occurs when sinus node IS reset)
- CP: PP’ = 2PP intervals (occurs when sinus node is NOT reset)
key:
- PP’ = interval from initial sinus P wave to next sinus p wave (following the premature beat)
- PP = normal P to P interval
Type of sinus pause expected after an atrial extrasystolic beat?
non-compensatory pause
- APCs usually reset the SAN → leads to NCP
Mechanism of blocked APC?
premature ectopic atrial beat:
- resets the SAN → get NCP
- is blocked at the level of the AVN → no conduction to V
*blocked APCs can be seen in normal individuals
clinical scenario for sick sinus syndrome (SSS)? (3)
- elderly pt w/ Afib
- sinus node dysfunction on EKG: sinus pause/arrest, sinus exit block, sinus bradycardia
- +/- intermittent tachycardia (“tachy-brady syndrome”)
What are the 4 types of sinoatrial exit block (SEB) & which can be diagnosed by surface EKG?
SEB subtypes are analogous to those of AVB:
- 1st degree*: fixed delay in sino-atrial conduction (SAC) time
- 2nd degree, type 1: SAC time prolongs w/ each cycle until conduction fails
- 2nd degree, type 2: fixed delay in SAC time with intermittent complete failure of conduction
- 3rd degree*: complete failure of sinus-to-atria conduction
*not diagnosable by surface EKG
