PGY4 - EKGs

Question 1

Answer 1

A Fib with WPW

• Rate > 200 bpm
• Irregularly irregular
• Changing QRS morphology
• Pathway:
  
  • Down normal- narrow QRS
  • Down accessory- wide QRS
• Treatment
  
  • No AV Nodal Blockers → VF
    
    • CCB, BB, dig, adenosine or amio
  • If unstable- cardioversion
  • If stable- procainamide or cardioversion

Question 2

VT vs AFib with WPW

Answer 2

Question 3

Answer 3

Antidromic atrioventricular re-entry tachycardia (AVRT)

= WPW + SVT in antidromic pattern

Age clues you in

Question 4

Brugada ALgorithm - I dunno, just review this shit

Answer 4

Question 5

Answer 5

AAI

• Atrial paced and sensing
• If native activity sensed then pacing is inhibited
• If no native activity sensed for predetermined time then atrial pacing initiated
• Used in sinus node dysfunction with intact AV conduction

Question 6

Answer 6

VVI

Ventricular pacing and sensing

Similar to AAI but ventricular

Used in chronic atrial impairment

Note LBBB Morphology

Question 7

Answer 7

DDD- pacing and sensing the atria and ventricles

• Most common
• Atrial pacing if no native atrial activity for set time
• Ventricular pacing if no native ventricle activity
• Atrial channel function suspended during a fixed periods following atrial and ventricular activity to prevent sensing activity or retrograde p waves as native atrial activity

A-V sequential pacing:

• Atrial and ventricular pacing spikes are visible before each QRS complex.
• There is 100% atrial capture — small P waves are seen following each atrial pacing spike.
• There is 100% ventricular capture — a QRS complex follows each ventricular pacing spike.
• QRS complexes are broad with a LBBB morphology, indicating the presence of a ventricular pacing electrode in the right ventricle.

Question 8

Magnet Mode

For Pacemaker

For AICD

Answer 8

Pacemaker - Goes to asynchronous mode

ICD - Deactivates ICD

Question 9

Answer 9

Undersensing

• Undersensing occurs when the pacemaker fails to sense native cardiac activity.
• Results in asynchronous pacing.
• Causes include increased stimulation threshold at electrode site (exit block), poor lead contact, new bundle branch block or programming problems.
• ECG findings may be minimal, although presence of pacing spikes within QRS complexes is suggestive of undersensing.

Question 10

Answer 10

Oversensing

• Oversensing means that the pacemaker thinks it is sensing myocardial electrical discharges but it’s a LIE.
• The pacemaker appropriately inhibits itself, which leads to inappropriate underpacing
• Oversensing = Underpacing
• Causes:
  
  • Large P or T waves, skeletal muscle activity, lead contact
    *

Question 11

Answer 11

Failure to Capture

• This means the pacemaker discharges a stimulus, but the myocardium does not depolarize.
• EKG = pacer spikes without an associated QRS complex
• Can be caused by…
  
  • lead dislodgement or malplacement
  • fibrosis or inflammation at the interface of the lead and the myocardium
  • pacemaker setting problems
  • capture threshold set too high
  • lead failure
  • battery depletion
  • recording system failure

Question 12

Answer 12

RVH

• RAD of +100 or more
• Dominant R wave in V1 (>7mm tall or R/S >1)
• Dominant S wave in V5 or 6 (>7mm deep or R/S <1)
• QRS duration < 120 ms

Question 13

Answer 13

Normal Peds EKG

• Heart rate > 100 beats/min
• Apparent right ventricular strain pattern:
  
  • T wave inversions in V1-3 (“juvenile T-wave pattern”)
  • Right axis deviation
  • Dominant R wave in V1
  • RSR’ pattern in V1
• Marked sinus arrhythmia
• Short PR interval (< 120ms) and QRS duration (<80ms)
• Slightly peaked P waves (< 3mm in height is normal if ≤ 6 months)
• Slightly prolonged QTc (≤ 490ms in infants ≤ 6 months)
• Q waves in the inferior and left precordial leads

Question 14

Answer 14

TCA

• Widened QRS
• QT prolongation (>100-sz, >160- ventricular arrhythmia),
• Right axis deviation of terminal QRS
  
  • Terminal R > 3 mm in aVR
  • R:S >0.7 in aVR

Question 15

LBBB STEMI Equivalent

Answer 15

LBBB is STEMI equivalent if:

• Hemodynamically unstable, acute HF
• Sgarbossa (a or b- c is questionable)
  
  • A. Concordant STE > 1 mm any lead
  • B. Concordant STD > 1 mm in V1-3
  • C. Discordant STE > 5 mm
• Smith/Revised Sgarbossa
  
  • Lead with > 1mm STE and proportionally excessive discordant STE (>25% of the depth ofpreceding S wave)

Question 16

Answer 16

Left Ventricular Aneurysm

• ECG Features​​​
  
  • Easy = Ant STE + Path Q Waves > 2 weeks after STEMI
  • T-waves have a relatively small amplitude in comparison to the QRS complex (unlike the hyperacute T-waves of acute STEMI)
  • Usually associated with well-formed Q- or QS waves
  • May exhibit concave or convex morphology
  • Most commonly seen in the precordial leads
  • ST elevation seen > 2 weeks following an acute myocardial infarction
• Clinical Significance
  
  • Ventricular aneurysms predispose patients to an increased risk of:
  • Ventricular arrhythmias and sudden cardiac death (myocardial scar tissue is arrhythmogenic)
  • Congestive cardiac failure
  • Mural thrombus and subsequent embolisation

Question 17

Answer 17

Cor Pulmonale

• RBBB
• Extreme right axis deviation (+180 degrees)
• S1 Q3 T3
• T-wave inversions in V1-4 and lead III
• Clockwise rotation with persistent S wave in V6

Question 18

Answer 18

Arrhythmogenic Right Ventricular Dysplasia (ARVD)

EKG Findings

• Epsilon wave (30%)
• T wave inversions in V1-2 (85%) Prolonged S-wave of 55 ms in V1-3

General

• Inherited myocardial disease associated with paroxysmal ventricular arrhythmias and sudden cardiac death
• Fibro-fatty replacement of RV myocardium, autosomal dominant

Clinical

• Symptoms due to ventricular ectopic beats or sustained V tach
  
  • palpitations, syncope, cardiac arrest, over time RV failure