Echo, MR, EKG, SVT Flashcards
What is the Brugada criteria used for?
stepwise approach for differentiating VT vs. SVT with aberrancy If any of the four criteria is positive –> VT if non of the criteria are positive –> SVT with abberancy
Define the Brugada Criteria?
- Absence of RS complex in all precordial leads
- R to S interval > 100ms in one precordial lead
- AV dissociation
- Morphology criteria for RBBB or LBBB present in precordial leads
*dominant R wave in V1 –> criteria for RBBB
*dominant S wave in V1 –> criteria for LBBB
*if any are positive –> VT
*all negative –> SVT
Common EKG features of VT:
- Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen.
- Brugada’s sign (The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms)
- AV dissociation (P and QRS complexes at different rates)
- Absence of typical RBBB or LBBB morphology
- Capture beats (occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.)
- Fusion beats (occur when a sinus and ventricular beat coincides to produce a hybrid complex.)
- Josephson’s sign (Notching near the nadir of the S-wave -RSR’ complexes with a taller left rabbit ear. This is the most specific finding in favour of VT. This is in contrast to RBBB, where the right rabbit ear is taller.)
- Extreme axis deviation (“northwest axis”)
- Very broad complexes (>160ms)
- QRS is positive in aVR and negative in I + aVF.
EKG findings of LVH:
- increased amplitude (voltage) of QRS
- supported (and strengthened) by presence of secondary ST-T wave changes
- Other: left atrial abnormality, LAD, and/or prolonged intrinsicoid deflection, prominent U waves may be present
EKG Criteria for LVH (Sokolow and Lyone):
Precordial leads
- Sv1 and R v5 or v6 > 35 mm
- R v5 or v6 > 25 mm
Limb leads
-R aVL > 11 mm
EKG Criteria for LVH (Romhilt and Estes Point system)
**5 or more = LVH, 4 or more = probably LVH**
Amplitude (any of the following) = 3 points
- Any limb lead R or S > 20 mm
- Sv1 or Sv2 > 30 mm
- Rv5 or Rv6 > 30 mm
ST-T change = 3 points (1 with digitalis)
Left atrial abnormality = 3 points
Left axis deviation (-30 or more) = 2 points
Intrinsicoid deflection = 1 point
EKG Criteria for LVH (Cornell)
Men: Ravl + Sv3 > 28 mm
Women: Ravl + Sv3 > 20 mm
EKG Criteria for left atrial abnormality
- Prominent notching of P-wave (especially L2) with P-wave duration > 0.12s
- Leftward shift of P-wave axis
- Increased duration and depth of terminal negative portion of P in V1 ( > 0.04 mm-sec)
Key characteristics of RVH
- R/S ratio in V1 > 1 and R wave > 5mm
- QR in V1
- RAD
- Right atrial enlargement
-S1Q3T3 pattern and S1S2S3 pattern
*S1S2S3 pattern due to RVH = (SII > SIII)
EKG criteria for Right atrial enlargement
- peaked P (amplitude > 2.5 mm) in leads II, III, and aVF
- Rightward shift in P-wave axis ( > +75)
- Increased area ( >0.06 mm/sec or amplitude > 1.5 mm) of initial positive portion of P wave in V1
Differential diagnosis of RAD
- RVH
- Lateral wall MI
- Left posterior hemiblock
- COPD
- Normal Young Adult
Differential diagnosis: Prominent R wave or R/S ratio in V1
- RVH
- Ventricular Pre-excitation (WPW)
- Posterior wall MI
- Hypertrophic Cardiomyopathy
- If qR pattern, incomplete RBBB with septal MI
- Normal Variant
EKG findings: Acute PE
- Rightward shift of the QRS axis ( > 90 or indeterminate)
- S1Q3T3 pattern
- Incomplete or complete RBBB (often transient)
- ST-segment deviation (depression or elevation) in V1-V2
- Sinus tachycardia, atrial flutter, atrial fibrillation
RBBB diagnostic criteria
- Broad QRS > 120 ms
- RSR’ pattern in V1-V3 (M-shaped QRS complex)
- Wide, slurred S wave in the lateral leads (I, aVL, V5-V6)
Causes of RBBB
- RVT / cor pulmonale
- PE
- Ischemic heart disease
- Rheumatic heart disease
- Myocarditis or cardiomyopathy
- Degnerative disease of the conduction system
- Congenital heart disease (e.g. ASD)
Incomplete RBBB criteria
-RSR’ patterin in V1-V3 with QRS duration < 120 ms
*Normal variant often seen in children (of no clinical significance)
RBBB pathophysiology
- activation of the RV is delayed as depolarization has to spread across the septum from the LV
- LV is activated normally, meaning that the early part of the QRS is unchanged
- Delayed RV activation produces a secondary R wave (R’) in the right precordial leads (V1-V3) and a wide, slurred S wave in the lateral leads
- Delayed activation of the RV also gives rise to secondary repolarization
EKG findings: Ostium Primum ASD
-rSR’s’ in lead V1
+
-Left axis deviation
*Normal axis = Ostium secundum
*Low atrial rhythm = sinus venosus ASD
What is Ashman phenomenon (Ashman beat)?
- occurs when a premature supra ventricular beat occurs before the right bundle branch has recovered from its refractory period –> results in the PVC being displayed as RBBB
- frequently occurs with PAC’s, however can also be seen in A-fib, atrial tachycardia as R-R intervals can vary
- No clinical significance, patient’s may feel palpitations
What is the significance of ST-depression that occurs only in the recovery period?
same diagnostic accuracy as ST-segment depression during exercise
When does ST-elevation usually show up on ETT?
What does this mean?
- Can be arrythmogenic if exercise continues.
- Can localize site of myocardial ischemia (unlike ST-depression) and usually indicates high-grade stenosis
What EKG findings preclude interpretation of exercise EKG?
- Paced ventricular rhythm
- Pre-excitation (WPW)
- LBBB
- Reduce specicity –> ST-T abnormalities, Digoxin use, LVH
What is one clinical feature differentiating SVT types?
Character of symptom onset
- sudden, abrupt onset and termination without any clear inciting factor –> AVNRT, AVRT
- gradual onset and resolution with a possible trigger (exercise) –> AT
Useful classification system for PSVT’s?
RP relationship
- Long R-P tachycardia = RP interval that is greater than half of the RR interval
Useful information to determine SVT type?
Telemetry strip at onset and termination
- Longer PR –> may indicate conduction down a slow AV nodal pathway and initiation of AVNRT or orthodromic AVRT
SVT diagnosis:
-P wave
AVNRT: Retrograde (caudocranial) atrial activation –> negative P waves in inferior leads
AT (some): craniocaudal activation –> positive P wave in inferior leads
Conduction around a fast-slow re-entry circuit occurring only once is called this?
echo beat
Define typical AVNRT
- 80-90% of AVNRT
- short R-P tachycardia ( < 70 msec)
- initiated by long PR interval
- Slow AV nodal anterograde conduction and Fast AV nodal retrograde conduction
- EKG findings:
- P waves often absent (embedded in previous QRS)
- Retrograde P waves may be present –> Pseudo r’ waves seen in V1
- Pseudo S waves may be seen in inferior leads (II, III, aVF)
Define Uncommon AVNRT
- 10% of AVNRT
- Fast AV nodal anterograde conduction - Slow AV nodal retrograde conduction
- EKG findings:
- P waves often visible after QRS
- QRS-P-T complexes
- P waves are visible between QRS and T wave
Define Atypical AVNRT
- 1-5% of AVNRT
- Slow AV nodal anterograde - Slow AV nodal retrograde conduction
- EKG findings:
- P wave appearing before QRS complex (often confused for sinus tachycardia)
SVT with R-P interval < 70 msec
Possible
- AVNRT (likely)
- AT (with short RP)
Excludes
- AVRT (requires activation of atria-ventricles)
How to differentiate between AT and AVNRT if RP < 70 msec?
AV blockade
- AVNRT -> P wave that blocks in the AV node with no R wave and termination of tachycardia
- AT -> termination highly unusual with AV blockade
Accessory pathways may be involved with tachycardia in what 3 circumstances:
- Orthodromic AVRT
- Antidromic AVRT
- Pre-excited tachycardias
EKG criteria for Left Posterior Fascicular Block (LPFB)?
- RAD ( > +90)
- rS complexes
- Small r waves with deep S waves in leads I and aVL
- qR complexes
- Small Q waves with tall R waves in leads II, III, aVF
- QRS normal or slightly prolonged
- Increased QRS voltage in limb leads
- No RVH or any other cause for RAD
EKG features of WPW?
PR interval > 120 msec QRS > 110 msec Delta wave ST-T wave discordant changes (opposite direction to the major component of the QRS complex)
Pseudo-infarction pattern (70% of patients)
-negatively deflected delta waves in the inferior / anterior leads or -prominent R wave in V1-V3 (mimicking posterior infarction)
What are the types of WPW?
Type A
- positive delta wave in all precordial leads with R/S > 1 in V1
Type B
- negative delta wave in leads V1 and V2
In what situation is no EKG evidence of WPW seen on EKG?
“concealed pathway”
- patients with retrograde-only accessory conduction will conduct only antegrade conduction via the AV node
- Patient’s still experience tachycarrhythmias as pathways still form part of a re-entry circuit
Define accessory pathway
electrical connections between the atrial and ventricular tissue that bypass the normal conduction system
What are the most commonly encountered / typical accessory pathways?
- short, rapidly conducting AV accessory pathways that cross the Tricuspid or Mitral annulus
- most commonly left sided pathways in normal hearts (Ebstein’s anomaly -> right sided)
If accessory pathway is “concealed,” when will it become visible on EKG?
slowing of AV nodal conduction (high vagal tone or following a PAC)
What two situations can an accessory pathway be “concealed”?
- incapable of conducting antegradely from atrium to the ventricles
- conduction down the accessory pathway takes longer than conduction down the AV node.
- Either due to:
- brisk AV nodal conduction
- large distance between the origin of the atrial impulse and the accessory pathway (left free-wall accessory pathway in sinus rhythm)
- Either due to:
Define of Orthodromic AVRT
- Most common form of AVRT
- narrow complex tachycardia
- RP interval > 70msec
- antegrade conduction down the AV node and -retrograde conduction up the accessory pathway
**Development of BBB ipsilateral to the accessory pathway usually increases RP interval; this is diagnostic of orthodromic AVRT and localizes the pathway to one side
Define Antidromic AVRT
- Pre-excited, wide complex tachycardia
- Antegrade conduction down the accessory pathway and Retrograde conduction up the AV node
- Dependent on AV node for tachycardia perpetuation –> Terminated with AV nodal blocking agents or Adenosine
What circumstance would AVRT not be terminated with AV nodal blockade?
Antegrade/Retrograde conduction via two separate accessory pathways
What is the treatment for asymptomatic patients with WPW?
- no treatment
- Consider assessment of the refractory period of the pathway (cardiac monitoring, exercise stress testing or EP study)
- High-risk professions (pilots, bus driver) should be test be risk stratified early
In what situations is cardiac ablation of accessory pathway indicated / reasonable in asymptomatic patients with no documented tachycardia?
EP study demonstrates high risk features *conduction to ventricles in A-fib with shortest RR interval of < 250msec
Accessory pathways can present in two ways?
Manifest -> producing a delta wave via antegrade conduction Concealed -> conducting retrograde only
How to identify accessory pathway location in manifest pre-excitation?
Identify QRS transition point *Left sided ( < V1 - RBBB) *Septal (V1 - V2) *Right sided ( > V2 - LBBB) Delta Wave Polarity of Inferior Leads *Anterior –> Positive in > 2/3 leads *Posterior –> Negative in > 2/3 leads
What are the indications for CCTA?
Symptomatic patients (typical angina) Low-to-Intermediate risk individuals
What is the differential for wide complex tachycardia?
- VT
- SVT with aberrant conduction due to BBB
- SVT with pre-excitation of teh ventricle due to antegrade conduction down an accessory pathway
What should therapy be initiated for hypertriglyceridemia?
What are the first line therapies?
- TG > 500
- Fenofibrate or Niacin
- Statins are second line
Define Atrial tachycardia
-least common form of PSVT (~10%) -long R-P tachycardia with P wave morphology and PR interval that are distinct from sinus rhythm -usually abnormal P-wave axis (inverted in the inferior leads II, III, aVF) -AV block may be present (generally a physiological response to rapid HR) -Not dependent on AV node –> will not terminate with AV block -May be periods of variable conduction with more P’s than QRS’s
Atrial tachycardia: -Diagnosis
-EKG findings -IV adenosine can be used acutely to promote AV block and expose P-waves -Automatic or micro-re-entrant focal rhythm would not be expected to terminate with adenosine -15-20% of AT’s can respond to IV adenosine.
Atrial tachycardia: -Treatment
-Often termination is spontaneous -Medical therapy (BB’s, CCB’s) often used for symptomatic relief if AT frequent -hemodynamic compromise –>cardioversion -Frequent, symptomatic episodes from a single focus with high AT burden –> catheter ablation (85-90% success rates)
EKG criteria: Left Anterior Fascicular Block (LAFB)
LAD (usually between -45 and -90) Small Q waves with tall R waves (= ‘qR complexes’) in leads I and aVL Small R waves with deep S waves (=’rS complexes’) in leads II, III, aVF QRS duration normal or slightly prolonged (80-110 ms) Prolonged R wave peak time in aVL > 45 ms Increased QRS voltage in the limb leads **QRS voltage in aVL may meet voltage criteria for LVH (R wave > 11 mm), but there will be no LV strain pattern
