Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medical > Echo, MR, EKG, SVT > Flashcards

Echo, MR, EKG, SVT Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

What is the Brugada criteria used for?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define the Brugada Criteria?

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Common EKG features of VT:

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

EKG findings of LVH:

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

EKG Criteria for LVH (Sokolow and Lyone):

A

Precordial leads

  • Sv1 and R v5 or v6 > 35 mm
  • R v5 or v6 > 25 mm

Limb leads
-R aVL > 11 mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

EKG Criteria for LVH (Romhilt and Estes Point system)

A

**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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

EKG Criteria for LVH (Cornell)

A

Men: Ravl + Sv3 > 28 mm

Women: Ravl + Sv3 > 20 mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

EKG Criteria for left atrial abnormality

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Key characteristics of RVH

A
  • 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

EKG criteria for Right atrial enlargement

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Differential diagnosis of RAD

A
  • RVH
  • Lateral wall MI
  • Left posterior hemiblock
  • COPD
  • Normal Young Adult
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Differential diagnosis: Prominent R wave or R/S ratio in V1

A
  • RVH
  • Ventricular Pre-excitation (WPW)
  • Posterior wall MI
  • Hypertrophic Cardiomyopathy
  • If qR pattern, incomplete RBBB with septal MI
  • Normal Variant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

EKG findings: Acute PE

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

RBBB diagnostic criteria

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of RBBB

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Incomplete RBBB criteria

A

-RSR’ patterin in V1-V3 with QRS duration < 120 ms

*Normal variant often seen in children (of no clinical significance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

RBBB pathophysiology

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

EKG findings: Ostium Primum ASD

A

-rSR’s’ in lead V1
+
-Left axis deviation

*Normal axis = Ostium secundum
*Low atrial rhythm = sinus venosus ASD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Ashman phenomenon (Ashman beat)?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the significance of ST-depression that occurs only in the recovery period?

A

same diagnostic accuracy as ST-segment depression during exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When does ST-elevation usually show up on ETT?

What does this mean?

A
  • Can be arrythmogenic if exercise continues.
  • Can localize site of myocardial ischemia (unlike ST-depression) and usually indicates high-grade stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What EKG findings preclude interpretation of exercise EKG?

A
  • Paced ventricular rhythm
  • Pre-excitation (WPW)
  • LBBB
  • Reduce specicity –> ST-T abnormalities, Digoxin use, LVH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is one clinical feature differentiating SVT types?

A

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
24
Q

Useful classification system for PSVT’s?

A

RP relationship

  • Long R-P tachycardia = RP interval that is greater than half of the RR interval
25
Q

Useful information to determine SVT type?

A

Telemetry strip at onset and termination

  • Longer PR –> may indicate conduction down a slow AV nodal pathway and initiation of AVNRT or orthodromic AVRT
26
Q

SVT diagnosis:

-P wave

A

AVNRT: Retrograde (caudocranial) atrial activation –> negative P waves in inferior leads

AT (some): craniocaudal activation –> positive P wave in inferior leads

27
Q

Conduction around a fast-slow re-entry circuit occurring only once is called this?

A

echo beat

28
Q

Define typical AVNRT

A
  • 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)
29
Q

Define Uncommon AVNRT

A
  • 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
30
Q

Define Atypical AVNRT

A
  • 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)
31
Q

SVT with R-P interval < 70 msec

A

Possible

  • AVNRT (likely)
  • AT (with short RP)

Excludes

  • AVRT (requires activation of atria-ventricles)
32
Q

How to differentiate between AT and AVNRT if RP < 70 msec?

A

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
33
Q

Accessory pathways may be involved with tachycardia in what 3 circumstances:

A
  • Orthodromic AVRT
  • Antidromic AVRT
  • Pre-excited tachycardias
34
Q

EKG criteria for Left Posterior Fascicular Block (LPFB)?

A
  • 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
35
Q

EKG features of WPW?

A

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)

36
Q

What are the types of WPW?

A

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
37
Q

In what situation is no EKG evidence of WPW seen on EKG?

A

“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
38
Q

Define accessory pathway

A

electrical connections between the atrial and ventricular tissue that bypass the normal conduction system

39
Q

What are the most commonly encountered / typical accessory pathways?

A
  • 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)
40
Q

If accessory pathway is “concealed,” when will it become visible on EKG?

A

slowing of AV nodal conduction (high vagal tone or following a PAC)

41
Q

What two situations can an accessory pathway be “concealed”?

A
  • 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)
42
Q

Define of Orthodromic AVRT

A
  • 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

43
Q

Define Antidromic AVRT

A
  • 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
44
Q

What circumstance would AVRT not be terminated with AV nodal blockade?

A

Antegrade/Retrograde conduction via two separate accessory pathways

45
Q

What is the treatment for asymptomatic patients with WPW?

A
  • 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
46
Q

In what situations is cardiac ablation of accessory pathway indicated / reasonable in asymptomatic patients with no documented tachycardia?

A

EP study demonstrates high risk features *conduction to ventricles in A-fib with shortest RR interval of < 250msec

47
Q

Accessory pathways can present in two ways?

A

Manifest -> producing a delta wave via antegrade conduction Concealed -> conducting retrograde only

48
Q

How to identify accessory pathway location in manifest pre-excitation?

A

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

49
Q

What are the indications for CCTA?

A

Symptomatic patients (typical angina) Low-to-Intermediate risk individuals

50
Q

What is the differential for wide complex tachycardia?

A
  • VT
  • SVT with aberrant conduction due to BBB
  • SVT with pre-excitation of teh ventricle due to antegrade conduction down an accessory pathway
51
Q

What should therapy be initiated for hypertriglyceridemia?

What are the first line therapies?

A
  • TG > 500
  • Fenofibrate or Niacin
    • Statins are second line
52
Q

Define Atrial tachycardia

A

-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

53
Q

Atrial tachycardia: -Diagnosis

A

-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.

54
Q

Atrial tachycardia: -Treatment

A

-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)

55
Q

EKG criteria: Left Anterior Fascicular Block (LAFB)

A

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

Medical (69 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions