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8. ECG > ECG tidbits > Flashcards

ECG tidbits Flashcards

1
Q

Q wave

A

first negative deflection preceding the R wave

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2
Q

R wave

A

first positive deflection associated with ventricular activation

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3
Q

S wave

A

first negative deflection following the R wave

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4
Q

Hyperkalemia pathophys of bradycardia

A

1) shifts resting membrane potential (RMP) to less negative value due to less intra vs extracellular gradient of K+, which also (as hyperK+ increases)

2) causes decrease in impulse conduction velocity of phase 0 (decreases Vmax) through myocardium, and

3) HyperK+ also decreases phase 3 (shortens repolarization) because increased extracellular K+ increases K+ conductance of Ikr channel currents causing more K+ to leave the cell – causes ST-T segement depression, peaked/tented T waves and shortens QT.

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5
Q

Aberration/Aberrancy

A

Abnormality of supraventricular impulse with abnormal or bizarre intraventricular conduction

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6
Q

Phasic aberrant ventricular conduction

A

temporary aberrant ventricular conduction or rate-dependent bundle branch block

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7
Q

Phase III aberrancy

A

early diastolic (tachycardia-dependent)

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8
Q

Phase IV aberrancy

A

late diastolic (bradycardia-depended)

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9
Q

Ashman’s phenomenon

A

when duration of refractory period is directly related to preceding cycle length (long-short). Long cycle length immediately before cycle terminating by aberrant QRS complex, usally RBBB morphology b/c refractory period of RB > LB (only with Afib?)

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10
Q

Chung’s phenomenon

A

premature complex causes atrial aberrant conduction may be manifested by wider, lower-amplitude p-wave

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11
Q

Acceleration-dependent (tachycardia-dependent) aberrancy

A

delayed ventricular conduction following APC (same as phase III aberrancy?)

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12
Q

Supranormal conduction

A

conduction better than expected of an APC

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13
Q

Decceleration-dependent (bradycardia-dependent)

A

aberrancy following longer interval (same as phase IV aberrancy?)

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14
Q

Concealed conduction

A

: Partial penetration of a sinus or ectopic impulse in the AV junction (Tilley) OR phenomenon of incomplete cardiac impulse conduction through specialized conduction tissue (AVN).

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15
Q

Retrograde impulse transmission of VPC into the AV node may cause

A

1) conduction delay,
2) conduction block,
3) pacemaker displacement,
4) enhanced conduction,
5) any combination (Moise)

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16
Q

Parasystole

A

arrhythmias characterized by,
1) varying coupling interval b/t ectopic (parasystolic) complex and dominant sinus complex,
2) common minimal time interval b/t interectopic intervals (longer interectopic intervals representing multiples of minimal interval) ectopic impulse independent of and “protected” from discharge by dominant sinus rhythm,
3) fusion complexes

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17
Q

Noncompensatory pause

A

when R-R interval encompassing an ectopic beat is less than R-R interval of 3 consecutive sinus beats – cause by retrograde conduction of ectopic beat resetting the sinus node – usually follows APC

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18
Q

Compensatory pause

A

R-R interval encompassing the ectopic beat is more than 2x normally conducted R-R interval. When ectopic focus does not travel retrograde and does not reset the sinus node and sinus rhythm continues undisturbed – usually follow VPC.

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19
Q

Re-entry

A

pathway where original impulse can return to re-excite part or all of the heart

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20
Q

Criteria for re-entry

A

3 criteria exist:
1) must be at least two conduction pathways (AV jxn or accessory pathway),

2) Pathways must have different conduction rates,

3) conduction block must occur in one direction at some time during reciprocal sequence (Tilley)

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21
Q

Types of accessory pathways

A

Bundles of Kent: accessory AV connections

James fibers’: AV nodal bypass tracts (associated with LGL syndrome)

Mahaim’s fibers: nodoventricular tracts

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22
Q

Accessory pathway syndromes

A

Lown-Ganong-Levine Syndrome (LGL): if atrial impulse conducted over James’ bypass fibers, short P-R interval with QRS complex of normal duration results (no delta wave)

Wolff-Parkinson-White Syndrome: paroxysmal tachycardia associated with ventricular pre-excitation

23
Q

Pre excitation

A

Delta wave: slurred/notched upstroke of widened QRS

24
Q

U wave

A

U-wave: (u-wave and large t-waves) associated with toxicity from class III antiarrhythmic drugs, heterogeneity of repolarization, positive deflection following t-wave. Repolarization of His-Purkinje cells

25
Q

J point

A

where QRS complex joins the ST segment

NEGATIVE deflection at this point indicates subendocardial ischemia of LV

26
Q

Osborn wave

A

POSITIVE deflection occurring between QRS complex and ST segment. Causes include hypothermia, hypercalcemia, brain injury, others

27
Q

Epsilon wave

A

Often occurs with ARVC/D in humans – terminal notch in QRS complex d/t slowed intraventricular conduction

28
Q

Shortened Q-T

A

associated with digoxin toxicity, hypercalcemia or hyperkalemia

29
Q

notched/sloppy R-wave descent

A

“MIMI” (microscopic intramural myocardial infarction)

30
Q

Sinoventricular rhythm

A

SA node continues to fire and impulse transmitted via internodal pathways to AV jxn and ventricles (e.g., hyperkalemia)

31
Q

Low R-wave amplitude DDX

A

pericardial effusion, pleural effusion, obesity, hypothyroidism, severe pulmonary dz, hypoalbuminemia (per Bruce Keene), pneumothorax, PTI, variations in blood viscosity and blood volume, malnutrition (ECGoftheMonth 1April2007

32
Q

Ventriculophasic sinus arrhythmia

A

when P-P’ intervals that encompass a QRS complex are shorter then P’-P intervals that do not encompass a QRS complex – may develop with 2nd AVB, complete AVB or with VPCs and full compensatory pause

33
Q

Ventriculophasic sinus arrhythmia pathophys

A

may be explained by 1) Bainbridge reflex (ECG of the Month JAVMA Sept 15 2011). Bainbridge reflex results in vagal inhibition with acceleration of SAN discharge OR

2) Ventricular contraction produces an increase in coronary blood supply to SAN, which accelerates the SAN discharge (Tilley).

34
Q

Decremental conduction

A

progressive decrease in conduction velocity when impulse enters region of slow conduction. Or: increased conduction time with increasing prematurity of a stimulus (Moise).

35
Q

Bix rule

A

States that atrial flutter should be suspected when P -wave (NOT T-wave per Moise) is equally spaced between two R-waves

36
Q

Use-dependency

A

greater antiarrhythmic effect of a drug with faster HR, reverse use-dependency = opposite: decreased affect at higher HR

37
Q

Dobies

A

Dobermans typically have deep Q-waves and widened R-waves

38
Q

Dogs w/ LBBB

A

should not have large q-wave

39
Q

Dogs w/ VSD

A

can have a Q-wave that is wide or contains high-frequency notching d/t abnormal early septal activation

40
Q

Dogs w/ TVD

A

splintered QRS complex

41
Q

Overdrive Suppression

A

prolonged suppression of SAN pacemaker cells proportional to rate and duration of a more rapidly discharging pacemaker (e.g., SSS) d/t increased activation of Na/K ATPase thus creating net outward Na current (hyperpolarizes) that suppresses spontaneous impulse formation in subsidiary pacemaker cells.

42
Q

QRS alternans

A

common finding of SVT – often rate-dependent and not related to underlying mechanism of SVT (ECG of the Month 15 June 2008); probably secondary to alternating prolongation of the refractory phase of the heart (Tilley)

43
Q

Idioatrial rhythm

A

develops as a result of a combination of an accelerated ectopic atrial focus coupled with depression of sinus impulse formation or conduction (ECG of the Month 1July 2008)

44
Q

Brody effect

A

variation in amplitude of the R wave that develops with changes in the intracardiac blood volume

45
Q

AV dissociation (interference dissociation)

A

Per Katz: AV dissociation describes any condition that impairs impulse transmission from atria to ventricles, whereas AV block refers to AV dissociation that is caused by depressed/diseased conduction (E.g., AV dissoc = 2:1 PAT with block, AV block = 2:1 type II 2nd degree AV block)

atrial and ventricular rhythms that are independent of each other and NOT complete AVB
* never a primary rhythm disturbance
* AV dissociation DOES NOT mean complete AVB is present whereas complete AVB indicates AV dissociation is present
* In AV dissociation sinus rate is slower than ectopic focus rate (junction rate) opposite with complete AVB

46
Q

Complete AV dissociation

A

separate pacemaking foci independent of each other

47
Q

Incomplete AV dissociation

A

when SA node impulses occasionally conduct to ventricle

48
Q

Wenckebach periodicity

A

progressive prolongation of AV nodal (or SA nodal) conduction until block occurs

49
Q

Group beating

A

progressive prolongation of PR interval occurs by decreasing increments so when PP interval is constant, the decreasing increments in PR interval cause slight acceleration of ventricular rate (RR interval).

50
Q

ST segment elevation

A

ischemia vs epicarditis, pericarditis

51
Q

Concertina effect

A

In patients with pre-excitation, as HR increases (& cycle length shortens) QRS complexes progressively narrow meanwhile PR interval lengthens (changes in QRS morphology are due to variability of the ventricular zone that undergoes pre-excitation)

52
Q

Concealed junctional extrasystoles

A

extrasystolic discharge in AV junction with both antegrade and retrograde conduction block (silent on surface ECG, need His bundle electrograms to definitively dx). Dx important b/c dx can mimic Type I or II 2nd degree AV block.

53
Q

Concealed junctional extrasystoles surface ECG clues

A

1) abrupt, unexplained lengthening of PR interval,

2) presence of apparent type I and II 2nd-degree AVB in same tracing,

3) Apparent type II block w/ normal appearing QRS complex,

4) manifestation (unveiled) junctional extrasystoles elsewhere

8. ECG (21 decks)

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