B P3 C14 ECG Flashcards
Pulmonary embolism causing acute RV pressure overload may generate characteristic ECG patterns including:
QR or qR pattern in the right sided leads
S1Q3T3 pattern
ST-segment deviation and T wave inversions in leads V1 to V3
Incomplete or complete RBBB.
Left Anterior Fascicular Block
Frontal plane mean QRS axis between −45 and −90 degrees
qR pattern in lead aVL
QRS duration <120 msec
Time to peak R wave in aVL ≥ 45 msec
Left Posterior Fascicular Block
Frontal plane mean QRS axis >90 degrees (or >110–120 degrees)
rS pattern in leads I and aVL with qR patterns in leads III and aVF
QRS duration <120 msec
Exclusion of other factors causing right axis deviation
CLBBB
- QRS duration ≥120 msec
- Broad, notched, or slurred R waves in leads I, aVL, V5, and V6
- Small or absent initial r waves in leads V1 and V2 followed by deep S waves
- Absent septal q waves in leads I, V5, and V6
- Prolonged time to peak R wave (>60 msec) in V5 and V6
CRBBB
QRS duration ≥120 msec
rsr′, rsR′, or rSR′, patterns in leads V1 and V2
S waves in leads I and V6 ≥40 msec wide
Normal time to peak R wave in leads V5 and V6 but >50 msec in V1
Most common pattern of bifascicular block
RBBB + LAFB
Conduction delay in the RBB plus delay in either the main LBB or in both the left anterior and the left posterior fascicle
Trifascicular block
ECG pattern of trifascicular block
Bifascicular block + evidence of prolonged conduction below the AV node
Occasionally the ECG in acute coronary syndromes involving the occlusion of the left anterior descending (LAD) coronary will show a paradoxical combination of ST depressions and prominent T waves, especially in the precordial leads, sometimes now referred to as _____
DeWinter’s sign
Necrosis of sufficient myocardial tissue can lead to _____ as a result of loss of electromotive forces in the infarcted area
Decreased R wave amplitude
or
Frank Q waves (typically >30 to 40 msec in duration in multiple leads)
Earliest ECG manifestations of STEMI.
Ischemic ST-segment elevation and hyperacute T wave changes
This development usually reflects spontaneous recanalization or good collateral circulation and is a positive prognostic sign.
Complete normalization of the ECG after Q wave infarction
Correlate strongly with severe underlying wall motion disorders (akinetic or dyskinetic zone), although not necessarily a frank ventricular aneurysm.
Persistent Q waves and ST- segment elevation seen several weeks or more after infarction
The presence of an _____ or similar type of multiphasic complex in the mid-left chest leads or lead I is another reported marker of an LV aneurysm
rSr′ pattern
Classic ECG marker of Prinzmetal’s variant (vasospastic) angina
Transient ST-segment elevation
ECG sign/patter in some patients with ischemic chest pain exhibit deep coronary T wave inversions in multiple precordial leads (e.g.,V1 through V4, I, and aVL), with or without cardiac biomarker level elevations.
LAD–T wave or Wellens’ pattern
Exercise-induced transient inversion of precordial U waves has been correlated with severe stenosis of the _____ coronary artery
LAD
_____ U waves are uncommon and are strongly associated with adverse cardiac events.
Negative U waves
Diagnostic criteria for early repolarization
(1) Prominent notch or J wave at the end of QRS complex or slur on the downstroke of the R wave
(2) Peak of the notch or J wave is 0.1 mV or greater in amplitude in two or more contiguous leads, excluding V1 to V3 (to avoid cases of Brugada pattern)
(3) QRS duration is normal
The sequence of LV endocardial activation, begins at three sites on the left side of the septum:
(1) Anterior paraseptal wall
(2) Posterior paraseptal wall
(3) Center of the left side of the septum
Ventricular septal activation begins on the left side and spreads across the septum from _____.
Left to right and from apex to base
Atrial activation begins with impulse generation in the atrial pacemaker complex in or near the sinoatrial node. Once the impulse leaves this pacemaker site, atrial activation proceeds _____ toward the lower portion of the right atrium (RA) and the AV node.
Anteriorly and inferiorly
This wave is generated by activation of the atria
P wave
This interval corresponds to the duration of atrioventricular (AV) conduction
PR interval
This wave is produced by the activation of the two ventricles
QRS complex
This wave reflects ventricular recovery.
ST-T wave
Normal Upper Limits for Durations of Electrocardiogram Waves and Intervals in Adults
P wave duration
PR interval
QRS duration
QT interval c (corrected)
P wave duration <120
PR interval <200
QRS duration <110-120
QT interval c (corrected) </= 440-450
Analysis of beat-to-beat changes in heart rate and related dynamics is termed ______
Heart rate variability
T wave inversion in leads V 1 to V 3 (sometimes referred to as the ________) is common among children and adolescents and in 1% to 3% of apparently healthy adults.
Persistent juvenile pattern
Diagnostic criteria for LAA
Prolonged P wave duration to >120 msec in lead II
Prominent notching of P wave, usually most obvious in lead II, with interval between notches of >40 msec
Ratio between duration of P wave in lead II and duration of PR segment >1.6
Increased duration and depth of terminal-negative portion of P wave in lead V 1 (P terminal force) so that the area subtended by it is >0.04 mm-sec
Leftward shift of mean P wave axis to between −30 and −45 degrees
Diagnostic criteria for RAA
Peaked P waves with amplitudes in lead II to >0.25 mV
Prominent initial positivity in lead V1 or V2 >0.15 mV
Increased area under initial positive portion of P wave in lead V1 to >0.06 mm-sec
Rightward shift of mean P wave axis to >+75 degrees
Diagnostic criteria for LVH
Sokolow-Lyon voltages:
SV 1 + RV 5 >3.5 mV
RaVL >1.1 mV
Cornell Voltage criteria:
SV 3 + RaVL >2.8 mV (for men)
SV 3 + RaVL >2.0 mV (for women)
Diagnostic criteria for RVH
Tall R in V 1 > 0.6 mV
Increased R/S in V 1 > 1
Deep S in V 5 > 1.0 mV
Deep S in V 6 > 0.3 mV
Differential diagnosis of tall R wave in V1
Displacement of heart toward right side of chest (dextroversion), congenital or acquired
Lateral or “true posterior” myocardial infarction
Duchenne muscular dystrophy
RVH (usually with right axis deviation)
Right ventricular conduction abnormalities
WPW patterns (caused by posterior or lateral wall preexcitation)
Localize
ST segment elevation (V1through V6) and/or in leads I and aVL
ST segment elevation V1 - V3
ST segment elevation V4-V6
ST segment elevation II, III, aVF
Right sided leads
ST segment elevation (V1through V6) and/or in leads I and aVL - acute transmural anterior or severe anterolateral wall ischemia
ST segment elevation V1 - V3 - anteroseptal or apical ischemia
ST segment elevation V4-V6 - apical or lateral ischemia
ST segment elevation II, III, aVF - inferior wall ischemia
Right sided leads - RV ischemia
ST-segment elevation in leads placed over the back of the heart, such as leads V7-V9
Posterior or posterolateral wall infarction
Posterior wall infarction can produce both inferior and posterolateral injuries, which may be indirectly recognized by reciprocal __________
ST-segment depression in leads V1 to V3.
Identify the culprit
ST-segment elevation in lead III exceeding that in lead II, particularly combined with ST-elevation in lead V 1(and additional right-sided chest leads)
Occlusion in the proximal to midportion of the RCA
Identify the culprit
The presence of ST-segment elevation in lead II equal to or exceeding that in lead III, especially in concert with ST-segment depressions in leads V 1 to V 3 or ST-segment elevation in leads I and aVL
Occlusion of the LCA or a distal occlusion of a dominant RCA.
________ should be considered when leads aVR and V1 show ST-segment elevation, especially in concert with diffuse prominent STsegment depression in other leads.
Left main (or severe multivessel) coronary artery disease
Differential Diagnosis of Noninfarction Q Waves
LBBB (slow R wave progression*)
WPW patterns
Differential Diagnosis of ST-Segment Elevation
Myocardial ischemia or infarction
Acute pericarditis
Brugada pattern (RBBB-like pattern and ST-segment elevations in right precordial leads)
Differential diagnosis of Deep T waves
CVA
Apical HCM
Takotsubo syndrome
Memory T waves - describe repolarization changes after depolarization changes caused by ventricular pacing, intermittent LBBB, intermittent WPW preexcitation, and other alterations of ventricular activation
________ refers to the relatively distinctive “scooped” appearance of the ST-T complex and shortening of the QT interval, which correlates with abbreviation of the ventricular action potential duration
Digitalis effect
Digitalis-related ST-T changes can be accentuated by an increased heart rate during exercise, with consequent ______ on stress testing
False-positive results
______ refers specifically to systemic effects (e.g., nausea, anorexia) or conduction disturbances and arrhythmias caused by drug excess or increased sensitivity.
Digitalis toxicity
Effects of Class 1A, Class III, Class 1A-like drugs
QRS and QT(U) prolongation
Effects of metabolic abnormalities
Hypercalcemia
Hypocalcemia
Hypercalcemia - shortened QT (shortens the ventricular action potential duration by shortening phase 2)
Hypocalemia - prolonged QT (prolongs phase 2)
Severe hypercalcemia (e.g., serum Ca 2+ >15 mg/dL) also can be associated with decreased T wave amplitude, sometimes with T wave notching; high takeoff of the J point/ST segment in leads V 1and V 2
Effects of hyperkalemia and hypokalemia
Hyperkalemia - narrowing and peaking (or tenting) of the T wave; QT interval is shortened; QRS begins to widen, and P wave amplitude decreases. PR interval prolongation; asystole, sometimes preceded by a slow undulatory (or sine wave) ventricular flutter-like pattern; occasionally induces ST e tions in the right precordial leads (V 1and V2)
Hypokalemia - ST depression with flattened T waves and increased U wave prominence
