Abnormal Ecg Flashcards
Right atrial overload (acute or chronic)
increase in P-wave amplitude (≥2.5 mm)
tall, peaked P waves in the limb or precordial leads.
Left atrial overload
a biphasic P wave in V1 with a broad negative component or a broad (≥120 ms), often notched P wave in one or more limb leads
Right ventricular hypertrophy
due to a pressure load (as from pulmonic valve stenosis or pulmonary artery hypertension) is characterized by
- a relatively tall R wave in lead V1 (R ≥ S wave), usually - with right axis deviation
; alternatively,
- there may be a qR pattern in V1 or V3R.
- ST depression and T-wave inversion in the
right to midprecordial leads are also often present.
This pattern, formerly called right ventricular “strain,” is
attributed to repolarization abnormalities in acutely or
chronically overloaded muscle. Prominent S waves may occur in the left lateral precordial leads.
.
Right ventricular hypertrophy due to ostium secundum–type atrial septal defects, with the accompanying right ventricular
volume overload, is commonly associated with an
incomplete or complete right bundle branch block pattern with a rightward QRS axis.
Acute cor pulmonale
e due to pulmonary embolism, for example, may be associated with a normal ECG or a
variety of abnormalities.
Sinus tachycardia is the most
common arrhythmia, although other tachyarrhythmias,
such as atrial fibrillation or flutter, may occur.
The QRS axis may shift to the right, sometimes in concert with the so-called S1Q3T3 pattern (prominence of the S wave in lead I, Q wave in lead III, with T-wave inversion in lead III).
Acute right ventricular dilation may also be
associated with slow R-wave progression and T-wave
inversions in V1–V4 simulating acute anterior infarction. A right ventricular conduction disturbance may
appear.
Chronic cor pulmonale
due to obstructive lung disease
usually does not produce the classic ECG
patterns of right ventricular hypertrophy noted above.
Instead of tall right precordial R waves, chronic lung
disease more typically is associated with small R waves
in right-to-midprecordial leads (slow R-wave progression) due in part to downward displacement of the diaphragm and the heart.
Low-voltage complexes are commonly present, owing to hyperaeration of the lungs
Left ventricular hypertrophy (LVH) increases the
amplitude of electrical forces directed to the left and posteriorly. In addition, repolarization abnormalities may cause ST-segment depression and T-wave inversion in leads with a prominent R wave. Right ventricular hypertrophy (RVH) may
shift the QRS vector to the right; this effect usually is associated with an R, RS, or qR complex in lead V1.
T-wave inversions may be present in right precordial leads
voltage criteria for left ventricular hyperthrophy
on the basis of the presence of tall left precordial R waves and deep right precordial S waves [e.g., SV1 + (RV5 or RV6)>35 mm].
Repolarization abnormalities (ST depression with T-wave inversions, formerly called the left ventricular “strain” pattern) may also appear in leads with prominent R waves.
However, prominent precordial
voltages may occur as a normal variant, especially in athletic or young individuals.
Left ventricular hypertrophy may increase limb lead voltage with or without increased precordial voltage (e.g., RaVL + SV3 > 20 mm in women and >28 mm in men).
The presence of left atrial abnormality increases the likelihood of underlying left ventricular hypertrophy in cases with borderline voltage criteria. (why??)
Left ventricular hypertrophy often progresses
to incomplete or complete left bundle branch
block.The sensitivity of conventional voltage criteria for
left ventricular hypertrophy is decreased in obese persons and in smokers. ECG evidence for left ventricular hypertrophy is a major noninvasive marker of increased
risk of cardiovascular morbidity and mortality, including
sudden cardiac death.
However, because of false-positive
and false-negative diagnoses, the ECG is of limited utility in diagnosing atrial or ventricular enlargement. More definitive information is provided by echocardiography
Complete bundle branch blocks
QRS interval cardiovascular morbidity and mortality: coronary heart disease (frequently with impaired left ventricular function),
hypertensive heart disease,
aortic valve disease, and
cardiomyopathy.
Bundle branch blocks may be
chronic or intermittent. A bundle branch block may be rate related; for example, it often occurs when the heart rate exceeds some critical value
Bundle branch blocks and depolarization abnormalities
secondary to artificial pacemakers not only affect
ventricular depolarization (QRS) but are also characteristically associated with secondary repolarization (ST-T) abnormalities T wave is typically opposite in polarity to the last deflection of the QRS
This discordance of the QRS–T-wave vectors
is caused by
the altered sequence of repolarization that
occurs secondary to altered depolarization.
primary repolarization abnormalities are independent of QRS changes and are related instead to
actual alterations in the electrical properties of the myocardial fibers themselves (e.g., in the resting membrane potential or action potential duration), not just to changes in the sequence of repolarization
primary ST–T-wave changes
Ischemia, electrolyte imbalance, and drugs such
as digitalis
Brugada pattern
A distinctive abnormality simulating right bundle branch
block with ST-segment elevations in the right chest leads
Partial blocks (fascicular or “hemiblocks”) in the left bundle system (left anterior or posterior fascicular blocks) generally do not prolong the
QRS duration substantially
but instead are associated with shifts in the frontal plane QRS axis (leftward or rightward, respectively).
Examples of bifascicular block
right bundle
branch block and left posterior fascicular block, right
bundle branch block with left anterior fascicular block,
and complete left bundle branch block
Chronic bifascicular block in an asymptomatic individual is associated with a relatively
low risk of progression to high-degree
AV heart block
new bifascicular block
with acute anterior myocardial infarction
carries a much
greater risk of complete heart block. Alternation of right
and left bundle branch block is a sign of trifascicular disease
LEFT ATRIAL ABNORMALITY
Prolonged P wave duration of >120 msec in lead II
Prominent notching of the P wave, usually most obvious in lead II, with an interval between the notches of >40 msec (p mitrale)
Ratio between the duration of the P wave in lead II and the duration of the PR segment of >1.6
Increased duration and depth of the terminal negative portion of the P wave in lead V1 (the P terminal force) so that the area subtended by it exceeds 0.04 mm-sec
Leftward shift of the mean P wave axis to between -30 and +45 degrees
RIGHT ATRIAL ABNORMALITY
Peaked P waves with amplitudes over 250 muV in lead II (p pulmonale)
Rightward shift of the mean P wave axis to above 75 degrees
Increased area under the initial positive portion of the P wave in lead V1 to >0.06 mm-sec
In patients with cardiac disease, the ECG finding of LVH correlates with more severe disease, including
higher blood pressure in hypertensives and greater ventricular
dysfunction in patients with hypertension or coronary artery disease.
In contrast, effective treatment of hypertension reduces ECG evidence of LVH and decreases
the associated risk of cardiovascular mortality.[61]
Patients with repolarization abnormalities have, on average, more severe degrees of LVH and more commonly have symptoms of left ventricular dysfunction, in addition to a greater risk of cardiovascular events.[61
Chronic obstructive pulmonary disease can induce ECG changes by producing
RVH, changes in the position of the heart within the chest, and hyperinflation of the lungs . QRS changes caused by the insulating and positional changes produced by hyperinflation of the lungs include reduced amplitude of the QRS complex, right axis deviation in the frontal plane, and delayed transition in the precordial leads (probably reflecting a vertical and caudal shift in heart position because of hyperinflation and a flattened diaphragm). Evidence of true RVH includes (1) marked right axis deviation (more positive than 110 degrees), (2) deep S waves in the lateral precordial leads
LEFT ANTERIOR FASCICULAR BLOCK
Frontal plane mean QRS axis of -45 to -90 degrees with rS patterns in leads II, III, and aVf
and a qR pattern in lead aVl
QRS duration less than 120 msec
LEFT POSTERIOR FASCICULAR BLOCK
Frontal plane mean QRS axis of 120 degrees RS pattern in leads I and aVl with qR patterns in inferior leads QRS duration of less than 120 msec Exclusion of other factors causing right axis deviation (e.g., right ventricular overload patterns, lateral infarction)
COMPLETE LEFT BUNDLE BRANCH BLOCK
QRS duration 120 msec
Broad, notched R waves in lateral precordial leads (V5 and V6 ) and usually leads I and aVl
Small or absent initial r waves in right precordial leads (V1 and V2 ) followed by deep S waves
Absent septal q waves in left-sided leads
Prolonged intrinsicoid deflection (>60 msec) in V5 and V6
COMPLETE RIGHT BUNDLE BRANCH BLOCK
QRS duration
120 msec
Broad, notched R waves (rsr
, rsR
, or rSR
patterns) in right precordial leads (V1 and V2 )
Wide and deep S waves in left precordial leads (V5 and V6 )
Criteria derived from the QRS complex are due to
both the high incidence of RVH when RAE is present , and the RV dispalcement by an enlarged right atrium
