8/5- Electrocardiography at the Bedside 2 Flashcards
Recap- Normal intervals:
- Normal PR interval:
- Normal QRS interval:
- Normal QTc interval:
- Normal PR interval: 3-5 small boxes = 120-200 ms
- Normal QRS interval: 2-3 small boxes = 80-120 ms
- Normal QTc interval: 9-11 small boxes = 360-440 ms
What may cause long PR?
Drugs
- Digoxin
- BB
- CCB
Ischemia or infarction;
Degeneration or calcification of AVN or His bundle
What may cause long QT?
- Drugs
- Electrolytes (low K, low Ca, or low Mg)
What are the ECG criteria for LVH? RVH? (Left/right ventricular hypertrophy)
Are these concentric or eccentric hypertrophy?
LVH:
- Left axis deviation
- R (V5/V6) + S (V1/V2) > 35 mm
RVH:
- Right axis deviation
- Tall R in V1/V2 (> 5 mm or R > S)
This is for concentric hypertrophy
What is this showing?
Left Ventricular Hypertrophy
- Deep S waves in V1 and V2
- Tall R waves in V5 and V6
What is this showing?
Right ventricular hypertrophy
- Right axis deviation “RAD” (from looking at leads 1 and aVF)
- Tall R in V1, V2: R>S or R > 5mm
(QRS are positive in V1 and V2!)
ECG signs of pressure vs. volume overload?
Pressure Overload:
- Concentric hypertrophy
- LVH or RVH
Volume Overload:
- Eccentric hypertrophy
- LBBB or RBBB
What are pathologic Q wave characteristics?
What are they indicative of?
- Small Q waves are normal in I, aVL, V5, and V6
Two features of pathologic Q waves
- Wider than 0.04 sec in duration
- Deeper than 1/3 of the R wave in same lead
Pathologic Q waves are indicative of old MI
Analyze this?
Pathologic Q waves
- Pathologic Q waves
- ST elevation
- Inverted T waves
What are some ST segment abnormalities (broadly)? What are these indicative of?
- ST depression: indicates sub-endocardial ischemia
- ST elevation: indicates acute myocardial infarction
What is the pathophysiologic difference between ST depression and ST elevation? on EKG?
What are the different types of ST segment depression?
- Downsloping
- Horizontal
- Upsloping
What is this showing?
Classical downsloping ST segment depression
- Lower than isoelectric line and keeps going down (Sub-endocardial ischemia)
ST depression most specific for sub-endocardial ischemia is:
A. Downsloping
B. Horizontal
C. Upsloping
ST depression most specific for sub-endocardial ischemia is:
A. Downsloping
B. Horizontal
C. Upsloping
What are some possible causes of ST segment elevation?
- Acute myocardial infarction
- Coronary vasospasm (Prinzmetal angina): artery only becomes smaller transiently as muscle of artery contracts
- Acute pericarditis
- Early repolarization
Differentiation of Acute MI and Pericarditis by ECG?
Acute MI:
- LOCALIZED ST elevation (only a few leads)
- Pathologic Q waves
- NO PR depression
Acute Pericarditis (inflammation throughout pericardium):
- DIFFUSE ST elevation
- NO pathologic Q waves
- PR depression
What is shown here?
Acute Anterolateral Myocardial Infraction
- ST segment elevations in leads I, aVL, and V2-V6
- Very marked elevation
What is shown here?
Acute Pericarditis
- Diffuse ST segment elevation in all ECG leads
- More subtle elevation
What is shown here?
PR segment depression in acute pericarditis
- Depressed PR segments between P and QRS
3 characteristics of Evolving Infarction?
- Pathologic Q waves
- ST elevation
- Inverted T waves
Evolution of Myocardial Infarction (EKG)
Characteristics that determine which phase of evolution the myocardial infarction is in?
- Acute MI:
- Evolving MI:
- Old MI:
- Acute MI: ST elevation ONLY
- Evolving MI: ST elevation AND T wave inversion or pathologic Q waves
- Old MI: pathologic Q waves only (never goes away)
(ST elevation typically subsides in 2-3 days; if it persists more than 14 days, should suspect ventricular aneurysm –)
(T wave normalization is variable… days or never)
Steps in evolution of myocardial infarction? Recovery?
- ST segment is elevated immediately
- Pathologic Q waves and T wave inversions appear at 8-12 hours
- ST segments normalize in 2-14 days
- Pathologic Q waves stay usually indefinitely
- T wave inversions are highly variable
In what conditions do we see T wave inversions?
- Myocardial ischemia
- LVH or RVH (called strain changes)
- LBBB or RBBB
- Digoxin (called digoxin effect)
*NOT specific for sub-endocardial ischemia
What characterizes “tall” T waves?
In what conditions do we see tall T waves?
T waves > 10mm in at least 2 chest leads
- Myocardial ischemia
- Acute myocardial infarction
- Hyperkalemia!!
What is this showing?
Progression of R waves in precordial leads
Steps in abnormal R wave progression?
- Early R/S transition:
- Late R/S transition:
Early R/S transition: bigger R waves in V1 and V2
Later R/S transition: smaller R waves in V5 and V6
(resulting in overall negative QRS complex)
Tall R waves in V1 and/or V2 may be present in which conditions/diseases?
- Old posterior myocardial infarction
- Right ventricular hypertrophy (RVH)
- Right bundle branch block (RBBB)
- Wolf-Parkinson-White (WPW)
- Duchenne muscular dystrophy
LVH ECG Criteria?
R (V5/V6) + S (V1/V2) > 35
and
LAD
RVH ECG Criteria?
R > 5 or R/S > 1 in V1/2
and
RAD
Pathologic Q waves are characterized how?
Indicative of?
Q > 0.04 ms or > 1/3 of R wave
- Indicative of OLD myocardial infarction
ST elevation seen in what conditions?
AMI, pericarditis or spasm
- Acute pericarditis if diffuse ST elevation, no pathologic Q waves, depressed PR
ST depression seen in what conditions?
ischemia (horizontal or downsloping ST); otherwise nonspecific
Peaked T is caused by what?
High K, AMI, or ischemia
Tall R in V1 is caused by what?
Post MI, RVH, RBBB, and WPW
Pathologic Q waves are characterized by all of the following except?
A.
-
