ECG Flashcards
List the limb lead interpretations:
I → left ventricle, lateral wall
II, III, and aVF → left ventricle, inferior wall (inferior ECG leads)
aVL → left ventricle, high part of the lateral wall
aVR → reciprocal of the left lateral side leads (II, aVL, V5 and V6)
List the precordial interpretations:
V1 and V2 → both ventricles, anterior wall
V3 and V4 → anterior wall of the left ventricle and parts of the septum
V5 and V6 → lateral wall of the left ventricle and apex of the heart
What is usually the paper speed of an ECG?
A paper speed of 25 mm/s 10mm/mVolts is usually used –> 1 mm = 0.04 s = one square
- -> one small box is 40msecs
- -> one big box (with five small) is 200msecs
- -> 10 mm vertically equals 1 mvolts
How to measure amplitude in ECG?
1 mm (vertical) = 0.1 mV = one square
How to measure HR from ECG?
If the QRS rhythm is regular (see determination of the heart rhythm below), then the heart rate can be estimated by dividing 300 by the number of large (5 mm) squares between successive QRS complexes,
How is the heart rhythm assessed on an ECG?
The heart rhythm is assessed by evaluating the frequency, regularity, and relationships between the P waves and QRS complexes.
What is the usual and abnormal QRS duration?
Normal duration: 0.07–0.10 seconds
Wide QRS: > 0.12 seconds or 3 small squares
What is a criteria for sinus rhythm?
Normal morphology of the P waves
A regular QRS complex follows every P wave.
Normal, constant PP and RR intervals
What leads can be used to make a rapid approximation of the axis?
A rapid approximation of the axis may be made by assessing the QRS complexes in leads I and aVF
List the coordinates for each limb leads:
I - 0 II - 60 III - 120 AvL - -30 AvF - 90 AvR - -150
What are the coordinates for left axis deviation?
-30 to -90 (only positive on lead I)
What are the coordinates for right axis deviation?
90 to 180 (only positive for aVF)
What are the coordinates for extreme right axis deviation?
-90 to -180 (I and aVF neg)
What are the coordinates for normal axis?
-30 to 90
What are the three causes of LAD?
Normal variant
Left anterior fascicular block
Left ventricular hypertrophy (rarely with LVH; usually axis is normal)
What are the causes of RAD?
Normal variant Right bundle branch block Right ventricular hypertrophy Left posterior fascicular block Dextrocardia
Where are p waves generated and seen in which leads?
Sinus node –> II, III, avF
What do an absence of p wave and an irregular rhythm indicate?
Atrial fibrillation (irregular irregular) Atrial flutter with variable block
What do an absence of p wave and a regular rhythm indicate?
May hidden retrograde p wave as seen in:
- supraventricular tachycardias
- ventricular tachycardia
How many boxes should a QRS be?
3 small boxes
What does a wide QRS usually indicate?
- bundle branch block
- ventricular tachycardia???
How many boxes is the PR segment?
5 small boxes
What can cause a long PR segment?
- increased vagal tone
- AV block
What is the effect of sympathetics on PR segment?
- shortened PR
What prolongs and shortens the QT segment?
Prolongs:
- hypocalcemia (tetany, numbness, spasms)
- antiarrythmics
Shortens:
- hypercalcemia (confusion; constipation)
What happens to T waves in ischemia?
Early ischemia: peaked T
Late ischemia : inverted T
What flattens T waves and introduces U waves?
hypokalemia
What is indicated by a ST depression?
subendocardial ischemia (NSTEMI)
What is indicated by a ST elevation?
transmural ischemia (STEMI/pericarditis)
What features can be seen in RBBB?
High QRS on V1, inverted T on V4, wide QRS
What features are present in LBBB?
High negative QRS, wide QRS, T inversion and positive elevations
What feature is noticeable in atrial flutter ECG?
v^v^v^v —> saw-tooth pattern in every single lead
What is indicated by wide QRS complexes that are close to each other (happening fast consecutively) with infrequent bumps in between them?
Ventricular tachycardia
bumps –> p wave
What kind of pattern is noticed in Torsades de Pointes?
Sinusoidal
Who is at increased risk for TdP?
Those with prolongues QT intervals bc of
- antiarrhythmic drugs
- congenital long QT syndromes
- antibiotics (erythro, quiniolones)
- hypokalemia
- hypomagnesemia
What can be seen in a PVC (premature ventricular contraction)?
Wide weird looking and sudden QRS
What happens in an ECG for a premature atrial contraction (PAC)?
- normal looking QRS that suddenly appears and is out of sync from the rhythm
What clue might indicate there was a limb lead reversal?
aVR is positive
usually negative because aVR looks away from usual atrial/ventricular traffic
How to calculate HR from ECG?
For Regular:
300 divided by the number of large boxes between two Rs
For Irregular:
multiply the number of R-R segments in 10 seconds (ie. 50 large boxes) by 6
T or F: sinus rhythm and normal sinus rhythm are not the same
T:
sinus rhythm just means that the HR is controlled by the sinus node (and does not specify about the rest of conduction)
What is normal sinus rhythm?
- has sinus rhythm (ie. lead I and II have positive P waves)
- every Q wave follows a QRS
- every QRS preceded by P wave
- PR interval less 0.12 - .2 seconds (ie. three to five small boxes)
- 60-100 beats per minute
What is the PR interval?
beginning of P wave to beginning of R wave
What would you see with a ectopic atrial rhythm?
inverted P wave - non-sinus rhythm
What would you expect to see in atrial fibrillation?
F-waves: no true p-waves but rather several small undulations
What is a quick way to see if axis is normal?
if QRS in leads I and II positive then normal
If lead I positive and lead II negative, what kind of axis is it?
left axis deviation (lead currents are leaving each other)
If lead I negative and lead II positive, what kind of axis is it?
right axis deviation
If both lead I and lead II are negative then what?
extreme axis deviation
What is the systematic way of interpreting ECGs?
- Calibration
- Rate
- Rhythm
- Axis
- Intervals
- Hypertrophy
- Infarcts
- ST elevation / ST depression
- T wave abnormalities
How long should QRS be?
less than .12ms (or less than 3 boxes)
What is the PR interval?
Time from atrial activation to ventricular activation (ie. beginning of Q wave)
What usually causes prolonged QRS?
bundle branch blocks, accessory bypass tracks, or non-specific QRS widening
What is QT internal?
beginning of ventricle depol. to end of ventricle repol.
roughly the length of ventricular systole
QTs are usually less than 50% of R-R interval
What would you expect for a right atrial hypertrophy?
Prominent right atrial P-wave waves at V1 >1.5 mm
Inferior leads –> large P waves (at lead II) >2.5 mm
(ie. II, III and aVF)
V1 sees large P wave
What would you expect for a left atrial hypertrophy?
Inferior leads at lead II –> long, notched P waves (RA, then LA firing) [like M shape] >110ms or >40ms peak to peak
V1 sees large late -ve P wave (more than 1 by 1 square)
What would you expect for a right ventricular hypertrophy?
Prominent right-sided R waves (V1)
R > S in V1 or R >7mm
Prominent left-sided S waves (V1)
RV strain pattern = ‘hockey stick’ ST/T changes
–> down-sloping ST depression (if upright QRS)=‘hockey stick’
–> up-sloping ST elevation (if down-going QRS)
–> Right axis deviation
What ECG features would be seen for a RBBB?
QRS > .12 secs (ie. 3 boxes)
V1 has rsr’, rsR’, rSR’, ‘bunny ears’ on right
Slurred S wave on left leads I and V6
–> fat, wide S wave
Due to : late depolarization of RV
slow, via ‘back alley’ cell conduction
What ECG features would be seen for a LBBB?
QRS > .12 sec (ie. three boxes)
V1-V3 either rS or QS
V6 Broad or notched R. bunny ears’ on left
No q waves in V5/6, I
What happens to conduction in an accessory tract or Wolff-Parkinson White Pathway?
fires ventricle early, but via slow ‘back alley’ working class muscle cells
- -> a normal QRS and a SLOW bypass activated QRS are initiated
- -> results in initial wide QRS = ‘delta wave’
- -> PR interval < 3 small squares = shortened
what is a Non-specific QRS widening?
Non-specific Intra-ventricular conduction delay
= No clear left / right bundle / no delta waves
How to calculate corrected QT?
QT (in seconds)/ (root of R-R interval)
What is normal QT?
in M, normal QTc <460ms
in F, normal QTc <480ms
What would you expect for a left ventricular hypertrophy?
Prominent left-sided R waves (V5,6)
Prominent right-sided S waves (V1)
__________________________
S in V1 + R in V5 or V6 ≥ 35 mm
R in aVL > 11 mm (9mm for females)
R in aVL + S in V3 >25mm (>20mm in females)
What kind of ECG feature is found for heart infarcts?
Q-waves:
at least 2 side-by-side leads
>40ms / 1mm wide (ie. one small box)
> ¼ of height of R wave
***Sometimes Q-wave in V1 OR V2 ALONE is enough to tell you there’s been a Septal infarct (1 lead with Q-wave is enough for V1,2)
R waves > S wave V1,2 suggest possible posterior infarct (can be RVH, normal variant, massive septal hypertrophy etc.)
***
What are the lead territories?
Lateral LV --> I, aVL Inferior LV --> II, III, aVF Septal LV --> V1,2 Mid Anterior LV --> V3,4 Antero-lateral LV --> V5,6 Posterior LV --> V8,9
What kind of ECG is noticed for sub-endocardial ischemia (NSTEMI)?
Marked ST depression + T waves abnormal
Why?–> diastolic theory: the ischemic cells in inner myocardium have more positive resting potential than neighboring outer myocardium cells –> so the current is from + ischemic to more negative normal cells (right, left, behind) which is the same direction of lead –> elevated PR segment (and the rest appears depressed)
or systolic theory: ischemic cells are less positive than normal cells during systole (ie. plateau phase) –> so away from lead –> ST depression
What kind of ECG is noticed for trans-mural ischemia (STEMI)?
ST elevation
Why?–> diastolic theory: the ischemic cells have more positive resting potential than neighboring cells –> so the current is from + ischemic to more negative normal cells (right, left, behind) which is opposite to the direction of lead –> depressed PR segment and the rest looks elevated
systolic theory: normal cells more positive than ischemic –> current from normal to ischemic –> same direction as lead –> ST elevation
If full thickness ischemia, when does the heart start to infarct?
After 20 minutes –> ST elevation
What is pathological ST elevation?
at least 2 side-by-side leads
>1-2mm elevation above P-R baseline
> usually convex upwards (‘tombstone’)
What is the ECG feature evolution in trans-mural MI?
- Basal state: ST segment at baseline
- “Hyperacute” T-waves (minutes)
- ST elevation (hours)
- Development of Q-waves, T inversion (1 to 2 days)
- ST normalizes, T wave inverted (days)
- ST & T normal, Q wave persists (weeks)
T or F: if there is a ST elevation at posterior leads there is mirror ECG with a ST depression at an anterior lead
T
Changes in inferior leads will have reciprocal changes in which leads?
lateral (ie lateral ST elevation = inferior ST depression)
If an anterior lead shows a ST depression, what could it be?
posterior STEMI
anterior NSTEMI
What would be clues for posterior STEMI?
1st hint would often be that there’s also acute inferior infarct (usually supplied by same coronary)
2nd hint is ST depression on opposite side of heart = V1,2
3rd hint would be Posterior Q waves starting = R>S in V1,2
Always try to get V8,9 to confirm!
T or F: ST elevations are specific to STEMI
F
can be seen in LVH (dominant –ve QRS in V1,2 with ‘strain pattern’ ‘hockey stick’ ST elevation common)
can be seen in pericarditis
can be seen as normal variant (young people with mild STE, large T waves)
T or F: T waves are specific to ischemia
F:
can be seen
metabolic changes (K+/Mg++/Ca++, pH, fever, etc.)
anything that affects depolarization (LVH, LBBB, pacemaker, WPW etc.)
For STEMI. reciprocal changes are always needed
F
