12. EKG introduction Flashcards
Know this this
know image
ECG waveforms
know this
ECG with heart tracings:
helps with readings
Just for reference
Cardiac conduction: to get your bearings
just FYI
Action potentials for Cardiac Myocytes
image from slide 3
Direction of electrical current flow by convention is from:
negatively to positively charged areas
At rest, cell surface is _____ charged
With depolarization, outside of cell becomes ____
Positive
Negatively
Direction of current outside cell moves toward the positive electrode of voltmeter during depolarization thus we see ______ defleciton
positive deflection
(refer to A and B)
When charge on outside surface of cell is homegenous there is no potential difference between positive and negative electrodes: we see volmeter at
zero
Refer to B
During repolarization of single cell, the end of cell initially depolarized is the _____ to repolarize thus current moves _____ to _____, away from positve electrode volemeter and registers negative deflection
First to depolarize
Negative to Positive
What is it that ECG is recording?
When depolarization spreads through the heart, each cell generates a force that can be measure in the skin
In an intact heart, sequence of repolarization is ______ to depolarization, as action potential duration is SHORTER near outer epicardium (last to depolarize)
OPPOSITE
Unlike single cell model, in double cell model, electircal deflection of depolarization and repolarization are usually oriented in
same direction
thus see + QRS and + T wave
What are my frontal referece limb leads?
Lead I, II, III
aVR, aVL, aVF
What are my 6 transverse/precordial leads?
V1- V6
Direction and magnitude of deflection on each lead depends on:
how cumulative electircal forces are aligned with the axes or leads
What are my unipolar leads?
no single negative pole/negative pole is composite reference of other avereaged leads:
aVR, aVF, aVL and V1-V6 are all unipolar
What do the aVR, aVL and aVF look like?
know these bitches
What do standard/bipolar limb leads look like?
Have single electrode as positive pole and a single electrode as negative reference
Einthovens Triangle
See image
Where is aVL on circle of Axes
-30 degress (upper right quad)
Where is lead I on circle of axes?
0 degrees, pointing right
Where is lead II on cirlce of axes?
+60 degrees (in lower right quad)
Whre is aVF in circle of axes?
+90 degrees (pointing directly down)
Where is Lead III on circle of axes?
+120 degress (in bottom left quad)
where is lead aVR on circle of axes?
-150 degrees (in upper left quad)
Electrical force directed toward + pole of a lead generates a ____ deflection
Force directed away from + pole results in _____ defelction
positive
negative
How is magnitude of deflection determined?
By how parellel electrical force is to the lead axis:
more parellel = GREATER magnitude of deflection in that lead
When forcei is perpendicular to a lead; get a flat line on recording
Sequence of events in cardiac depolarization
- Depolarize atria (starts at SA node)
- Depolarize setpum from L–> R
- Depolarize anteroseptal region of myocardium; towards apex
- Depolar bulk of ventricle myocardium… from ENDO to EPI
- Depolarize posterior part of base of Left ventricle
- Ventricles are now polarized
Inital septal depolarization is directed anteriorly:
left to right; toward V1 and away from V6
As lateral wall LV depolarized, electrical forces of thick LV outweigh RV and depolarization is directed:
leftward and posteriorly towards V6
Intially, as septal is depolarized we see a small _____ in V1 and small ____ in V6
As lateral wall depolarizes, we see a subsequent large ____ in V1 and large ____ in V6
small r in V1
small q in V2
large S in V1
large R in V6
Verticle axis measures _____ in standard 1mm = ___
Horizonal measures____ in 1mm = ____
voltage; 1mm= -.1mV
time; 1mm= 0.04 seconds
**IG use every 5th line = .2 seconds
What is normal hearth rhythm determined by
termed sinus rythm with intact AV conduction
initiated by depolarization of sinus node and conduction to ventricles
Normal EKG:
Every P followed by:
Upright P present in leads:
PR interval between:
followed by QRS
upright P in I, II, III
PR interval btwn 120 and 200 ms
LImits for bradycardia and sinus tachycardia
bradycardia is <60
tachycardia is >100
Trick to approximate HR on grid paper
Count off large (5mm) boxes between 2 consecutive QRS using sequence:
300, 150, 100, 75,60,50
How to calculate irregular rhythm
count # of QRS durign 6 secs and multiply by 10
Way to find HR
[25mm/sec x 60sec/min] / mm between beats
Calculate PR interval:
what is normal
onset of P to onset of QRS
0.12 to 0.2 seconds
Define QRS interval and normal time
beginning to end of QRS
QT interval and normal value
onset of QRS until end of T wave
(QT corrected: measured QT/square of RR interval)
QTc
What is the mean QRS axis?
ave of instantatneous electrical forces generated during ventricular depolarization in FRONTAL plane
Normal: -30 to +90 degrees
Left axis deviation: negative to -30
Right axis deviation: Positive to +90
How to do Rough, rapid estimation of axis
Evaluate QRS in leads I and II
if net QRS positive in both leads; upward deflection>negative defection; aixs is normal range between -30 and +90
Calculating axis: geometric method
Use Lead I and II
Inspection method of calculating axis
Find axis perpendicular to isoelectric lead (will be a flat line on the read)
Then find the largest QRS to see if it’s + or -
What do we expect to see in a P wave for Right atrial activation/enlargement?
left atrial activation/enlargement?
Right:
II: increaed RA
V1: increased RA and
Left:
II: double hill
V1:large decrease of LA
What does a normal P wave look like IN lead II and V1
This is P wave… whats going on?
Left atrial activation/enlargement
This is a P wave, whats going on?
Right atrial enlargement
What happens in LVH?
increase amplitude of electircal forces directed to left and posteriorly.
Repolarization abnormalities–> result in ST segment depression and T wave inverion in leads with promiment R wave
What changes to QRS do we see in LVH?
ST segement depression
T Wave inversion causing promient R wave
What do we see in a RVH?
shift QRS vector to the right leading to a R, RS or qR complex in lead V1
possible T wave inversions in right precarodial leads
Key ECK measurements for LVH
S in V1 plus R V5 OR
V6 >35mm OR
R in aVL >11mm, or R in I >15mm
Key ECG measures for RVH
R>S in V1 and right axis deviation
Whats going on with this dude?
Note tall R wave in V1
right axis deviation
T wave inversion V1-V3
***RVH****
When do we see an S1 Q3 pattern in EKG
With acute or chornic right ventricle overload sydromes
or severe right ventcile pressure overload
Interuption of Left Anterior fasicular division or LAD results in:
intial inferior (1) followed by domiant superior (2) direction of activation.
Interruption of Left posterior Fascicle or division LPD results in:
intial superior (1) followed by dominant inferior (2) direction of activation.
If you see wide QRS: think LBBB or RBBB and check V1 and V6
Review image
Image on left is V1
on right is V6
Dx?
Right Branch Bundle Block
Image on left is V1
Image on right is V6
Dx?
Left Branch Bundle Block
Criteria for RBBB?
QRS complex over .12 sec
RsR’ (Mshaped) QRS comples in V1
Widended or ‘slurred’ S wave in leads I and V6
Criteria for LBBB
QRS greater then .12 sec
widened or ‘slurred’ R wave in leads I and V6
Prominent QS or rS in leave V1
Dx?
RBBB;
see QRS more then .12 (means L or R BBB)
RsR’ (M shaped) QRS in V1
Widened S wave in V6 and I
Dx?
LBBB
QRS over .12 (can be Rt or LEft)
widened R wave on I and V6
Prominent QS or rS in lead V1
With predominant subendocardial ischemia; the ST vector is director toward:
inner layer of afftected ventricle and ventricular cavity
Leads overlying it should record ST depression
With ischemia involving outer ventricular (transmural or epicardial) injury, we see:
ST vector is directed OUTWARD and overlying leads record ST segment elevation
Recipricol ST segment depression can appear in conralateral leads
Acute ischemia can alter ventricular AP by inducing lower RMP and decreaed amplitude of phase 0… what can we see reflected in ECG
deviation of ST segment
(effects create a voltage gradient between ischemic and normal cells at dif phases in cardiac cycle)
In MI we see ______ in leads I, aVL, and V2-V6
ST segment elevation
Subendocardial Ischemia will cause ____
ST depression
In and ST elevated MI, unless reperfusion of occluded artery is achieved we have irreversible necrosis and will eventually develop:
Pathologic Q wave in overlying infarcted tissue (nectrotic tissue can’t generate electric force)
Why do we get Pathologic Q wave?
Lead over necrotic tissue (from MI) detects currents from health tissue on opposite regions of ventricle directed away from infarct thus a downward deflecting Q wave
See a small Q wave defelcting down that is 20 ms long and at 20% QRS height.. is there any pathology associated with this?
No: small initial Q waves can be normal as long as they are >40ms and low magintude of >25% QRS
–are not localized to single lead but can see them in anatomical grouping
What changes do we see in ST segments in Anterior lateral infarcts?
ST seg ELEVATION in I, aVL and precordial leads
along with
ST depression in II, III and aVF
What changes do we see with acute inferior (or poseterior) infarcts?
Recipricol ST segment depression in leads V1-V3
What would a normal varient with early repolarization look like on ECG?
ST elevation most markeldy in V4 and recipricol ST depression and PR depression are absent (while these are present in ischemia dn pericarditis… escpecially in lead aVR)
