Cardiology Lectures 1 and 2 -- EKG Flashcards
Define EKG
A voltmeter that records electrical voltages at the skin surface generated by the depolarization of heart muscle
Single cell model: voltmeter reading for a cell that has initially depolarized
Single cell model: voltmeter reading for a cell that has depolarizaed halfway
Peak
Single cell model: voltmeter reading for a fully depolarized cell
Returned to baseline (since no more current)
Single cell model: effect of switching polarity of the voltmeter on the reading
Flips wave upside down
Voltmeter reading (in theory) for myocyte repolarization of a single cell
Why is the voltmeter curve for repolarization upright in an actual voltmeter?
Last cells to depolarize are actually the first cells to repolarize
General location of chest electrodes
In 4th and 5th intercostal spaces
Define a lead
A recording electrical activity between 2 points on the body
Number of leads in a complete ECG
12
Deflection recorded when a depolarization current is directed towards the + electrode of a lead
Upward (positive) deflection
Deflection recorded when a depolarization current is directed away from the positive electrode
Downward (negative) deflection
Wave recorded when the wave of depolarization moves perpendicularly to the lead in question
Biphasic (partially positive and partially negative) waveform or a straight line
(NOTE: not very helpful)
Number of limb leads
6
Plane of measurement of limb leads
Frontal plane (i.e. no depth perception; only up-down and lateral)
Number of precordial (chest) leads
6
Plane of chest leads
Transverse plane (i.e. provides depth perception)
Directionality of unipolar limb leads
Towards the limbs from the heart
Names of unipolar leads and locations
aVR = right arm
aVF = left leg/foot
aVL = left arm
Name and directionality of bipolar limb leads
I = right arm –> left arm
II = right arm –> left leg
III = left arm –> left leg
Result of overlaying the 6 limb leads
Axial Reference System is established
Location relative to the heart of the 6 chest leads
On the anterior and left lateral aspect of the chest
3 major deflections that represent a heartbeat
P wave
QRS complex
T wave
The first chambers to depolarize
Right and left atria
What event does the P wave represent
Atrial depolarization (right, quickly followed by left; superimposed)
What event does the QRS complex represent?
Ventricular contraction
5 different possible shapes of the QRS complex
- QRS
- RS
- R only
- QS
- RSR’
Define the Q wave
The first downward deflection of the QRS
Define the R wave
The first upward deflection whether or not a Q wave is present
Define the S wave
Any downward reflection following the R wave
Normal resting state
Surfaces of myocardial cells homogenously charged
No electrical activity detected by ECG leads
First portion of ventricle to depolarize
Left side of mid portion of interventricular septum
Direction of electrical current from left side of mid portion of interventricular septum during ventricular depolarization
Toward the right ventricle and interiorly
Leads that perceive the depolarization through the left side of the mid portion of the interventricular septum
aVL
aVF
Wave that aVL detect upon depolarization of the left mid portion of the interventricular septum
Q wave (initial downward deflectoin)
What wave does aVF detect upon left mid interventricular septum depolarization
R wave (initial upward deflection
Directionality of the overall charge as the lateral walls of the ventricles are depolarized
Forces of the thicker LV outweigh those of the right, so the arrow’s orientation is increasingly directed towards the LV
What phase does the T wave represent?
Ventricular repolarization
Define the ST segment
The line between the QRS complex and the T wave that should normally be isoelectric (same as baseline)
When may the ST segment move up or down?
When the heart is lacking oxygen
Define the P-R interval
Time from start of P wave to the start of the QRS complex
Define the QT interval
Time from start of the QRS complex to the end of the T wave
Vertical axis of an ECG
Voltage in mV
1 mm = 0.1 mV
Horizontal axis of an ECG
Time (ms)
1 small box = 40 ms
1 large box = 0.2 sec
NOTE: assuming a normal paper speed of 25 mm/sec
8 steps in the sequence of analysis of an EKG
- Check voltage calibration
- Heart rhythm
- Heart rate
- Intervals (PR and QT)
- Mean QRS axis
- Abnormalities of the P wave
- Abnormalities of the QRS
- Abnormalities of the ST segment and T wave
3 examples of abnormalities that can arise in an abnormal QRS complex
Hypertrophy
Bundle branch block
Infarction
How to calibrate ECG voltage
1.0 mV (i.e. 10 small boxes) vertical signal at the beginning and/or end of the tracing to document normal voltage calibration has been used
When is doubling the calibration of the ECG useful?
If a condition, such as PC effusion, muffles the signal to produce small voltage waves (need to see them better)
4 criteria to have a normal sinus rhythm
- Every P wave is followed by a QRS complex
- Every QRS complex is preceded by a P wave
- P wave is upright in leads I, II, III
- PR interval is >0.12 sec (3 small boxes)
What happens if not all 4 criteria for a sinus rhythm are fulfilled?
There is an arrhythmia
First method of determining HR from an ECG
Count the number of boxes between two adjacent QRS complexes (i.e. between two beats).
Note that the standard paper speed is 25 mm/sec, so use this equation
Use method1 to determine the HR of this ECG
HR = (25 mm/sec x 60 sec/min) / 23 mm per beat = 1500 mm/min / 23 mm/beat = 65 bpm
Method 2 of determining HR from an ECG
“Count off method” = memorize this sequence:
300 - 150 - 100 - 75 - 60 - 50
Start at an R wave that is on a dark line and assign each subsequent dark line to the right with a number from this descending sequence. Where the next R wave falls is the HR.
Advantage and disadvantage of Method 2 for determining HR
Advantage = faster (most commonly used in busy wards)
Disadvantage = less accurate than method 1
Method 3 of determining HR from an ECG
There is usually a 3 sec marker on the ECG. Count the number of QRS complexes in this interval and multiply by 20 to get the HR.
Normal PR interval
0.12 - 0.20 sec
(3 - 5 small boxes)
2 conditions that may cause PR interval decrease
Preexcitation syndrome
Junctional rhythm
One condition that may cause PR interval increase
First degree AV block
What does the QT interval indicate?
Represents the time for ventricular depolarization and repolarization.
Estimates the duration of the cardiac action potential (so increased action potential duration = increased QT interval)
Effect of high HR on QT interval
At high heart rates, the heart needs to repolarize faster so the QT interval tends to shorten
Effect of low HR on QT interval
At low heart rates, the heart does not need to rush so it takes its time repolarizing and the QT tends to lengthen
2 methods to correct for QT interval for HR
Bazett’s formula
Rapid rule
Bazett’s formula for QT interval correction
QTc = “Qtcorrected (for heart rate)”
QTc = QT interval in ms / √ R-R interval (in sec)
Normal QTc
Normal QTc ≤ 0.44 sec
Rapid rule for QT interval correction for HR determination
If the QT interval is less than ½ the R-R interval, then the QT is within normal range
This technique only works at normal heart rates (60-100bpm)
What is the danger of an abnormally long QT interval?
May predispose patients to lethal cardiac rhythm disturbances
2 conditions that cause a decrease in QT interval
Hypercalcemia
Tachycardia
6 conditions that can cause an increase in the QT interval
- Hypocalcemia
- Hypokalemia
- Hypomegnesemia
- Myocardial ischemia
- Congenital QT interval increase
- Toxic drug effect (i.e. certain anti-arrhythmic drugs)
What is the mean QRS axis?
A vector that represents the average of the instantaneous electrical forces generated during the sequence of ventricular depolarization as measured in the frontal plane (the limb leads)
Blue section = normal area of axis
Effect of heart orientation on QRS axis
Effect of ventricular hypertrophy on QRS axis
Shift towards the hypertrophied side
Effect of myocardial infarction on QRS axis
Points away from the infarction
3 causes of left axis deviation
- Inferior wall myocardial infarction
- Left anterior fascicular block
- Left ventricular hypertrophy (sometimes)
3 causes of right axis deviation
- Right ventricular hypertrophy
- Acute right heart strain (i.e. massive pulmonary embolism)
- Left posterior fascicular block
First step for determining QRS axis
Start with lead I:
Is the QRS + or - ?
If + then the vector of depolarization is heading towards the + electrode of lead I (so between -90°and + 90°) = good (no right axis deviation)
If - then the vector of depolarization is heading towards the - electrode of lead I = right axis deviation
Second stop for determining QRS axis
Move on to lead II:
Is the QRS + or - ?
If + then the vector of depolarization is heading towards the + electrode of lead II (so between -30°and + 150°)
If -, then left axis deviation
What is normal range ofr QRS axis
If QRS is + in both I and II, then the axis vector must lie between -30° and + 90°
Leads that see P wave best
Leads II and V1
Define right atrial enlargement representation on an ECG and which lead best perceives it
Height greater than 2.5 mm in lead II
Define left atrial enlargement representation on an ECG and which lead perceives it best
Negative P in V1 > 1 mm wide and 1 mm deep
4 important abnormalities of QRS complex
- Ventricular Hypertrophy
- Bundle branch blocks
- Fascicular Blocks
- Pathologic Q waves in Myocardial Infarction
Effect of right ventricular hypertrophy on ECG waves
Chest leads V1 and V2 (which overlie the RV) record greater than normal upward deflections (R wave greater than S wave)
Effect of right ventricular hypertrophy on QRS axis
Increased RV mass shifts the mean axis to the right –> Right axis deviation
Effect of left ventricular hypertrophy on ECG waves
V5 and V6 (which overlie the LV) record greater than normal upward deflections (Taller than normal R waves)
Other side of the heart (V1 and V2) demonstrate the opposite (deeper than normal S waves
Effect of left ventricular hypertrophy on QRS axis
Increased LV mass may shift the mean axis to the left = Left axis deviation
Define a bundle branch block and its potential cause
Interruption of conduction through the right or left bundle branches
May develop from ischemic or degenerative damage
Effect of bundle branch blockage on electrical activity and QRS complex
Cells of that ventricle must rely on relatively slow myocyte to myocyte spread of electrical activity traveling from the unaffected ventricle
Prolongs depolarization and widens the QRS complex
Normal QRS duration
Less than or equal to 0.10 sec (2.5 small boxes)
Effect on QRS duration by a complete bundle branch block
QRS > 0.12 sec (> 3 small boxes)
Effect on QRS duration by an incomplete bundle branch block
QRS between 0.10 - 0.12 sec
Give the progression of the directionality of the electrical activity during a left bundle branch blockade
Complete depolarization of the right ventricle –> slow myocyte to myocyte depolarization towards the left ventricle
Give the progression of the directionality of the electrical activity during a right bundle branch blockage
Complete depolarization of the left ventricle –> slow myocyte to myocyte depolarization towards the right ventricle
Effect of fascicular blockage on mean axis
Marked alteration (no details)
How is myocardial necrosis represented in an ECG
Pathologic Q waves
In what leads do pathologic Q waves develop
In leads overlying the infarcted tissue
Reason why pathologic Q waves occur
- Necrotic muscle does not generate electrical forces
- ECG electrode over the necrotic region picks up electrical currents from the healthy tissue on the opposite region of the ventricle
- Therefore, Q waves are permanent evidence of an old trans-mural infarction
Where can Q waves be physiological
It is normal to have small Q waves in leads V6 and aVL (from normal septal depolarization)
How are physiological Q waves represented in an ECG
Physiologic Q waves are short in duration (<0.04 sec) and are not deep (< 25% of the total QRS height)
ECG representation of a pathological Q wave
Width ≥ 1 small square
Depth > 25% to total height of QRS complex
Leads involved in anteroseptally-localized infarction
V1
V2
Leads involved in anteroapically-localized infarction
V3
V4
Leads involved in anterolaterally-localized infarction
I
aVL
V5
V6
Leads involved in inferiorly-localized infarction
II
III
aVF
Why isnt aVR involved in readings for infarctions?
Electrical forces are normally directed away from the right arm
How to detect posteriorly-localized infarction
- Chest leads V1 and V2 are directly opposite the posterior wall –> record the inverse of what leads placed on the back would record
- Taller than normal R waves in leads V1 and V2 are the equivalent of pathologic Q waves in the diagnosis of posterior MI
3 ST-segment and T-wave abnormalities
- Transient Myocardial Ischemia
- Acute ST segment Elevation MI (STEMI)
- Acute Non-ST Segment Elevation MI (NSTEMI)
Common ECG manifestations of transient myocardial ischemia
Reversible deviations of the ST segments (usually ST depression) and T waves (usually inversions)
Sequence of ECG changes in acute ST-segment elevation MI
Note: These changes are recorded in the leads overlying the zone of infarction
Typically, reciprocal changes are observed in the leads opposite that site
When does acute non-ST-segment elevation MI occur?
When the thrombus is only partially occlusive
ECG manifestations of non-ST-segment elevation MI
ST-segment depressions and/or T wave inversions in the leads overlying the affected myocardium
Q waves do not develop as typically only the sub-endocardium is involved
ECG manifestations of pericarditis
Diffuse ST segment elevation in most leads except aVR and V1
PR segment depression
What does diffuse ST segment elevation signify in the event of pericarditis?
Reflects inflammation of adjacent myocardium
What does PR segment depression reflect in the event of pericarditis?
Reflects abnormal atrial repolarization
