All Decks Flashcards
Delay or prevent the conduction of depolarization
What three types?
Heart Blocks
SA Node
AV node
Bundle Branches
This, when unhealthy, may temporarily fail to pace for at least 1 cycle
May resume pacing in step with the previous rhythm
Long pause may induce an escape contraction from an automaticity focus
Sinus Block
A group of arrhythmias caused by SA node dysfunction associated with unresponsive supraventricular automaticity foci
No escape contractions
Sick Sinus Syndrome
This can develop from sick sinus syndrome
—> intermittent episodes of SVT and sinus bradycardia
Bradycardia-Tachycardia Syndrome
Prevent or eliminate conduction from the atria to the ventricles
Three types that get worse
AV Block
First, Second and Third Degree
Prolonged PR interval >0.20 seconds (>5 small boxes)
PR remains consistently lengthened from cycle-to-cycle
P-QRS-T sequence is normal in every cycle
Constant, normal P-wave
First Degree AV Block
Two types of second degree AV blocks
2nd degree Wenckebach (type I) AV Block
2nd degree Mobitz (type II) AV blocks
PR Interval gradually lengthens in each successive cycle until the P wave fails to conduct to the ventricles (no QRS complex after P wave)
P-P wave intervals are regular and constant
2nd Degree Wenckebach AV Block
Totally blocks a number of paced atrial depolarizations (P waves) before conduction to the ventricles is successful
2:1, 3:1, or higher ratios of P waves: QRS complexes
PR intervals prolonged with a SUDDEN dropped QRS complex
P-P wave intervals are regular
2nd Degree Mobitz AV block
Total block of conduction to the ventricles. Atrial depolarizations are not conducted to the ventricles
Atria and ventricles are completely INDEPENDENTLY pacing
An automaticity focus below the complete block escapes to pace the ventricles at its inherent rate
P-P intervals remain regular and constant
Complete 3rd Degree AV Block
Block of conduction in the right or left bundle branches
The blocked bundle branch delays depolarization to the ventricle it supplies
Bundle Branch Block
Ventricles do not depolarize simultaneously -> produces the “widened QRS” appearance on the ECG
Each QRS complex is of normal duration but they superimpose on each other causing a widened QRS with two peaks
What does R’ represent?
Bundle Branch Block
R’ represents delayed depolarization of the blocked ventricle
Widened QRS
Greater than or equal to 3 small boxes (0.12 seconds or more)
Right Bundle Branch Block
V1 and V2 (look for bunny years)
Left ventricle depolarizes punctually, so the R represents left ventricular depolarization and the R’ represents delayed right ventricular depolarization
Widened QRS
R: left Ventricle
R’: Right Ventricle
Left Bundle Branch Blocks
V5 and V6 (look for bunny ears)
The left ventricular depolarization is delayed, so the right ventricle depolarizes punctually R, and the R’ represents delayed left ventricular depolarization
Widened QRS
R: Right Ventricle
R’: Left Ventricle
Direction of depolarization as it passes through the heart
Direction and magnitude of a depolarization
Axis
Vector
This conducts depolarizations from the endocardium (inside lining of the heart) to the epicardium (outside)
Ventricular Depolariation
These are special connections in the ventricle which transmit depolarizations from the endocardium to they myocardial cells
Purkinje Fibers
Sum of all small vectors of ventricular depolarization
Mean QRS Vector
Since the left ventricle is larger than the right ventricle, where does the mean QRS vector point normally?
DOWN and to the LEFT
How does ventricular hypertrophy effect the mean QRS vector?
More tissue that will change the magnitude and direction of the vector
Which direction will the vector point during hypertrophy?
The vector will point towards the hypertrophied side
How does myocardial infarction effect mean QRS vector?
Blockage of one or more of the coronary arteries results in necrosis of tissue due to lack of oxygen and blood.
No vectors are derived from dead tissue so the mean QRS vector veers AWAY from an area of necrotic tissue
P wave represents the depolarization and contraction of both atria, we examine the P wave for evidence of what?
Enlargement includes both hypertrophy and dilation
Atrial Enlargement
Which lead do you look at for atrial enlargement?
Lead V1 is directly over the atria, so the P wave in V1 is the best source for atrial enlargement
With atrial enlargement, the P wave is usually….?
Diphasic (both positive and negative)
The chest electrode that records lead V1 is….
Positive
Right Atrial Enlargement criteria
A diphasic P wave in lead V1 with a large, often peaked initial component tells us that the right atrium is probably hypertrophied and dilated compared to the left atrium
If the height of the P wave in any LIMB lead (especially Lead II) exceeds 2.5mm (0.25mV) - amplitude - even if not diphasic, suspect right atrial enlargement.
(2.5 small boxes or more)
Point P waves are also called…
They are tall (>2.5mm) = Right Atrial Enlargement
P Pulmonale
Left Atrial Enlargement criteria
Terminal portion of a diphasic P wave in V1 is large and wide
Terminal component of a diphasic P wave in lead V1 is usually negative
P wave duration is greater than or equal to 0.12 seconds (3 small boxes or larger) in LEAD II
This is also called P-Mitrale
Bi-Atrial Enlargement criteria
Both left and right atrial enlargment
BLUF: tall p-wave in Lead II that is widened
In right ventricular hypertrophy (RVH) there is a large…..in lead V1
What about the S wave?
R Wave
The S wave in lead V1 is SMALLER than the R wave in RVH
When RVH is present, there is a large R wave in lead V1 that becomes……
Progressively smaller in the chest leads V2, V3 and V4
Enlarged right ventricle adds more vectors to the right side, so there is a right axis deviation
How is the S wave in Lead V1 with left ventricular hypertrophy
DEEPER in lead V1 (left axis deviation is present)
Lead V1 is a right-sided leaded. LVH produces a large positive depolarization away from V1 hence creates large negative S wave
How is R in LVH?
Tall R in lead V5
Lead V5 is over the left ventricle, so the increased depolarization is going toward the electrode of V5 when there is LVH
Result is more positive depolarization going toward the positive electrode of V5 which produces a tall R wave in that lead
Sokolow-Lyon Criteria
Diagnosing LVH on an ECG
S wave V1 + R wave V5
If the depth (in mm) of the S wave in V1 + R wave (in mm) of the R wave in V5 >35mm, then LVH is present
In LVH, which limb leads are ideal to check that may have a characteristic where the T wave has a gradual downslope and a steep return to the baseline, making it assymmetrical
Left chest leads V5 or V6
Characterized by depression of the ST segment
What is the pathology?
Ventricular Strain
Increased resistance from a narrowed valve or from hypertension causes ventricle strain leading to hypertrophy (muscle working harder against resistance)
Depressed ST segment with an upward hump in the middle
Which lead would indicate right ventricular strain and left ventricular strain?
V1 - right VS
V5 - left VS
Overall guideline to check for cardiac hypertrophy
- Check lead V1 to see if the P waves are diphasic for atrial enlargement
- Check R wave in lead V1 or right ventricular hypertrophy
- Check S wave depth + R wave height in lead V5 for left ventricular hypertrophy
Which coronary curves around the right ventricle?
Right Coronary Artery
Which coronary curves around the left atrium?
Left circumflex
Which coronary artery supplies blood to the left ventricle?
Left Anterior Descending
What is the source of life-threatening ventricular arrythmias?
Hypoxic ventricular foci near the infarction
What is cardiac ischemia, how is it characterized on the ECG, and what can it symptomatically cause?
Decreased blood supply from the coronary arteries
Characteristic sign of ischemia on an ECG is the INVERTED T-Wave
Cardiac ischemia alone can cause chest pain known as angina
T wave changes are most pronounced in which leads?
T Wave inversion in which leads are pathological?
V1-V6
V2-V6
Wellens Syndrome
Marked T wave inversions in leads V2 and V3
STENOSIS of the left anterior descending artery
Cardiac Injury
Indicates an acute infarct
Injury is characterized by ST SEGMENT ELEVATIONS
Brugada Syndrome
Hereditary condition that can cause sudden death in individuals without heart disease
Right Bundle Branch Block + ST segment elevation V1-V3
ST segment elevations have a peaked downsloping shape
Acute Pericarditis
Diffuse ST segment elevations that are flat or slight concave (middle sags down)
Diffuse PR depressions
ST Segment depressions (in leads where the QRS is upright) indicates compromised coronary blood flow until proven otherwise
This may indicate….
Subendocardial infarction
Positive stress test
Cardiac necrosis: diagnosis of myocardial infarction is usually based on the presence of significant Q waves produced by an area of necrosis in the wall of the left ventricle
What is the criteria for significant Q waves?
Greater than or equal to 0.04 seconds (1 small box) in duration and/or Q wave is 1/3 (height and depth) of the entire QRS complex
4 general ares of left ventricular infarctions
Anterior/septal
Inferior
Lateral
Posterior
Lateral MI leads
Lead I, V5, V6
Occlusion of the left circumflex
Inferior MI leads
II, III, aVF
Occlusion of the terminal branch of either right or left coronary artery
Anterior/septal MI leads
V1, V2, V3, V4
Occlusion of the left anterior descending
Always check V1 and V2
ST Elevation and Q waves (anterior infarct)
ST depression and large R waves (posterior infarct)
The ECG diagnosis of infarction is generally NOT VALID in the presence of….
Left bundle branch block
Why? = unable to tell if there are ST segment elevations or concerning depressions
NEW Left bundle branch block
A new left bundle branch block along with clinical correlation may be indicative of an acute infarctions
If area of infarction causes injury/necrosis of left bundle branch, may cause a left BBB
Prolonged QT interval is a marker for…
Ventricular arrythmias such as torsades de pointes and also a risk factor for sudden cardiac death
QT interval is DEPENDENT on heart rate
The faster the heart rate, the shorter the QT interval
Prolonged if QT interval is greater than 1/2 R-R distance
What is the QTc?
Normal is 450ms
Men greater than 450ms
Females greater than 470ms
Low Voltage ECG
Defined as a QRS amplitude of:
<5mm (0.5mV) in limb leads (I, II, III, aVR, aVF)
<10mm (1.0mV) in chest leads V1-V6
Etiologies for Low Voltage ECG
Amyloidosis, sarcoidosis, pericardial effusions, COPD, obesity, anasarca
Early Repolarization
Greater than or equal to 0.1mV J-point elevation in 2 or more adjacent leads with either a slurred or notched morphology
ASYMPTOMATIC patient
More prevalent in young, athletic patients
Electrical Alternans
Alternating amplitude of the QRS complexes in any or all leads (due to shifting fluid)
MCC: pericardial effusion
Slow (“poor”) R wave progression
R wave height normally becomes progressively taller from leads V1 through V6
Remains smaller than the S wave height OR remains at low amplitude across the entire precordium
Etiologies: lead placement, MI, LVH, LBBB, WPW pattern, chronic pulmonary disease, normal variant
S1Q3T3 Syndrome (Pulmonary Embolism)
S1: large S wave in lead I
Q3: Q wave in lead III
T3: Inverted T wave in lead III
Other possible ECG findings:
Sinus tachycardia (MC)
St depression in lead II
Transient right axis deviation
T wave inversion V1-V4
Hyperkalemia
Peaked T waves
P wave widening and flattening with eventual disappearance
QRS widening
Cardiac arrythmias develop such as ventricular fibrillation
Hypokalemia
T wave flattening and/or inverted
U wave appearance
Cardiac arrhythmias develop
Hypercalcemia
Short QT interval
(Normal QT interval is <1/2 R-R distance)
QTc is less than 430
Hypocalcemia
Prolonged QT interval
