Module 4- basic ECG & Arrhythmia Flashcards
ST Segment Elevation Myocardial Infarction
STEMI
Penetrates entire myocardial wall.
ST Segment elevation of 1mm or more in more than one lead that looks at the same ventricular wall segment
results in “Q” waves (wider than 1mm)
Ventricular Flutter
150-300 bpm
as flutter waves become smaller, fibrillation more imminent.
Ventricular Fibrillation
150-500 bpm
grossly irregular waveform with various amplitudes
Torsade de pointes
type of VT showing cycles of alternation QRS polarity.
Ventricular Tachycardia (VT)
3 or more Premature Ventricular Contractions occur in succession exceeding 100-250 bpm
Widened QRS complex
ST segments and T waves may not be distinct.
Premature Ventricular Tachycardia (PVC)
Widened QRS (greater than .12s)
can also be interpolated
either a RBBB or LBBB or near normal morphology
-impulse of ventricular origin before next expected sinus beat, SA activity is unaffected (impulse is unable to penetrate AV node)
3rd degree AV block
complete heart block
All sinus and SV impulses fail to conduct through AV node to ventricles. (Latent subsidiary pacemaker is needed)
Atrial rate is different from Ventricular rate. (no consistent PR interval)
2nd degree AV block type II (Mobitz II)
Occasionally a P wave in not conducted to the ventricles.
PR interval is constant
2nd degree AV block type I (Wenckebach)
Impulse from the atria becomes harder and harder to propagate to ventricles.
Progressive prolongation of P wave
PR interval is longest right before dropped beat and shortest right after
QRS complex’s cluster into groups separated by non-conducted P waves
First Degree AV block
Refractory period of the AV node is delayed
PR interval exceeds .20s
P waves can be buried in preceding T waves
Ventricular Arrhythmia’s are:
Ventricular tachycardia
Ventricular flutter
Ventricular fibrillation
Atrioventricular conduction defects are:
First degree (Mobitz I) AV block Second degree (Mobitz II) AV block Second degree (Wenckebach) Third degree (complete heart block)
Supraventricular Arrhythmias are:
When PAC's occur in succession Atrial fibrillation and flutter AV nodal re-entry tachycardia AV re-entry tachycardia Atrial tachycardia
Atrial fibrillation with Irregular RR response
Absence of discernible P waves
QRS normal
T wave obscured by f(fibrillatory) waves
Atrial Fibrillation
Both atria beat chaotically not allowing ventricles to fill completely.
No P wave, Variable R-R interval
impulse reach ventricles in excess of 140-180 bpm
most common adult arrhythmia
Atrial Flutter
Slower more organized rhythm than fibrillation
Atria contract faster than ventricles
f(flutter) waves appear
Usually associated with AV block
Premature Atrial Contraction (PAC)
Originates in ectopic focus outside the SA node
Can come suddenly and then terminate, 3 or more in a row indicated SV tachycardia.
140-220 bpm
P wave may be premature and hidden in preceding T wave
P wave contours differ
Hyperkalemia
Tall, peaked, narrow T waves in precordial leads
Precordial leads
“chest leads”
provide a horizontal view of the heart
V1-V6
Hypokalemia
Flattened T waves
appearance of U waves in anterior Precordial leads (V2, V3)
ST depression
Hypercalcemia
Shortened QT interval
Hypocalcemia
Prolonged QT interval
Digoxin Toxicity
produces significant ECG changes
ST scooping depression
mild PR prolongation
Left bundle branch block (LBBB)
failure to conduct an impulse through the left bundle branch.
lead V1 will have a deep S wave
large RR in V6 with duration of .12s
Fascicular block
failure to conduct an impulse through the left anterior-superior fascicle, or the left posterior-inferior fascicle branches off of the Left bundle branch.
Right bundle branch block (RBBB)
failure to conduct an impulse through the right bundle branch.
RSR’ pattern- secondary R wave in V1- QRS duration .12s
Slurred S wave in V6
Sinus tachycardia
rhythm exceeding 100 bpm
Sinus arrhythmia
Exaggeration of the normal heart rate during respiration
Sinus Bradycardia
less than 60 bpm
Sinus rhythm
60-100 bpm
fairly regular and continuous
Components of the cardiac conduction system
SA node AV node Bundle of His Left and right bundle branches Purkinje fibers
P wave
First waveform in a cycle
represents atrial depolarization
.12 s
PR interval
beginning of the P wave to the beginning of QRS complex
represents impulse transversing the AV node
QRS complex
Ventricular depolarization
ST segment
Low electrical activity following ventricular depolarization
(sensitive indicator of ischemia during myocardial infarction)
For end of QRS to beginning of T wave
T wave
Ventricular repolarization
QT Interval
From the beginning of the QRS to the end of the T wave
ventricular depolarization and repolarization
Shortens as heart rate quickens, lengthens as heart rate decreases
indicator of predisposition to ventricular arrhythmias
U wave
Deflection following T wave
origin uncertain
Non- ST Segment Elevation Myocardial Infarction
NSTEMI
Does not penetrate entire width of the myocardium. ECG changes variable but include:
- Downsloping ST segment depression of 1mm or more
- T wave inversion
- or both
Right atrial enlargement (RAE)
Tall peaked P wave
associated with right ventricular hypertrophy
Left atrial enlargement (LAE)
Biphasic P wave “double hump”
Longer duration of P wave in some leads
Left ventricular hypertrophy (LVH)
Increase R wave height in ECG leads that reflect left ventricular potential
