EKG Flashcards
EKG Limb leads
Standard: I, II, III
Augmented: AVF, AVL, AVF
Precordial Leads
V1-V6
Bipolar limb lead charges
Lead I: R to L arm, L arm positive = electrical activity over top of heart
Lead II: R arm to L leg, L leg positive
Lead III: L leg to L arm, both leads positive
Augmented Limb Lead charges
aVR = right arm positive
aVL = left arm positive
aVF = left leg positive
Lateral leads
AVL
I
V5
V6
Inferior leads
II
III
AVF
Anteroseptal leads
V1-V4
Anterolateral leads
V3-V6
I
AVL
Anterior leads
V3-V4
Inferolateral leads
II
II
AVF
V5-V6
Precordial lead polarity
Each lead is positive, all pass through AV node
V1 and V2 are negative deflections
V3-V6 become more positive w/ peak positive ~ V4
Precordial leads and vasculature
RCA: II, III, AVF
LAD: I, AVL
V1-V6
CX: I, AVL, V5-V6
Septal leads
V1-V2
P wave time interval
<0.12
PR interval
0.12-0.20
QRS wave
<0.12
QT Interval
0.34-0.43
Q wave
When at least 1/3 as high as the R wave => transmural MI
RS line
Activation of posteriobasal ventricle portion
J point
Transition point from S wave to T wave
transition from horizontal to verticle axis
ST segment
Elevation or depression is a hallmark sign of ischemia, CAD, or STEMI
0.08-0.12 seconds long
Prolonged QT
Pathological slowing of electrical activity
May allow for depolarization before complete repolarization -> go into an arrhythmia
Cause by some Abx -> Macrolides, fluroquinolones, azole antifungals
T wave abnormalities
Indicate ischemia
U wave
Purkinje fiber repolarization
Prominent U waves: hypokalemia, hypercalcemia, thyrotoxicosis, or epiniphrine exposure
Methods to calculate rate
- Count # R waves in 6 seconds, x10
- 300-150-100, 75-60-50
- Count number of small squares between R waves, and divide into 1500
SVT
Supreventricular tachycardia
150-200 bpm
Prolonged PR interval
AV block - 1st and 2nd degree Type 2
Irregular PR interval
Sinus arrhythmia
Wandering pacemaker
AV block - 2nd degree Type 1
Lack of PR interval
A-fib
Atrial flutter
Complete heart block - 3rd degree
Ventricular rhythm
Second degree AV block types
Type 1 - Wenckebach
-PR interval gets progressively longer until QRS doesn’t occur
Type 2
-PR interval fixed, but sometimes a QRS doesn’t occur
Third degree AV block
P waves and QRS complexes are independent of each other
Impulses are not traveling past the AV node
Conduction delays
Widened QRS (anything > 0.12)
3 types:
- Left bundle branch block
- Right bundle branch block
- Intraventricular conduction delay
Right bundle branch block
R ventricular depolarization occurs more slowly than L vent due to R bundle branch blockage
Get “rabbit ears” in leads over RV - V1 and V2
Left bundle branch block criteria
QRS > 0.12
Dominant S in V1
Broad R in I, AVL, V5-V6
Absent Q in I, V5-V6
T wave inversions
-Dubin’s criteria = QS or rS in V1 w/ RsR in V6
Dubin’s criteria
For LBBB
V1 => QS or rS comples
V6 => RsR
Not a definite thing
LBBB considerations
Cannot Dx LVH or ischemia w/ a LBBB
MI until proven otherwise
LBBB on exercise stress test => increased mortality rate and cardiac events
Bundle branch block causes
LBBB - scar tissue/dead spot
RBBB - PE
Intraventricular conduction delay (IVCD)
QRS > 0.12
Doesnt meet criteria for a specific bundle branch block
QRS Axis
Shows where the main vector of electrical activity is going
Axis goes toward hypertrophy, away from ischemia
Dubin’s thumb up/thumbs down
To determine axis
Look at QRS in leads I (lateral = left) and aVF (inferior = right)
Whichever is up wins = axis deviation towards that side
Both up = normal
Best leads to check for hypertrophy
Atrial leads
II, III, AVF, V1 (biphasic)
P Pulmonale
R atrial enlargement
Lead II
-P wave is taller and overlaps more w/ LA as RA takes longer to depolarize
V1 - P wave is >1.5mm
P Mitrale
LA enlargement
Lead II shows P wave >0.12 seconds, w/ a possible notch in the middle
P wave inversion
Leads II, III, AVF
ectopic atrial and junctional rhythms
Right ventricular hypertrophy
Large R wave in V1 that gets smaller as you move towards V6
Should accompany RAE and deviated axis (I and AVF)
Left ventricular hypertrophy
V1 = deep S wave
V5 = Tall R wave
S wave (V1) voltage + R wave (V5) >35mm = LVH
Also may have inverted/asymmetrical/depressed T wave in lateral leads (I, AVL, V5-V6)
Ventricular strain
Associated w/ ventricular hypertrophy
Depression of ST segment
RV strain = V1
LV strain = V5-V6
EKG analysis
Rate
Rhythm
Axis (I, AVF)
P waves (V1, II)
R waves (V1-V6)
Hypertrophy (R: V1-V6, L: V1 and V5)
Strain (R:V1, L:V5-V6)
EKG markers of ischemia
Pathologic Q waves
Poor R wave progression (V1-V6)
ST segment elevation/depression
T wave abnormalities
ST elevation or depression
Depressed ST (also inverted T) => coronary ischemia
ST elevation => MI, hypokalemia, or digitalis toxicity
Non-ST Elevation Infarction
ST depression and T wave inversion
After infaction has resolved/fibrosis occurs, ST returns to baseline but T wave remains inverted
ST Elevation Infarction
Initial ischemia shows ST depression, peaked then inverted T waves
Infarction shows ST elevation and Q waves appear
Fibrosis shows normal T waves and ST segments, but Q waves may persist
Sinus Arrhythmia
Only rate changes - synchronizes w/ respiratory cycle
No need for treatment
Sinus Pause/Arrest
Pause between 2 seconds and 2 minutes
Tx: pacemaker, atropine
Healthy heart, myocarditis, MI, digitalis toxicity
Sinus bradycardia
<60 bpm
Caused by BB, digoxin
Only Tx w/ HTN or dizziness
Tx: atropine, pacemaker (long-term)
Sinus Tachycardia
>100 bpm
Caused by anemia, thyrotoxicosis, fever, pain, exercise
Tx underlying cause, CCB, BB
Supraventricular Tachycardia
Originates above HIS w/ reentry into AV node
Can be caused by PVC/PAC
palpitation, dizziness, syncope, SOB, anxiety, angina
Tx: vagal maneuvers, Adenosine, Cardioversion, IV BB/CCB
Prevent: BB, CCB, digoxin, SVT ablation
Paroxysmal supraventricular tachycardia (PSVT)
140-240 bpm
P buried in QRS, QRS narrow and normal
Tx: BB
Wolff-Parkinson-White Syndrome (WPW)
>200 bpm
Electrical pathway shortcut
Causes A-fib, can cause V-fib
EKG: Delta wave on QRS beginning
Tx: Ablation, BB, CCB, Flecainide, Adenosine w/ acute episodes
Paroxysmal Atrial Tachycardia (PAT)
150-250 bpm
P wave morphology varies from sinus rhythm
Usually transient, doesn’t need Tx
Tx: vagal maneuvers, Adenosine, cardioversion, digoxin
Premature Atrial Contractions (PAC)
P waves vary, precursor to A-fib
Common w/ MI, Cardiomyopathy, Mitral valve dx
Tx: BB
Wandering Atrial Pacemaker
45-100 bpm
Need 3 or more distinct P waves - multifocal A-tach
No Tx
Occurs w/ heart dx, COPD
Multifocal Atrial Tachycardia (MAT)
>100 bpm
3 or more distinct P waves, no hemodynamic instability
Occurs w/ lung dx, COPD, acute MI, sepsis
Tx: BB, CCB
Atrial Fibrillation
110-170 bpm, irregularly irregular
No P waves, possible ST depression
Prevent Thromboemboli ( Warfarin w/ INR between 2-3)
Control Rate/Rhythm
Rate: CCb, BB, Digoxin
Rhythm: Class 1a, 1c, and 3 - usually amiodarone
Atrial Flutter
250-350 atria, 150 ventricle - regularly irregular
Precipitates CHF, A-fib
Tx: ASA, Ablation, Class 1a, BB, CCB, Digoxin
Junctional escape/Accelerated junctional rhythm
40-60 bpm escape, 60-100 bpm accelerated
Inferior MI, Digoxin toxicity
Narrow QRS w/ retrograde/absent P waves
No treatment
Junctional Tachycardia
150-250 bpm
Initiated by PAC, no P wave
Acute Tx: Vagal maneuvers, Adenosine
Long-term Tx: BB, CCB, Class 1a/1c/3 antiarrhythmics
First degree AV block
Inferior MI, Digitalis toxicity, hyperkalemia, increased vagal tone, acute rheumatic fever, myocarditis
EKG: PR Interval > 0.20
Tx: none needed, monitor progression to 2/3 degree
Second-degree AV Block
Type 1: Wenckebach
- Transient, longer PR interval until QRS dropped
- No Tx, monitor
- MI, digitalis toxicity
Type 2: after acute anterior MI
- Rate varies, QRS wide, PR normal until dropped QRS
- Tx: permanent pacemaker
Third Degree AV Block
Digitalis toxicity, acute infection, MI, Conductive tissue degeneration
Vent rate is slower than atrial rate
Tx: Pacer
Premature Ventricular Contractions (PVC)
Rate varies, P obscured by QRS w/ PVC, QRS wide
Tx if: MI, continuously multifocal, > 6 PVC/min
Tx: Lidocaine, procainamide, amiodarone, replace electrolytes
R on T phenomenon - R PVC wave lands on normal T wave, causes Torsades
Ventricular Tachycardia
Ischemia and electrolyte abnormalities, MI, congenital defect, dilated cardiomyopathy, hypertrophic cardiomyopathy
No P wave, Wide QRS, rate regular
>30 seconds = hemodynamic instability - life-threatening
Pulse: Cariovert, amiodarone
Pulseless: Defibrillate then amiodarone
Torsade de Pointes
Lengthened QT, electrolyte imbalance, myocardial ischemia
Tx: synchronous cardioversion, replace electrolytes, overdrive pacing
Ventricular Fibrillation
Sudden cardiac death - no output
Tx: Defibrillate and ACLS, treat underlying cause, ICD
Idioventricular rhythm
Dying heart rhythm
No P, widened QRS
Ischemia/infarction, pacemaker failure, metabolic imbalance
Tx: Pacemaker, improve C.O. and rhythm, atropine
Pulseless Electrical Activity (PEA)
electrical activity w/ no mechanical response - no pulse
Tx: epi, atropine, CPR
Posterior MI
Mirror image of septal MI
Large R wave, no Q waves
ST-segment depression, not elevation
Upright T waves
Digitalis/Digoxin
Therapeutic levels cause a scooped ST depression across all leads
Toxicity = increases automaticity and decreases AV conduction
-heart block, A-tach, PAC/PVC, PAT, Atrial/Junctional tachyarrhythmias
Hyperkalemia
Peaked “Eiffel tower” T waves
Flat and wide P
Wide QRS
Can cause V-fib
Hypokalemia
U waves
Flattened/inverted T waves
Ventricular foci irritation - Torsades, VT, VF
Hypercalcemia
Short QT interval
J waves
Hypocalcemia
Prolonged QT - T barely finishes before next P
Hypomagnesemia
Prolonged QT
Torsades
Frequent PVC/PAV
Ventricular and Atrial tachyarrhthmias
Hypothermia
Osborn (J waves) - positive deflection at J site after QRS
Slow heart and metabolic rate
J waves indicate ventricular depolarization abnormality
Pulmonary embolus
Sinus tach most common
S1Q3T3 - prominent S in I, Q and T abnormal in III
Right axis deviation, RBBB, T inversions in V1-V4
