intro to EKG Flashcards
test that measures
the electrical activity of the heart
EKG
purpose of an EKG
Detects arrhythmias, heart
attacks, and other heart-related issues
Provides critical information
about heart rhythm, structure, and
electrical activity
blood flow is blocked
infarction
blood flow is reduced
ischemia
electrical pathway
SA node (Sinoatrial
node) → AV node (Atrioventricular node) → Bundle of His → Right and Left bundle branches → Purkinje fibers
Atrial depolarization, small upward deflection
P wave
Ventricular depolarization, large upward and downward
deflection
QRS complex
Ventricular repolarization, small upward deflection
T wave
Time taken for the electrical impulse to travel from the SA node to the AV node
PR interval
Total time for ventricular depolarization and repolarization
QT interval
Represents the period when the ventricles are depolarized
ST segment
inverted P wave
impulse from AV node instead of SA node (travels in reverse
direction from AV to SA then rest of ventricles)
what does p wave look like in V1
In V1, typically biphasic and similar size of positive and negative deflections
p wave too tall
right atrial enlargement
p wave too wide or notched
p wave biphasic
left atrial enlargement
PR interval normal
less than 0.20 secs (one big box)
PR interval bigger than 0.20
first degree AV block
short PR
WPW delta wave
first deflection of QRS downward
Q wave
QRS duration normal
< 3 small boxes
QRS duration > 0.12 seconds
BBB
broad, monophasic R
waves in leads I and V6
LBBB
RSR’ pattern (rabbit ears)
in V1 and wide slurred S in V6
RBBB
QT interval = normal
< half the distance of
R-R interval, 0.4-.44 secs
flat T wave
hypokalemia
broad peaked T wave
hyperkalemia or hyper acute of acute ischemia
deep symmetric T waves
ischemia
U wave present
Think hypokalemia, bradycardia, or medications (Digitalis, Amiodarone)
U wave prominent
higher likelihood of lethal
arrhythmia (Torsades)
Negative U-waves
ischemia, HTN, valvular disease, or RVH
one small box
0.04 sec
3 small boxes
0.12 secs
5 LARGE boxes
1 second
5 small boxes
one LARGE box
0.20 secs
Comprised of 10 physical electrodes
12-lead EKG
6 precordial (chest) leads:
V1, V2, V3, V4. V5, V6
4 limb leads
I, II, III, aVR, aVL, aVF
II, III, aVF
inferior
V1, V2
septal
I, aVL, V5, V6
lateral
V3, V4
anterior
V1-V4
anteroseptal
I, aVL
high lateral
Tall R waves in V1, V2, ST depression in V3, V4
Get posterior EKG = V7, V8,
V9
posterior
Blockage in posterior descending artery
- 80% of people this is supplied by RCA
- 10% by Left circumflex
- 10% by both
* Standard 12-lead does not reveal
- Look for ST-depression in reciprocal anterior leads
* Run a posterior EKG
- Place V7, V8, V9 electrodes on back, mirroring V4-V6
- Look for ST elevation or depression in V7-V9
posterior MI
if impulse moving towards lead
upward deflection
if impulse moving away
negative deflection
If main deflection of QRS is (+)
in both leads I and aVF
normal axis
- Normal variant in children, young and thin
adults - RVH
- COPD without RVH
- Left posterior fascicular block
- Lateral wall MI
- WPW pattern
causes of RAD
Slow heart rate (less than 60 bpm)
bradycardia
- Normal variant in older, obese adults
- LVH
- Elevated diaphragm = ascites,
pregnancy - Left anterior fascicular block
causes of LAD
Fast heart rate
(greater than 100 bpm)
tachycardia
Irregular, rapid atrial rhythm
atrial fibrillation
Life- threatening arrhythmia
originating in the ventricle
ventricular tachycardia
ST elevation or depression, pathologic Q waves
myocardial infarction (heart attack)
- Rate: Less than 60 bpm
- Causes: Vagal stimulation, medications (beta- blockers), athletic
heart - EKG: Normal sinus rhythm but
slower rate
sinus bradycardia
- Rate: More than 100 bpm
- Causes: Exercise, fever, anxiety, hypovolemia, anemia
- EKG: Normal P waves and QRS
complexes, just faster
sinus tachycardia
- Rate: Irregular
- Causes: Breathing pattern-related,
normal variant in young and healthy
individuals - EKG: Varying P-P intervals, but
consistent QRS complex
sinus arrhythmia
irregularly irregular
No discernable p-waves
Chaotic pattern
Can be bradycardic, normal,
or tachycardic
Causes: HD, Hyperthyroidism, ETOH
atrial fibrillation
regularly irregular
No p-waves
Atrial flutter waves = sawtooth pattern
Causes: HD, post-surgery, PE
atrial flutter
Narrow complex tachycardia
Rate = 150-250 bpm
Absent p-waves or hidden within the T
Causes: Re-entry circuits, in young, healthy patients typically
supraventricular tachycardia (SVT)
Rate: 40-60 bpm (escape rhythm)
* Causes: SA node dysfunction, AV node as the pacemaker
* EKG: Inverted or absent P waves, normal QRS
junctional rhythm
- Rate: 60-100 bpm
- Causes: Digoxin toxicity, beta agonists, MI
- EKG: Same as junctional rhythm, but faster rate
Accelerated Junctional Rhythm
Rate = 100-250 bpm
* Wide QRS complexes, rapid
rate, no p-waves
* Causes: ischemic HD, MI
ventricular tachycardia: Vtach
Rapid, erratic electrical
activity with no coordinated
contraction, no identifiable
QRS complexes or p-waves
* Causes: heart attack,
electrical disturbances
ventricular fibrillation: VFib
Rate: Depends on underlying rhythm.
* Causes: Caffeine, stress, ischemia.
* EKG: Early, wide, bizarre QRS complexes without preceding P
wave.
premature ventricular contractions (PVCs)
Rate: Depends on underlying rhythm
* Causes: Idiopathic, thyroid, anxiety, pregnancy, caffeine, stimulants
* EKG: an early p-wave, atria contracting too early, occurs from
ectopic tissue in atria
premature atrial contractions (PACs)
prolonged PR interval (greater than 3 small boxes)
* Rate: Normal
* Causes: Often benign, could be BB
1st degree heart blocks
Mobitz Type I (Wenckebach) = PR interval steadily increases then
QRS dropped
* Mobitz Type II = PR interval stays constant and then QRS
dropped
second degree heart block
Rate: atrial rate faster than ventricular rate
* Causes: severe damage to AV node or Bundle of His
* No relationship between p-waves and QRS (complete A-V
disassociation), ventricular contractions are not a result of atrial
activity, like 2 divorced people in same house not communicating
3rd degree (complete heart block)
Prominent voltage = think LVH
If aVL amplitude >11mm
If S in V1 + R in V5 or V6 >
35mm
Any R wave + any S-wave in
precordial leads >45mm
left ventricular hypertrophy (LVH)
R-wave height > S-wave depth
in V1
OR
R-wave in V1 >/= 7mm
Usually with RAD
right ventricular hypertrophy (RVH)
left ventricle depolarizes late
LBBB
right ventricle depolarizes late
RBBB
LAD
Small Q1, deep S3
S wave bigger than R wave in II, III, aVF in absence of MI
left anterior fascicular block (LAFB)
May have normal axis or shift to right
I and aVL small R/deeper S waves
II, III, aVF small Q waves/taller R waves
Rare and hard to diagnose
left posterior fascicular block (LPFB)
“Slurring” of the QRS as it begins its upstroke
Can see in SVT secondary to WPW syndrome = reentry tachycardia
delta waves
Sequence of Changes Ischemia/Infarct
T-wave first inverts within first 1-2 minutes of ischemia (only see on telemetry)
Then T-wave becomes upright and peaked (hyperacute T-waves)
Then ST elevation occurs (signs of injury)
Q-waves then develop (indicates infarct = cells dying) = can also be present with old MI
Always try to get prior EKG!
ST-segment elevation
Indicates acute myocardial injury
Definition = Clinical symptoms consistent
with ACS (generally of ≥ 20 minutes
duration) with persistent (> 20 minutes)
ECG features in ≥ 2 contiguous leads of:
* ≥ 2.5 mm (i.e ≥ 2.5 small squares)
ST elevation in leads V2-3 in men
under 40 years, or ≥ 2.0 mm (i.e ≥ 2
small squares) ST elevation in leads
V2-3 in men over 40 years
* ≥ 1.5 mm ST elevation in V2-3 in
women
* ≥ 1 mm ST elevation in other leads
* New LBBB (LBBB should be
considered new unless there is
evidence otherwise)
STEMI
Reciprocal Changes in STEMI
PAILS
Anterior infarct = inferior reciprocal changes
Inferior infarct = lateral reciprocal changes
Septal infarct = posterior reciprocal changes
Etc.
Non-ST-segment elevation = indicates ischemia or previous infarction
- ST or T wave inverted
NSTEMI
Sgarbossa Criteria
In 1996, Dr. Elena B Sgarbossa first
described criteria to diagnose
infarction in setting of LBBB
- Concordant ST elevation ≥1mm
in ≥ 1 lead
o Any lead where QRS is positive, if
ST elevation at least 1mm in same
direction = 5 points - Concordant ST
depression ≥ 1mm in ≥ 1 lead in
V1-V3
o If ST depression at least 1mm in
same drection of QRS = 3 points - Discordant ST elevation ≥ 5mm
o The ST segment will shift in the
opposite direction of the main QRS
vector, elevation at least 5mm = 2
points
Any concordant shift could represent
underlying injury (STEMI),
essentially score of 3 or more indicates
AMI
what do you see on EKG of hyperkalemia and what medication do you give them
- peaks in T wave
- calcium gluconate
- Irregular, but p-waves
present! - 3 different p-wave
morphologies - Causes: COPD,
hypoxia, pulmonary
hypertension - Management: O2,
treat underlying
condition, rate control
Multifocal Atrial Tachycardia (MAT)
Positive for anterior
STEMI
2% of acute LAD
occlusions
Upsloping ST
depression and peaked
T waves in precordial
leads
De Winter
- Clinical syndrome
- Biphasic or deeply inverted T waves V2, V3
+ recent chest pain that has resolved
Highly specific for critical stenosis of
LAD
Can have normal to mildly elevated
cardiac markers
Prime example of why patients need
serial EKGs
wellens
EKG Troubleshooting/Pitfalls
- Electrode Placement Errors: Can cause misinterpretation of leads
- Artifact: Motion, electrical interference, poor skin contact
- Common Mistakes: Not assessing the rhythm, missing key changes like
ST elevation/depression
Electrical alternans
Large pericardial effusion = heart is shifting back and forth
o Obesity
o COPD
o Pleural or pericardial effusion
o Myocardial infiltration – amyloidosis, sarcoidosis
o Hypothyroidism
- Low voltage
- Widespread ST elevation
- Spodick’s sign = downsloping of TP segments, best in II and
V4-V6
o Can see in acute MI sometimes as well
pericarditis
Acute stress → catecholamine surge → SNS activation → microvascular
spasm
takotsubo
- J (Osborn) waves
- PR, QRS, and QT prolongation
hypothermia
- Genetically inherited sodium channelopathy
- Most common men, FH of sudden death <45yo, typically asymptomatic
- Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave
- Type 1 = wide and large J waves, most concerning
- Type 2 = has >2mm of saddleback shaped ST elevation
- Type 3 = either type 1 or 2, but with <2mm elevation
brugada syndrome
Presence simply means patient is on
Digoxin, not consistent with toxicity
Dig effect = downsloping ST depression, biphasic T waves, short QT interval
“Hockey stick” or”Salvador Dali’s
mustache” sign
digoxin
- Normal QT should be < ½ RR interval
- Congenital long QT syndrome
- Antiarrhythmics Ia, Ic, and III
- Antipsychotics
- Antiemetics
- Quinolones
- Macrolides
- Hypocalcemia
- Hypothyroidism
- Hypothermia
- Associated with increased risk of sudden cardiac death
prolonged QT
