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EKGs - short

Normal PR segment length
0.12 - 0.2 sec
3 - 5 small boxes
Normal QRS interval
0.06 - 0.1 sec
1 - 3 small boxes
Normal QT interval
40% of cardiac cycle
Normal P amplitude & duration
< 0.12 sec (3 small boxes)
< 0.25 mV (2.5 small boxes)
Positive P waves in?
left lateral (I, aVL, V5, V6) & inferior (II, III, aVF); usually most positive in II
& most negative in aVR
Often biphasic P in?
Tall R waves in?
left lateral (I, aVL, V5, V6) & inferior (II, III, aVF)
Q waves in?
in one or several of left lateral leads (I, aVL, V5, V6), sometimes in inferior leads (II, III, aVF)
T wave positive in?
Usually in leads w/ tall R waves; left lateral (I, aVL, V5, V6) & inferior (II, III, aVF)
R atrium enlargement?
Leads II (parallel) & V1 (perpendicular; biphasic)
1) P wave > 0.25 mV in II, III, aVF
aka "p pulmonale"
p pulmonale?
RA enlargement, almost always related to pulmonary system; usually causes backup into the ventricle & atria, causing enlargement of atria
L atrium enlargement?
1) V1 terminal portion, P > 1mm below line
2) Terminal portion of P > 0.04 sec (1 small box)
"p mitrale"
p mitrale
LA enlargement due to mitral valve issue
RVH - criteria
1) R > S in V1
2) R progressively smaller from V1-V6
3) S > R in V6
- will cause right axis deviation
(also tall R in III)
LVH - precordial criteria
1. V5: R > 26 mm
2. V6: R > 18 mm
**3. S (V1 or V2) + R (V5 or V6) > 35 mm (best)
4. V6 R > V5 R
axis is not a great indicator (L axis shift)
Sensitivity is low, specificity is high
LVH - limb criteria
1. aVL: R > 13 mm
2. aVF: R > 21 mm
3. I: R > 14 mm
4. R (I) + S (III) > 25 mm
2º repolarization in ventricular hypertrophy - criteria?
1. Down-sloping ST segment depression
2. T wave inversion (R +, T -)
Tends to be most evident in leads most affected by size change
RVH = V1, V2
LVH = V5, V6
causes of arrhythmias
HISDEBS: hypoxia, ischemia/irritability, SNS, drugs, electrolytes, bradycardia, stretch (hypertrophy/enlargement)
symptoms of arrhythmias
none, "palpitations," light-headedness, syncope, angina, HF, sudden death
Types of arrhythmias
1. Sinus origin
2. Ectopic
3. Re-entrant (abnormally shaped path)
4. Conduction blocks (blocked signal)
5. Pre-excitation (shortcut in pathway)
Arrhythmias - 4 quick questions
1. Normal P waves?
2. Wide QRS? (> 0.12 sec indicates pacemaker below Bundle of His)
3. One P for every QRS?
4. Normal rate & rhythym?
Sinus arrhythmia
Appearance is ALMOST NORMAL:
Respiratory - Circulatory interaction
Sinus arrest - criteria
Rate: Regular or Bradycardia
P wave: Normal
QRS: Normal
Conduction: Normal
Rhythm: Irregular: length of pause ≠ multiple of normal rate (random)
Junctional Escape Beat/Rhythym - criteria
Rate: Bradycardia
P wave: Absent or Inverted P; if present, may occur during or after the QRS
QRS: Normal
Conduction: Escape beat: P-R interval < 0.12 seconds (if P present)
Rhythm: Irregular when it occurs (late)
If occurs 3 or more times in a row, is considered junctional escape rhythm
Sinus exit block - criteria
Rate: Regular or Bradycardia
P wave: Normal
QRS: Normal
Conduction: Normal
Irregular: length of pause = multiple of normal rate
(Signal blocked leaving SA node; block is exactly equal to multiple of rate - one or more impulses "missed")
PACs (premature atrial contractions/atrial premature beats) - criteria
Rate: Regular underlying rate
P wave:
Abnormal - they originate from an ectopic pacemaker
QRS: Normal
Normal (except for PACs)
Irregular when PACs occur (early)
PJCs (Premature Junctional Contractions)
AKA: Junctional Premature Beats
Rate: Regular underlying rate
P wave:
Absent or Inverted (like junctional escape)
QRS: Normal
PJC: P-R interval < 0.12 seconds (if P waves are present)
Irregular when PJCs occur (early)
PSVT (Paroxysmal Supraventricular Tachycardia) AKA: AV nodal Re-entrant Tachycardia
Rate: Tachycardia (usually 150 - 200)
P wave: Absent or Inverted (like junctional escape)
QRS: Normal (may be wide, pseudo R')
Conduction: P-R interval < 0.12 seconds (if P)
Rhythm: Regular (abrupt onset and termination)
Carotid massage: slows or terminates
Atrial flutter
Rate:Atrial 250-350
Ventricular: 100 -175
P: Irregular or absent, often "saw tooth"
QRS: Normal
Conduction: AV Block (2:1 > 3:1, 4:1)
Rhythm: Regular (usually)
- Often underlying cardiac disease
Carotid massage: increases block
Atrial fibrillation
Rate: Atrial 400-650;
Ventricular usually 120 - 180
P wave: Not present; often wavy baseline
QRS: Normal
Conduction: Variable AV conduction
Rhythm: Irregularly Irregular
- chaotic, unpredictable depolarizations w/i atrium, no atrial kick
- CAD, HTN, COPD, etc.
Carotid massage: may slow ventricular rate
MAT (Multifocal Atrial Tachycardia):
Rate: Atrial varies, Ventricular 100-200
P wave: ≥ 3 different 'P' waves
QRS: Normal
Conduction: AV conduction, P-R intervals vary
Rhythm: Irregularly irregular
Carotid massage: no effect
Etiology: longstanding COPD, etc.
Wandering Atrial Pacemaker
Rate: Atrial & Ventricular 45 - 100 (slow MAT)
P wave: ≥ 3 different 'P' waves
QRS: Normal
Conduction: P-R intervals vary
Rhythm: Irregularly irregular
Carotid massage: no effect
PAT (Paroxysmal (episodic) Atrial Tachycardia)
Rate: 100 - 200; Ventricular 1:1 (or 2:1, 3:1, 4:1)
P wave: Usually present, abnormal
QRS: Normal
Conduction: P-R interval varies (dt ectopic sites)
Rhythm: Regular (warm up &/or cool down)
Carotid massage: no effect, or only mild slowing
1:1 ratio of normal:PVC
2:1 ratio of normal:PVC
PVCs (Premature Ventricular Contractions)
Rate: Regular underlying rate (usually)
P wave: Absent (or abnormal) in PVC
QRS: PVC: wide > 0.12 seconds; shape is bizarre; T wave inversion
Conduction: Normal before & after PVC
Rhythm: Irregular; may occur in singles, couplets or triplets
Reasons to worry about PVCs?
- Frequency increasing
- Runs of 3 or more consecutively
- Multiple PVC foci
- R-on-T Phenomenon
- PVC in acute MI
Multiple PVC foci
Beats 1 and 4 are sinus in origin. The other three beats are PVCs. The PVCs differ from each other in shape (multiform), and two occur in a row.
PVC - R on T
A PVC falls on the T wave of the second sinus beat, initiating a run of ventricular tachycardia.
Ventricular tachycardia
Rate: 120 - 200 usually
P wave: Usually absent (unrelated to the QRS)
QRS: Wide & bizarre shape (PVCs)
Conduction: No correlation between 'P' if present and QRS
Rhythm: Regular or Irregular
* Cannon A waves may be present
Carotid massage: no effect
Ventricular Fibrillation
Rate: Not attainable
P wave: Obscured by ventricular waves
QRS: No true QRS
Conduction: Chaotic electrical activity
Rhythm: Irregularly Irregular
Accelerated Idioventricular Rhythm
Rate: 50 - 100 (usually slow)
P: Obscured by V waves - SA node is slower than faster ventricular pacing
Conduction: Ventricular only
Rhythm: Regular
- benign rhythm sometimes seen in acute MI/early after reperfusion. Rarely sustained, does not progress to vfib, rarely requires treatment
Torsades de Pointes
Rate: 120 - 200 usually
P wave: Obscured by ventricular waves
QRS: Wide QRS - "Twisting of the Points"
Conduction: Ventricular only
Rhythm: Slightly irregular
1º AV block
Rate: Normal (usually)
P wave: Normal
QRS: Normal
Conduction: P-R interval is > 0.2 seconds (delay)
Rhythm: Regular
2º AV Block - Wenckebach/Mobitz Type I
Rate: Normal or Bradycardia
P wave: Normal & constant P-P interval
QRS: Normal
Conduction: P-R interval is progressively longer until P wave is blocked; the cycle begins again
Rhythm: Irregular
2º AV Block - Mobitz Type II
Rate: Bradycardia
P wave: Normal & constant P-P interval
QRS: Normal or widened (usually associated with a bundle branch block)
P-R interval normal or prolonged (constant); some P waves are not conducted to ventricles (varies)
3º AV Block
Rate: Atrial 60-100; Ventricular 30-45
P wave: Normal with constant P-P interval ("marching through")
QRS: Usually widened (depends on location of escape pacemaker)
Conduction: Atrial & Ventricular activities are unrelated (complete block)
Rhythm: Irregular
Bundle branch blocks - general criteria
Due to changes related to the block, cannot say there is hypertrophy - BBB will make it look like hypertrophy

Rate: Regular or Bradycardia
P wave: Normal usually
QRS: Wide > 0.12 seconds
Conduction: Block occurs in the right or left bundle branches (or both)
Rhythm: Regular usually
Right bundle branch block (RBBB)
Right ventricular depolarization is delayed
- QRS complex > 0.12 seconds
- RSR′ in V1 and V2 (rabbit ears) with ST segment depression and T wave inversion
- Reciprocal changes in V5, V6, I, and aVL.
Left bundle branch block (LBBB)
LV depolarization is delayed
- Wide QRS > 0.12
- Broad (+/- notched) R waves, ST depression & T-wave inversion in I, aVL, V5, V6
- Broad S waves in V1, V2
- Left axis deviation may be present
MI evolution: three phases
Acute Onset: T-wave Peaking (Hyperacute T)(T > ½ R wave)
A Few Hours Later: T-wave Inversion; ST Elevation (STEMI)/NSTEMI; "tombstone sign"
Last: (days/weeks) Significant Q-wave (true infarct)
Ischemic signs
- ST elevation or ST depression:
> 1mm related to baseline (0.08 s (2 boxes) after QRS)
- Also symmetric T-wave inversion in multiple precordial leads
no Q wave or ST elevation
- T wave inversion
- elevated cardiac enzymes (CPK-MB, troponin)
- high risk for later infarction!
Other causes of T-wave inversion?
LBBB: asymmetrical (with wide, upsloping +/- notched QRS); may mask ischemia & bury Q or P
LVH: asymmetrical
Other causes of ST elevation
evolving transmural MI, Prinzmetal's angina, J point elevation, acute pericarditis, acute myocarditis, hyperkalemia, PE, Brugada syndrome, hypothermia
ST-elevation in MI - characteristics
ST segment and T wave merge into each other without a clear demarcation between them.
Prinzmetal's Angina
- ST elevation w/o infarction & ischemia
- Angina that occurs unprovoked at rest (coronary artery spasm) +/- underlying CAD
- Provide nitroglycerin & ST returns to baseline
Significant Q waves?
1) Q wave depth ≥ 1/3 the height of the R in the same QRS
2) Q wave duration > 0.04 seconds (1mm)
Ignore Q waves in?
aVR - almost always has significant-appearing Q waves!
Insignificant Qs common in?
Small Qs in I, AVL, V5 & V6 , II, III
- Due to depolarization of septum
Posterior infarct - reciprocal changes in?
V1 (poss. V2)
- large R = large Q
- upright T (T inversion)
Inferior infarct - arteries & leads?
RCA or distal LAD
- Reciprocal changes in anterior and left lateral leads.
Inferior infarct - with time?
May lose Q-wave significance within 6 months
Lateral infarct - arteries & leads?
LCX or diagonal branch of LAD
I, aVL, V5, V6
- Reciprocal changes in inferior leads.
Anterior infarct - arteries & leads?
I, V2, V3, V4
- Reciprocal changes in inferior leads.
Posterior infarct - arteries & leads?
- RCA distal branches
- Reciprocal changes in V1 (poss. V2)
ST-segment depression, tall R wave
anterior infarct
inferior infarct
lateral infarct
posterior infarct
RVH v. posterior MI
Both may have tall R waves in V1 & V2, but only RVH will have right axis deviation
conduction block of 1 of 3 LBB fascicles
aka fascicular block
L anterior hemiblock
L axis deviation (dt impulse wrapping around from behind)
- Normal QRS duration, ST & T-wave
- Left axis deviation (-30º & -90º)
- No other causes of axis deviation (LVH, LBBB)
L posterior hemiblock
R axis deviation dt flow from anterior fascicle (wrapping around behind)
- Normal QRS duration, ST and T-wave
- Right axis deviation (+90º & +180º)
- No other cause of axis deviation (RVH, MI)
bifascicular block
RBBB + either L hemiblock:
RBBB - wide QRS, RSR' V1 & V2
(RBBB by itself, usually no axis deviation)
- L Anterior - Left axis deviation
- L Posterior - Right axis deviation
RBBB - underlying
May be otherwise normal (sometimes in athletes)
LBBB - underlying
Usually underlying cardiac disease
Bundle blocks evident?
All the time, or only w/ increased HR
Incomplete BBB
no QRS & lead changes - not quite meeting criteria
Wolff-Parkinson-White Syndrome (WPW)
- Bypass pathway (bundle of Kent) between atria & ventricles
- No pause at AV node - short PR interval
- Delta Wave: Slurred initial upstroke of R
Short PR interval < 0.12 seconds
Wide QRS > 0.1 second with delta wave
WPW risks
- PSVT dt reentrant pathway present; may be narrow QRS if via AV node & back up Kent, or wide (& hard to distinguish from V tach) if via Kent & back up AV node
- a fib - Kent acts as free conduit for chaotic atrial activity; may lead to V fib
Intranodal James fibers bypass AV node
- PR interval less than 0.12 seconds
- Normal QRS width
- No delta wave.
Risks of LGL
Not really; mostly reduced CO during stress as no time for atrial kick, impaired filling
- Evolution of (1) peaked T waves, (2) PR prolongation & P wave flattening, & (3) QRS widening.
- Ultimately, the QRS complexes and T waves merge to form a sine wave, and ventricular fibrillation may develop.
- ST segment depression
- Flattening (or inversion) of the T wave
- Appearance of a U wave.
shortened QT
Prolonged QT
- risk of R on T leading to Torsades de Points
causes of long QT
- Medications: many antiarrhythmics, tricyclic antidepressants, quinolone antibiotics, etc.
- hypocalcemia
- Inherited disorder: Long QT Syndromes
Digitalis/Digoxin - indications
- Increase contractility
- Slows AV junction conduction
- Used to tx HF
Digitalis effect - therapeutic levels
Asymmetric ST depression, flat/inverted T-wave
Digitalis toxicity
- enhances automaticity --> tachyarrhythmias
- slowed AV conduction --> AV blocks
- PAT with block MC
DIFFUSE flat or concave ST elevation
- A large effusion can cause low voltage and electrical alternans.
pericardial effusion
1) low voltage - diffuse smaller waves
2) electrical alternans - axis changes w/ each beat; large QRS then small QRS
- Low voltage,
- Right axis deviation (RVH),
- poor R wave progression
- P pulmonale (right atrial enlargement;
tall P >2.5 in II) & abnormal P in V1) - "barrel chest" - increase AP diameter
Acute pulmonary embolism
Signs may include:
- RVH, RBBB (blood not getting through dt clot)
- Arrhythmias (s. tach & a fib MC)
- S1Q3: large S in lead I, deep Q wave ONLY in lead III (if deep Q in several, then infarct)
Brugada syndrome
structurally normal hearts
- autosomal dominant, M > W
- Resembles RBBB; ST elevation & RSR' in leads V1, V2, and V3.
- can cause fast polymorphic V tach (looks like torsades de pointes).
- ICD required (b-blockers no help)
Common in athletes
- sinus bradycardia as low as <30 bpm
- ST elevation in precordial w/ T flattening or inversion.
- LVH, sometimes RVH criteria
- Incomplete RBBB
- 1º or Wenckebach AV block.
- Arrhythmias (junctional, wandering atrial pacemaker)
Osborne waves (ST elevation- abrupt ascent at J point & sudden plunge back to baseline) prolonged intervals, sinus bradycardia, slow atrial fibrillation. Beware of muscle tremor artifact.
CNS disease
Diffuse T wave inversion, with T waves typically wide and deep; U waves.
Indications for stress test
- eval CP/ro CAD
- eval >40 w/ risk factors for CAD
- assess pt response to interventions
- ?eval asx adults who want to start vigorous exercise (lots of false +)
criteria for selection of pts for stress test
- sx classic, atypical, or not at all angina-like?
- established CAD?
- functional tolerance to exercise?
stress test - contraindications
- angina at rest
- uncontrolled HF
- acute systemic illness
- severe aortic stenosis
- hypertrophic cardiomyopathy (sudden death)
- ability to walk/exercise
- caution if systolic > 200 or diastolic > 120; risk of hemorrhagic stroke!
normal physiological response to stress test
- incr SNS
- incr CO
- incr skeletal mm perfusion
- incr O2 extraction
- decr PVR
- incr systolic BP
stress test - pt preparation
- DC meds which may interfere (b-blockers, CCBs, digoxin, nitrates)
- no food, smoking, drink 2-4 hrs before
- pretest EKG
- pretest BP
stress test - finished when?
1) pt cannot tolerate dt compliance or sx
2) 90% of max HR reached
3) Significant EKG changes
stress test - positive when?
Horizontal or down-sloping ST depression (> 1mm & > 0.08 sec); earlier occurrence in test, more significant;
or exercise-induced hypotension, severe arrhythmia, or areas of heart w/ reduced blood
ST segment elevation - reasons
- With an evolving infarction
- In Prinzmetal's angina.
ST segment depression
- With typical exertional angina
- In a non-Q wave infarction.

- positive stress test.
- J point elevation
- Acute pericarditis
- Acute myocarditis
- Hyperkalemia
- Pulmonary embolism (S1Q3)
- Brugada syndrome
- Hypothermia
coronary cath - reasons?
testing & interventions; can be used w/ balloon angioplasty or stenting
Transesophageal or transthoracic - 2D or 3D, Doppler, basically ultrasound of heart; can see movement of blood, valve regurgitation - can see valves & cardiomyopathies very well
Ashman phenomenon
Aberrant conduction of a supraventricular beat commonly seen in patients with atrial fibrillation; wide SV beat after a QRS complex that is preceded by a long pause.
How to interpret an EKG
1) Identify all waves & segments
2) Calculate rate
3) Determine intervals (PR, QT, QRS)
4) QRS axis
5) Hypertrophy & enlargement
6) Rhythm (normal P, wide QRS, P:QRS ratio, regular rhythm?)
7) Coronary artery disease
8) Other weird stuff