Like this study set? Create a free account to save it.

Sign up for an account

Already have a Quizlet account? .

Create an account

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

Please allow access to your computer’s microphone to use Voice Recording.

Having trouble? Click here for help.

We can’t access your microphone!

Click the icon above to update your browser permissions and try again


Reload the page to try again!


Press Cmd-0 to reset your zoom

Press Ctrl-0 to reset your zoom

It looks like your browser might be zoomed in or out. Your browser needs to be zoomed to a normal size to record audio.

Please upgrade Flash or install Chrome
to use Voice Recording.

For more help, see our troubleshooting page.

Your microphone is muted

For help fixing this issue, see this FAQ.

Star this term

You can study starred terms together

Voice Recording