EKGs - short

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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?

III, V1

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
Rate INCREASES with INSPIRATION (IN=IN)

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
Rhythm:
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
Conduction:
Normal (except for PACs)
Rhythm:
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
Conduction:
PJC: P-R interval < 0.12 seconds (if P waves are present)
Rhythm:
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

bigeminy?

1:1 ratio of normal:PVC

trigeminy?

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
QRS: Wide QRS
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)
Conduction:
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
Criteria:
- 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
Criteria:
- 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

NSTEMI

no Q wave or ST elevation
- T wave inversion
- ST DEPRESSION
- 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
II, III, aVF
- 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?

LAD
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

Hemiblock

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

Lown-Ganong-Levine

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

Hyperkalemia

- 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.

Hypokalemia

- ST segment depression
- Flattening (or inversion) of the T wave
- Appearance of a U wave.

Hypercalcemia

shortened QT

Hypocalcemia

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

pericarditis

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

COPD

- 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)

Hypothermia

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.

Also:
- 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

echocardiogram

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

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