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ECG Strip Interpretation

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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 P amplitude & duration
< 0.12 sec (3 small boxes)
< 0.25 mV (2.5 small boxes)
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
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.
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
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
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
Other causes of ST elevation
evolving transmural MI, Prinzmetal's angina, J point elevation, acute pericarditis, acute myocarditis, hyperkalemia, PE, Brugada syndrome, hypothermia
RBBB - underlying
May be otherwise normal (sometimes in athletes)
LBBB - underlying
Usually underlying cardiac disease
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
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
anterior leads
V2, V3, V4
left lateral leads
I, aVL, V5, V6
inferior leads
II, III, aVF
right ventricular leads
aVR, V1
Lead I - angle
+0º
left lateral
Lead II - angle
+60º
inferior
Lead III - angle
+120º
inferior
Lead aVF - angle
+90º
inferior
Lead aVR - angle
-150º - "la la land"
right ventricular
Lead aVL - angle
-30º
left lateral
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)
< 2.5 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)
PR interval represents?
atrial depolarization & transmission through AV junction; supraventricular
QT interval represents?
Beginning of Q to end of T, ventricular depolarization → ventricular repolarization
Basic steps to interpret EKG
1) Identify all waves & segments
2) Calculate the rate
3) Determine intervals
4) Determine QRS axis
5) Recognize hypertrophy & enlargement
Waveform & orientation of I?
+0º
predominantly + (L arm +, R arm -)
left lateral
Waveform & orientation of II
+60º
predominantly + (R arm -, L Leg + (think "ll=LL")
inferior
Waveform & orientation of III
+120º
typically biphasic (L arm -, L Leg +)
inferior
Waveform & orientation of aVR
-150º "la la land"
predominantly - (R arm +, all others -); center of heart → R arm
right ventricular
Waveform & orientation of aVL
-30º
typically biphasic (L arm +, all others -); center of heart → L arm
left lateral
Waveform & orientation of aVF
+90º
predominantly + (both legs +, both arms +); center of heart → feet
inferior
Normal axis?
I +
aVF +
Right axis deviation?
I -
aVF +
Extreme right axis deviation?
I -
aVF -
Left axis deviation?
I +
aVF -
R atrium enlargement?
Leads II (parallel) & V1 (perpendicular; biphasic)
1) P wave > 2.5 mm in II, III, aVF
aka "p pulmonale"
Precise axis determination?
Look for most biphasic wave - it will be perpendicular to this.
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 (most useful)
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 bradycardia - criteria
HR < 60 bpm
Sinus tachycardia - criteria
HR > 100 bpm
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
vagal stimulation
PNS stimulation - slows conduction through AV node; not if suspected carotid plaques
- valsalva, squatting, etc.
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 (narrow)
Conduction: Variable AV conduction, P-R intervals vary
Rhythm: Irregularly irregular
- Various unpredictable atrial pacing sites
- Etiology: Often severe lung disease, longstanding COPD, etc.
Carotid massage: no effect
Wandering Atrial Pacemaker
Rate: Atrial & Ventricular 45 - 100
P wave: ≥ 3 different 'P' waves
QRS: Normal
Conduction: P-R intervals vary
Rhythm: Irregularly irregular
- slower form of MAT
Carotid massage: no effect
PAT (Paroxysmal (episodic) Atrial Tachycardia)
Rate: 100 - 200; Ventricular response 1:1 (or 2:1, 3:1, 4:1)
P wave: Usually present, abnormal
QRS: Normal
Conduction: P-R interval varies (due to ectopic sites)
Rhythm: Regular (may see warm up &/or cool down); unlike abrupt stop/start of PSVT; may be hard to distinguish
Carotid massage: no effect, or only mild slowing
MC ventricular arrhythmia?
PVCs - common in healthy people
bigeminy?
1:1 ratio of normal:PVC
trigeminy?
2:1 ratio of normal:PVC
PVCs (Premature Ventricular Contractions)
Rate: Regular underlying rate (usually); may happen occasionally in otherwise normal heart
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 (usually slow)
P wave: Obscured by ventricular waves (occur during ventricular contraction) - SA node slower than faster ventricular pacing than should be
QRS: Wide QRS
Conduction: Ventricular only
Rhythm: Regular

- benign rhythm that is sometimes seen during acute MI or 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) - slowing at the AV
Rhythm: Regular
2º AV Block - Wenckebach or Mobitz Type I
Rate: Normal or Bradycardia
P wave: Normal morphology & 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 morphology & 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:
- Wide QRS
- RSR' in V1, V2 ("bunny ears") with ST depression and T wave inversion
- Late S waves in I, aVL, V5, V6 (reciprocal changes)
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" (similar shape) - often associated with heart attack

Last: (days to weeks later)
- 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
J-Point elevation
(often <40)
At rest, returns to baseline if exercising
Flat, very distinct T wave
NO CLINICAL SIGNIFICANCE!
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)
+
- Anterior - Left axis deviation
- Posterior - Right axis deviation
RBBB - underlying
May be otherwise normal (sometimes in athletes)
LBBB - underlying
Usually underlying cardiac disease
Bundle branches evident?
All the time, or only w/ increased HR
Incomplete BBB
no QRS & lead changes - not quite meeting criteria
Wolff-Parkinson-White Syndrome (WPW)
- By-pass 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 and P wave flattening, and (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
RVH, RBBB
- Blood not getting through dt clot
Arrhythmias
S1Q3: large S in lead I, deep Q wave ONLY in lead III (if deep Q in several, then infarct)
- sinus tach & a fib MC arrhythmias
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
Common in athletes
- sinus bradycardia as low as <30 bpm
- ST segment elevation in the precordial leads with T wave 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.
**Mobitz Type I or Wenckebach Atrioventricular Block*****likely due to increased parasympathetic nerve activity. There is a progressive increase of the PR interval until finally a beat occurs with no conduction to and no action potential occurring in the ventricles. There is no conduction from the atria to the ventricles and a "dropped beat" occurs. The ratio of conducted to non-conducted beats can vary.
*Mobitz type II atrioventricular block*
1.sudden failure of conduction from the atria to the ventricles.
2.There is no progressive elongation of the PR interval as in Wenckebach
3.The fourth P wave is not followed by a QRS complex - action potentials never reach the ventricles.
4.This can lead to complete atrioventricular block and compromised heart function due to an excessively slow ventricular rate and low cardiac output.
*Complete Heart Block.*
1.Damage to the atrioventricular node, bundle of His or both bundle branches could cause a complete failure of conduction from the atria to the ventricles.
2.Note that the P waves are occurring regularly. Similarly, the R waves are occurring regularly, but at a much slower rate than the P waves. There is no predictable, consistent relationship of P wave to R wave occurrence.
In a premature atrial beat the P wave occurs earlier than expected (arrows in Figure 30), but it is followed by the usual waveforms.
*Junctional premature beat*
The fourth beat originates in the lower part of the atria near the junction of the atria with the ventricles (Figure 31). What feature of the P wave suggests that it originates in the lower part of the atria
2.Negative P wave indicates atrial depolarization from "bottom, up" rather than the usual progression from the sinoatrial node down.
In paroxysmal atrial tachycardia (Figure 32) there is a run of closely spaced heartbeats that originate in the atria, although not necessarily in the sinoatrial node. There is a P wave preceding each QRS complex.
*Atrial flutter*
Action potentials travel an abnormal, circular, usually counterclockwise path in right atrial myocardium affected by drug toxicity or disease. This repetitive travel around a loop results in depolarization of the atria at a rate of about 300/minute
*Atrial fibrillation*
ventricular depolarizations are irregularly spaced (Figure 34). Since the atrial electrical activity is random and chaotic, there is no organized depolarization wave front and no P waves. Likewise, there is no effective atrial contraction, although that is not measured by the ECG
*Wolff-Parkinson-White (WPW)*
In WPW there are abnormal muscular connections from the atria to the ventricles (bundles of Kent), bridging the annulus fibrosus. These accessory pathways lead to earlier than normal ventricular activation.
* Premature ventricular beat*
There is no preceding P wave because the premature ventricular beat originates within a ventricular muscle focus
2.Its shape and long duration are related to the slower moving, less organized wave front of depolarization when the conduction system does not distribute the
*Ventricular Tachycardia*
There is no P wave preceding each R wave since the ventricular depolarizations are arising from ventricular muscle.
2.Pumping becomes inadequate and circulatory collapse with shock may occur. Ventricular tachycardia can deteriorate into ventricular fibrillation and death.
In ventricular fibrillation ventricular electrical activity is random and chaotic. There is no organized, sequential wave of depolarization.
NSR (Normal Sinus Rhythm)
Sinus bradycardia
Sinus tachycardia
Premature atrial complex (PAC)
Paroxysmal atrial tachycardia (PAT)
Atrial flutter (A-flutter)
Atrial fibrillation (A-fib)
Premature ventricular contractions (unifocal PVCs)
PVC (couplets)
bigeminy or trigeminy
V-tach
V-tach
Ventricular fibrillation (V-fib)
Asystole
First degree AV block
Second degree AV block type 1
Second degree AV block type 2
Third degree AV block
Third degree AV block
Junctional rhythm
Idioventricular rhythm
Myocardial ischemia
Myocardial infarction
Multifocal PVCs
Atrial Flutter
Atrial Fib
Polarized
Resting state is called the ___ state.
Repolarizing
When a cell returns to its original negative charge, it is ___.
Insulated
The atria and ventricals are electrically ___ from each other.
Bi
Limb leads are __-polar in electrical potential.
Precordial
Chest leads are called ___ leads.
Uni
Chest leads are _-polar in electrical potential.
Center
The reference point for unipolar, precordial leads in near the __ of the heart.
P
To monitor the atrial rate of the heart, count the ___ waves.
Augmented
The letter "A" in AVf = ___.
Pacemaker
The only cells the are autorythmic are ___ cells.
U
The second of a spit T wave is called a ___ wave.
Taller
T waves are ___ than P waves and asymetric.
Perkinje fibers
The isoelectric line between the P wave and the QRS is when the impulse is traveling through the ___.
Pause
The isolelectric line that makes up the ST segment is the __ before ventrical repolarization.
J
The upstroke just after QRS is the __ mark.
T
The QT interval begins before Q and ends after the __ wave.
Left
LL or AVf lead is usually locacated below and to the __ of the heart.
Left arm
aVl = ___ location of lead.
Sternum
Leads V1 and V2 straddle the ___.
Sinus
SA node is the pacemaker of the heart and is the norce of ___ rhythm.
Triangle
Limb leads create a ___ shape in the frontal (vertical) plane.
Horizontal
Precordial (chest) leads view the heart on the ___ plane.
Voltage
"V" in aVr = ___.
II
Lead ___ is used for continous ECG monitoring.
Fast or slow
First question to ask when looking at an ECG = ___.
Regular or Irregular
Second question to ask when looking at an ECT = ___.
3rd
With a __ degree heart block, no communication takes place between the artia and ventricals.
2nd
___ degree heart block is characterized by partical communication between atria and ventricals.
Ectopic
Superventrical tach is intiated by an ___ pacemaker.
Escape
A non-sinus impluse generations is called an ___ pacemaker.
Ectopic tachycardia
Top = AV; Bottom = Ventricular origin*
100
Tachycardia is HR greater than __.
P
To check whether atrial rhythm is irregular, use calipers to measure distance between ___ waves.
R
To check whether verntricular rhythm is irregular, use calipers to measure distance between ___ waves.
P
If atria and ventricular rhythm is associated like it should be, every QRS will have a __ wave.
Irregular
Premature complexes are ectopy, commly cause rhythm to be ___.
Arrest
An irregular rhythm in which the SA node fails to fire, this phenomenon is called sinus ___.
Sinus Arrest
Flat line sandwhiched between a regular rhythm is an irregular process called ___.
Notched
First image is a ___ P wave.
Wide, notched
Second P wave is both ___ and ___.
Biphasic
Third P wave is ___.
SA node
All these P waves lack __ impulse generation.
Inverted
This P' wave is ___.
First degree heart block
Delay between P and QRS (3rd arrow) is seen with what condition?
I
This type of heart block is 2nd degree type ___, with increasing delays due fatiged AV node.
Weinke-bach
A. P gets further away from QRS until QRS is dropped. This is called ___.
PR
A has an increasingly prolonged ___ interval until QRS is dropped.
QRS
B. indicates a repeated and complete drop of what complex?
2, II
Both A and B are sub-types of __ degree, type __ heart block.
Third
This is an example of ___ degree heart block.
Nothing
What is wrong with this ECG?
Biphasic
These P waves are __, usually due to L atrial enlargement.
P wave
Hmmm. Something's missing.
Weinke-bach
This abnormal ECG is called ___.
Atrial flutter
This is called ___.
Peaked
Increases R atrial pressure/dilation causes a ___ P wave.
Notched
Increases L atrial pressure/dilation causes a ___ P wave.
Biphasic
Both R and L atrial dilation causes a ___ P wave.
Flutter
Atrial __ waves are seen at P wave rates <350
F
Flutter waves are __ (letter) waves and occur when atrial rates are between 250-350 beats per min.
Sawtooth
F waves replace normal P waves is called ___ waveform.
Dysrhythmia
Cycles of slowing and speeding HR is called Sinus ___.
Wandering atrial
P waves that change in appearance due to shifting impulse generation from SA to AV nodes is called ___ pacemaker.
PAC
An early atrial impulse generated outside the SA node causes a ___.
Premature atrial
PAC stands for ___ complex.
Ectopic
Abnormal location for impulse generation is call an ___ site.
Normal
Two questions to ask about P waves. Do they have a ___ appearance? Does one come before every QRS?
QRS
Two questions to ask about P waves. Do they have a normal appearance? Does one come before every ___?
P
Most __ waves are round and upright when normal.
P'
P waves that originate from the atria and not the SA node are called __ waves.
SA
PAC's, wandering pacemaker, and atrial tachycardia all lack ___ impulse generation.
P'
Peaked, notched T waves can be observed when __ wave becomes buried in the T wave. (i.e. atrial tach)
Ectopic
P' waves are ___ in impulse generation.
f
Lowercase __ waves are used for chaotic fibrillary contractions that are >350 beats per min.
Inverted
Atria contract bottom up (inverted) and produce an ___ P' wave when impulse is generated from AV node or L atria.
First
Prolonged PR intervals is an example of ___ degree heart block.
Ventricles
Heart blocks occur when impulse from SA node fails to make it to the ___.
2
There are __ types of second degree heart block.
II
2:1, 3:1, or 4:1 atria to ventricle contraction ratios are seen with 2nd degree, type __ heart block.
I
2nd degree heart block type ___ is characterized by variable heart block patterns with increasing delay.
Pumping
ECG limitation = can tell how well the heart is ___.
Aorta
Coronary arteries are the main blood supply for the heart and originate in the base of the ___.
BP
__ = CO x Peripheral vascular resistance
CO
___ = HR x SV
Sympathetic
NE and E are the neurotransmitters of the ___ nervous system. (Fight or flight)
Parasympathetic
Ach is the neurotransmitter of the ___ nervous system. (Rest and Digest)
Na, K, Ca
Three cations responsible for electrical conduction are __, ___, and ___ (abv).
150
Ventricular tach begins at ___ beats per minute.
Ectopic pacemaker
Ventricular tach is the result of impulse creation from an ___.
100
Junctional tach begins at __ beats per minute.
Atrial fib
Example of totally irregular (irregularly irregular) rhythm with no consistency = ___.
II
Use lead __ to determine regularity.
Appearance
P waves that continually change in ___ have a wandering impulse origin within the atria.
Normal
___ progression of impulse from AV to perkinje fibers gives QRS complex above.
Tall
__ QRS complexes (seen above) are the result of ventricular hypertrophy or conduction problems.
thyroid
Fat or fluid in chest, and hyper____ can cause low voltage QRS (seen above).
Supraventricular
Wide bizarre QRS complexes (above) are associated with ___ impulse generation.
Conduction
The wide QRS (above) is an example of aberrant ventricular ____.
Delta
Abnormal slurring (A) of this QRS complex is called a ___ wave.
Preexitation
The condition represented above is called ventricular ___.
Pacemaker
Arrow points to ___ spike seen preceding this wide abnormal QRS.
Opposite
QRS complexes are ___ the direction of the T wave = ventricular dysrhythmias.
Pre-excitation
___ (above) result from a ectopic ventricular impulse before the SA can fire. Note QRS is wide.
Idioventricular
Slow (20), ____ escape rhythm is pictured above with a wide QRS from ___ (same) pacemaker.
Tachycardia
3 PVC's in a row (above) is Ventricular ___, also with wide QRS and an ectopic ventricular pacemaker.
Torsades de pointes
Multiple PVC's with rotating ventricular ectopic pacemakers (above) are called __.
Third degree heart block
Name above condition.
V. Fib
Name above ventricular condition.
Asystole
Name above condition.
Normal
Name above condition
Q wave.
What is missing in every cycle?
...
PVC
Name above condition.
Tachycardia
This person is in ventricular ___.
V fib
This person is in ___.
QRS
Ventricular ectopic pacemakers cause abnormal ___ complexes.
QRS
Intraventricular blocks can cause abnormal ___ complexes.
QRS
Ventricular hypertrophy can cause abnormal ___ complexes.
QRS
Cardiac pacemakers can cause abnormal (ventricular) ___ complexes.
Aberrant
If one bundle branch recovers slow from previous impulse, ___ conduction results with a widened QRS.
Delayed
Widened QRS during aberrant conduction occurs because one bundle branch impulse is ___.
Opposite
Ventricular dysrhythmias are identifiable when the QRS is in the ___ direction of the T wave.
R'
Bundle branch block creates an abnormal upward deflection after the QRS called the __ wave.
Pre-excitation
A partial premature ventricular contraction is also called ____.
Compensatory pause
When the overall rhythm is not disturbed after a PVC, a ___ is needed to keep the rate regular.
Junction
The AV node is also known as the AV ___, thus ___al (same) tachycardia, etc.
Multifocal
___ PVC's have many pacemaker sites.
Paroxysmal
A brief or transient electrical disturbance is called ___.
Retrograde
Inverted P waves are associated with ___ depolarization of the atria.
Idioventricular
When the foci of a ventricular pacemaker (20 beat/min) is unknown, it's called a ___ rhythm.
Trigeminal
PVC's that occur every three contractions are termed ___.
Polymorphic
___ V-tach has multiple ectopic pacemakers.
Standstill
Ventricular ___ occurs when when the ventricles take a couple of beats off.
Pulseless
___ electrical activity occurs when the and impulse fires but no contraction occurs.
Disassociation
AV ___ occurs with third degree heart block. Atria and ventricles beat independently.
Second, 1
Think AV fatigue, lengthening PR leading to dropped QRS in ___ heart block Type ___.
Wenckebach
Second degree heart block Type 1 is A.K.A. ___.
P wave
Supra-ventricular tachycardia is characterized by an absent ___.
V. Tach
Three or more PVC's in a row is termed ___.
Wider, shorter
P' is __ than P due to its location closer to the AV node.
Shorter
The PR segment is ___ because the impulse has less distance to travel. The pacemaker is closer to the AV node.
PR
The ___ interval encompasses the entire impulse from SA through the Perkinje fibers.
Missing
When you evaluate the PR interval, it can be either ___, short, long, or irregular in length.
Short
When you evaluate the PR interval, it can be either missing, ___ long, or irregular in length.
Long
When you evaluate the PR interval, it can be either missing, short, ___, or irregular in length.
Irregular
When you evaluate the PR interval, it can be either missing, short, long, or ___in length.
Pre-excitation
Shorter PR intervals can lead to ___ of the ventricles.
Supraventricular
In pre-excitation of the ventricles, the impulse is premature and located ___.
SA node
lies in posterior wall of RA near inlet of the SVC
SA node
aka the pacemaker of the heart; generates electrical impulses automatically and regularly
AV node
relays electrical impulses from atria into ventricles
AV node
delays transmission of electrical impulses and allows time for the Atria to contract
Bundle of His
distal part of AV junction, lies in upper part of inter-ventricular septum, connecting AV node with 2 bundle branches
0.03, 0.05
Once electrical impulses enter bundle of His they travel more rapidly on their way to bundle branches, taking ____ to ____ seconds
Perkinje Fibers
these spread widely throughout ventricles beneath endocardium in the myocardium
Electrical Impulses
___________ result of brief, but rapid flow of positively charged ions (primarily Na and K ions and to a lesser extent, Ca ions) back and forth across the cardiac cell membrane
polarization
this phase, represented by the T-wave, is the heart at rest; there is no stimulation, contraction, or measurable activity
depolarization
this phase is the discharge of electrical energy or contraction that follows the impulse
atrial
___ depolarization = P-wave
ventricular
____ depolarization = QRST-wave
repolarization
represented by the T-wave; it is the phase of electrical recovery of the heart when the cells recharge
P-wave
represents firing of SA node and depolarization (contraction) of atria.
QRS complex
represents journey of electrical impulse from AV node through Purkinje Network (no > than 0.20 seconds)
T-wave
represents repolarization (relaxation) of the ventricles; cells recharge themselves in preparation for another impulse
baseline
follows U wave; heart is polarized or at rest
isoelectric
the baseline is also know as the ____ line
PR Interval
time required for impulse to travel from SA node, through atria to AV node (no more than 0.12 seconds). (measure from beginning of P to beginning of Q) (helps identify bundle branch block)
ST elevation
indicates myocardial infarction
ECG
recording of electrical impulses associated with cardiac contraction and relaxation
time, voltage
What two things are recorded by ECG?
25 mm/sec
What is the standard paper speed of an ECG recording?
dry, hair, oil
When applying electrodes, make sure skin is _____, any overabundance of ____ is clipped, and remove excess skin ____ with alcohol
bony, folds, scar, breast, muscle, apex
Avoid applying electrodes:
_____ areas
Skin _____
____ tissue
_____ tissue
_____ mass
Heart ____
highest, stump
When placing leads on pts with amputations, place lead in ______position on limb/away from ______
artifacts
abnormal waves and spikes in an ECG that result from sources other than electrical activity of heart and interfere with or distort component of ECG
the machine
What is the least likely cause of an artifact?
somatic tremors
can occur in tense or nervous patients or those shivering from cold and give ECG a finely or coarsely jagged appearance
electrodes, paste
Loose _____ - or ones in poor electrical contact with skin because of insufficient or dried electrode _____ can cause multiple sharp spikes and waves in the ECG
Sinus Rhythm
Rhythm: Normal
Rate: WNL
Complexes: present
Reflects normal functioning conduction system without interference of any bodily symptoms or diseases
Sinus Arrhythmias
Rhythm: Irregular
Rate: 60-100bmp
Complex: present
Treatment usually not needed
Sinus Bradycardia
Rhythm: regular
Rate: below 60bpm
Complex: Present
Sinus Tachycardia
Rhythm: regular
Rate: >100bpm
Complex: present
Atrial Flutter
Rhythm: regular
Rate: 250-350 bpm
Complex: QRS is Present, no P wave
Appearance of "sawtooth"
Atrial Fibrillation
Rhythm: irregular
Rate: 375-700 bpm
Complex: QRS is slightly present or normal, no P wave
PVC
Rhythm: regular and irregular
Rate: same as rhythm
Complex: will be stretched, present, or unidentifiable with no P wave
Ventricular Tachycardia
Rhythm: regular
Rate: >100 bpm
Complex: not present, but widened, no P wave
AED
When V-tach is pulselesss - should be treated with _______
Ventricular Fibrillation
Rhythm: Irregular
Rate: >300 bpm
Complex: not identifiable
defibrillation
Treatment for V-Fib is immediate _____, ventilation and lidocaine
Asystole
Rhythm: none
Rate: none
Complex: none
AKA: "flat line"
pacemaker
mechanical device that stimulates heart muscle to contract by creating an electrical current and delivering that current to muscle via specialized wire in the heart
jugular, subclavian
Temporary Transvenous Pacemaker is placed using a wire inserted through ____ or _____ vein.
external pacemaker
Used in emergency situations when pacing must be instituted rapidly. Systems use adhesive pads, placed on the anterior and posterior walls of chest over heart. External power source delivers electrical current through chest wall to heart.
cardioversion
External electrical stimulation that interrupts irregular conduction pattern of heart and restores it to normal sinus rhythm (must have some heart rate present)
cardioversion
Shock (25 jules) that momentarily stops electrical cardiac activity, allowing a normal pacemaker to take over. (changes one rhythm to another)
Continuous cardiac monitoring required for at least 24 hours after procedure
Only treats a-fib and a-flutter
adenosine
this medication can be used in place of cardioversion
defibrillation
stops the heart temporarily to allow normal rhythm to begin by delivering electrical shock to the heart through paddles placed on chest at base and apex of heart
LOC, ECG
After successful defibrillation, monitor ___, ___ pattern, BP, P and R rates at frequent intervals
U-wave
usually only seen in children, if seen in adults there is something wrong (i.e. potassium levels)
block
if an ECG stip is missing a QRS, but the rhythm can be "marched out" equally, the the pt has a heart _____.
A-fib
rhythm that is most worrisome because it can lead to stroke; heart quivers but doesn't pump causing the blood to pool producing blood clots
pulseless
Only defib a pt in v-tach if they are ____.
code cart monitor
In ICU, if a code cart is needed, which monitor should you use?
spike
Pt with a pacemaker will have a ____ between the P and Q wave.
bipolar lead
type of ECG lead that measures the flow of electrical current in two directions at the same time; consists of leads I, II, and III
input, signal process, output
three purposes of ECG
input
Standard, augmented, input, precordial---which of these is not a lead
Einthoven triangle
consists of RA, LA, LL leads, the RL lead is the ground.
decreased, increased
If a pt is in shock, the blood pressure is ____ and the heart rate is _____.
cardioversion
used on a patient with a-fib
sa node not firing
Why would a patient need a pacemaker?
mid-axillary
Where is V6 placed?
4th intercosal, right sternal border
Where is V1 placed?
atrial kick
slight pause of impulse between SA and AV so the blood has time to push into the ventricles
sodium pump
causes contraction by making sodium and potassium ions switch places across the membrane
depolarization
when the heart is working (PQRS)
repolarization
when the heart is at rest (T)
atrial
P is ____ activity
ventricular
QRS complex and T-wave is ____ activity
round
P wave should be ____ with a QRS immediately followin
v-tach
3 PVCs together can leed to _____.
PVC
ventricular activity that is wide and bazarre
low fowlers
what position would you put a pt in for an ECG that had CHF, COPD or any other condition in which they can't lie flat?
equal
When measuring, atrial and ventricular should be ____
monitor heart for 24 hours
After cardioversion, what is the most important nursing implication?