CV2 EKG - Junct + Vent Rhythms, 12 Lead Acquistion, Axis Dev

arrhythmias sustained or originating in the AV junction (4)

*Premature Junctional Contractions

*Junctional Escape Complexes and Rhythm

*Accelerated Junctional Rhythm

*Paroxysmal Junctional Tachycardia

characteristics of arrhythmias sustained or originating in the AV junction

*Inverted or absent P Waves in Lead II

*PRI of < 0.12 Seconds

Normal QRS Complex Duration

junctional rhythms originate from 

electrically active tissue with automaticity in the junction between the atria and the ventricles, typically near the AV node 

intrinsic rate of AV node

40-60 bpm 

p waves morphologies in junctional rhythms

premature junctional contractions

rate

rhythm

pacemaker site

p waves

PRI

QRS

rate = depends

rhythm = depends

pacemaker site = ectopic focus in AV junction

p waves = inverted; may occur after QRS

PRI = normal except for early beat

QRS = usually normal

PJC

rate

rhythm

pacemaker site

p waves

PRI

QRS

junctional rhythm

rate

rhythm

pacemaker site

p waves

PRI

QRS

rate = 40-60

rhythm = regular 

pacemaker site = AV junction 

p waves = absent, inverted or after QRS

PRI = often can’t measure

QRS = usually normal 

junctional rhythm

junctional escape rhythms

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = </= 40 

rhythm = regular 

pacemaker site = AV junction 

p waves = absent, inverted, may occur after QRS

PRI = often cannot measure

QRS = usually normal 

junctional escape rhythm

accelerate junctional rhythm

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = 60-100

rhythm = regular 

pacemaker site = AV junction 

p waves = inverted, may occur after QRS

PRI = often cannot measure

QRS = normal 

accelerated junctional rhythm

junctional tachycardia

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = 100-180

rhythm = regular

pacemaker site = AV junction 

p waves = inverted, may be after QRS

PRI = often cannot measure

QRS = normal 

junctional tachy

AV node reentrant tachycardia occurs due to

an electrical “short circuit” contained within the AV node

AVNRT is characterized by

*Very rapid rates (usually 150-250)

*Regular with no beat-to-beat variability

*P waves difficult to discern.  If present, may be buried in QRS complex (arrows).

*PR interval usually prolonged

AVNRT

AVNRT

AV reentrant tachycardia is different than AVNRT because

it occurs due to an electrical “short circuit”, but in AVRT the short circuit is not contained to the ventricle.

In patients with AVRT, communication between the atria and ventricles may happen either via the

AV node or via a pathological accessory pathway

In AVRT, conduction may be 

orthodromic or antidromic

orthodromic AVRT is

*Antegrade conduction (normal) via AV node and His bundle

*Retrograde conduction via accessory pathway

orthodromic AVRT is the most

common form of AVRT (90%)

orthodromic AVRT may be initiated by 

PVCs; ECG features are nearly identical to an AVNRT

antidromic AVRT is

*Antegrade conduction via accessory pathway

*Retrograde conduction via AV node and His bundle

antidromic AVRT can also be initiated by ___ and is ___

PVCs; rare (~10%)

**on ECG = if present, P waves are inverted.  PR interval will be prolonged

orthodromic AVRT

antidromic AVRT

Patients who have pathological accessory conduction pathways between atrium and ventricle tend to have

abnormal baseline features on their ECG, even when not experiencing an arrhythmia.

These conditions are called preexcitation syndromes, named because the ventricle is

depolarized earlier than usual by antegrade conduction through the accessory pathway

There are two commonly recognized preexcitation syndromes:

Wolff-Parkinson-White syndrome

*Lown-Ganong-Levine syndrome

WPW syndrome involves

*Accessory pathway via the Bundle of Kent

*Bridges fibrous tissue between atrium and ventricle, providing an electrical connection

*Usually remote from the AV node

*Can be on either left or right side of heart

criteria for WPW syndrome

wolff-parkinson-white syndrome

lown-ganong-levine syndrome consists of 

*Accessory pathway historically thought to be James bundle (James fibers)

*Connect atria to distal AV node or proximal His bundle

caveat with LGL syndrome is

*electrophysiology data casts some doubt on this mechanistic hypothesis and has had difficulty identifying a consistent accessory pathway in LGL patients

The ECG findings of Lown-Ganong-Levine syndrome are

more subtle than those of WPW

The only characteristic baseline finding of LGL syndrome

is a short PR interval <120 ms

WPW vs LGL syndromes

Arrhythmias Originating Within the AV Junction (AV blocks)

located = at the AV Node, at the Bundle of His, or below the Bundle of His

*First-Degree AV Block

*Type I Second-Degree AV Block

*Type II Second-Degree AV Block

*Third-Degree AV Block

first degree AV block 

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = depends on underlying rhythm

rhythm = usually regular

pacemaker site = SA node or atrial

p waves = normal

PRI = > 0.20 seconds

QRS = usually <0.12 seconds

first degree AV block

first degree AV block

etio

clinical significance

treatment

*Etiology

• Delay in the conjunction of an impulse through the AV node.

• May occur in healthy hearts, but often indicative of ischemia at the AV junction.

*Clinical Significance

• Usually not significant, but new onset may precede a more advanced block.

*Treatment

• Generally, none required other than observation.

• Avoid drugs that may further slow AV conduction.

type I second degree AV block

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = atrial, normal; ventricular, normal to slow

rhythm = atrial, regular; ventricular, irregular

pacemaker site = SA node or atrial

p waves = normal, some P waves; not followed by QRS

PRI = increase until QRS is dropped, then repeats

QRS = usually, <0.12 seconds

type I second degree AV block

Conduction Pattern in Type I Second Degree

type I second degree AV block

etio

clinical significance

treatment

*Etiology

• Also called Mobitz I, or Wenckebach.

• Delay increases until an impulse is blocked.

• Indicative of ischemia at the AV junction.

*Clinical Significance

• Frequently dropped beats can result in cardiac compromise.

*Treatment

• Generally, none required other than observation.

• Avoid drugs that may further slow AV conduction.

• Treat symptomatic bradycardia.

Mobitz 1 or Wenkebach is 

type I second degree AV block

type II second degree AV block

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = arial, normal; ventricular, slow

rhythm = may be regular or irregular

pacemaker site = SA node or atrial 

p waves = normal, some p waves not followed by QRS

PRI = constant for conducted beats, may be > 0.21 seconds

QRS = normal or > 0.12 seconds

type II second degree AV block

2:1 AV block

narrow vs wide QRS in second degree AV blocks

Narrow QRS favors final diagnosis of 2^nd degree type I

Wider QRS favors final diagnosis of 2^nd degree type II

conduction Ratios in Type II Second Degree Heart Block

type II second degree AV block 

etio

clinical significance

treatment

*Etiology

• Also called Mobitz II or Classic.

• Intermittent block of impulses.

• Usually associated with MI or septal necrosis.

*Clinical Significance

• May compromise cardiac output and is indicative of MI.

• Often develops into full AV blocks.

*Treatment

• Avoid drugs that may further slow AV conduction.

• Treat symptomatic bradycardia.

• Consider transcutaneous pacing.

third degree AV block

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = atrial, normal; ventricular, 40-60

rhythm = both atrial and ventricular regular

pacemaker site = SA node and AV junction or ventricle

p waves = normal, with no correlation to QRS

PRI = no relationship to QRS

QRS = 0.12 seconds or > 

third degree AV block 

third degree AV block

etio

clinical significance

treatment

*Etiology

• Absence of conduction between the atria and the ventricles

• Results from AMI, digitalis toxicity, or degeneration of the conductive system.

*Clinical Significance

• Severely compromised cardiac output.

*Treatment

• Transcutaneous pacing for acutely symptomatic patients.

• Treat symptomatic bradycardia.

• Avoid drugs that may further slow AV conduction.

arrhythmias Originating in the Ventricles

*Ventricular Escape Complexes and Rhythms

*Accelerated Idioventricular Rhythm

*Premature Ventricular Contractions

*Ventricular Tachycardia

*Related Dysrhythmia

*Ventricular Fibrillation

*Asystole

Artificial Pacemaker Rhythm

ventricular escape rhythm/idioventricular escape complex

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = 25-40

rhythm = escape complex, irregular; escape rhythm, regular

pacemaker site = ventricle

p waves = non

PRI = none

QRS = > 0.12 seconds, bizarre

ventricular escape rhythm/idioventricular escape complex

ventricular escape rhythm/idioventricular escape complex

etio

clinical significance

tx

*Etiology

• A subtype of ventricular escape rhythm that frequently occurs with MI.

• Ventricular escape rhythm with a rate of 60–110.

*Clinical Significance

• May cause decreased cardiac output if the rate slows.

*Treatment

• Does not usually require treatment unless the patient becomes hemodynamically unstable.

• Primary goal is to treat the underlying MI.

premature ventricular contractions (PVCs)

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = underlying rhythm

rhythm = interrupts regular underlying rhythm 

pacemaker site = ventricle

p waves = none

PRI = none

QRS = >0.12, bizarre 

PVCs

PVCs etio

*Single ectopic impulse resulting from an irritable focus in either ventricle.

*Causes may include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid–base disturbances, electrolyte imbalances, or as a normal variation of the ECG.

*May occur in patterns

*Bigeminy, trigeminy, or quadrigeminy.

*Couplets and triplets.

bigeminy 

every other

trigeminy

every third (2 normal QRS, 1 PVC)

quadrigeminy

every fourth (3 normal QRS, 1 PVC)

bigeminy PVCs

trigeminy PVCs

PVC couplets

PVCs clinical significance

*Malignant PVCs

• More than 6/minute, R on T phenomenon, couplets or runs of ventricular tachycardia, multifocal PVCs, or PVCs associated with chest pain.

*Ventricles do not adequately fill, causing decreased cardiac output.

ventricular tachycardia

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = 100-250

rhythm = usually regular 

pacemaker site = ventricle 

p waves = if present, not associated with QRS

PRI = none

QRS = >0.12 seconds, bizarre 

ventricular tachycardia

vtach etio and clincial significance

*Etiology

• 3 or more ventricular complexes in succession at a rate of >100.

• Causes include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid–base disturbances, or electrolyte imbalances.

• VT may appear monomorphic or polymorphic

*Clinical Significance

• Decreased cardiac output, possibly to life-threatening levels.

• May deteriorate into ventricular fibrillation.

torsades de pointes is 

polymorphic VT 

torsades de pointes typically occurs in

*nonsustained bursts.

• Prolonged Q–T interval during “breaks.”

• QRS rates from 166–300.

• RR interval highly variable.

torsades de pointes can be exacerbated by

by administration of antihistamines, azole antifungal agents and macrolide antibiotics, erythromycin, azithromycin, and clarithromycin

vfib 

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = no organized rhythm

rhythm = no organized rhythm

pacemaker site = numerous ventricular foci 

p waves = usually absent

PRI = none

QRS = none 

vfib

vfib etio and clinical significance

*Etiology

• Wide variety of causes, often resulting from advanced coronary artery disease.

*Clinical Significance

• Lethal dysrhythmia with no cardiac output and no organized electrical pattern.

asystole

asystole etio and clinical significance

*Etiology

• Primary event in cardiac arrest, resulting from massive myocardial infarction, ischemia, and necrosis.

• Final outcome of ventricular fibrillation.

*Clinical Significance

• Asystole results in cardiac arrest.

• Poor prognosis for resuscitation.

artifical pacemaker rhythm

rate 

rhythm

pacemaker site

p waves

PRI

QRS

rate = varies with pacemaker

rhythm = may be regular or irregular

pacemaker site = depends upon electrode placement

p waves = none produced by vent pacemakers, pacemakers spike

PRI = if present, varies

QRS = > 0.12 seconds, bizarre 

artificial pacemaker rhythm

causes of artifact

patient movement

cable movement

electrical interference

an accurate ECG should have

*Negative aVR

• aVR should be negative

• If aVR is upright, check for reversed limb leads

*One complete cardiac cycle in each lead

*Proper calibration

*Appropriate speed

the hexaxial system is represented by

a circle

• each lead has a positive (+) half and a negative (–) half

the hexaxial system has an

Isoelectric lead: 90°angle from the dividing line between the positive and negative halves of the lead.

–This lead is neither positive nor negative.

–Each lead has a corresponding isoelectric lead.

On the ECG..

The positive vector will be taller or more positive.

The negative vector will appear deeper or more negative.

If the vector is exactly isoelectric, it will fall

directly on the isoelectric lead.

Four quadrants of the hexaxial system:

–Normal

–Left

–Right

–Extreme right

Causes of right axis deviation

*Normal in adolescents and children

*Right ventricular hypertrophy

*Left posterior hemiblock

*Dextrocardia

*Ectopic ventricular beats and rhythm

Causes of left axis deviation

*Left axis deviation (LAD):

• Left anterior hemiblock (LAH)

• Ectopic ventricular beats and rhythms

*Most frequent cause of LAD is LAH.

You tell axis deviation using

lead I and aVF

lead I + 

aVF + 

normal 

lead I +

aVF - 

left axis deviation 

lead I -

aVF +

right axis deviation 

lead I -

aVF - 

extreme right axis deviation 

identify axis

lead I +

avf +

normal