Dysrhythmias

Front 1

Define Automaticity

Back 1

Intrinsic property of specialized, pacemaker cells that dictates that they will spontaneously depolarize to a threshold voltage in a rhythmic, repeated fashion.

Rate at which the tissue reaches threshold (slope of Na+ influx in phase 4 depol) determines its sponteneous rhythm


--SA node fastest(60-100 bpm)
--AV node (50 bpm)
--Purkinje fibers (40 bpm)

Front 2

Define Escape Beat

Back 2

As a result of automaticity, tissue in a subsidiary pacemaker fires to depolarize the heart when a pacemaker fails

EBs are LATE (not pre-mature!) beats, occurring later than the regular pacemaker would have

EBs TERMINATE A PAUSE caused by a slowed sinus rhythem (return of HR after brief flatline)- EBs = good!

EBs prevent asystole and prevent the HR from becoming too slow when SA node firing is impaired

--Hierarchical order of EBs

--Slower than the usual beat

Front 3

Junctional Escape Beats

Back 3

JUNCTIONAL ESCAPE BEATS: Protective back-up mech that maintains a heart rate and CO when SA node or AV node conduction fail (asystole)

Arise from the AV node or proximal bundle of His

SLOW and LATE w/ 40-60 bpm

Tags:
-No P waves evident b/c impulse originates below atria
-normal QRS b/c still using Purkinje system

Front 4

Aberrant conduction

Back 4

ABERRANT CONDUCTION: Rate related impairment of conduction down one of the bundle branches

Results from differential recovery (refractory period) of the two bundle branches

Follows a premature stimulus

Mimics a premature ventricular beat

Example:
RBBB with wide QRS
--> RV depol occurs via slow cell to cell conduction
--> INCONSISTENT pattern since right bundle is functional

Front 5

Reentry Tachycardia

Back 5

1) Requires specific substrates
-Dual pathway (functional or anatomic division in conduction system)
-Region of slowed conduction
-Region of unidirectional block

2) Allows establishment of sustained tachycardia

3) Occurs at any level of the conduction system, or myocardium

REENTRY TACHYCARDIA: usually follows a premature stimulus from coming from above

A circus movement of the wave front causes depolarization of the distal tissues each time the circuit is completed

*Macroreentry- large circuit involving considerable area (atrial flutter)
*Microreentry - small circuit (ventricular tachy)

Front 6

Abnormalities of electrical function can produce clinical sequelae in two ways:

Back 6

Remember: CO = SV x HR

CO FALLS if the heart goes
--TOO FAST (too little time in diastole, SV falls) or
--TOO SLOW (SV can only become so large, so CO falls d/t fall in HR)

*CO can be maintained between HR of 40-160bpm, but will fall if the rate is higher or lower

Front 7

Ventricular Escape Beat

Back 7

Widened QRS complex b/c NOT using the purkinje system, conduction is occurring cell-to-cell (slower)
- No P wave
- comes late

Front 8

Escape beat

Back 8

Escape beat:

--no P wave

--delayed QRS wave b/c ventricular contraction is d/t AV node which takes longer to reach threshold

--AV node has shallower phase 4 and will take longer to depolarize ventricles

Front 9

Aberrant conduction

Back 9

Aberrant conduction:

--Right bundle branch depolarizes slower than left.

--Small segment time when LBB is in relative refractory period and the RBB is in an absolute refractory period

--If an early beat occurs at this time the ECG will look like a RBBB where every beat appears wide

Front 10

Fusion beat

Back 10

Fusion beat:

Ventricular depolarization resulting from impulses that originated at two different sites.

WPW syndrome: fusion of impulses from AV node and from the ectopic tissue.

Front 11

Compensatory pause

Back 11

Compensatory pause:

--Defining marker for PVC

--Found when sinus rhythm is uninterrupted by the PVC

--The P wave that occurs during or immediately following PVC is NOT conducted, creating a pause

--After an irregular beat there is a pause before the next beat so that the rhythm remains the same as it was before the irregular beat

Front 12

SA node dysrythmias
Sinus tachycardia:

Back 12

Sinus tachycardia:

--MC dysrythmia

--Caused by fever, anemia or exercise

--innappropriate sinus tachycardia: the SA node is set too fast, which results in heart dilation

--Can lead to CHF, but can be reversible with treatment

Front 13

SA node dysrythmias
Sinus bradycardia:

Back 13

Sinus bradycardia:

Often occurs in a person in very good shape with a distensible heart (ie marathon runner)

These hearts have a high SV and so the heart does not need to increase HR to maintain CO.

Also seen in
-patients on beta-blockers
-elderly patients

Front 14

SA node dysrythmias
Premature atrial contractions (PAC):

Back 14

Premature atrial contractions (PAC):

--Area in the atria which depolarizes spontaneously, sends a second wave front through the atria that results in an irregular p wave.

--After irregular beat, the SA node is reset

--The next beat occurs at a regular sinus cycle rate with no compensatory pause.

--Early p wave, an irregular p shape, and the next beat occurring in sinus rhythm.

Front 15

Atrial flutter:

Back 15

Atrial flutter:
-Irritable focus of atrial automaticity fire a PAC

-Circus rhythm of atrial depolerization

-Only some P waves make it through AV node b/c the circus cycle is so fast

-Produces a "sawtooth atrial wave" on ECG

-AV node able to maintain HR consistent with life

Front 16

Carotid massage: A-Flutter vs. A-Fib

Back 16

Carotid massage: vagally-med slowing of AV conductioon

In A-flutter: causes an incremental drop in ventricular response (QRS)(ie 1:3--> 1:4, thus slow the rate of depolarization)

In A-fib: causes a gradual slowing of ventricular response

Front 17

Atrial Fibrillation:
600-1000/min to AV node

Back 17

Atrial Fibrillation:
“Electrical anarchy” where every atrial cell depolarizes independently

No True P waves, just a wavering baseline

Underlying pathology - always dilated atria!!

Irregularly, irregular ventricular response rhythm (random AV nodal conduc, not in a set pattern like A-flutter)

No two QRS complexes occur at the same distance from each other on ECG

Disorganized contraction, thrombi, emboli likely

Increased O2 demand

Front 18

Atrioventricular Block:

Back 18

Atrioventricular Block:

--AV node receives signals from above that it can’t handle.

--There is normal SA node rhythm.

Front 19

Three classes of AV Block:

Back 19

Three classes of AV Block:

1st degree- all beats conduct through AV node from the SA node, so every P wave will occur
--> However the conduction is slowed there is a long PR interval

2nd degree- only some beats make it through the AV node

3rd degree- no beats make it through

Front 20

Type I Mobitz AV Block:
Lesion above bundle of His

Back 20

Type I Mobitz AV Block:

SA node functions normally

PR intervals progressively prolonged

Predictable Pattern

P wave not follwed by QRS
PR interval- Progressively longer, then drops a QRS

Tx: generally, nothing
Dysrhythmia meds aren’t used anymore

Front 21

Type I Mobitz AV Block:
Rule regarding the increment change in the PR interval:

Back 21

Type I Mobitz AV Block:
The change in PR length between the first two beats of the set is the greatest.
Length of time b/w the first two QRS peaks is greatest.
R-R interval becomes shorter between beats

Front 22

Type II Mobitz AV Block:
Lesion below bundle of HIS

Back 22

Type II Mobitz AV Block:

Dropped P waves with no pattern

More dangerous than Type I b/c more likely to lead to total heard block

Unpredictable, follows no particular pattern

Low CO, so syncope (faint)

Tx: Kill the AV node with heat and put in a pacemaker
No meds

Front 23

3rd degree AV block:

Back 23

3rd degree AV block:

Atrium is beating regularly, but the ventricle is NOT beating with the same rhythm

Ventricular escape rhythms rescue ventricular depolerization

The two chambers are uncoordinated

Front 24

AV Nodal Dysrhythmias:
AV nodal (junctional) premature beats:

Back 24

AV nodal (junctional) premature beats:

AV node phase 4 is faster than SA node

Causes a premature, narrow QRS w/o P wave before it

Benign

Front 25

WPW Pre-Excitation Syndrome

Back 25

Conduction from the SA node and an anatomical bypass tract, but AV node conducts the signal slower

The same signal goes through the AV node and then through the His-Purkinje system, overtaking the signal that went through the bypass tract.

Produces Fusion beat:
1. short PR (bypass tract conducts faster in atria)
2. delta wave (first wide portion of the QRS complex.)
3. wide QRS

Tx: catheter to burn the bypass tract with high frequency energy.

Front 26

Two possible scenarios:
Short PR makes WPW a good setup for reentry tachycardia:

Back 26

Short PR makes WPW a good setup for reentry tachycardia:

1. Premature beat from the SA node could go through the AV node and then pass retrograde back through the bypass tract, causing a narrow QRS complex.

2.The beat could pass through the bypass tract and then retrograde through the AV node, causing a wide QRS complex b/c the signal doesn’t travel through the His-Purkinje fibers.

Front 27

AV nodal reentry tachycardia (microreentry tachycardia):

Back 27

AV nodal reentry tachycardia (microreentry tachycardia):

MC AV rhythm disturbance

Functional divide of AV node: one side has longer refractory period than the other, setting up a reentry circuit

a PAC conducts down fast portion of the AV node and then retrograde up the slow

Narrow QRS, w/ NO delta wave

Signal can be inverted, but it’s usually incorporated into the QRS

Looks like NARROW-COMPLEX TACHYCARDIA

Always supraventricular

AV nodal tachy = junctional tachycardia.

Front 28

Premature Ventricular Contractions:

Back 28

Premature Ventricular Contractions:

Similar to PAC’s, but with a compensatory pause

Everyone has these, which is fine in normal hearts, problematic in diseased hearts esp. when accompanies by ischemia

Accelerated phase 4 in the ventricular tissue, but NOT in the His-Purkinje system.

TAGS:
Early, wide QRS
Next P wave comes right when it should since SA node not reset

Compensatory pause b/w the crazy beat and the next, normal one

Front 29

PVC Categories:

Back 29

PVC Categories:
1. PVC
2. Couplet- 2 PVC’s in a row
3. Triplet/ventricular tachycardia- 3 PVC’s in a row: “3-beat run of ventricular tach”
(monomorphic, polymorphic)
4. Bigeminy- every other beat is a PVC
5. Trigeminy- every third beat is a PVC

Front 30

Monomorphic Ventricular Tachycardia

Back 30

Ventricular Tachycardia:

3+ PVC’s in a row - classified as monophoric if
all the beats are arising from the same location

Front 31

Polymorphic Ventricular Tachycardia

Back 31

Torsades-de-pointe (turning on point):

Wide QRS that gets bigger, then smaller, then bigger, then smaller, etc.

Always assoc. w/ QT prolongation

Life threatening and should be treated aggressively

Front 32

Ventricular Fibrillation

Back 32

V-Fibrillation:

Ischemic event -> fibrillation -> no CO -> die

You lose all coordinated contraction in fibrillation, meaning you can’t pump CO needed to survive

Incompatible with life, defibrillation must be proptly carried out

This is the rhythm in most terminal events

This is the putative cause of most cases of sudden cardiac death

May result following period of v-tach or spontaneously