cardiac arrhythmias chapter 13 - core

Cardiac Arrhythmias

Bioengineering 6000 CV PhysiologyECG

Cardiac Activation Sequence and ECG


Cardiac Activation Sequence: Moving Dipole

Oriented from active to inactive tissueChanges location and magnitudeGross simplification





• Oriented from active to inactive tissue

• Changes location and magnitude

• Gross simplification













P wave

Atria Contract

P P PQ

PQ

RP wave PQ Segment Q wave R wave



























PQ

R

STP

Q

R

SP

Q

R

SP

Q

R

ST

Ventricles Contract

S wave ST Segment T wave The end

Arrhythmia Substrate

Normal Reentry

Stimulus

+=

Unidirectional conduction

Chapter 13 Cardiac Arrhythmias and Their Electrocardiographic Interpretation 153

Phenomenon of Re-entry—“CircusMovements” as the Basis forVentricular Fibrillation

When the normal cardiac impulse in the normal hearthas traveled through the extent of the ventricles, it hasno place to go because all the ventricular muscle isrefractory and cannot conduct the impulse farther.Therefore, that impulse dies, and the heart awaits a newaction potential to begin in the atrial sinus node.

Under some circumstances, however, this normalsequence of events does not occur. Therefore, let usexplain more fully the background conditions that caninitiate re-entry and lead to “circus movements,” whichin turn cause ventricular �brillation.

Figure 13–14 shows several small cardiac musclestrips cut in the form of circles. If such a strip is stimu-lated at the 12 o’clock position so that the impulse travelsin only one direction, the impulse spreads progressivelyaround the circle until it returns to the 12 o’clock posi-tion. If the originally stimulated muscle �bers are still ina refractory state, the impulse then dies out becauserefractory muscle cannot transmit a second impulse. Butthere are three di�erent conditions that can cause thisimpulse to continue to travel around the circle, that is,to cause “re-entry” of the impulse into muscle that has already been excited. This is called a “circus movement.”

First, if the pathway around the circle is too long, bythe time the impulse returns to the 12 o’clock position,the originally stimulated muscle will no longer berefractory and the impulse will continue around thecircle again and again.

Second, if the length of the pathway remains constantbut the velocity of conduction becomes decreasedenough, an increased interval of time will elapse beforethe impulse returns to the 12 o’clock position. By thistime, the originally stimulated muscle might be out of

the refractory state, and the impulse can continuearound the circle again and again.

Third, the refractory period of the muscle mightbecome greatly shortened. In this case, the impulse couldalso continue around and around the circle.

All these conditions occur in di�erent pathologicalstates of the human heart, as follows: (1) A long pathwaytypically occurs in dilated hearts. (2) Decreased rate ofconduction frequently results from (a) blockage of thePurkinje system, (b) ischemia of the muscle, (c) highblood potassium levels, or (d) many other factors. (3) A shortened refractory period commonly occurs inresponse to various drugs, such as epinephrine, or afterrepetitive electrical stimulation. Thus, in many cardiacdisturbances, re-entry can cause abnormal patterns ofcardiac contraction or abnormal cardiac rhythms thatignore the pace-setting e�ects of the sinus node.

Chain Reaction Mechanism of Fibrillation

In ventricular �brillation, one sees many separate andsmall contractile waves spreading at the same time indi�erent directions over the cardiac muscle. The re-entrant impulses in �brillation are not simply a singleimpulse moving in a circle, as shown in Figure 13–14.Instead, they have degenerated into a series of multiplewave fronts that have the appearance of a “chain reac-tion.” One of the best ways to explain this process in �brillation is to describe the initiation of �brillation byelectric shock caused by 60-cycle alternating electriccurrent.

Fibrillation Caused by 60-Cycle Alternating Current. At acentral point in the ventricles of heart A in Figure 13–15,a 60-cycle electrical stimulus is applied through a stimulating electrode. The �rst cycle of the electricalstimulus causes a depolarization wave to spread in alldirections, leaving all the muscle beneath the electrodein a refractory state.After about 0.25 second, part of thismuscle begins to come out of the refractory state. Someportions come out of refractoriness before other

Absolutelyrefractory

Absolutelyrefractory

Relativelyrefractory

LONG PATHWAY

NORMAL PATHWAY

Figure 13–14

Circus movement, showing annihilation of the impulse in the shortpathway and continued propagation of the impulse in the longpathway.

Stimuluspoint Dividing

impulses

Blockedimpulse

BA

Figure 13–15

A, Initiation of �brillation in a heart when patches of refractory mus-culature are present. B, Continued propagation of �brillatoryimpulses in the �brillating ventricle.

Diseasedtissue

Ventricular Arrhythmias

Life Saving Devices

Deadly Arrhythmias

Leads

Right Atrium

Right Ventricle

Pacemaker

Pacemaker

Treatment for Ventricular Tachycardia

VF Defibrillation pulse Normal rhythm

Implantable Cardioveter Defibrillator (ICD)

Automatic External Defibrillator (ICD)

Treatment for Ventricular Fibrillation

Atrial Arrhythmias

Increasing PrevalenceGreater Risk with Age

Cause 20% of All Strokes

TriggeringFoci

Atrial Septum

SuperiorVena Cava

InferiorVena Cava

LeftAtrium

PulmonaryVeins

RightVentricle

LeftVentricle

RightAtrium

MappingCatheter

AblationCatheter

RF Ablation of AF Termination of AF

- Atrial Dilation- Fibrosis

Triggers

AF Begets AF

StructuralRemodeling

ElectricalRemodeling

- Ectopic Foci- Hypertension- Aging- Heart Valve Disease- Heart Failure

- Slowed Conduction- Increased Excitability

ECG

ECG

Atr

ial E

GM

Atr

ial E

GM

Atrial Fibrillation

Sinus Rhythm

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Ventricular Fibrillation (VF)Ventricular Tachycardia (VT)

VT Anti-tachycardia pacing Normal rhythm

Normal Conduction

cardiac arrhythmias chapter 13 - core

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