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Causes of Cardiac Arrythmias

This term refers to a change from a normal, regular, automatic, heart beat and rhythm to an irregular beat and rhythm.

1. Abnormalities of impulse generation

A. Change of normal automaticity

I.   Normal sinus node pacemaker (see figure 104b) failure in disease states.
II.  Normal sinus node excessively rapid due to sympathetic nerve stimulation.

Figure 104b
click to enlarge


B.   Pacemaker in His Bundle-Purjinke system (see figure 104b) may control cardiac rhythm as escape pacemakers or when sympathetic activity is increased.

I.   Sinus bradycardia (see figure 16 and 17) or AV block of atrial impulses to a rate lower than intrinsic rate of His-Purjinke pacemaker.

II.  Abnormal conditions like ischemia (inadequate oxygen level due to coronary atherosclerosis causing reduced blood flow) or drug (medication) treatment increases rate of firing of His-Purjinke system pacemaker to overcome the sinus node rate.

C.   Abnormal automaticity in Purjinke cells ,which are involved in a heart attack with ischemic fibers (reduced oxygen).

D. Triggered activity is single or repetitive firing of a myocardial cell or a group of cells caused by reexcitation (afterdepolarization which occurs after repolarization has begun). Repolarization is the electrochemical process of cell recovery after excitation of the heart muscle.

I.  There are two kinds of afterdepolarization:

a. early
     Causes of early afterdepolarization include:

1.  low potassium blood levels
2.  slow heart rate (see figure 16)
3.  drug toxicity (i.e. quinidine causing torsades de pointes form of ventricular tachycardia, see figures 6, 13).


b. late (delated afterdepolarization occur after the cell has repolarized).
These may cause rapid firing or triggered activity due to:

1.  premature beats
2.  increased calcium blood levels
3.  increased adrenaline levels
4.  digitalis toxicity (see figure 4)

2. Abnormalities of impulse conduction

a. Slowing of conduction and block (see figure 17)

b. Unindirectional block and reentry (causes):

1.  Anomalous AV Connections that cause a short PR interval and wide QRS (see figures 1, 3a). This additional, anomalous pathway promotes rapid heart beats called supraventricilar tachycardia. When this pathway is destroyed, the tachycardia never reoccures (see figure 3b).

c.  Ordered reentry
d.  Random reentry

3. Combined abnormalities of impulse generation and conduction

 

4. NORMAL OR ABNORMAL IMPULSE INITIATION

Automatic Rhythms Normal Mechanism
Cardiac cells that normally are capable of developing spontaneous diastolic (phase 4) depolarization are called pacemaker cells. When pacemaker cells manifest spontaneous diastolic depolarization
(Fig. 16-1)


and thus are responsible for generating the cardiac rhythm, the rhythm
is classffied as an automatic rhythm. Normally, the dominant pacemaker
of the heart is in the sinus node, which in adults fires at a rate of 60 to 100 beats per minute. Cells capable of developing spontaneous diastolic depolarization (i.e., of manifesting automaticity) also are normally found in the specialized fibers in the atria, the atrioventricular (AV) junction, and the His-Purkinje system. The normal rate of impulse formation in adults by these ectopic pacemakers is 40 to 60 beats per minute in the AV junction (the AV node and His bundle).
Normal rates of more distally located ectopic pacemakers are probably
20 to 40 beats per minute in the bundle branches. These ectopic (i.e.,
nonsinus) pacemakers also are called latent or escape pacemakers for
two related reasons:

(1) The normal intrinsic rate of these pacemakers is lower than that of the dominant pacemaker, the sinus node, and
(2) spontaneous diastolic depolarization of these latent or escape
pacemakers normally is suppressed by the more rapid rate of the sinus node pacemaker through the active process of overdrive suppression.
Only when the sinus rate slows below the intrinsic rate of these ectopic pacemakers does "the next one in line" warm up and fire (see also "Automaticity," below).

Arrhythmias of the Sinus Node

An arrhythmia occurs when the sinus node pacemaker fires at a rate
above 100 beats per minute (sinus tachycardia) (Table 1) or at a rate below
60 beats per minute (sinus bradycardia) and is still the dominant
pacemaker of the heart.

Tachycardia

Mechanism

Origin

Rate Range, bpm

AV or VA Conduction

Sinus tachycardia Automatic (normal) Sinus node >100 1:1

Sinus nod reentry

Reentry

Sinus node and right atrium

?110-180

1:1 or variable

Atrial fibrillation

Reentry

Atria

260-450

Variable

 

Fibrillatory conduction

Pulmonary veins, SVC

?

Variable

Atrial flutter

Reentry

Right atrium, left atrium (infrequent)

240-350, usually 300 ± 20

2:1 or variable

Atrial tachycardia

Reentry

Atria

150-240

1:1, 2:1, or variable

 

Automatic (normal or abnormal)

Atria

?

?
 

Triggered (DADs) 2° to digitalis toxicity

Atria

150-240

1:1, 2:1, or variable

 

 

     

AV nodal reentry tachycardia

Reentry

AV node with an atrial component

120-250, usually 150-220

1:1

AV reentry (WPW or concealed accessory AV connection)

Reentry

Circuit includes accessory AV connection, atria, AVnode, His, Purkinje system, ventricles

140-250, usually 150-220

1:1

Accelerated AV junctional tachycardia

Automatic or ? triggered (? digitalis toxicity)

AV junction (AV node and His bundle)

61-200, usually 80-130

1:1 or variable

Accelerated idioventricular rhythm

Abnormal automaticity

Purkinje fibers

>60-?

Variable, 1:1, or AV dissociation

Ventricular tachycardia

Reentry

Ventricles

120-300, usually 140-240

AV dissociation, variable, or dissociation

 

Automatic (rare) (normal or abnormal)

Ventricles

?

Variable, 1:1, or AV dissociation

Bundle branch reentrant tachycardia

Reentry

Bundle branches and ventricular septum

160-250, usually 195-240

AV dissociation, variable, or 1:1

Right ventricular outflow tract

? Triggered (DADs)

Right ventricular outflow tract

120-220

AV dissociation, variable, or 1:1

Torsades de pointes tachycardia

? Triggered (EADs) (with reentry)

Ventricles

>200

AV dissociation

Table 1

These are called arrhythmias resulting from normal automaticity, since the ionic mechanism causing the pacemaker depolarization is unchanged from the normal sinus rhythm. A sinus tachycardia is usually an appropriate response to a precipitating factor (e.g., exercise, fever, hypotension), although on occasion it may be inappropriate, as in the presence of a sympathetic dysautonomia (inappropriate sinus tachycardia). By contrast, sinus bradycardia often reflects an abnormality not only of the sinus node pacemakers (they are too slow) but also of the latent pacemakers (when the sinus rate slows abnormally, they do not escape). Sinus bradycardia may be due to an intrinsic abnormality of pacemaker cells, a parasympathetic dysautonomia (inappropriate sinus bradycardia), or an extrinsic factor such as suppression of automaticity by drug therapy (e.g., a beta blocker, a Ca2~ channel blocker, or an antiarrhythmic agent). Fro some patients, sinus bradycardia, particularly when it is present only at rest, may simply reflect a normal response to increased vagal tone, as in a well-trained athlete. Marked beat-to-beat variations in cycle length of the sinus rhythm, which are due virtually always to the influence of vagal tone on the pacemaker cells of the sinus node, also is considered an arrhythmia (sinus arrhythmia) even if the overall sinus rate is normal.