Cardiac Muscle Arrhythmias Part 1 1

Abnormal ECG's
Arrhythmias to be covered: Heart Blocks, Fibrillations, Premature Beat, Wandering
Pacemaker, Multifocal Atrial Tachycardia, Atrial Escape Rhythm, Junctional Escape
Rhythm, Retrograde Atrial Depolarization, Ventricular Escape Rhythm, Ventricular
Parasystole Tachy-arrhythmias, Supraventricular Tachycardia Paroxysmal, Ventricular
Tachycardia, Long QT Syndrome, Torsades de Pointes, Atrial and Ventricular Flutter,
Wolff- Parkinson-White Syndrome, Lown-Ganong-Levine Syndrome, Sick Sinus
Syndrome

Note: normally HR is slightly higher during inhalation and slightly slow during exhalation.

Heart Blocks

Usually caused by compromise in blood flow to the conduction system of the heart. These lead
to arrhythymias aka dysrhythmias.

SA block. There are two cell populations in the SA node. A core group of cells that generate
sinus depolarization called “P cells” and outer layer group that transmits the signal to the
conduction fibers. These outer layer cells are called “T cells”

There are three types of SA blocks. Type 1 or 1st degree: slow transmission from P cells to the
T cells. This is undetectable in a 12 lead EKG and can be only seen with specialized
physiological tests.

Type II or 2nd degree: There is an intermittent drop out of the P wave and QRS complex. See
figure below.

Type III or 3rd degree: Total failure of the SA node to generate depolarization, therefore no P
waves. Junctional automaticity focus will escape overdrive suppression and emit a Junctional
Escape beat. Heart rate is slower. See figure below

Type II
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Type III

Three types of AV blocks

First degree AV block: prolonged PR interval, a delay in the conduction from atria to
ventricles. It’s not really a block, per se, but rather a delay in conduction. The abnormality is
thought to be within the AV node. Normal hearts can have this block. Typically patient will
have no symptoms. This block can be associate with a higher risk of atrial fibrillation.

Second degree AV block: all QRS complexes proceeded by P waves but not all P waves are
followed by QRS complexes. Sometimes the action potentials don't make it to the AV node.
There are two basic types of second degree AV blocks: Wenckebach aka Mobitz (Type 1)
AV block and Mobitz (Type 2) AV block. The difference is where the issue is within the AV
system.

Wenckebach secondary AV block

With a Wenckebach secondary AV block the PR segment gets progressively longer, then after
about 3 cycles, the QRS is missing. Then the pattern starts all over. This type of block is
considered benign and the patient will typically have no symptoms. The type of block almost
always has to do with some abnormality within the AV node itself.
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Mobitz secondary AV block, (there are subtypes of these designated by ratios)

With a Mobitz secondary AV block, a QRS complex will follow the P wave only every 2 or 3
P waves. This is more serious than the Wenckebach 2o AV block and may progress rapidly to a
third degree 2o block. The type of block almost always has to do with an abnormality below
the AV node, e.g., His bundle.

Symptoms could be syncope, dizziness, chest pain if block is related to myocarditis or

ischemia. But some patient may present no symptoms.
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Third degree AV block: complete conduction block between SA node and AV node. Atria
and ventricles contract independently and in an uncoordinated way. Some QRS complexes are
not preceded by P-waves. Symptoms in the patient will be severe bradycardia and syncope.
This type of blockage is the most common condition that requires an artificial pace maker. The
site of block could be the AV node or the pathway below the node.
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Bundle Branch Block: either the left or right bundle branch may be blocked. The bundle
branches conduct the electrical impulse simultaneously to the right and left ventricles resulting
in the R peak of the QRS is one sharp peak. If one of the bundles is blocked, then the
depolarization of the ventricle whose bundle is blocked progresses more slowly because it is no
longer progressing through the specialized conducting fibers but rather through the regular
myocardiocytes. This will result in a widening of the QRS complex and will likely lead to a
double R wave peak. Patient typically have no symptoms with a bundle branch block. If
symptoms are present, it will be syncope and bradycardia. LBBB: Left Bundle Branch Block;
RBBB: Right Bundle Branch Block.

RBBB
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LBBB

Normal V1 – V6 leads.
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Hemiblock: a failure to conduct a cardiac impulse down one division of the left bundle branch,
such as an anterior or posterior divisions. LAHB: Left Anterior Hemiblock, LPHB: Left
Posterior Hemiblock. Therefore, the patient would have one part of the left ventricle (anterior
or posterior) depolarizing before the other part (anterior hemiblock, posterior hemiblock). One
of the most common causes of hemiblocks is coronary artery disease. Hemiblocks can also be
associated with myocardial infarction. Hemiblocks in and of themselves are typically
asymptomatic. However, the underlying cause such as coronary artery disease or myocardial
infarction will cause the patient to present symptoms.
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Fibrillation

This occurs when there is total loss of coordinated depolarization of atrial or ventricular muscle
therefore no coordinated contraction. Fibrillation, whether atrial or ventricular, involve the
rapid discharge from numerous irritable automaticity foci, which suffer from entrance block,
therefore they are parasystolic. They cannot be overdrive-suppressed, they all pace at once very
rapidly.

Normally following contraction, the depolarization has nowhere to go because the entire
ventricle is in a refractory period.

Atrial Fibrillation
The most common cardiac arrhythmia (irregular heart beat). It may cause no symptoms, but it
is often associated with palpitations, fainting, chest pain, or congestive heart failure. AF
increases the risk of stroke; the degree of stroke risk can be up to seven times that of the
average population, depending on the presence of additional risk factors (such as high blood
pressure).
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Ventricular Fibrillation
Ventricular fibrillation is the most commonly identified arrhythmia in cardiac arrest patients.
This arrhythmia can degenerate into asystole (flatline).

Loss of consciousness occurs 4-5 seconds following ventricular fibrillation.

Common cause of VF: ischemia to the conduction portion of the heart (Purkinje fibers)

Defibrillation: shocks the ventricles causing synchronized refractory period. This needs to be
done within one minute or so of VF. Too much longer than that, the lack of blood to the
heart muscle causes the heart muscle to weaken.

CPR helps keep the blood flow to the heart muscle, which significantly lengthens the
defibrillation window.

Cardioversion: causing some types of arrhythmia of the heart to return to sinus rhythm, i.e.,
normal rhythm using antiarrhythmic drugs (pharmacological or chemical cardioversion), or
synchronized electrical cardioversion. Verb: to cardiovert.

Synchronized electrical cardioversion involves the use of an electrical device, defibrillator,

which will deliver the appropriate amount of low level joules to the heart at the appropriate
time during the heart rhythm, which is during the depolarization of the atria or ventricle. In the
ventricle delivery would be at the R wave when the cycle is in absolute refractory period. If the
joules are delivered during relative refractor period (repolarization, T wave), this could lead to
fibrillation. In the event of ventricular fibrillation, one would use nonsynchronized delivery of
high level of joules; and it matters not when the delivery is done since there is no pattern of
electrical activity with which so synchronize, hence the term “nonsynchronized”. When this is
done, it is not considered “cardioversion”, but instead is called “defibrillation”. So the
defibrillator can either cardiovert the heart by way of a synchronized delivery of joules or
defibrillate the heart with a nonsynchronized delivery of joules.
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Asystole. In common vernacular, known as flat line EKG. This indicates no electrical activity
of the heart. Unlike what you would see in the movies, asystole cannot be treated with a
defibrillator since there is no electrical activity to alter by delivery of joules. It is treated by
CPR and the administration of a vasopressor such as epinephrine. Survival rate is less than 2
percent.

Cardiac arrest. Patient will have no pulse because the heart is not pumping blood. Several
things can cause cardiac arrest, ventricular fibrillation, ventricular tachycardia, asystole,
pulseless electrical activity (PEA).

PEA is when there is electrical activity of the heart but no pulse in the patient. For whatever
reason, the cardiac muscle cells are not contracting in response to the electrical
depolarization. Tension pneumothorax can cause PEA.

Two types of cardiac arrests: shockable and non-shockable. Shockable, which means can be
treated with joules -Ventricular fibrillation, ventricular tachycardia. Non-shockable, which
means cannot be treated with joules - Asystole and PEA.

Survival rates are as high as 90 percent if a victim of sudden shockable cardiac arrest is
defibrillated within one minute. The survival rate is around 70 percent if defibrillation
occurs within four minutes. If delivered 10 minutes after cardiac arrest, the survival rate
drops to two percent.

Defibrillator devices typically use direct current (DC). Earlier versions of DC devices
delivered about 360 Joules. The energy traveled in one direction from one electrode to another.
These are called monophasic devices. Newer versions are biphasic. They deliver Joules in
rapid alternating pulses, reversing field of the pads, one cycle of alteration being 10
milliseconds. They are able to be effective with less energy using only about 200 Joules. There
is less damage to the heart with the reduced energy. Some defibrillator devices use a modified
alternating current (AC). They use about the same amount of energy as the biphasic devices.

Implantable Cardioverter-Defibrillator (ICD).

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Classification of antiarrhythmic drugs.

Classification of antiarrhythmic drugs are based on mechanism of action, although this has limitation since some drugs
act via multiple mechanisms or the mechanism may not be known at all. This classification system is called the
Vaughan Williams classification.

The type of antiarrhythmic drug administered to the patient depends on what type of arrhythmia the patient has. Note
that a risk of using antiarrhythmics is that they can cause more life threatening antiarrhythmias. Example, treatment of
a non-life threatening tachycardia may cause fatal ventricular arrhythmia. Dosing is critical.

Class I: sodium blockers, with the exception of lidocaine, most of these drugs are rarely used because they can cause a
more lethal dysrhythmia. Lidocaine is the go-to drug for any dysrhythmia following myocardial infarction because it
preferentially binds to sodium channels in ischemic tissue. 80% of patients with MI’s will go into some sort of
arrhythmia.
Ia: moderately inhibits sodium voltage-gated channels, in addition to their effect on the voltage-gated sodium
channels, slow repolarization by inhibiting potassium efflux. It also increases the effective refractory period
(ERP). They are procainamide, quinidine, disopyramide.

Ib: weakly inhibits sodium voltage-gated channels, in addition to their effect on the sodium voltage-gated channels,
accelerate cellular repolarization by increasing potassium efflux, and decrease the duration of the action potential
and the refractory period. It also decreases the effective refractory period (ERP). They are lidocaine, phenytoin
(also used as an antiseizure drug) and mexiletine.

Ic: strongly inhibits the voltage-dependant sodium channels and prolong the depolarization phase, have little effect on
the repolarization phase. Has no effect on effective refractory period (ERP). They are flecainide, propafenone.
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Class II: beta adrenergic blockers. Slows SA node rhythm. Propranolol, Esmolol.
Class III: potassium channel blockers. Amiodarone.
Class IV: Calcium blockers, slows AV conduction. Verapamil.
Class V: Variable mechanisms. Digoxin (a type of digitalis), Adenosine, Magnesium Sulfate.

Other arrhythmias

Premature Beat
A premature beat originates in an irritable automaticity focus that fires spontaneously,
producing a beat earlier than expected in the rhythm.

Causes of irritable automaticity foci:

Epinephrine
Increased sympathetic stimulation
Caffeine, amphetamines, cocaine, any beta 1 receptor stimulants
Excess digitalis, some toxins, ethanol
Hyperthyroidism
Stretching of the heart muscle
Hypoxia (COPD, compromised coronary circulation, anemia, hypovolemic or cardiogenic
shock, pulmonary embolus, pneumothorax)
Hypokalemia
Mitral Valve Prolapse
Myocarditis