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CARDIAC ARRYTHMIA
is any of a group of conditions in which the electrical activity of the heart is irregular, faster, or slower
than normal
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- Normal HR, should be in a moderate speed (velocity) SA, is slow AT, should be rapid, Purkinje
should be very fast
If one of these criteria is not followed, then the definition of Cardiac arrhythmia is diagnosed
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ARRYTHMIA
Increased Atomicity/accelerated automaticity
- The normal trigger of the SA node, is constantly stimulated by Na+ K+ influx, however, when
epinephrine(Catecholamine)is stimulating SA-node  it will fire more AC of the SA node and
this will lead to sinus tachycardia
Trigger atomicity
- What happens, is that spontaneous depolarization, it can happen that it can lead to an extra
depolarization either early depolarization or later delayed depolarization due to abnormal
membrane exchange(Loading of catecholamine or ischemic injuries) during resting potential
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due to ischemic heart disease
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During inspiration phase, Vagus is inhibited and HR is
going up, and vice versa
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Sinus tachycardia Excessive stimulation of SA node, this means that it will produce more
frequently and fires earlier and rapidly, this will mean that the P wave is presented earlier

Sinus bradycardia Due to athletes that decreases their Vagal tone, hypothyroidism, hypothermia,
choleostasis jaundice due to bile salts accumulate in the SA node
P wave, is showing less frequency, as well as longer pauses, asymptomatic
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Sinus syndrome, tachybrady syndrome, sick sinus syndrome Due to infarction or serious injury
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Atrial fibrillation
- >350
It means there is more than one ectopic foci in the atrium, that is simultaneously trying to take control of
the conductivity, there would then be more depolarized vector and sends different places especially to
each other
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And AV not is specialized in slow conduction
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The diameter of AV node is also smaller, as well as having resting membrane
potential -60 mv, compare to other which is -90mv resting potential, voltage gated calcium channels
prefer more -90mv
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Purkinje cells, right after AV node, are larger and is arranged oriented along the current flow, here is
more gap junction between cells, and larger diameter, and the current pass more efficiently
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This junctional can be either
Junctional tachycardia
Junctional bradycardia
- Junctional block/Nodal block/Heart blocks
Due to some Ca++ channels not working, this will lead to PR interval prolong (more than 0,2 second)
First degree block, common causes are MYOCARDITIS, Acute MI (inferior MI) electrolyte imbalance,
medications (CCB, beta blocker, digoxin, cholinesterase i)

Second degree block  is when the first electrical conduction is firing, but the second conduction will be
blocked and the third conduction will be fired, therefore, there will be an absence of QRS complex

The first degree HB (Mobitz I or wenkebach) is that every P wave is followed by QRS with sometimes
one delay, it can happen, that it will be progressive prolongation PR interval until there is no QRS
complex
Second Degree HB (Mobtiz II or Hay)some P wave is followed by QRS and some P wave is not followed
by QRS (may experience, Stokes-adams attack, cardiac arrest, sudden cardiac death, treatment is
pacemaker), PR interval is however stable, and not progressively prolonged
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Third degree block/complete heart block/complete junctional block/, when there is no conduction
through AV node, and there will be a new pacemaker will probably produce 40 Bpm,
(poor prognosis if not treated, most common cause is coronary ischemia, P wave is appeared here and
there on ECG without any relation with QRS complexNarrow complex escape rhythm (<0
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The current will go through bundle of kent, but the conduction goes also to AV conduction but then
there could not reenter so they continue forward with the conductions to bundle of his
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Treatment, carotid massages that can produce strong vagal tone, and can complete the cycle and normal
sinus rhythm, IV verapamil

VENTRICULAR ARRYTHMIAS
Common causes is when foci cells stimulates, if ischemia, gives little oxygen to the cardiac disuse, the
membrane will not be balanced and the it will produce less ATP and will not work probably
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Also Ca++
will be leaked inside
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Monomorphic ventricular tachycardia, all the beats look the same because the impulse is either being
generated from increased automaticity of a single point in either the left or the right ventricle, or due
to a reentry circuit within the ventricle
Common causes
- myocardial scarring from a previous myocardial infarction
- include right ventricular dysplasia
- Right and left ventricular outflow tract VT
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Common causes
- abnormalities of ventricular muscle repolarization
- QT prolongation
- sotalol and amiodarone

VENTRICULAR PREMATURE BEATS/
There is action potential firing abnormal vectors in ventricular muscle tissue and fires in another
direction, which will leave to upside down QRS complex and wider QRS complex,
Usually benign
VENTRICULAR FLUTTER
More specifically a tachycardia affecting the ventricles with a rate over 250-350 beats/min, It has been
considered as a possible transition stage between ventricular tachycardia and fibrillation, and is a
critically unstable arrhythmia that can result in sudden cardiac death
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This condition results in cardiogenic shock and cessation of effective blood circulation
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