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Heart rythm disorders Old medicine

Heart Rhythm disorders
Cardiac dysrhythmia (also known as arrhythmia and irregular
heartbeat) is any of a large and heterogeneous group of conditions in
which there is abnormal electrical activity in the heart. The heartbeat
may be too fast or too slow, and may be regular or irregular.
Coordination of heart work is provided by heart’s main features:
automatism, excitation, transmission, and contraction, which
disorders cause arrhythmias.
1. Arrhythmias developed at automatism disorder
Heart automatism is revealed by sinus node and by transmission
system ability to generate impulses. In this regard, the most
spontaneously active is sinus node. Other parts of transition system
have as less capacity to generate impulses as far they are from sinus
node. In normal conditions in these cells action potential is generated by
receiving excitation from higher automatism capacity cells. On this basis
the transmission system cells “fail” to reveal their automatism. Sinus
node (in the right atrium) initiates and regulates the cardiac rhythm,
this means, it is the primary hearts' pacemaker.
This node discharges electric current (An electrical discharge is the
passage of electrical current through a material which normally does
not conduct electricity) through the atria causing them to contract. The
electric current then passes through the atrioventricular (AV) node
which lies within the lower interatrial septum. Electrical impulses pass
from here into the Purkinje's network, along the right and left bundles of
His, and excite the ventricular muscles causing their contraction. The
conduction system and myocardium have a nerve supply and are
hormone sensitive (to catecholamines), which allows regulation of the
heartbeat according to different activities, stress and excitement.
A. Tachycardia and bradycardia An arrhythmia is a disorder of the
heart rate (pulse) or heart rhythm, such as beating too fast
(tachycardia), too slow (bradycardia), or irregularly.
Tachycardia is a fast heart rhythm arising from the sinus node so called
P -cells, the normal primary pacemaker of the heart. That is, the heart
rhythm is arising from the normal location but at an inappropriately
high rate. This symptom is signed e.g. at high temperature of body, at
the action of mediators of sympatic nervous system (catecholamines dopamine, adrenaline and noradrenaline). Causes of sinus tachycardia
may be: heart inflamative, ischemic, infective or toxic injury.
Tachycardia at heart overload is frequently of compensative manner.
Tachycardia may be developed by extracardial causes (Anemia,
volume depletion, hypoxia etc.) and they also frequently may be
Heart contractions become more frequent at those pathological
processes with nervous system activation and catecholamine surplus
release. Tachycardia is very characteristic at thyreotoxicosis. It
develops also at fever, because warm blood excitates sinoatrial node. As
usual, increased temperature for 1 Celsius causes heart beat increase for
8 - 10 in minute.
At deceleration of impulse generation in sinoatrial node (e.g. at vagus
nerve excitation) impulse generation is decreased and bradycardia is
Heart work slow down – bradycardia can be caused by heart injury as
well as by extracardial reasons. Frequently bradycardia is caused by,
e.g. vagus nervus centre excitation at intracranial pressure increase or
kinetosis. Bradycardia can be developed also by all diseases that cause
bile acid transmission to blood (cholemia) because acids excitate vagus
nervus and inhibit sinus node function.
Tachycardia is characterized by T-P interval decrease on ECG
(electrocardiogram), and bradycardia – by increase of this interval.
B. Extrasystolic Arrhythmia
Extrasystoles are essentially extra beats, or contractions, which interrupt
the normal regular rhythm of the heart. They occur when there is
electrical discharge from somewhere in the heart other than the sinoatrial node. It may take place when sinus node automatism is decreased
or when ectopic sites impulse initiation capacity is increased as well as
at potential difference formation, e.g. at non synchronous repolarization
at local ischemia, or cardiac glycoside poisoning.
Extrasystoles are classified as sinusoidal (nomotopic), atrial, atrioventricular or ventricular extrasystoles (VEs) according to their site of
origin. Initiated extra waves are spread towards paradoxical directions
that are revealed on the structure of ECG.
a) At sinusoidal (nomotopic) extrasystoles pacemaker is in sinus node,
QRST complex is preceded by positive atrial P waves. ECG differs from
normal only by T-P interval decrease before extrasystole. In response to
decreased diastole duration, ventricle is not fully filled with blood that
decreases pulse wave of heart.
b) Atrial extrasystole is initiated when ectopic excitement site is
localized in atrium. They are premature P waves which look different
from a normal P wave; are characterized by P wave deformation (two
phases, negativity) preceding QRST complex and by prolonged interval
after extrasystole.
c) At atrio-ventricular extrasystole excitement from the node is spread
towards both: atrium and ventricles. As excitement in atrium is spread
retrogradely (from bottom to top), P wave is negative. According to the
place of impulse generation P wave can precede, combine or follow
QRST complex. In this case QRST complex is usually normal because
excitement is spread normally trough bundles of Hiss to myocardiocytes.
When additional impulse is generated in the middle or upper site of
node, diastolic interval after extrasystole is a bit increased. If the
impulse is generated in the lower part of the node, compensative pause
is signed after the exrtrasystole.
d) At ventricular extrasystoles additional impulse is generated in any
part of ventricular transmission system. It may be spread differently
according to where and which phase of heart it was generated. When
impulse is spread in non ordinary manner, Ventricular extrasystoles
(VEs) are wide, abnormally-shaped QRS complexes, excitement can not
reach atrium and P wave is not observed in ECG. Extrasystoles
occurring at every second or third beat are called bigeminy or
trigeminy respectively. Seldom we can meet interpolated extrasystole
(A ventricular contraction that occurs between two normal heartbeats). It
is not followed by compensative pause.
When extrasystoles become more frequent compensative pause is
observed. This is because, when impulse coming from sinus node
reaches ventricle it is in the absolute refraction phase after extrasystole
and can not respond to electric current.
When frequently repeated, group extrasystoles are initiated, they fully
restrain physiological rhythm, and paroxysm tachycardia is developed.
Risk factors for extra systoles
 Can occur in normal hearts, where the prevalence of extrasystoles
increases with age
 Hypertension
 Heart disease, including acute myocardial infarction, valvular heart
disease, cardiomyopathy, ventricular hypertrophy and cardiac
 Electrolyte
hypomagnesaemia, hypocalcaemia
 Drugs, including digoxin, tricyclic antidepressants, cocaine
 Alcohol excess
 Infection
 Stress
 Hyperthyroidism
 Stimulants such as caffeine may have a role, although this has not
been proven for ventricular extrasystoles
2. Arrhythmias developed at transmission disorders
Impulse transmission disorder in transmission system is called heart
block. Excitement transmission can be interrupted in different parts of
the system, according to which heart block following types are differed:
A. Sinoauricular block - electric signals are hindered from sinus
node to atrium (such kind of block develops at vagus nervus
excitation, miocardiodystropies, electrolyte balance disorders in
B. Atrioventricular block - impulse transmition is hindered in
atrioventricular node. They differ full or none full atrioventricular
block. The last is divided into 3 types:
1. I degree block – Atrioventricular node transmits every impulse to
the ventricles but they are delayed from 0.08 0.12 sec (normally),
to 0.2 -0.5 sec P-Q interval on ECG.
2. II degree block – P-Q interval is becoming more and more
prolonged until VII – IX wave of excitation is omitted. The next
cycle P-Q interval is normal but increasing again gradually until
blockage of one of impulses.
3. At III degree none full block every II or III impulse is omitted, on
ECG every II or III QRS complex is not observed.
4. Full atrioventruicular block (IV degree block according to some
authors) is developed when the node does not transmit any
excitation impulse to ventricles. In this case atrium and ventricles
contract according to their independent rhythm. Non full block
transition to full block is immensely important, when impulses
coming from sinus node are totally inhibited. Slow diastolic
depolarization in third grade pacemaker appears after some tome
after full blockage. This period is called preautomatric pause. At
full asystole developed during the pause brain is not provided with
blood, loss of consciousness and cramps are signed. (MorganAdams – Stocks Syndrome). In this period death may be signed
though frequently ventricles start contraction again by the
prevalence of their automatism, symptom disappears. The
syndrome may be many times repeated.
C. Right or left brunch block of bundle of Hiss – characterized by
electric current disorder in any branch of Hiss bundle. (In this case
impulse is transmitted to left or right ventricle, to second ventricle
impulse can be transmitted to intraventricular partition. That’s why
ventricles contract non synchronously.
3. Atrial and ventricular Arrhythmia
Heart muscle certain sites non synchronic, chaotic contraction is
revealed by palpitation and flutter.
Atrial fibrillation: In atrial fibrillation, the electrical activity of the heart
is uncoordinated, with electricity traveling about the upper chambers in
a chaotic fashion, causing the upper chambers to quiver (like a "bag of
worms") and contract inefficiently or not at all. Atrial fibrillation is
common particularly in the elderly and those with heart disease. It is
also common in patients with heart valve disease who may require
surgery to repair or replace the mitral valve. There are a variety of
treatment options for atrial fibrillation, including drugs, an ablation -- a
non-surgical technique which eliminates the abnormal heart tissue with a
catheter, or surgery in some cases.
Atrial flutter: Atrial flutter causes a rapid but coordinated electrical
stimulation of the upper chamber of the heart, often leading to a rapid
pulse. The atria are stimulated so quickly that they can not contract or
squeeze. This arrhythmia is due to a loop of electricity in the upper
chambers of the heart. It is often curable with ablation.
Wolff-Parkinson-White syndrome: This is a special type of
supraventricular tachycardia. This syndrome involves episodes of a
rapid heart rate (tachycardia) caused by abnormal electrical connection
in the heart. In people with Wolff-Parkinson-White syndrome, there is
an extra (accessory) connection between the top and bottom chambers of
the heart. Wolff-Parkinson-White occurs in approximately 4 out of
100,000 people, and is one of the most common causes of fast heart rate
disorders (tachyarrhymthmias) in infants and children.
Fibrillation is where electrical signals in the ventricles fire in a very fast
and uncontrolled manner. This causes the lower chambers to quiver, and
not pump blood. If the person does not receive immediate medical
attention and a normal rhythm is not restored quickly, the patient will
suffer from brain and heart damage and die. Patients who survive this
Ventricular Tachycardia is a rapid, regular heartbeat arising in the
ventricles, the bottom chamber of the heart. When it occurs, it's usually
fatal. About 400,000 people a year die from it. The treatment of choice
for this invariably includes an implantable defibrillator and or
medication and or interventions like ablation to try to minimize or limit
the number of shocks.