Cardiac dysrhythmia

Cardiac arrhythmia

Classification and external resources

Ventricular Fibrillation or V-Fib, an example of cardiac

ICD-10 I47. - I49.

ICD-9 427

DiseasesDB 15206

MedlinePlus 001101

MeSH D001145

Cardiac dysrhythmia (also known as arrhythmia) is a term for any of a large and heterogeneous group of conditions in which there
is abnormal electrical activity in the heart. The heart beat may be too fast or too slow, and may be regular or irregular.
Some arrhythmias are life-threatening medical emergencies that can result in cardiac arrest and sudden death. Others cause symptoms
such as an abnormal awareness of heart beat (palpitations), and may be merely annoying. Still others may not be associated with any
symptoms at all, but may predispose the patient to potentially life threatening stroke or embolism.
Some arrhythmias are very minor and can be regarded as normal variants. In fact, most people will on occasion feel their heart skip a
beat, or give an occasional extra strong beat; neither of these is usually a cause for alarm.[1]
Proarrhythmia is a new or more frequent occurrence of pre-existing arrhythmias, paradoxically precipitated by antiarrhythmic
therapy, which means it is a side effect associated with the administration of some existing antiarrhythmic drugs, as well as drugs for
other indications. In other words, it is a tendency of antiarrhythmic drugs to facilitate emergence of new arrhythmias.
The term sinus arrhythmia refers to a normal phenomenon of mild acceleration and slowing of the heart rate that occurs with breathing
in and out. It is usually quite pronounced in children, and steadily decreases with age. This can also be present during meditation
breathing exercises that involve deep inhaling and breath holding patterns.
Manifestations
The term cardiac arrhythmia covers a very large number of very different conditions.The most common symptom of arrhythmia is an
abnormal awareness of heartbeat, termed palpitations. These may be infrequent, frequent, or continuous. Some of these arrhythmias
are harmless (though distracting for patients) but many of them predispose to adverse outcomes.
Some arrhythmias do not cause symptoms, and are not associated with increased mortality. However, some asymptomatic arrhythmias
are associated with adverse events. Examples include a higher risk of blood clotting within the heart and a higher risk of insufficient
blood being transported to the heart because of weak heartbeat. Other increased risks are of embolisation and stroke, heart failure and
sudden cardiac death.
If an arrhythmia results in a heartbeat that is too fast, too slow or too weak to supply the body's needs, this manifests as a lower blood
pressure and may cause lightheadedness or dizziness, or fainting.
Some types of arrhythmia result in cardiac arrest, or sudden death.
Medical assessment of the abnormality using an electrocardiogram is the best way to diagnose and assess the risk of any given
arrhythmia.
Main article: Electrical conduction system of the heart
Each heart beat originates as an electrical impulse from a small area of tissue in the right atrium of the heart called the sinus node or
Sino-atrial node or SA node. The impulse initially causes both of the atria to contract, then activates the atrioventricular (or AV) node
which is normally the only electrical connection between the atria and the ventricles , which can be called as main pumping chambers.
The impulse then spreads through both ventricles via the Bundle of His and the Purkinje fibres causing a synchronised contraction of
the heart muscle, and thus, the pulse.
In adults the normal resting heart rate ranges from 60 to 80 beats per minute. The resting heart rate in children is much faster.
Bradycardias

Normal sinus rhythm, with solid black arrows pointing to normal P waves representative of normal sinus node function, followed by a
pause in sinus node activity (resulting in a transient loss of heart beats). Note that the P wave that disrupts the pause (indicated by the
dashed arrow) does not look like the previous (normal) P waves- this last P wave is arising from a different part of the atrium,
representing an escape rhythm.
A slow rhythm, (less than 60 beats/min), is labelled bradycardia. This may be caused by a slowed signal from the sinus node (termed
sinus bradycardia), a pause in the normal activity of the sinus node (termed sinus arrest), or by blocking of the electrical impulse on its
way from the atria to the ventricles (termed AV block or heart block). Heart block comes in varying degrees and severity. It may be
caused by reversible poisoning of the AV node (with drugs that impair conduction) or by irreversible damage to the node.
Bradycardias may also be present in the normally functioning heart of athletes or other well conditioned persons.
Tachycardias - Any resting heart rate faster than 100 beats/minute is labelled tachycardia. Tachycardia may result in
palpitation, however, tachycardia is not necessarily an arrhythmia. Increased heart rate is a normal response to physical
exercise or emotional stress. This is mediated by the sympathetic nervous system on the sinus node, and is called sinus
tachycardia. Other things that increase sympathetic nervous system activity in the heart include ingested or injected
substances such as caffeine or amphetamines, and an overactive thyroid gland (hyperthyroidism).
Tachycardia that is not sinus tachycardia usually results from the addition of abnormal impulses to the normal cardiac cycle.
Abnormal impulses can begin by one of three mechanisms: automaticity, reentry or triggered activity. A specialised form of re-entry
problem is termed fibrillation.
Automaticity - Automaticity refers to a cardiac muscle cell firing off an impulse on its own. All of the cells in the heart have the
ability to initiate an action potential, however, only some of these cells are designed to routinely trigger heart beats. These cells are
found in the 'conduction system' of the heart and include the SA node, AV node, Bundle of HIS and Purkinje fibers. The sinoatrial
node is a single specialized location in the atrium which has a higher automaticity (a faster pacemaker) than the rest of the heart, and
therefore is usually responsible for setting the heart rate, and initiating each heart beat.
Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus, and is by definition a
pathological phenomenon. This may cause a single premature beat now and then, or, if the ectopic focus fires more often than the
sinoatrial node, it can produce a sustained abnormal rhythm. Rhythms produced by an ectopic focus in the atria, or by the
atrioventricular node, are the least dangerous dysrhythmias; but they can still produce a decrease in the heart's pumping efficiency,
because the signal reaches the various parts of the heart muscle with different timing to usual and can be responsible for poorly
coordinated contraction.
Conditions that increase automaticity include sympathetic nervous system stimulation and hypoxia. The resulting heart rhythm
depends on where the first signal begins: if it is the sinoatrial node, the rhythm remains normal but rapid; if it is an ectopic focus,
many types of dysrhythmia may ensue.
Re-entry - Re-entry arrhythmias occur when an electrical impulse recurrently travels in a tight circle within the heart, rather than
moving from one end of the heart to the other and then stopping.[2] Every cardiac cell is able to transmit impulses in every direction,
but will only do so once within a short period of time. Normally, the action potential impulse will spread through the heart quickly
enough that each cell will only respond once. However, if conduction is abnormally slow in some areas, part of the impulse will arrive
late and potentially be treated as a new impulse. Depending on the timing, this can produce a sustained abnormal circuit rhythm. Re-
entry circuits are responsible for atrial flutter, most paroxysmal supraventricular tachycardia, and dangerous ventricular tachycardia.
By analogy, imagine a room full of people all given these instructions: "If you see anyone starting to stand up, then stand up for three
seconds and sit back down." If people are quick enough to respond, the first person to stand will trigger a single wave which will then
die out; but if there are stragglers on one side of the room, people who have already sat down will see them and start a second wave,
and so on.
Fibrillation - When an entire chamber of the heart is involved in a multiple micro-reentry circuits, and therefore quivering with
chaotic electrical impulses, it is said to be in fibrillation. Fibrillation can affect the atrium (atrial fibrillation) or the ventricle
(ventricular fibrillation); ventricular fibrillation is imminently life-threatening.
Atrial fibrillation affects the upper chambers of the heart, known as the atria. Atrial fibrillation may be due to serious underlying
medical conditions, and should be evaluated by a physician. It is not typically a medical emergency.
Ventricular fibrillation occurs in the ventricles (lower chambers) of the heart; it is always a medical emergency. If left untreated,
ventricular fibrillation (VF, or V-fib) can lead to death within minutes. When a heart goes into V-fib, effective pumping of the blood
stops. V-fib is considered a form of cardiac arrest, and an individual suffering from it will not survive unless cardiopulmonary
resuscitation (CPR) and defibrillation are provided immediately.
CPR can prolong the survival of the brain in the lack of a normal pulse, but defibrillation is the only intervention which can restore a
healthy heart rhythm. Defibrillation is performed by applying an electric shock to the heart, which resets the cells, permitting a normal
beat to re-establish itself.
Triggered beats - Triggered beats occur when problems at the level of the ion channels in
individual heart cells result in abnormal propagation of electrical activity and can lead to
sustained abnormal rhythm. They are relatively rare, but can result from the action of anti-
arrhythmic drugs.
Classification of common cardiac arrhythmias
Arrhythmia may be classified by rate (normal, tachycardia, bradycardia), or mechanism (automaticity, reentry, fibrillation).
It is also appropriate to classify by site of origin:
Atrial
• Premature Atrial Contractions (PACs)
• Wandering Atrial Pacemaker
• Multifocal atrial tachycardia
• Atrial flutter
• Atrial fibrillation (Afib)
Junctional arrhythmias
• Supraventricular tachycardia (SVT)
• AV nodal reentrant tachycardia is the most common cause of Paroxysmal Supra-ventricular Tachycardia (PSVT)
• Junctional rhythm
• Junctional tachycardia
Atrio-ventricular
• AV reentrant tachycardia occurs when a re-entry circuit crosses between the atria and ventricles somewhere other than the
AV node:
○ Wolff-Parkinson-White syndrome
○ Lown-Ganong-Levine syndrome
Ventricular
• Premature Ventricular Contractions (PVC) sometimes called Ventricular Extra Beats (VEBs)
○ Premature Ventricular beats occurring after every normal beat are termed ventricular bigeminy
○ PVCs that occur at intervals of 2 normal beats to 1 PVC are termed PVCs in trigeminy
○ Three premature ventricular grouped together is termed "A Run of PVCs", runs lasting longer than 3 beats are
generally referred to as ventricular tachycardia
• Accelerated idioventricular rhythm
• Monomorphic Ventricular tachycardia
 • Polymorphic ventricular tachycardia
• Ventricular fibrillation
Heart blocks
These are also known as AV blocks, because the vast majority of them arise from pathology at the atrioventricular node. They are the
most common causes of bradycardia:
• First degree heart block, which manifests as PR prolongation
• Second degree heart block
○ Type 1 Second degree heart block, also known as Mobitz I or Wenckebach
○ Type 2 Second degree heart block, also known as Mobitz II
• Third degree heart block, also known as complete heart block
Diagnosis
Cardiac dysrhythmias are often first detected by simple but nonspecific means: auscultation of the heartbeat with a stethoscope, or
feeling for peripheral pulses. These cannot usually diagnose specific dysrhythmias, but can give a general indication of the heart rate
and whether it is regular or irregular. Not all the electrical impulses of the heart produce audible or palpable beats; in many cardiac
arrhythmias, the premature or abnormal beats do not produce an effective pumping action and are experienced as "skipped" beats.
The simplest specific diagnostic test for assessment of heart rhythm is the electrocardiogram (abbreviated ECG or EKG). A Holter
monitor is an EKG recorded over a 24-hour period, to detect dysrhythmias that may happen briefly and unpredictably throughout the
day.
A more advanced study of the heart's electrical activity can be performed to assess the source of the aberrant heart beats. This can be
accomplished in an Electrophysiology study. A minimally invasive procedure that uses a catheter to "listen" to the electrical activity
from within the heart, additionally if the source of the arrhythmias is found, oftentimes the abnormal cells can be ablated and the
arrhythmia can be permanently corrected.
Treatment
Because arrhythmias are such a heterogeneous group of conditions, treatment needs to be carefully selected by a patient with their
physician. Some arrhythmias require no treatment at all. Others require immediate emergency treatment if death is to be avoided.
Treatments include physical maneuvers, antiarrhythmic drugs, other drugs, electricity, and electro or cryo cautery.
[edit] Physical manoeuvres
A number of physical acts can increase parasympathetic nervous supply to the heart, resulting in blocking of electrical conduction
through the AV node. This can slow down or stop a number of arrhythmias that originate above or at the AV node (see main article:
supraventricular tachycardias). Parasympathetic nervous supply to the heart is via the vagus nerve, and these maneuvers are
collectively known as vagal manoeuvres.
[edit] Antiarrhythmic drugs
See main article on antiarrhythmic agents.
There are many classes of antiarrhythmic medications, with different mechanisms of action and many different individual drugs within
these classes. Although the goal of drug therapy is to prevent arrhythmia, nearly every antiarrhythmic drug has the potential to act as a
pro-arrhythmic, and so must be carefully selected and used under medical supervision.
[edit] Other drugs
A number of other drugs can be useful in cardiac arrhythmias.Several groups of drugs slow conduction through the heart, without
actually preventing an arrhythmia. These drugs can be used to "rate control" a fast rhythm and make it physically tolerable for the
patient.Some arrhythmias promote blood clotting within the heart, and increase risk of embolus and stroke. Anticoagulant medications
such as warfarin and heparins, and anti-platelet drugs such as aspirin can reduce the risk of clotting.
[edit] Electricity
Dysrhythmias may also be treated electrically, by applying a shock across the heart — either externally to the chest wall, or internally
to the heart via implanted electrodes.
Cardioversion is either achieved pharmacologically or via the application of a shock synchronised to the underlying heartbeat. It is
used for treatment of supraventricular tachycardias. In elective cardioversion, the recipient is usually sedated or lightly anesthetized
for the procedure.
Defibrillation differs in that the shock is not synchronised. It is needed for the chaotic rhythm of ventricular fibrillation and is also
used for pulseless ventricular tachycardia. Often, more electricity is required for defibrillation than for cardioversion. In most
defibrillation, the recipient has lost consciousness so there is no need for sedation.
Defibrillation or cardioversion may be accomplished by an implantable cardioverter-defibrillator (ICD).
Electrical treatment of dysrhythmia also includes cardiac pacing. Temporary pacing may be necessary for reversible causes of very
slow heartbeats, or bradycardia, (for example, from drug overdose or myocardial infarction). A permanent pacemaker may be placed
in situations where the bradycardia is not expected to recover.
Electrical cautery - Some cardiologists further sub-specialise into electrophysiology. In specialised catheter laboratories, they use
fine probes inserted through the blood vessels to map electrical activity from within the heart. This allows abnormal areas of
conduction to be located very accurately, and subsequently destroyed with heat, cold, electrical or laser probes.
This may be completely curative for some forms of arrhythmia, but for others, the success rate remains disappointing. AV nodal
reentrant tachycardia is often curable. Atrial fibrillation can also be treated with this technique (e.g. pulmonary vein isolation), but the
results are less reliable.