Cardiac arrhythmia is 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 arrhythmia 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 arrhythmias 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, an
endovascular procedure that uses a catheter to "listen" to the electrical activity from within the heart, additionally if the source of the arrhythmias is found, often the abnormal cells can be ablated and the arrhythmia can be permanently corrected. '''' (TAS) instead uses an electrode inserted through the
esophagus to a part where the distance to the posterior wall of the
left atrium is only approximately 5–6 mm (remaining constant in people of different age and weight). Transesophageal atrial stimulation can differentiate between
atrial flutter,
AV nodal reentrant tachycardia and orthodromic
atrioventricular reentrant tachycardia.
Differential diagnosis Normal electrical activity Each heartbeat originates as an electrical impulse from a small area of tissue in the right
atrium of the heart called the
sinus node or sinoatrial node (SA node). The impulse initially causes both atria to contract, then activates the
atrioventricular node (AV node), which is normally the only electrical connection between the atria and the
ventricles (main pumping chambers). The impulse then spreads through both ventricles via the
bundle of His and the
Purkinje fibers causing a synchronized contraction of the heart muscle and, thus, the pulse. In adults, the normal resting heart rate ranges from 60 to 90 beats per minute. The resting heart rate in children is much faster. In athletes, however, the resting heart rate can be as slow as 40 beats per minute, and be considered normal. The term
sinus arrhythmia refers to a normal phenomenon of alternating mild acceleration and slowing of the heart rate that occurs with breathing in and out respectively. 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.
Bradycardias A slow rhythm (less than 60 beats/min) is labelled
bradycardia. This may be caused by a slowed signal from the sinus node (sinus bradycardia), by a pause in the normal activity of the sinus node (sinus arrest), or by blocking of the electrical impulse on its way from the atria to the ventricles (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 endurance athletes or other well-conditioned persons. Bradycardia may also occur in
some types of seizures.
Tachycardias In adults and children over 15, resting heart rate faster than 100 beats per minute is labeled
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 called sinus tachycardia. Other conditions 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) or
anemia. 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, re-entry, or triggered activity. A specialized form of re-entry which is both common and problematic is termed fibrillation. Although the term "tachycardia" has been known for over 160 years, bases for the classification of arrhythmias are still being discussed.
Heart defects Congenital heart defects are structural or electrical pathway problems in the heart that are present at birth. Anyone can be affected by this because overall health does not play a role in the problem. Problems with the electrical pathway of the heart can cause very fast or even deadly arrhythmias.
Wolff–Parkinson–White syndrome is due to an extra pathway in the heart that is made up of electrical muscle tissue. This tissue allows the electrical impulse, which stimulates the heartbeat, to happen very rapidly. Right
ventricular outflow tract tachycardia is the most common type of ventricular tachycardia in otherwise healthy individuals. This defect is due to an electrical node in the right ventricle just before the pulmonary artery. When the node is stimulated, the patient will go into ventricular tachycardia, which does not allow the heart to fill with blood before beating again.
Long QT syndrome is another complex problem in the heart and has been labeled as an independent factor in mortality. There are multiple methods of treatment for these including cardiac ablations, medication treatment, or lifestyle changes to have less stress and exercise.
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 heartbeats. 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 that 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 heartbeat. 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 than 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-entrant 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. Every cardiac cell can transmit
impulses of excitation in every direction but will do so only once within a short time. Normally, the
action potential impulse will spread through the heart quickly enough that each cell will respond only once. However, if there is some essential heterogeneity of
refractory period or if conduction is abnormally slow in some areas (for example in heart damage) so the myocardial cells are unable to activate the fast sodium channel, 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. As a sort of
re-entry, vortices of excitation in the myocardium (
autowave vortices) are considered to be the main mechanism of life-threatening cardiac arrhythmias. In particular, the
autowave reverberator is common in the thin walls of the atria, sometimes resulting in
atrial flutter. Re-entry is also responsible for most
paroxysmal supraventricular tachycardia, and dangerous
ventricular tachycardia. These types of re-entry circuits are different from
WPW syndromes, which utilize abnormal conduction pathways. Although
omega-3 fatty acids from
fish oil can be protective against arrhythmias, they can facilitate re-entrant arrhythmias.
Fibrillation When an entire chamber of the heart is involved in multiple micro-re-entry circuits and is, 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. An affected individual 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 that 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 a sustained abnormal rhythm. They are relatively rare and can result from the action of anti-arrhythmic drugs, or after
depolarizations. ==Management==