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 main article: automatic tachycardia 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 the method of cardiac rhythm management depends firstly on whether the affected person is stable or unstable. treatments may include physical maneuvers, medications, electricity conversion, or electro- or cryo-cautery. in the united states, people admitted to the hospital with cardiac arrhythmia and conduction disorders with and without complications were admitted to the intensive care unit more than half the time in 2011. physical maneuvers several 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 several 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 maneuvers. antiarrhythmic drugs main article: 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. other drugs 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 the 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. electricity arrhythmias 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 synchronized to the underlying heartbeat. it is used for the 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 synchronized. 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 arrhythmias 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-specialize into electrophysiology. in specialized 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 by heat, cold, electrical, or laser probes in a process called catheter ablation. this procedure may be completely curative for some forms of arrhythmia, but for others, the success rate remains disappointing. av nodal reentrant tachycardia is often curable by ablating one of the pathways in the av node (usually the slow pathway). atrial fibrillation can also be treated, by performing a pulmonary vein isolation, but the results are less reliable. research arrhythmias due to medications have been reported since the 1920s with the use of quinine. in the 1960s and 1970s problems with antihistamines and antipsychotics were discovered. it was not until the 1980s that the underlying issue, qtc prolongation was determined.