Causes of heart racing
Atrial fibrillation (AF)
Atrial fibrillation (AF) is the most common arrhythmia encountered in patients. When the atria fibrillate, they beat at 400-600 beats per minute. Because this is so fast, the atria just quiver rather than help fill the ventricles. AF arises from the left atrium in about 90% of patients – the pulmonary veins (PV) being the most common source. Until recently, we assumed that atrial muscle stopped right where the PVs met the left atrium. We now know that threads of atrial tissue called fascicles can go up into the PVs for some distance. These fascicles are where AF originates. When the fascicle starts rapid autonomous firing, the impulses follow the PVs to the left atrium and causes AF.
Atrial flutter (AFl)
Atrial flutter (AFl) is a common rhythm disturbance where the atria beat at about 300 beats per minute. This rate is too fast for the AV node to conduct each of them to the left ventricle. Therefore heart rate is kept physiologic at the expense of AV synchrony. The result is that cardiac efficiency is diminished somewhat
Supraventricular tachycardia (SVT)
SVT is a fast heart rhythm involving at least part of the atrium and/or the AV node. SVT is caused by a reentrant pathway in about 90% of patients and an atrial focus with either abnormal automaticity or triggered activity in the remaining 10% of patients. The exact mechanism of SVT can only be determined by an electrophysiology or EP study.
AV Node Reentry (AVNRT)
In this most common form of SVT, comprising 60-70% of cases, AVNRT involves a reentrant circuit that actually is part of the AV node complex. The AV node in such patients involves longitudinal dissociation producing a fast pathway and a slow pathway. AVNRT occurs when a premature beat blocks in one pathway and then traverses the other slowly enough so that when it reaches the far end of the first pathway, it can turn around and conduct retrograde to the top again producing reentry. Usually the slow pathway is the one used antegrade to the ventricle and the fast pathway to return to the atrium, but rarely the circuit is reversed or even consists of two different slow pathways. Usually these different pathways are very near the main part of the AV node, but they may occur at some distance either on the right or left side of the heart. These pathways never are hereditary as far as we know.
AV Reentry (AVRT)
This is the second-most common form of SVT comprising about 30% of cases. AVRT involves an accessory pathway usually not close to the AV node. These accessory pathways (AP) are present since birth and result from incomplete separation of the atrium from the ventricle. Embryologically, the atrium and ventricle are in direct continuity. As the fetus ages, connective tissue grows septating the atrium from the ventricle completely except for the AV node. When this septation process is incomplete, an AP is created. Only about 1% of accessory pathways are hereditary. They can allow conduction from the atrium to the ventricle only, from the ventricle to the atrium only or bidirectionally. When the AP allows conduction from the atrium to the ventricle or bidirectionally then the Wolff-Parkinson-White syndrome (WPW) is said to exist. These APs can cause SVT through reentry. Usually an ectopic beat blocks in the AP then engages the AV Node with sufficient slowing that the reentrant impulse can then reenter the AP and produce SVT. However, the reentrant circuit can be reversed on even involve two APs without participation of the AV node. Most of these APs are located just underneath the endocardium of the heart, but occasionally are located closer to the epicardium, usually within the coronary sinus.
The least common type of SVT involves one or more irritable foci that have formed after birth in one of the atria. These spots usually form around the tricuspid or mitral valves. They can also form within the pulmonary veins or along the crista terminalis (a ridge running around inside of the right atrium). They are virtually never hereditary. They may occur by themselves or with other arrhythmias such as atrial flutter or atrial fibrillation. Patients with atrial tachycardia are more likely to have hypertension or structural heart disease than patients with other types of SVT.
Ventricular tachycardia (VT)
Ventricular Tachycardia (VT) arises from the ventricles. It may arise from the right ventricle or the left ventricle. It can be caused either by an irritable focus or by a reentrant circuit in the heart muscle or involving the normal bundle branches. If the ventricles are structurally normal, then curative ablation is feasible and frequently disire. If the ventricles have been damaged by scar tissue and/or weakened then VT is potentially life-threatening and an implantable cardiac defibrillator (ICD) is usually required. However if frequent episodes of VT occur trigerring ICD shocks inspite of antiarrhythmic drugs, then ablation may also be required.
Ventricular fibrillation (VF)
Ventricular fibrillation (VF) is a life threatening arrhythmia that unless caused by a reversible cause such as a heart attack, has a high likelihood of recurrence and requires an ICD, since medications are seldom effective. Only in very rare cases where VF recurs frequently triggering shocks from the ICD in spite of antiarrhythmic drugs is ablation of the beats that trigger the VF an option.
Torsades de Pointes
Torsades de Pointes is a chaotic ventricular rhythm disturbance usually caused by medications or by an inherited abnormality causing prolongation of the QT interval. Since it can be fatal, pacemakers or even defibrillators may be required. There is not currently a role for ablation.
Multifocal atrial tachycardia (MAT)
Multifocal atrial tachycardia (MAT) is a tachycardia caused by multiple atrial foci occurring as a consequence of pulmonary disease per se of the medications used to treat it. It occurs most commonly in patients with COPD. Most patients do not have symptoms from MAT, since the heart rates are usually not very fast (130-150 beats per minute). When treatment improves lung function, MAT usually goes away. Heart rhythm medications may be tried in rare patients. Ablation is very rarely required and seldom effective given the fact that multiple foci exist.
Every person alive has ectopic beats. These extra beats may arise from irritable spots in the atrium (PACs), from the AV node itself (PJCs) or most commonly from the ventricles (PVCs). Sometimes these ectopic beats produce a pulse that the patient can feel as an extra beat. In other cases, the ectopic beat does not generate a significant pulse beat since the ventricle has not had time to fill with much blood and the stroke volume of that beat is very small. However, the ectopic beat prevents the next normal sinus beat creating a pause that the patient feels as a skip. Some patients feel these ectopic beats while others do not. Symptoms caused by them can be palpitations, dyspnea, light-headedness, chest pain, fatigue, or the need to cough. Sometimes these ectopic beats can trigger an arrhythmia like atrial fibrillation or SVT. Usually patients are afraid that these ectopic beats will produce a cardiac arrest, stroke, or myocardial infarction. However in virtually every situation, they are nothing more than a nuisance. The treatment of ectopic beats, therefore, does not prolong life since they do not shorten life. Therefore in patients who are asymptomatic, there is seldom the need to treat them. The only exception to this is in patients who have many (usually more than 20,000 daily) PVCs when rarely a cardiomyopathy results. This so-called tachycardiomyopathy is reversible when the PVCs are treated with antiarrhythmic drugs or ablation.
Patients who are symptomatic with ectopic beats when reassurance is insufficient may be treated with antiarrhythmic drugs, pacing (when bradycardia is etiologic usually when pacing is indicated for another reason) or by ablation usually assisted by a 3D mapping system.