While<unk>  can sometimes go unnoticed, its onset is often marked by characteristic sensations of the heart feeling like it is beating too fast or hard. Such sensations usually last until the episode resolves, or until the heart rate is controlled.<unk>  is usually well-tolerated initially (a high heart rate is for most people just a normal response to exercise), however, people with other underlying heart diseases (such as coronary artery disease) or poor exercise tolerance may rapidly develop symptoms, such as shortness of breath, chest pain, lightheadedness or dizziness, nausea and, in some patients, nervousness and feelings of impending doom. Prolonged<unk>  with fast heart rates may lead to decompensation with loss of normal heart function (heart failure). This may manifest as exercise intolerance (exertional breathlessness), difficulty breathing at night, or swelling of the legs and/or abdomen. Complications Although often regarded as a relatively benign heart rhythm problem,<unk>  shares the same complications as the related condition atrial fibrillation. There is paucity of published data directly comparing the two, but overall mortality in these conditions appears to be very similar. Rate related Rapid heart rates may produce significant symptoms in patients with pre-existing heart disease and can lead to inadequate blood flow to the heart muscle and even a heart attack. In rare situations,<unk>  associated with a fast heart rate persists for an extended period of time without being corrected to a normal heart rhythm and leads to a tachycardia-induced cardiomyopathy. Even in individuals with a normal heart, if the heart beats too quickly for a prolonged period of time, this can lead to ventricular decompensation and heart failure. Clot formation Because there is little if any effective contraction of the atria there is stasis (pooling) of blood in the atria. Stasis of blood in susceptible individuals can lead to the formation of a thrombus (blood clot) within the heart. A thrombus is most likely to form in the atrial appendages. A blood clot in the left atrial appendage is particularly important as the left side of the heart supplies blood to the entire body through the arteries. Thus, any thrombus material that dislodges from this side of the heart can embolize (break off and travel) to the brain's arteries, with the potentially devastating consequence of a stroke. Thrombus material can, of course, embolize to any other portion of the body, though usually with a less severe outcome. Sudden cardiac death Sudden death is not directly associated with<unk> . However, in individuals with a pre-existing accessory conduction pathway, such as the bundle of Kent in Wolff-Parkinson-White syndrome, the accessory pathway may conduct activity from the atria to the ventricles at a rate that the AV node would usually block. Bypassing the AV node, the atrial rate of 300 beats/minute leads to a ventricular rate of 300 beats/minute (1:1 conduction). Even if the ventricles are able to sustain a cardiac output at such a high rates, 1:1 flutter with time may degenerate into ventricular fibrillation, causing hemodynamic collapse and death.
Atrial flutter
Ventricular flutter
Sinus arrhythmia
Supraventricular tachycardia
Atrial fibrillation
Ventricular fibrillation
Left bundle branch block
Junctional tachycardia