Atrial tachycardia is a form of supraventricular tachycardia (SVT) usually seen in patients with structural heart abnormalities but can be seen in patients with structurally normal hearts. Unlike other SVTs, atrial tachycardia does not depend upon the atrioventricular junction or accessory pathways for initiation or maintenance.
Typical with most SVTs, atrial tachycardia exhibits a narrow QRS complex tachycardia. A narrow complex tachycardia is defined as a QRS complex <120 milliseconds. A compound this short illustrates the rapid activation of the ventricles, which indicates that the arrhythmia is originating above the ventricles.
Heart rates are highly variable in atrial tachycardia producing a rate usually between 100-250. The rhythms of atrial tachycardias are commonly regular, but irregular variants can be seen. P wave morphology is highly variable and can indicate the location and origin of the arrhythmia. The arrhythmias can originate in either the left or right atrium, superior vena cava and as well as some lesser common areas such as the hepatic veins and noncoronary aortic cusp. The basic anatomy of the heart is vital to consider the origins of reentrant circuits. The orifices of the vena cava, coronary sinus, and pulmonary veins are common anatomical sites where reentry can occur.
Atrial tachycardia can manifest itself in patients with both anatomically normal and anatomically abnormal hearts. The structure of the patient’s heart can be responsible for specific variants. In hearts, reentrant variations, typically present in hearts that accommodate the reentrant conduction, such as in the orifices of the vena cava, coronary sinus, and pulmonary veins.
Atrial tachycardia can present secondary to a triggering event or conditions. Hypoxia, catecholamine release, alcohol, drug use, and even exercise can trigger atrial tachycardia. Iatrogenic versions are seen following ablation procedures; most commonly originating from gaps in the ablation lines. 
Atrial tachycardia is a less common form of SVT, accounting for 5-15% of diagnosed SVTs. Atrial tachycardia is seen in all age ranges but tends to present more in older patients. There is no known ethnic or racial association but appears more commonly in patients with known triggering risk factors (see etiology).
The pathophysiology of atrial tachycardia can vary depending on the origin of the arrhythmia, which can be determined through electrophysiology mapping to elucidate the source of the sickness. Reentrant atrial tachycardias can manifest due to an anatomical provenance or an iatrogenic origin, commonly by postsurgical scar tissue or post ablation gaps.
Patients with structurally normal hearts typically display atrial tachycardia thanks to increased tissue automaticity. P wave location can provide insight into the anatomical area of the enhanced tissue, but electrophysiologic mapping is crucial for the exact position. Atrial tachycardias provoked by increased tissue automaticity display a ‘warm-up phenomenon’ in which the atrial rate accelerates to its peak rate upon initiation of the arrhythmia.
Atrial tachycardia, with trigger origins, result from an electrolyte disturbance after an action potential. The error occurs by a calcium influx, originating from the other action potential, which causes depolarization. If the depolarization is significant enough, to reach the threshold, an action potential is generated. If this event is isolated, it may only result in an atrial ectopic beat, but if this electrolyte disturbance continues, it will produce a tachycardic arrhythmia. Catecholamine imbalance and digitalis toxicity are common trigger sources. Triggered atrial tachycardia can originate in one location in the atria or from multiple sites, which can result in a regular or irregular rhythm.
Patients with atrial tachycardia can be asymptomatic or symptomatic. If asymptomatic, the patient’s arrhythmia will be found incidentally on an EKG or any rhythm recorder. Patients who present symptomatically may complain of dizziness, palpitations, dyspnea, lightheadedness or chest pain. The patient’s atrial tachycardia could be a manifestation of an underlying condition. Patients must be worked up for underlying pathologies. For example, multifocal atrial tachycardia is most commonly elicited by an underlying chronic obstructive pulmonary disease (60%). The hypoxemia and increased bronchodilator use, which in turn causes increased catecholamine release, is thought to initiate multifocal atrial tachycardia.
When encountering a patient with atrial tachycardia, it is essential to get a thorough medical history. It is vital to ask about any cardiac surgery or procedures. Make a note of any family history of cardiac conditions or sudden death. Also, review the patient’s current medications as well any over the counter supplementation. Finally, ask about any illicit drug abuse, alcohol abuse or environmental or workplace exposures.
A thorough physical exam is required to work up and rule out other possible triggering conditions. Accurate vitals are essential to determine if the patient is hemodynamically stable. Cardiac reviews such as an EKG and an echocardiogram are crucial in identifying the source of the arrhythmia and establishing the sites of structural heart defects precipitating the malady.
The first step in the evaluation of a patient in atrial tachycardia is to obtain a 12 lead EKG. Ideally, the patient should also have a baseline EKG to compare against the abnormal. By reading the EKG, you should be able to determine the type of atrial tachycardia. Additionally, the morphology and the pattern of the P waves in the EKG could help you spot the location or locations of the origin of the arrhythmia. With a positive or biphasic P wave in aVL, one can infer right atrial origin (88% sensitivity, 79% specificity). With a positive P wave in lead V1, one can assume left atrial origin (93% sensitivity, 88% sensitivity).
Once the EKG is obtained, and the arrhythmia is determined, basic labs should be drawn to work up any underlying pathology that could be causing this arrhythmia. Additionally, an echocardiogram should be performed to look for any structural heart defects that could be causing this problem.
If the atrial tachycardia is found to be primary in nature, electrophysiology mapping should be done to precisely determine the origin and pattern to the arrhythmia. Mapping is crucial if the patient wants to undergo an ablation procedure to resolve their arrhythmia.
Another option, typically for patients with paroxysmal events, is home telemetry. This process would be useful in patients who are symptomatic but have a normal EKG, lab workup and echocardiogram. 24-hour monitoring can catch the arrhythmia and provide valuable information to its etiology.
Hemodynamic stability is the first step in determining treatment for a patient with atrial tachycardia. According to the 2015 American College of Cardiology , American Heart Association and the Heart Rhythm Society, first line management for hemodynamically unstable atrial tachycardia is IV Adenosine. If Adenosine is ineffective or not possible (due to no IV access for example), synchronized cardioversion is warranted. Adenosine is also the first line treatment for patients with paroxysmal atrial tachycardia.
For a hemodynamically stable patient, according to the same guidelines as above, first line management is IV beta-blockers, IV Diltiazem or IV Verapamil.  IV amiodarone or IV ibutilide can be used if the IV beta blockers or IV diltiazem/verapamil are ineffective.
In chronic management of atrial tachycardia beta blockers, diltiazem and verapamil can be used in their oral forms. In patients without structural heart defects or ischemic heart disease, flecainide or propafenone can be used. Patients can be managed on amiodarone  or sotalol. Digitalis is another option for patients with chronic atrial tachycardia. Digitalis toxicity can cause atrial tachycardia, but if handled and dosed properly, digitalis can be useful in managing this condition.
Cardioversion can also be used for patients who have refractory atrial tachycardia or atrial tachycardia which has been difficult or unable to control pharmacologically. Another non-pharmacologic treatment used in refractory cases is treatment by radiofrequency catheter ablation. After mapping, the atrial tachycardia’s origin can be targeted. The ablation technique is aimed at correcting the arrhythmia and curing the condition. Experienced centers have noted success rates >90% with complication rates around 1%.
Differential diagnoses for symptomatic atrial tachycardia are primarily other arrhythmias. In order to identify different rhythms, a 12 lead EKG will need to be obtained and read accurately. A full workup needs to be completed to establish if the arrhythmia is secondary to another condition.
Atrial tachycardia is not considered a life-threatening condition. Lifestyle modifications need to be implemented to prevent atrial tachycardia from being triggered again if that was the cause. Caffeine, alcohol, and situations that cause stress or anxiety should be avoided. Adequate and regular sleep is recommended. Prolonged states of atrial tachycardia can cause long term effects on the heart such as cardiac remodeling. Atrial tachycardia typically is more difficult to control the more prolonged time the heart stays in the arrhythmia, so it is essential to correct the arrhythmia or underlying issue as quickly as possible.
Atrial tachycardia does not have many complications from the arrhythmia itself, but many of the difficulties come from the treatment methods. Chronic atrial tachycardia can cause cardiac remodeling, which could lead to pump dysfunction and heart failure.
Many complications can occur from cardiac ablation, most commonly bleeding from the site of insertion. Other complications to be aware of is mechanical trauma to the heart itself; such as damage to the heart vessels, the valves or even puncture the wall of the heart. Another feared complication of ablation is to create another arrhythmia, which could also cause the patient to become unstable. If the normal conduction is damaged enough, a pacemaker may be required to manage the new arrhythmia.
Complications from medication used to treat atrial tachycardia (see drugs classes side effects and contraindications). Cardioversion has its own set of possible complications. Complications can range from as benign as minor burning of the skin to severe arrhythmias and even asystole (see cardioversion complications).
Atrial tachycardia is caused by a problem in the heart’s conduction system which coordinates the heartbeat. The issue in atrial tachycardia is the heart is beating too fast. Patients can experience this event with or without symptoms. Common symptoms include palpitations, dizziness, lightheadedness and passing out. If you feel any of the symptoms for more than a brief period, you should seek medical attention.
Tests for atrial tachycardia include an EKG which shows the rhythm of the heart. Other tests include a Holter monitor or a loop recorder which records the heart's rhythm for a longer period.
Treatment for atrial tachycardia includes medications to slow the heart rate down or adjust the heart rhythm. Another method is cardioversion which shocks the heart back into a normal rhythm. Another way of treatment is an ablation procedure in which the area of the heart producing the abnormal signals in heated and destroyed.
In a patient with unstable atrial tachycardia, all healthcare staff must work together effectively for optimal care for the patient. Communication, proper training and clear team roles are essential in any rapid response team or code blue situation. A study at Vancouver General Hospital showed that nurses felt the team performed better after training and with assigned team roles. Before practice, many nurses noted that it was unclear who the team leader was and who had which functions. It is essential to have these skills and roles established at any institution caring for patients with conditions, such as atrial tachycardia, who could become unstable.
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