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Tachycardia refers to rapid beating of the heart. By convention it defined as a heart rate greater than 100 beats per minute in adults. Tachycardia may be normal, such as in exercise and stress, or abnormal, such as in cardiac arrhythmias. However, depending on the mechanism of the tachycardia and the health status of the person, tachycardia may be harmful and require medical treatment. In extreme cases, tachycardia can be life threatening.
The condition can be associated with anxiety.
Tachycardia can be harmful in three ways. First, if the heart is pumping too fast for an extended period of time it will change the balance of oxygen and carbon dioxide in the hemoglobin in the blood; this is normal during exercise but when resting this is quite dangerous. Second, when the heart beats too rapidly, it may pump blood less efficiently as there is less time for the myocardium to relax between contractions. Third, the faster the heart beats, the more oxygen and nutrients the heart requires. This may leave patients feeling out of breath or cause angina in those suffering from ischemic heart disease.
- 1 Haemodynamic responses
- 2 Autonomic and endocrine causes
- 3 Cardiac arrhythmias
- 4 Treatments
- 5 See also
- 6 References
- 7 Further reading
- 8 External Links
The body contains several feedback mechanisms to maintain adequate blood flow and blood pressure. If blood pressure decreases, the heart beats faster in an attempt to raise it. This is called reflex tachycardia.
This can happen in response to a decrease in blood volume (through dehydration or bleeding), or an unexpected change in blood flow. The most common cause of the latter is orthostatic hypotension (also called postural hypotension), a sudden drop of blood pressure that occurs with a change in body position (e.g., going from lying down to standing up). When tachycardia occurs for this reason, it is called postural orthostatic tachycardia syndrome (POTS).
Autonomic and endocrine causes
An increase in sympathetic nervous system stimulation causes the heart rate to increase, both by the direct action of sympathetic nerve fibers on the heart and by causing the endocrine system to release hormones such as epinephrine (adrenaline), which have a similar effect. Increased sympathetic stimulation is usually due to physical or psychological stress (the so-called "fight or flight" response), but can also be induced by stimulants such as amphetamines.
- Main article: Arrythmias (heart)
The 12 lead ECG can help distinguish between the various types of tachycardias, generally distinguished by their site of pacemaker origin:
- Sinus tachycardia, which originates from the Sino-atrial (SA) node, near the base of the superior vena cava
- Ventricular tachycardia, any tachycardia which originates in the ventricles.
- Supraventricular tachycardia (SVT), which is a tachycardia paced from the Atria or the AV node. SVT rhythms include:
- Atrial fibrillation
- AVNRT or AV nodal reentrant tachycardia
- AVRT or AV reentrant tachycardia
- Junctional tachycardia
It is sometimes useful to classify tachycardias as either narrow complex tachycardias (often referred to as supraventricular tachycardias) or wide complex tachycardias. "Narrow" and "wide" refer to the width of the QRS complex on the ECG. Narrow complex tachycardias tend to originate in the atria, while wide complex tachycardias tend to originate in the ventricles. Tachycardias can be further classified as either regular or irregular.
- Main article: Sinus tachycardia
The most common type of tachycardia is sinus tachycardia, which is the body's normal reaction to stress, including fever, dehydration, or blood loss (shock). It is a technical narrow complex tachycardia. In the absence of heart disease, it tends to have a narrow QRS complex on the ECG. Treatment is generally directed at identifying the underlying cause.
- Main article: Ventricular tachycardia
Ventricular tachycardia (VT or V-tach) is a potentially life-threatening cardiac arrhythmia that originates in the ventricles. It is usually a regular, wide complex tachycardia with a rate between 120 and 250 beats per minute. Ventricular tachycardia has the potential of degrading to the more serious ventricular fibrillation. Ventricular tachycardia is a common, and often lethal, complication of a myocardial infarction (heart attack).
Exercise-induced ventricular tachycardia is a phenomenon related to sudden deaths, especially in patients with severe heart disease (ischaemia, acquired valvular heart and congenital heart disease) accompanied with left ventricular dysfunction. A case of a death from exercise-induced VT was the death on a basketball court of Hank Gathers, the Loyola Marymount basketball star, in March 1990.
- Main article: Supraventricular tachycardia
Atrial fibrillation is one of the most common cardiac arrhythmias. It is generally an irregular, narrow complex rhythm. However, it may show wide QRS complexes on the ECG if a bundle branch block is present. At high rates, the QRS complex may also become wide due to the Ashman phenomenon. It may be difficult to determine the rhythm's regularity when the rate exceeds 150 beats per minute. Depending on the patient's health and other variables such as medications taken for rate control, atrial fibrillation may cause heart rates that span from 50 to 250 beats per minute (or even higher if an accessory pathway is present). However, new onset atrial fibrillation tends to present with rates between 100 and 150 beats per minute.
AV nodal reentrant tachycardia (AVNRT)
AV nodal reentrant tachycardia is the most common reentrant tachycardia. It is a regular narrow complex tachycardia that usually responds well to vagal maneuvers or the drug adenosine. However, unstable patients sometimes require synchronized cardioversion. Definitive care may include catheter ablation.
AV reentrant tachycardia
AV reentrant tachycardia (AVRT) requires an accessory pathway for its maintenance. AVRT may involve orthodromic conduction (where the impulse travels down the AV node to the ventricles and back up to the atria through the accessory pathway) or antidromic conduction (which the impulse travels down the accessory pathway and back up to the atria through the AV node). Orthodromic conduction usually results in a narrow complex tachycardia, and antidromic conduction usually results in a wide complex tachycardia that often mimics ventricular tachycardia. Most antiarrhythmics are contraindicated in the emergency treatment of AVRT, because they may paradoxically increase conduction across the accessory pathway.
Junctional tachycardia is an automatic tachycardia originating in the AV junction. It tends to be a regular, narrow complex tachycardia and may be a sign of digitalis toxicity.
Treatment of tachycardia is usually directed at chemical conversion (with antiarrythmics), electrical conversion (giving external shocks to convert the heart to a normal rhythm) or use of drugs to simply control heart rate (for example as in atrial fibrillation).
The treatment modality used depends on the type of tachycardia and the hemodynamic stability of the patient. If the tachycardia originates from the sinus node (sinus tachycardia), treatment of the underlying cause of sinus tachycardia is usually sufficient. On the other hand, if the tachycardia is of a potentially lethal origin (ie: ventricular tachycardia) treatment with anti arrhythmic agents or with electrical cardioversion may be required. Below is a brief discussion of some of the main tachyarrhythmias and their treatments.
The electrocardiac management of atrial fibrillation and atrial flutter is either through medications or electrical cardioversion. Pharmacologic management of these arrhythmias typically involves diltiazem or verapamil as well as beta-blocking agents such as atenolol. The decision to use electrical cardioversion depends heavily on the hemodynamic stability of the presenting patient; in general those patients who are unable to sustain their systemic functions are electrically converted although conversion to a normal sinus rhythm can be performed with amiodarone. An interesting type of atrial fibrillation which must be carefully managed is when it appears in combination with Wolff-parkinson White. In this case, calcium channel blockers, beta-blockers and digoxin must be avoided to prevent precipitation of ventricular tachycardia. Here, procainamide or quinidine are often used. Of note: patients who have been in atrial fibrillation for more than 48 hours should not be converted to normal sinus rhythm unless they have been anti-coagulated to an INR of 2-3 for at least 4 weeks.
In the case of narrow complex tachycardias (juntional, atrial or paroxysmal), the treatment in general is to first give the patient adenosine (to slow conduction through the AV node) and then perform vagal maneuvers to slow the rhythm. If this does not convert the patient, amiodarone, calcium channel blockers or beta-blockers are commonly employed to stabilize the patient. Again as in atrial fibrillation, if a patient is unstable, the decision to electrially cardiovert him/her should be made.
With wide complex tachyarrhythmias or ventricular tachyarrhythmias, in general most are highly unstable and cause the patient significant distress and would be electrically converted. However one notable exception is monomorphic ventricular tachycardia which patients may tolerate but can be treated pharmacologically with amiodarone or lidocaine.
Above all, the treatment modality is tailored to the individual, and varies based on the mechanism of the tachycardia (where it is originating from within the heart), on the duration of the tachycardia, how well the individual is tolerating the fast heart rate, the likelihood of recurrence once the rhythm is terminated, and any co-morbid conditions the individual is suffering from.
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