comes from the Greek words tachys
) and kardia
(of the heart
). Tachycardia typically refers to a heart rate that exceeds the normal range for a resting heartrate (heartrate in an inactive or sleeping individual). In humans, the upper threshold of a normal heart rate is usually based upon age, sometimes it can be very dangerous depending on how hard the heart is working and the activity:
- 1-2 days: >159 beats per minute (bpm)
- 3-6 days: >166 bpm
- 1-3 weeks: >182 bpm
- 1-2 months: >179 bpm
- 3-5 months: >186 bpm
- 6-11 months: >169 bpm
- 1-2 years: >151 bpm
- 3-4 years: >137 bpm
- 5-7 years: >133 bpm
- 8-11 years: >130 bpm
- 12-15 years: >119 bpm
- >15 years - adult: >100 bpm
When the heart beats rapidly, the heart pumps less efficiently and provides less blood flow to the rest of the body, including the heart itself. The increased heart rate also leads to increased work and oxygen demand for the heart (myocardium), which can cause a heart attack (myocardial infarction) if it persists. This occurs because the decreased flow of necessary oxygen to the heart causes myocardial cells to begin to die off. Acutely, this leads to angina; and chronically to ischemic heart disease.
The body has 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). Fever, hyperventilation and severe infections can also cause tachycardia, primarily due to increase in metabolic demands.
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. This is the basis for the so-called Fight or Flight response, but such stimulation can also be induced by stimulants such as ephedrine, amphetamines or cocaine. Certain endocrine disorders such as pheochromocytoma can also cause epinephrine release and can result in tachycardia independent nervous system stimulation. Hyperthyroidism can also cause tachycardia.
Types of tachycardia (cardiac arrhythmias)
An electrocardiogram (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
- AV nodal reentrant tachycardia (AVNRT)
- AV reentrant tachycardia (AVRT)
- Junctional tachycardia
Tachycardias may be classified as either narrow complex tachycardias
(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.
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.
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 (ischemia, 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. Both of these rhythms normally last for only a few seconds to minutes (paroxysmal tachycardia)
, but if VT persists it is extremely dangerous, often leading to ventricular fibrillation.
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 the Valsalva maneuver 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 antiarrhythmics), 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 syndrome. 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. This is to help prevent blood clots embolizing from the heart chambers to the rest of the body where they can cause adverse events like a stroke. In the case of narrow complex tachycardias (junctional, atrial or paroxysmal), the treatment in general is to first give the patient adenosine (to slow conduction through the AV node) and then perform Valsalva 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 electrically 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.