Everything about Tachycardia totally explained
Tachycardia refers to rapid beating of the
heart. By convention it's 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.
Tachycardia can be harmful in three ways. First, if the heart is pumping too fast for an extended period of time it'll 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's 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.
Haemodynamic responses
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 (for example, going from lying down to standing up). When tachycardia occurs for this reason, it's called
postural orthostatic tachycardia syndrome (POTS).
Fever,
hyperventilation and
infection leading to
sepsis are also common causes of tachycardia, primarily due to increase in
metabolic demands and compensatory increase in heart rate.
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.
Endocrine disorders such as
pheochromocytoma can cause epinephrine release and tachycardia independent of the nervous system.
Hyperthyroidism is also known to cause tachycardia.
Cardiac Arrhythmias
The 12 lead
ECG can help distinguish between the various types of tachycardias, generally distinguished by their site of pacemaker origin:
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.
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.
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.
Both of these rhythms normally last for only a few
seconds to
minutes
(paroxysmal tachycardia), but if VT persists it's extremely dangerous, often leading to
ventricular fibrillation.
SVT Rhythms
Atrial 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
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
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.
Treatments
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. 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 shouldn't be converted to normal sinus rhythm unless they've been anti-coagulated to an INR of 2-3 for at least 4 weeks.
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 vagal maneuvers to slow the rhythm. If this doesn't 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's 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.
Further Information
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