Tachycardia
The increased heartbeat leads to increased myocardial oxygen demand, which accounts for the shortness of breath felt during an acute coronary event. Acute oxygen deficiency leads to angina; chronic oxygen deficiency causes ischaemic heart disease and may lead to myocardial infarction.
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 (e.g., going from lying down to standing up). When tachycardia occurs for this reason, it is 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 Cardiac Arrhythmias 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.
"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). In the absence of heart disease, it tends to have a narrow QRS complex on the ECG.
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.
At high rates, the QRS complex may also become wide due to the Ashman phenomenon. 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.
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).
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. In this case, calcium channel blockers, beta-blockers and digoxin must be avoided to prevent precipitation of ventricular tachycardia.
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.