As described earlier, the sinus node , a structure in the high right atrium, depolarizes typically 60 to 90 times per minute sending a sinus electrical impulse throughout both atria to the AV node. In brief, this leads to synchronized biatrial contraction before ventricular contraction forces blood out of the heart into the circulation.
The AV node , a structure that sits in the middle of the heart, is normally the only electrical connection between the atria and the ventricles. The AV node serves as a traffic signal, controlling the rate of electrical impulses from the atria allowed to reach the ventricles, limiting the danger of 1 to 1 conduction of fast rhythms from the atrium to the ventricles.
The electrical impulse that travels through the AV node eventually travels via a specialized network of fibers, known as the left and right bundle branches , to ultimately enter the ventricular muscle at its terminal ends, the Purkinje fibers. Figure 1. Illustration of the normal conduction system. The sinus node, located in the high right atrium depolarizes and sends an electrical impulse through both atrium typically at a frequency of 60 — 90 beats per minute.
In order for this impulse to reach the ventricles in normal hearts, it must traverse the AV node where it encounters a normal minimal delay before it continues its path to the ventricles via the bundle branches. A slow heart rate, or bradycardia less than 60 beats per minute , does not necessarily imply a cardiac rhythm problem. Many individuals can have a slow sinus rhythm, known as sinus bradycardia , at baseline or at times of rest, including sleep.
Professional athletes or physically active persons can frequently have resting heart rates in the 40 beats per minute range. If this bradycardia is symptomatic or inappropriately slow for the conditions i. We will be covering two of the most common bradyarrhythmias:.
Supraventricular tachycardia, or SVT , refers to fast heart rhythms that originate from above the ventricles, hence the term. Typically physicians consider heart rates above beats per minute as rapid, and classify them as tachycardia. Palpitations can be caused by extra beats from either the lower ventricular or upper heart chambers atria , and not necessarily from sustained fast rhythms, or tachycardias.
These palpitations can last from seconds to hours. Supraventricular tachycardias are generally not life-threatening, but their symptoms can be dehabilitating to patients. Other symptoms experienced during an episode of SVT include dizziness, shortness of breath, chest pain, and light-headedness. Patients may report these symptoms worsening with exercise, anxiety, or caffeine ingestion. Loss of consciousness, or syncope, is rarely due to an SVT, and it necessarily implies seeking prompt medical attention.
Occasionally patients may not experience any symptoms during an episode of SVT. Your physician can diagnose and differentiate an SVT from other rapid heart rhythms via an electrocardiogram EKG obtained during the episode.
In these situations hour Holter monitors or event monitors can be useful to catch the event. Medications can be used to treat many patients with SVT. These medications are dictated by the type of SVT and the coexisting medical conditions patients may have.
The most common class of medications for SVT include:. Medications for the treatment of SVT can act to slow conduction from the top atria to the lower ventricles by decreasing conduction at the AV node including b-blockers and calcium channel blockers or by acting directly on the atrial or ventricular tissue as with antiarrhythmics.
A special procedure, called an electrophysiology study EPS and radiofrequency ablation RFA can be an alternative to medication to treat many patients who are either intolerant of medication side effects or who have recurrent symptomatic breakthrough episodes on medications. Supraventricular tachycardias are typically classified by their origin and mechanism of perpetuation.
In general terms, an SVT is due to either a reentrant circuit continuous loop or a focal firing of irritable tissue. A reentrant circuit is sustained by tracts of heart muscle cells that allow an electrical impulse to self-perpetuate in an endless loop. Figure 2. Depiction of a reentry circuit mechanism of tachycardia versus an abnormal focus. In a reentry circuit, the electrical impulse travels in a loop of excitable tissue, self-perpetuating the rhythm disturbance.
In a focal tachycardia, a particular site of myocardial tissue abnormally fires at a rate typically faster than the sinus node, suppressing the normal mechanism of cardiac depolarization. Ventricular tachyarrhythmia is a term designated to those tachycardias, or fast heart rhythms, that originate from the lower ventricles.
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