An Overview of the Workings and Afflictions of the SA Node
As a student finishing up her first year at the University of Pennsylvania, I am ecstatic to be starting a summer of research on heart models and cardiac arrhythmia therapy here on campus. In this publication I will be posting updates as my cardiology journey ensues — sharing what I learn and discover along the way. This is my first blog publication so bear with me as I struggle to figure this thing out! Most of all, thanks for reading and I hope that by the end of the summer I can contribute something meaningful to the field of medicine.
When tackling complex issues in biology, one must first know the fundamentals of the body part in question. Two of the most important anatomical structures of the human heart are the sinoatrial (SA) and atrioventricular (AV) nodes. The SA node controls the natural, intrinsic heart rate. The AV node is the structure through which all electrical signals from the atria are conducted to the ventricles.
The SA node itself contains a patch of pacemaker cells surrounded by a fringe of conducting tissue. The pacemaker cells in the center exhibit automaticity. Automaticity is the random leakage of ions across the cardiac cell membrane. These leakages cause small deflections in the cardiac cell transmembrane potential until a certain threshold potential is reached, causing the cell to depolarize. This depolarization can be depicted on the action potential. Once it has fired off, the cell doesn’t stop — depolarization is an all-or-nothing type deal — and it causes surrounding cells to depolarize as well. This wave of electrical impulse travels from the SA node in the high right atrium all the way to the ventricular apex, causing the intervening chambers to contract and thus pump blood. In other words, the SA node is the body’s natural pacemaker.
I learned that when things go wrong in the SA node, the consequences are a slower-than-normal heart rate along with potentially debilitating symptoms. A slowed heart rate is clinically known as bradycardia and has a cutoff value of approximately 40 beats per minute. Symptoms include syncope, dizziness, and fatigue. Thankfully, many patients with structural abnormalities in their SA nodes never present with such symptoms, and those that do can be evaluated by the electrophysiology study. In fact, most symptomatic cases can be attributed to SA nodal disease without performing the EP study at all.
When the EP study is conducted, three values are measured to assess the health of the SA node: sinus node recovery time (SNRT), sinoatrial conduction time (SACT), and intrinsic heart rate (IHR).
Sinus node recovery time is based on the concepts of automaticity and overdrive suppression. Pacing is performed in the high right atrium of the heart and then abruptly stopped, causing a long pause until the next natural heart beat. The amount of time it takes for the SA node to fire off on its own after rapid pacing can indicate its relative health. The longer the pause, the more likely that the SA node is diseased or structurally abnormal. Abnormal values for SNRT vary from patient to patient, so there are corrections to the SNRT to account for these differences.
Sinoatrial conduction time is a measure of the SA node’s ability to conduct electrical impulses. The high right atrium receives a single premature impulse — an extrastimulus. The time is takes for the next electrical signal to be detected — the return cycle length — is measured. This is the amount of time it takes for the extrastimulus impulse to travel through the conducting tissue surrounding the pacemaker cells, fire off the pacemaker cells once, then travel back out of the conducting tissue. Thus,
return cycle length = 2SACT + BCL
where BCL is the basic cycle length. In other words, BCL is the amount of time between the intrinsic beats of the SA node. If the pacemaker cells fire off once, then one basic cycle length passes.
Lastly, intrinsic heart rate is the natural heart rate without any influence from the autonomic nervous system. The autonomic nervous system controls the involuntary functions of the body, while the somatic nervous system is associated with voluntary movements. The autonomic and somatic nervous systems make up the peripheral nervous system. The autonomic nervous system consists of sympathetic and parasympathetic nerves. The former controls the body’s “fight or flight” response. The latter controls the body’s ability to “rest and digest.” In other words, they have opposite effects on the body, depending on which is more active at a given time.
The SA node itself contains both sympathetic and parasympathetic fibers, so it is greatly affected by autonomic influence. Autonomic influence is diminished by the administration of certain types of drugs, including pranolol and atropine. If the resulting intrinsic heart rate is higher or lower than normal, then SA nodal disease is suspected to be present. If the resulting IHR is normal, then any symptoms previously attributed to SA nodal disease might actually be due to a dysautonomia. Dysautonomias are caused by imbalances in sympathetic and parasympathetic fibers of the autonomic nervous system. Normal IHR is calculated by the equation
IHR (beats/min) = 118.1-(0.53 x age)
which was devised by Anthony D. Jose and D. Collison.
