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Sinoatrial (SA) Arrest is a heart condition in which the sinoatrial node temporarily pauses in electrical impulse production, preventing the heart from contracting.[1] It is typically a mild and insignificant condition and only rarely becomes serious. The sinoatrial node is a group of pacemaker cells along the right atrium and superior vena cava. It creates the electrical impulse responsible for the myocardial tissue contracting to create a heart beat. It is often referred to as the natural or dominant pacemaker of the heart.[2]
A sinoatrial arrest can be identified on an electrocardiogram, a device that can monitor the electrical activity of the heart, by a gap in P waves that lasts for at least 2 seconds up to a few minutes. This temporary gap in P waves is what differentiates SA arrest from other SA dysfunctions. The length of a sinoatrial arrest has no relationship to the original rhythm of the sinoatrial nodes’s impulse production. This arrest is either followed by an escape rhythm, a beat produced by a latent (or backup) pacemaker, or the continuation of standard rhythm.[1]
Symptoms, causes, and treatment of SA arrest vary greatly and range from being asymptomatic to resulting in a cardiac arrest. It can be caused by everyday stress or serious problems with the lungs, blood stream, or heart.
Symptoms
[edit]It is very common for SA arrest to be asymptomatic. The continuation of standard rhythm, however, can feel like heart palpitations to many individuals. Some can experience dizziness or loss of consciousness, called an adam-stokes attack.[3]
While most instances of SA arrest are mild and treatable, asystole, a very serious cardiac arrest, can occur if no latent pacemaker creates an escape rhythm, but this is extremely uncommon.[4]
Causes
[edit]There are a wide range of causes for a sinoatrial arrest. SA abnormalities and complications are often acquired, but can be inherited through genetic mutations. The most common cause of SA arrest is high vagal tone, or increased activity of the vagal nerve. It is common for young individuals to have a high vagal tone caused from stress and high stimulation.[4]The Vagal Nerve is part of the parasympathetic nervous system and is responsible for many “unconscious” functions of the heart, lungs, and digestive system.[5] Sympathetic nerves increase SA rate during increased activity (stress, exercise) while parasympathetic information from the vagal nerve, decreases SA rhythm at rest.[6]
More dangerous causes of SA dysfunction are age, Idiopathic fibrosis (unknown scarring on the lungs)[7], ischaemia (blocked arteries that prevent adequate blood and oxygen flow)[8], myocarditis (inflamed heart muscle)[9], and Digoxin toxicity (an overdose of digoxin, a drug used for heart failure)[10][1]. While these are less common, they should be taken seriously and involve more complicated treatments.
Treatment
[edit]Atropine or isoproterenol are often administered through an IV or injection for immediate relief. Both drugs are commonly used to treat bradycardia and increase heart rate.[3]
Long term treatment for sinoatrial arrest depends on the underlying condition that caused the dysfunction. An attack due to high vagal tone does not require treatment but a 24 hour electrocardiogram watch is recommended.
Physiological Mechanism
[edit]A sinoatrial arrest is often inconsequential because there are multiple physiological mechanisms that can keep the heart beating. These “backup” pacemakers, referred to as latent pacemakers, produce electrical impulses until the sinoatrial node can recover. The beats produced from these form what is called an escape rhythm.[4] Parts of the heart that act as latent pacemakers include the atrial myocardium, cells around the atrioventricular node, and the His-Purkinje network.
Atrial myocardium
[edit]The atrial myocardium is the heart’s first response to a sinoatrial arrest because it has the fastest rate of depolarization. Parts of the atrial myocardium can create impulses at a rate of 60 beats per minute. This escape rhythm, referred to as an atrial rhythm, has P-waves different from the sinus P-wave, but are efficient in producing a heart beat.[4]
Cells around the atrioventricular node
[edit]The second response to a SA arrest are the cells specifically around the atrioventricular node. They can produce a rhythm of 40 beats per minute to create what is called a junctional rhythm.[4]
His-Purkinje network:
[edit]The final response is the His-Purkinje network. They are electrical conductors that have a rate of depolarization of 20-40 beats per min. The branches of the network both receive and send the impulses that create an escape rhythm called ventricular rhythm.[4]
See Also
[edit]References
[edit]- ^ a b c Da Costa, D. (2002-03-02). "ABC of clinical electrocardiography: Bradycardias and atrioventricular conduction block". BMJ. 324 (7336): 535–538. doi:10.1136/bmj.324.7336.535.
- ^ "UpToDate". www.uptodate.com. Retrieved 2019-11-07.
- ^ a b "What is sinus arrest?". ECGalert. Retrieved 2019-11-07.
- ^ a b c d e f "Sinoatrial arrest & sinoatrial pause (sinus pause / arrest)". ECG learning. Retrieved 2019-11-07.
- ^ Berntson, Gary G.; Cacioppo, John T.; Quigley, Karen S. (1993). "Respiratory sinus arrhythmia: Autonomic origins, physiological mechanisms, and psychophysiological implications". Psychophysiology. 30 (2): 183–196. doi:10.1111/j.1469-8986.1993.tb01731.x. ISSN 1469-8986.
- ^ "Sinus Node Dysfunction: Practice Essentials, Background, Pathophysiology". 2019-10-21.
{{cite journal}}: Cite journal requires|journal=(help) - ^ "Idiopathic Pulmonary Fibrosis | the lung association". www.lung.ca. Retrieved 2019-11-07.
- ^ "What Is Ischemia?". WebMD. Retrieved 2019-11-07.
- ^ "Myocarditis - Symptoms and causes". Mayo Clinic. Retrieved 2019-11-07.
- ^ "Digoxin Toxicity - What You Need to Know". Drugs.com. Retrieved 2019-11-07.