![]() History of trauma to the head or neck via fall or another mechanism, especially in the setting of anticoagulation use, may increase suspicion for underlying intracranial hemorrhage. Care should be taken to rule out other potential causes of sinus arrhythmia while taking history. If present, symptoms such as shortness of breath, lower extremity edema, dyspnea on exertion, or peripheral neuropathy are likely due to some underlying cause and not sinus arrhythmia. It is rare for patients with sinus arrhythmia to display symptoms. The finding is normal and found at a higher prevalence in younger individuals. Lack of sinus arrhythmia may be a sign of underlying chronic disease requiring further investigation. Sinus arrhythmia is a common incidental finding seen on presenting EKGs. On EKG, this is represented by an interval shortening between the QRS and subsequent P wave. The increased stroke volume triggers a carotid baroreceptor response. Currently theorized mechanisms suggest that ventriculophasic sinus arrhythmia results due to a prolonged cardiac filling resulting in increased stroke volume. However, they demonstrate correlations between premature ventricular contractions. The ventriculophasic sinus arrhythmia, when present, typically occurs in patients with third-degree AV block. One case report associated the finding with a traumatic intracerebral hemorrhage, which authors associated with vasospasm, hypoxia, or increased intracranial pressure. Some have reported this finding with underlying heart disease or associated with digitalis overdose. While it can occur within healthy individuals, more often, this type correlates with underlying pathology. ![]() The two differ in that nonrespiratory sinus arrhythmia is not associated with the respiratory cycle. In nonrespiratory sinus arrhythmia, electrocardiograms will appear similar to the respiratory type. They found that in patients with diabetes, there is a reduction in sinus arrhythmia, which investigators attributed to the autonomic effects of the disease. More recently, investigators have evaluated the effects of diabetes mellitus on sinus arrhythmia. The study suggested that baroreceptor signaling plays an important role in the generation of respiratory sinus arrhythmia. This concept was supported by a later study that successfully mimicked the respiratory cycle via stimulation of baroreceptors in the carotid artery with cycles of phased neck suction at the frequency of normal respiration. During the respiratory cycle, inspiration inhibits vagal tone leading to an increase in sinus rate, while expiration increases vagal tone resulting in a decreased rate. The study suggested that mediation of sinus arrhythmia occurs through vagal stimulation. Administration of hyoscine butylbromide resulted in the reduction of sinus arrhythmia, while atenolol reduced vagal tone, prolonging the mean R-R and increasing sinus arrhythmia. One study attempted to evaluate the influences of vagal and sympathetic efferent activity on sinus arrhythmia through the administration of hyoscine butylbromide and atenolol. Some studies suggest there may be some relationship between heart failure and other systemic conditions. Some studies have begun to associate sinus rhythm with obesity, diabetes mellitus, and hypertension, while others continue to support a reduction in sinus arrhythmia when these conditions are present. Recently, there has been controversy regarding the underlying pathogenesis of sinus arrhythmia. It is a normal alteration in cardiac rhythm generated from the stimulation of the vagus nerve and changes in cardiac filling pressures during respiration. Respiratory sinus arrhythmia is a common finding. These include respiratory-phasic, nonrespiratory-nonphasic, and nonrespiratory-ventriculophasic sinus arrhythmia. Investigation on the pathogenesis of sinus arrhythmia continues but three main theorized mechanisms exist at this time.
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