![]() ![]() This may be a 24-hour test (which has a very low yield but may be mandated by the insurer prior to longer term monitoring). The next step should be to obtain ambulatory monitoring. The resting electrocardiogram is usually unrevealing or demonstrates nondiagnostic abnormalities without symptoms. ![]() What diagnostic tests should be performed?Ĭorrelation of diagnostic electrocardiographic abnormalities is what is necessary to best guide management decisions. A resting bradycardia on examination is usually not associated with symptoms in patients with SND. Physical examination is rarely helpful in establishing a diagnosis. Thyroid disease must be ruled out because it requires specific treatment, which generally results in resolution of the arrhythmia problem. These patients are asymptomatic, are often young, and are usually in excellent physical condition and athletic. The differential diagnosis of SND includes chronically high vagal tone. History Part 3: Competing diagnoses that can mimic Sick Sinus Syndrome. There are rare familial cases of SND that may manifest in younger patients, some of which may be associated with long Q–T syndrome. SND is usually diagnosed in the seventh and eighth decades of life, with an average age of 65 in a few studies. In addition, the criteria for defining a heart rate or pause as abnormally slow are more dependent on the association of symptoms than an arbitrary number. The prevalence of SND is not known because so many patients are asymptomatic. More unusual symptoms may include cognitive abnormalities, periodic polyuria (related to atrial distention with release of atrial natriuretic peptide experienced with or immediately after paroxysmal atrial tachycardia or atrial fibrillation), and thromboembolic phenomena (from bradycardia-induced hypoperfusion of a stenotic vessel or embolic related to atrial fibrillation).Īs many times symptoms are present without electrocardiographic findings and nonspecific electrocardiographic findings present without symptoms, the correlation of electrocardiographic abnormalities with symptoms is paramount in establishing a causal relationship to best determine the most appropriate therapeutic approach. They may include palpitations (due to PACs, paroxysmal atrial tachycardias, or atrial fibrillation), fatigue (from bradycardia or chronotropic incompetence), light-headedness, or syncope (from pauses). Symptoms are diverse, corresponding to a broad range of electrocardiographic manifestations. The recordings may have been prompted as a part of the routine exam (ECG), or in the case of monitoring, prompted by findings found on a 12-lead ECG or by symptoms. The typical patient with SND presents with arrhythmias detected via electrocardiogram (ECG), ambulatory monitoring 24-hour recording, prolonged electrocardiographic event monitoring, or outpatient telemetry recordings (see diagnostic tests below). Extrinsic causes are addressed with assessment of medications, blood tests (for thyroid abnormalities), and evaluation for associated autonomic dysfunction, if suspected. The absence or presence of symptoms is not necessary for the diagnosis of SND, though it is the determinant of therapeutic recommendations. Usually there is underlying (intrinsic) physiologic substrate for SND if pharmacologic therapy causes SND, though it might not be clinically apparent or significant. If the first manifestation of the SND is with pharmacologic therapy that may be discontinued or there exists an alternative drug, cessation of the drug and observation with prolonged monitoring may be appropriate to differentiate between intrinsic and extrinsic SND. Sometimes the SND is solely due to the drug but other times may unmask or exacerbate intrinsic SND. SND may first manifest after initiation of antiarrhythmic drugs. Another is the inability to achieve 80% of the predicted maximal heart rate when adjusted for age. One is the inability to achieve a maximal exercise heart rate of 100 bpm. There exist varying quantitative criteria for defining chronotropic incompetence. ![]()
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