If the cause is due to decreased vagal activity, it is usually hard to treat and one may consider radiofrequency catheter ablation. IST and POTS īeta blockers are useful if the cause is sympathetic overactivity. Beta-blockers can be used to slow the rate, but most patients are usually already treated with beta-blockers as a routine regimen for AMI. Tachycardia in the presence of AMI can reduce coronary blood flow and increase myocardial oxygen demand, aggravating the situation. Patients with sustained sinus tachycardia reflects a larger infarct that are more anterior with prominent left ventricular dysfunction, associated with high mortality and morbidity. Sinus tachycardia can present in more than a third of the patients with AMI but this usually decreases over time. Patients who are unresponsive to such treatment can undergo catheter ablation to potentially repair the sinus node. In patients with inappropriate sinus tachycardia, careful titration of beta-blockers, salt loading, and hydration typically reduce symptoms.
Beta blockers may be used to decrease tachycardia in patients with certain conditions, such as ischemic heart disease and rate-related angina. Treatment for physiologic sinus tachycardia involves treating the underlying causes of the tachycardia response. Usually, in women with no heart problems, this syndrome is characterized by normal resting heart rate but exaggerated postural sinus tachycardia with or without orthostatic hypotension. Main article: Postural orthostatic tachycardia syndrome Postural orthostatic tachycardia syndrome.Acute inflammatory demyelinating polyradiculoneuropathy.Intake of stimulants such as caffeine, theophylline, nicotine, cocaine, or amphetamines.Acute coronary ischemia and myocardial infarction.Sinus tachycardia is usually a response to physiological stress, such as exercise, or an increased sympathetic tone with increased catecholamine release, such as stress, fright, flight, and anger. Sinus tachycardia accompanying a myocardial infarction may be indicative of cardiogenic shock. Rapid rates, though they may be compensating for ischemia elsewhere, increase myocardial oxygen demand and reduce coronary blood flow, thus precipitating an ischemic heart or valvular disease. If the heart rate is too high, cardiac output may fall due to the markedly reduced ventricular filling time. It is often a resulting symptom of a primary disease state and can be an indication of the severity of a disease. 3.3 Postural orthostatic tachycardia syndrome.
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