It can have harmful effects in two ways. First, when the heart beats too rapidly, it performs inefficiently (since there is not enough time for the ventricles to fill completely), causing blood flow and blood pressure to diminish. Second, it increases the work of the heart, causing it to require more oxygen while also reducing the blood flow to the cardiac muscle tissue, increasing the risk of ischemia and resultantly infarction.

Tachycardia is a general symptomatic term that does not describe the cause of the rapid rate. Common causes are autonomic nervous system or endocrine system activity, hemodynamic responses, and various forms of cardiac arrhythmia.

Autonomic and endocrine causes

An increase in sympathetic nervous system stimulation causes the heart rate to increase, both by the direct action of sympathetic nerve fibers on the heart, and by causing the endocrine system to release hormones such as epinephrine (adrenaline) which have a similar effect. Increased sympathetic stimulation is usually due to physical or psychological stress (the so-called "fight or flight" response), but can also be induced by stimulants such as amphetamines.

Endocrine disorders such as pheochromocytoma can cause epinephrine release and tachycardia independent of the nervous system.

Hemodynamic responses

The body contains several feedback mechanisms to maintain adequate blood flow and blood pressure. If blood pressure decreases, the heart beats faster in an attempt to raise it. This is called reflex tachycardia

This can happen in response to a decrease in blood volume (through dehydration or bleeding), or an unexpected change in blood flow. The most common cause of the latter is orthostatic hypotension (also called postural hypotension), a sudden drop of blood pressure that occurs with a change in body position (e.g., going from lying down to standing up). When tachycardia occurs for this reason, it is called postural orthostatic tachycardia syndrome (POTS).

Tachycardic arrhythmias

An electrocardiogram tracing can distinguish several different forms of rapid abnormal heartbeat:

If the heart's electrical system is functioning normally, except that the rate is in excess of 100 beats per minute, it is called sinus tachycardia. This is caused by any of the factors mentioned above, rather than a malfunction of the heart itself.

Supraventricular tachycardia (SVT) occurs when an abnormal electrical impulse originates above the ventricles, but instead of causing a single beat and a pause, it travels in circles and causes many rapid beats. To distinguish SVT from Sinus Tachycardia one must simply look at the rate: If the rate of contraction is more than 150 bpm, then it is considered SVT. Otherwise it is Sinus Tachycardia. Ventricular tachycardia (VT or "V-tach") is a similar phenomenon occurring within the tissue of the ventricles, causing an extremely rapid rate with poor pumping action. Both of these rhythms normally last for only a few seconds (paroxysmal tachycardia), but if VT persists it is extremely dangerous, often leading to ventricular fibrillation.

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Tachycardia associated with moxifloxacin
From British Medical Journal, 1/6/01 by Martin Siepmann

The fluoroqinolone grepatloxacin has been associated with tachycardia in animals and humans.[1 2] It was eventually withdrawn from use owing to prolongation of the QT interval. Another fluoroquinolone, moxifloxacin (Avalox, Bayer Vital), was introduced in Germany in September 1999 and two months later in the United States. The chemical structure of moxifloxacin is similar to that of grepafloxacin, and both drugs have a broad spectrum of activity against bacteria, including Gram positive bacteria. Up to March 2000 about one million patients have been treated with moxifloxacin, and half of them have been evaluated for adverse events (Bayer Vital, personal communication). We describe the first case of tachycardia associated with moxifloxacin.

A 49 year old non-febrile man was prescribed moxifloxacin for sinusitis and bronchitis. About 45 minutes after taking the daily dose of 400 mg moxittoxacin he developed tachycardia (120 beats per minute). About 60 minutes before taking the moxittoxacin he had taken 500 mg aspirin for a headache. He described the tachycardia as "thumping" palpitations, which he had never before experienced. The symptoms lasted for 45 minutes. Tachycardia did not recur when moxifloxacin was restarted. The patient has no history of cardiovascular disease and regularly exercised on cycle and rowing machines. The day before the tachycardia an electrocardiogram was recorded that gave normal results (sinus rhythm 75, no abnormal changes).

We informed the German Federal Institute for Drugs and Medical Devices and the Drug Commission of the German Medical Profession. They cited 19 other reported cases of tachycardia in association with moxifloxacin.

The underlying mechanism may be vasodilatation either directly or indirectly owing to release of histamine with reflex tachycardia. These effects have been described for fluoroquinolones such as flosequinan.[3 4] Tachycardia could also be due to prolongation of the QT interval. Prolongation (QT interval [is greater than] 450 milliseconds) has been documented in 38 patients treated with 400 mg moxifloxacin daily.[5]

Competing interests: None declared.

[1] Stahlmann R, Schwabe R. Safety profile of grepatloxacin compared with other fluorochinolones. J Antimicrob Chemother 1997;40(suppl A):83-92.

[2] Lode H, Vogel F, Elies W. Grepafloxacin: a review of its safety profile based on clinical trials and post marketing surveillance. Clin Ther 1999;21:61-74.

[3] Takayama S, Hirohashi M, Kato M, Shimada H. Toxicity of quinolone antimicrobial agents. J Toxicol Environ Health 1995;45:1-45.

[4] Janssen MC, Smits P, Reyenga J, Thien T. Acute effects of flosequinan (BTS 49465) in untreated moderate to severe hypertension. J Hum Hypertens 1995;9:363-8.

[5] Balfour JA, Lamb HM. Moxifloxacin. A review of its clinical potential in the management of community-acquired respiratory tract infections. Drugs 2000;59:115-39.

Martin Siepmann, Wilhelm Kirch, Institute of Clinical Pharmacology, Medical Faculty, Technical University, 01307 Dresden, Germany

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