Tuesday, July 3, 2012

Brachycardia/Bradycardia

    Types of Bradyarrhythmias

    A bradyarrhythmia is a slow heart rhythm that is usually caused by disease in the heart’s conduction system. Types of bradyarrhythmias include:
    • Sinus node dysfunction: Slow heart rhythms due to an abnormal SA node.
    • Heart block: A delay or complete block of the electrical impulse as it travels from the sinus node to the ventricles. The level of the block or delay may occur in the AV node or HIS-Purkinje system. The heartbeat may be irregular and slow.
[Abstract] The significance of sinus bradycardia (SB) in clinically healthy, non-endurance-trained, middle-aged and older persons is unknown. From 1,172 normal volunteers, aged 40 to 96 years, enrolled in the Baltimore Longitudinal Study of Aging, 47 subjects, aged 58 ± 13 years, with SB (less than 50 beats/min) were identified by rest electrocardiography and were compared with a group of control subjects matched for age and sex. The prevalence of unexplained SB was approximately 4% and was nearly identical in men and women. At the latest follow-up examination, after a mean follow-up of 5.4 years, the SB group had a higher prevalence of associated conduction abnormalities (first-degree atrioventricular [AV] block, left-axis deviation, and complete or incomplete right bundle branch block) than the control group (43% vs 19%, p <0.05). On maximal treadmill exercise testing, performed in 44 patients within 1 visit of their most recent examination showing SB, maximal heart rate (157 ± 18 beats/min) did not differ significantly from that of control subjects (163 ± 19 beats/min); exercise duration, however, was greater in the former group, 11.0 ± 2.8 vs 9.7 ± 3.1 minutes (p <0.05). No patients with SB had syncope, high-degree AV block or other manifestation of sick sinus syndrome during follow-up. Angina pectoris, myocardial infarction, congestive heart failure or cardiac death occurred in 8% of patients with SB and 11% of control subjects over the observation period (difference not significant). Thus, unexplained SB in apparently healthy, nonathletic subjects older than 40 years is associated with certain abnormalities of AV or intraventricular conduction, but does not signify chronotropic incompetence with exercise and does not appear to adversely influence long-term cardiovascular morbidity or mortality.

Research generally shows that caffeine increases blood pressure in some people (James, 1994; Nurminen, Nittynen, & Vapaatalo, 1999).

Bichler, Swenson and Harris (2006) found a link between caffeine+taurine, arterial blood pressure and brachycardia.

[Abstract] Red Bull energy drink has become extraordinarily popular amongst college students for use as a study aid. We investigated the combined effects of Red Bull’s two active ingredients, caffeine and taurine, on short term memory. Studies on the effects of these two neuromodulators on memory have yielded mixed results, and their combined actions have not yet been investigated. In this double-blind study, college student subjects consumed either caffeine and taurine pills or a placebo and then completed a memory assessment. Heart rate and blood pressure were monitored throughout the testing period. The combination of caffeine and taurine had no effect on short term memory, but did cause a significant decline in heart rate and an increase in mean arterial blood pressure. The heart rate decline may have been caused by pressure-induced bradycardia that was triggered by caffeine ingestion and perhaps enhanced by the actions of taurine.


[Abstract] The mechanisms by which caffeine typically elevates blood pressure (BP) in humans have not been previously examined using a placebo-controlled design. Accordingly, oral caffeine (3.3 mg/kg body weight, equivalent to 2 to 3 cups of coffee) was given on 2 days and a placebo was given on 1 day to 15 healthy young men using a double-blind, crossover procedure. All 3 test sessions were held during a week ofcaffeine abstinence. Multiple measurements were made on subjects at rest (baseline values) and over a 45-minute interval after ingestion of caffeine for BP, heart rate, systolic time intervals and thoracic impedance measures of ventricular function. Baseline measurements were highly reliable for each subject across all sessions and yielded means for placebo vs caffeine days that were not different. Caffeine increased systolic and diastolic BP (p < 0.01) and decreased heart rate (p < 0.05). The pressor effect was due to progressively increased systemic vascular resistance and resulted in greater stroke work (p < 0.01). There was no indication that caffeine increased cardiac output or contractility. These actions of caffeine were replicable when each caffeine day was tested separately against the placebo day. These results suggest that caffeine use by persons with cardiovascular diseases should be examined to determine whethercaffeine's enhancement of vascular resistance may contribute to systematic hypertension and/or create excessive demands for cardiac work.


Northcote et al. (1989) have a short description of two athletes with bradycardia.

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