PubMed · 9047495
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A Nishikado, T Oki. 1996. [Sinus arrhythmia].. https://pubmed.ncbi.nlm.nih.gov/9047495/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Respiration is a powerful modulator of heart rate variability, and of baro- and chemoreflex sensitivity. Abnormal respiratory modulation of heart rate is often an early sign of autonomic dysfunction in a number of diseases. In addition, increase in venous return due to respiration may help in maintaining blood pressure during standing in critical situations. This review examines the possibility that manipulation of breathing pattern may provide beneficial effects in terms not only of ventilatory efficiency, but also of cardiovascular and respiratory control in physiologic and pathologic conditions, such as chronic heart failure. This opens a new area of future research in the better management of patients with cardiovascular autonomic dysfunction.
The high-frequency (HF) component of the heart rate variability (HRV) is regarded as an index of cardiac vagal responsiveness. However, when vagal tone is decreased, nonneural mechanisms could account for a significant proportion of the HF component. To test this hypothesis, we examined the HRV spectral power in 20 patients with mild chronic heart failure (CHF) and 11 controls before and during ganglion blockade with trimethaphan camsylate (3-6 mg/min iv). A small HF component was still present during ganglion blockade, and its amplitude did not differ between CHF patients and controls. The average contribution of nonneural oscillations to the HF component was 15% (range 1-77%) in patients with CHF and 3% (range 0. 7-30%) in healthy controls (P < 0.005). During controlled breathing at 0.16 Hz, however, it decreased to 1% (range 0.2-13%) in healthy controls and 5% (range 1-44%) in CHF patients. Our results indicate that the HF component can significantly overestimate cardiac vagal responsiveness in patients with mild CHF. This bias is improved by controlled breathing, since this maneuver increases the vagal contribution to HF without affecting its nonneural component.
Typical atrial flutter may now be definitely treated in a single session. However, the very meaning of the term, atrial flutter, is confusing because it is a multiple entity. In fact, flutters may be classified with respect to their electrocardiographic and electrophysiological features. In addition to typical common atrial flutter with biphasic, predominantly negative F waves in the inferior leads and positive F waves in V1 due to an anticlockwise macro-reentry circuit localised to the right atrium, there are other forms which may be described as typical in that they pass through the cavo-tricuspid isthmus. They include typical flutter with inverted rotation, short loop inferior flutter and flutter with a double reentry circuit. In 2001, it would seem licit to call all flutters which do not pass through the cavotricuspid isthmus atypical, independently of their surface ECG appearances. The term flutter still refers to a continuous electrical activity with absence of an isoelectric line in at least one lead but with extremely variable ECG features. They may be classified as flutter on pre-existing lesions, with right or left atrial macro-reentry circuits. The ECG appearance is then that of very atypical flutter. More recently, flutters with circuits passing through the coronary sinus have been described. Ablation of the muscle of the coronary sinus seems to be able to treat this type of flutter, the prevalence of which is not yet known.