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At least 19 recordsLinked to original sources
PubMed1976

Variation of respiratory sinus arrhythmia with age.

Respiratory sinus arrhythmia was measured on 24 male subjects whose ages ranged from 21 to 65 yr, using a technique in which respiration was coupled to heart rate, so that there were 6 heartbeats per inspiration and 6 heartbeats per expiration. This voluntary cardiorespiratory coupling reduced the variance of heart rates measured at various points in the respiratory cycle. Fourier analysis was used to obtain the fundamental of heart rate and respiratory volume. A high correlation coefficient (-0.83) was found between percent of variation of heart rate from the average heart rate (PB) and the age of the subject. Linear regression analysis performed on these data produced the equation: PB = 23.2-0.35 (age). Since sinus arrhythmia at the low respiratory frequencies used probably reflects the viability of the cardiorespiratory control systems, we believe this provides a simple noninvasive method for the study of the overall competence of the system responsible for respiratory sinus arrhythmia.

Adult↗
PubMed1975

[The effect of the tidal volume on the sinus arrhythmia of the heart].

The sinus arrhythmia of the human heart was investigated in its relation to the tidal volume under resting conditions in the course of the day, in voluntarily changed tidal volume, under atropine medication and during physical work. In resting conditions it was found that nearly 40% of the sinus arrhythmia is of respiratory origin, and that no respiratory influence is demonstrable any longer at sufficient doses of atropine. Under physical load, the sinus arrhythmia is diminished in spite of the enlarged tidal volume. In this case, an additional smoothing influence to the sinus arrhythmia has to be assumed.

Adult↗
PubMed1978

Sinus arrhythmia in acute myocardial infarction.

Sinus arrhythmia, defined by means of a calculation of variance of the R-R interval on admission to hospital, was present in 73 of 176 patients admitted to a coronary care unit with acute myocardial infarction. These patients had a lower hospital mortality. They tended to have a higher incidence of inferior infarction, and a lower incidence of anterior infarction, and to have smaller infarcts as measured by the Norris index. The main difference between patients with sinus arrhythmia and without sinus arrhythmia related to heart rates on admission to hospital, the patients with the former having slower heart rates at that time.

Acute Disease↗
PubMed1976

Respiratory sinus arrhythmia in man: effects of carotid sinus baroreceptor stimulation.

1. The role played by the carotid sinus baroreflex in the genesis of the respiratory sinus arrhythmia (RSA) was studied in nine healthy subjects. The carotid sinus baroreceptors were stimulated by the application of subatmospheric to the neck. 2. Reducing the normal respiratory arterial pressure oscillations and changing the phase between the pressure oscillations and the respiration did not affect the RSA. 3. Stimuli applied during expiration only, augmented the arrhythmia, while inspiratory stimulation was without any effect. 4. It is suggested that changes in the arterial baroreflex set point and/or gain during the respiratory cycle contribute to RSA in man.

Adult↗
PubMed1978

Development of sinus arrhythmia during sleeping and waking states in normal infants.

The development of variability in heart rate (HR) due to respiration (sinus arrhythmia; SA) has been examined in normal infants from birth through the first 6 months of life. Two aspects of HR variation were examined: the absolute variation at the median respiratory frequency, or extent of sinus arrhythmia (XSA), and the degree to which HR follows respiration regardless of the absolute amount of variation, or coherence of sinus arrhythmia (CSA). Extent of sinus arrhythmia tended to be highest in quiet sleep (QS), lower in active or REM sleep (AS), and lowest in waking (AW), especially after 2 months of age. Extent declined at 1 month of age in QS, but rose over the first 6-month period in all states. During this same period, CSA was also highest in QS, lower in AS, and lowest in AW. Coherence in QS also declined at 1 month and rose between 1 and 6 months; however, no age effects were found in other states. Heart rate was negatively correlated with XSA, but less so with CSA. Sleep state appears to have a significant effect on cardiorespiratory coupling, and this coupling undergoes dramatic changes at 1 month in QS.

Arrhythmia, Sinus↗
PubMed1976

Respiratory sinus arrhythmia in man: relation to cardiovascular pressures.

The relationship of respiratory sinus arrhythmia (RSA) to the accompanying oscillations of cardiovascular pressure has been studied in five healthy subjects. Tidal volume (VT) of 1.0, 1.5, and 2.0 1 at the breathing rate of 6 c-min-1 were used as reference. With identical VT oesophageal pressure was varied by negative inspiratory pressure (NIP) and intermittent positive-pressure ventilation (IPPV). Compared with control, NIP with 1.01 significantly increased RSA, the oscillations of brachial artery pressures (PBA), and the net filling pressures of the ventricles. IPPV did not significantly change the variations of PBA but reduced RSA and the respiratory variations of the right ventricular end-diastolic net pressure. During control breathing and with NIP the acceleration of heart rate during inspiration was associated with rising PBA and rising net filling pressures of both ventricles. The results indicate that RSA may be elicited by cardiovascular reflexes due to changes in venous filling of the heart rather than by the variations in systemic arterial pressure.

Adult↗
PubMed1976

Respiratory sinus arrhythmia in man: relation to cardiovascular pressures.

The relationship of repiratory sinus arrhythmia (RSA) to the accompanying oscillations of cardiovascular pressures has been studied in five healthy subjects. Tidal volumes (VT) of 1.0, 1.5, and 2.0 1 at a breathing rate of 6 c-min(-1) were used as reference. With identical VT, oesophageal pressure was varied by negative inspiratory pressure (NIP) and intermittent positive-pressure ventilation (IPPV). Compared with control, NIP with 1.01 significantly increased RSA, the oscillations of brachial artery pressures (PBA), and the net filling pressures of the ventricles. IPPV did not significantly change the variations of PBA but reduced RSA and the repiratory variations of the right ventricular end-diastolic net pressure. During control breathing and with NIP the acceleration of heart rate during inspiration was associated with rising PBA and rising net filling pressures of both ventricles. The results indicate that RSA may be elicited by cardiovascular reflexes due to changes in venous filling of the heart rather than by the variations in systemic arterial pressure.

Adult↗
PubMed1976

Sinus arrhythmia in man: influence of tidal volume and oesophageal pressure.

The effect of tidal volume (VT) and of the intrathoracic pressure (Poes) on the respiratory sinus arrhythmia (RSA) was studied in healthy subjects. They breathed into a spirometer with a VT of 1, 1.5, and 2 1, at a standardized, slow respiratory rate, 6-min-1 (A). Poes was varied by (B) adding a negative inspiratory pressure (NIP) of 5 cm of water and by (C) intermittent positive pressure ventilation (IPPV) at identical VT and respiratory frequency. In separate study (D), intermittent negative pressure ventilation (INPV) was induced by applying negative pressure on the thorax. In A, increasing VT provoked an augmented RSA by a more marked tachycardia as well as bradycardia. On increasing the amplitude of Poes in B, RSA was somewhat more marked due to a lower minimum heart rate. Whem comparing respiratory cycles that had similar Poes but a different VT, the larger VT caused a slight increase in the RSA amplitude due to a more marked deceleration of the heart rate. IPPV almost abolished RSA, whereas INPV did not reduce the arrhythmia. It is concluded that pulmonary stretch reflexes to a minor extent contribute to RSA, whereas the hypothesis of a central nervous origin does not gain support. Cardiovascular reflexes remain the main possible cause of RSA.

Adult↗
PubMed1975

Sinus arrhythmia in man: influence of tidal volume and oesophageal pressure.

The effect of tidal volume (VT) and of the intrathoracic pressure (Poes) on the respiratory sinus arrhythmia (RSA) was studied in healthy subjects. They breathed into a spirometer with a VT of 1, 1.5, and 2 1, at a standardized, slow respiratory rate, 6-min-1 (A). Poes was varied by (B) adding a negative inspiratory pressure (NIP) of 5 cm of water and by (C) intermittent positive pressure ventilation (IPPV) at identical VT and respiratory frequency. In a separate study (D), intermittent negative pressure ventilation (INPV) was induced by applying negative pressure on the thorax. In A, increasing VT provoked an augmented RSA by a more marked tachycardia as well as bradycardia. On increasing the amplitude of Poes in B, RSA was somewhat more marked due to a lower minimum heart rate. When comparing respiratory cycles that had similar Poes but a different VT, the larger VT caused a slight increase in the RSA amplitude due to a more marked deceleration of the heart rate. IPPV almost abolished RSA, whereas INPV did not reduce the arrhythmia. It is concluded that pulmonary stretch reflexes to a minor extent contribute to RSA, whereas the hypothesis of a central nervous origin does not gain support. Cardiovascular reflexes remain the main possible cause of RSA.

Adult↗