Chest
Volume 125, Issue 2, February 2004, Pages 683-690
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Opinions/Hypotheses
Respiratory Sinus Arrhythmia: Why Does the Heartbeat Synchronize With Respiratory Rhythm?

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Respiratory sinus arrhythmia (RSA) is heart rate variability in synchrony with respiration, by which the R-R interval on an ECG is shortened during inspiration and prolonged during expiration. Although RSA has been used as an index of cardiac vagal function, it is also a physiologic phenomenon reflecting respiratory-circulatory interactions universally observed among vertebrates. Previous studies have shown that the efficiency of pulmonary gas exchange is improved by RSA, suggesting that RSA may play an active physiologic role. The matched timing of alveolar ventilation and its perfusion with RSA within each respiratory cycle could save energy expenditure by suppressing unnecessary heartbeats during expiration and ineffective ventilation during the ebb of perfusion. Furthermore, evidence has accumulated of a possible dissociation between RSA and vagal control of that heart rate, suggesting differential controls between the respiratory modulation of cardiac vagal outflow and cardiac vagal tone. RSA or heart rate variability in synchrony with respiration is a biological phenomenon, which may have a positive influence on gas exchange at the level of the lung via efficient ventilation/perfusion matching.

Section snippets

Pulmonary Gas Exchange and RSA

In our earlier study,7 we postulated that “RSA has a function to improve the pulmonary gas exchange, synchronizing the heartbeat with respiratory rhythm.” In the representative RSA in a dog, the clustering of heartbeats during inspiration and their scattering during expiration are observed (Fig 2). With RSA, as the instantaneous blood volume circulating in the pulmonary circulation depends on the corresponding heart rate, the relationships between alveolar gas and capillary blood undergoing

Chemoreflex and RSA

The response of RSA to hypoxia and hypercapnia provides the physiologic compensation against the turbulence/stressor challenged from outside the organism (Fig 1). RSA is easily influenced by such factors as cardiopulmonary function, pattern of breathing, sleep/wakefulness, anesthesia, body position, age, gender, species, and many other variables. In an RSA investigation, these variables must be strictly controlled. Therefore, the authors used unanesthetized, conscious dogs for this purpose,

Hypercapnia

The central chemoreceptors, respiratory center, and effector organs serve to maintain Paco2 within a range of 37 to 43 mm Hg in healthy humans. Representative tracing during acute hyperoxic hypercapnia15 is shown in Figure 4,left. During progressive hypercapnia lasting approximately 3 min, the partial pressure of end-tidal CO2 increased from 36 to 55 mm Hg, and, concomitantly, the tidal volume and respiratory rate increased from 230 to 850 mL and from 18 to 22 breaths/min, respectively. Both

Hypoxia

The bilateral carotid bodies located in the bifurcation of the internal and external carotid arteries serve primarily as the peripheral chemoreceptor. They sense the arterial Po2, and that information is transmitted to the respiratory center in the brainstem, which regulates depth and frequency of respiration.

A representative tracing during acute isocapnic hypoxia16 is shown in Figure 4, right. During progressive hypoxia lasting approximately 5 min, O2 saturation of arterial blood decreased

Hypercapnia vs Hypoxia

The influences of hypoxia and hypercapnia28 on the amplitude of RSA at a comparable level of minute ventilation of 15 L/min were significantly different. RSA was attenuated with hypoxia, whereas it was augmented with hypercapnia. According to the concept of permissive hypercapnia in patients with respiratory distress who have been treated with mechanical ventilation, a considerable level of hypercapnia (ie, 50 to 70 mm Hg) is permitted as long as their oxygenation is maintained.29 Therefore,

Mechanisms of RSA

Heart rate is determined by the firing frequency of the sinus node of a cardiac pacemaker. This frequency is determined by the balance between the cardiac sympathetic and vagal activities to the sinus node. The activity of the cardiac vagal nerve is assumed to be modulated by respiration, and hence the sinus node activity is secondarily modulated by the respiratory rhythm. Regarding the genesis of RSA, both the respiratory and circulatory centers in the brainstem appear to be responsible.

Clinical Significance of RSA

The magnitude of RSA is assessed as the amplitude of the high-frequency component of the fluctuation of the R-R interval (0.15 to 0.80 Hz), utilizing the frequency analysis of heart rate variability on electrocardiography. For an accurate assessment in short-term electrocardiography recording, an examinee's tidal breathing should be standardized due to the frequency-dependent characteristic of RSA.4647 When a frequency analysis of heart rate variability is performed with 24-h ambulatory

Conclusions

Respiratory-circulatory interactions similar to RSA are widely observed in birds, fish, and mammals.59 In spontaneously breathing ducks, respiration-related oscillations in heart rate, which is similar to RSA in mammals, are observed.60 In resting fish, gills are ventilated by a pulsatile water flow throughout the respiratory cycle, and the heartbeat occurs in 1:1 synchrony with respiration, resulting in a coincidence of the periods of maximum flow rate of blood and water across the gills.61

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