Respiratory Sinus Arrhythmia- Why Does the Heartbeat Synchronize With Respiratory Rhythm?

 

 

Respiratory sinus arrhythmia (RSA) :

It is a naturally occurring variation in heart rate that occurs during a breathing cycle. Heart rate increases during inspiration and decreases during expiration.

It is one of the physiologic interactions between respiration and circulation, where heart rate variability in synchrony with respiration, by which the R-R interval on an ECG is shortened during inspiration and prolonged during expiration occurs.

A clustering of heartbeats (R waves of an ECG) during inspiration and a scattering during expiration are clearly seen.

CLINICAL SIGNIFICANCE:

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.

Scheme showing the conceptual effects of RSA (top) and its inversion (bottom) on the relationship between alveolar gas volume and capillary blood flow during inspiration (left) and expiration (right). Curved horizontal arrows and vertical arrows indicate the volume of blood flow circulating in the pulmonary capillary bed and the direction of alveolar gas interfacing with the pulmonary capillary blood. V/Q = ventilation/perfusion.

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. Moreover, projections from the cerebral cortex, limbic system, and other parts of the brain to the brainstem should exist.

In mammals, the following two major mechanisms have been recognized for generating RSA:

1. direct modulation of the cardiac vagal preganglionic neurons by central respiratory drive;   The cardiac vagal efferent fibers are fired preferentially during expiration, and this respiratory-related activity is maintained even after the vagal nerve is resected at the peripheral to the recording site.The vagal efferent fibers are more powerfully excited during expiration by stimulating the arterial chemoreceptors and baroreceptors.Respiratory modulation could also be mediated by gating of the excitatory reflex inputs into the preganglionic neurons. Indeed, the membrane potential of cardiac vagal preganglionic neurons has been demonstrated to be hyperpolarized during each inspiration due to the arrival of an acetylcholine-mediated inhibitory postsynaptic potential, which makes neurons less amenable to excitatory inputs during inspiration.
2. and inhibition of cardiac vagal efferent activity by lung inflation.On the other hand, afferent activity arising in the lungs is also an important mechanism with which to generate RSA.Lung inflation inhibits cardiac vagal efferent activity and evokes tachycardia by stimulating the pulmonary C-fiber afferents (ie, pulmonary stretch receptors). This effect may be so strong that it reverses the bradycardia evoked by arterial chemostimulation into a tachycardia. The efferent cardiac vagal nerve plays the major role in the genesis of RSA, whereas the contribution of the cardiac sympathetic nerve seems to be minimal. During inspiration, as described above, the activity of the efferent cardiac vagal nerve is almost abolished. Hence, the R-R interval on an ECG is shortened. In contrast, during expiration, the activity of the efferent cardiac vagal nerve reaches its maximum, thus extending the R-R interval. The difference in the R-R interval between inspiration and expiration can be regarded as an indication of the magnitude of RSA, which is assumed to reflect the cardiac vagal outflow within its physiologic range.Accordingly, the magnitude of RSA has been widely used as a clinical measure of cardiac vagal activity. A neural basis for RSA has been demonstrated by its elimination or substantial attenuation following cervical vagotomy, ganglionic blockade, cholinergic blockade, and heart transplantation.

 

Abridged from CHEST journal.