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During inspiration, there is an increase in neural activity in the sympathetic fibers of cardiac autonomic nerves. Conversely, during expiration, the neural activity increases in the vagal fibers. The heart rate responds quickly when the vagal stimulation stops because acetylcholinesterase rapidly hydrolyzes the released ACh from the vagus nerves. This quick response allows the heart rate to vary rhythmically at the respiratory frequency. On the other hand, norepinephrine released periodically at the sympathetic endings is removed slowly. Therefore, the rhythmic variations in sympathetic activity during inspiration do not cause significant oscillatory changes in heart rate. Consequently, respiratory sinus arrhythmia is primarily caused by changes in vagal activity. In fact, enhancing vagal tone exaggerates respiratory sinus arrhythmia.

Stretch receptors in the lungs are stimulated during inspiration, leading to a reflex increase in heart rate. This reflex involves the afferent and efferent limbs located in the vagus nerves. Additionally, intrathoracic pressure decreases during inspiration, increasing venous return to the right side of the heart. The resulting stretch in the right atrium triggers the Bainbridge reflex. After a time delay required for the increased venous return to reach the left side of the heart, left ventricular output increases, raising arterial blood pressure. In turn, this rise in blood pressure reduces the heart rate through the baroreceptor reflex.

Respiratory cardiac arrhythmia is also influenced by central factors. The respiratory center in the medulla directly affects the cardiac autonomic centers. In studies involving heart-lung bypass, where the chest is opened, the lungs are collapsed, and venous return is diverted to a pump-oxygenator while maintaining constant arterial blood pressure, rhythmic movement of the rib cage indicates activity in the medullary respiratory centers. This movement is often accompanied by rhythmic changes in heart rate at the respiratory frequency. It is highly likely that this respiratory cardiac arrhythmia is induced by a direct interaction between the respiratory and cardiac centers in the medulla.

The response of the heart to peripheral chemoreceptor stimulation demonstrates the complex interactions that can occur when one stimulus simultaneously excites two organ systems. Stimulation of carotid chemoreceptors consistently increases both the rate and depth of ventilation. However, it only slightly affects the heart rate under normal circumstances. The extent of the ventilatory response determines whether the heart rate increases or decreases due to carotid chemoreceptor stimulation. Mild stimulation of respiration caused by chemoreceptor stimulation moderately decreases the heart rate, while more pronounced stimulation only slightly increases it. If the pulmonary response to chemoreceptor stimulation is blocked, the heart rate response may be greatly exaggerated, as described later.

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Recordings from cardiac autonomic nerves reveal that neural activity increases in the sympathetic fibers during inspiration and increases in the vagal fibers during expiration. The heart rate response to cessation of vagal stimulation is very quick because, as already noted, ACh released from the vagus nerves is rapidly hydrolyzed by acetylcholinesterase. This short latency enables the heart rate to vary rhythmically at the respiratory frequency. Conversely, the norepinephrine released periodically at the sympathetic endings is removed very slowly. Therefore, the rhythmic variations in sympathetic activity that accompany inspiration do not induce any appreciable oscillatory changes in heart rate. Thus respiratory sinus arrhythmia is brought about almost entirely by changes in vagal activity. In fact, respiratory sinus arrhythmia is exaggerated when vagal tone is enhanced.
Fig. 18.8 ). Stretch receptors in the lungs are stimulated during inspiration, and this action leads to a reflex increase in heart rate. The afferent and efferent limbs of this reflex are located in the vagus nerves. Intrathoracic pressure also decreases during inspiration and thereby increases venous return to the right side of the heart (see ). The consequent stretch of the right atrium elicits the Bainbridge reflex. After the time delay required for the increased venous return to reach the left side of the heart, left ventricular output increases and raises arterial blood pressure. This rise in blood pressure in turn reduces the heart rate through the baroreceptor reflex.
Central factors are also responsible for respiratory cardiac arrhythmia. The respiratory center in the medulla directly influences the cardiac autonomic centers (see
Fig. 18.8). In heart-lung bypass studies, the chest is opened, the lungs are collapsed, venous return is diverted to a pump-oxygenator, and arterial blood pressure is maintained at a constant level. In such studies, rhythmic movement of the rib cage attests to the activity of the medullary respiratory centers, and is often accompanied by rhythmic changes in heart rate at the respiratory frequency. This respiratory cardiac arrhythmia is almost certainly induced by a direct interaction between the respiratory and cardiac centers in the medulla.
The cardiac response to peripheral chemoreceptor stimulation illustrates the complex interactions that may ensue when one stimulus excites two organ systems simultaneously. Stimulation of carotid chemoreceptors consistently increases ventilatory rate and depth (see ), but ordinarily it changes the heart rate only slightly. The magnitude of the ventilatory response determines whether the heart rate increases or decreases as a result of carotid chemoreceptor stimulation. Mild chemoreceptor-induced stimulation of respiration decreases the heart rate moderately; more pronounced stimulation increases the heart rate only slightly. If the pulmonary response to chemoreceptor stimulation is blocked, the heart rate response may be greatly exaggerated, as described later.