The act of breathing fulfils the essential need for acquiring oxygen and removing carbon dioxide. But it is only with the close co-operation of the cardiovascular system that oxygen can reach every tissue in the body. For many years it has been known that cardiac and respiratory control systems interact and influence one another to maintain homeostasis in the face of changing demands for increased blood flow and oxygenation. Changes in environment (e.g. diving) and the demands of exercise require that the response of these control systems is quick and efficient.

As well as these major cardiovascular adjustments more subtle interactions also occur. These include changes in the cardiorespiratory interactions by temperature and long-term blood pressure fluctuations (see Kitney & Rompelman, 1980, for review). The best known interaction, and one which has been used extensively in clinical investigations, is the breath by breath modulation of the heart rate, called respiratory sinus arrhythmia (RSA). This can be defined as the rapid increase in heart rate which occurs during the inspiratory phase of respiration, and the subsequent slowing of the heart during expiration.

Fig. 33.1 shows two examples of RSA recorded in the barbiturate anaesthetized cat. The top trace in each panel shows a low-pass filtered version of the instantaneous heart rate (Hyndman, 1980). Below are integrated (‘leaky integrator’ low-pass filter) electromyographic (EMG) recordings from the external (inspiratory, IEMG) and internal (expiratory, EEMG) intercostal muscles recorded from intercostal spaces T4 and T8 respectively.