Fractal ventilation enhances respiratory sinus arrhythmia

BACKGROUND: Programming a mechanical ventilator with a biologically variable or fractal breathing pattern (an example of 1/f noise) improves gas exchange and respiratory mechanics. Here we show that fractal ventilation increases respiratory sinus arrhythmia (RSA) – a mechanism known to improve ventilation/perfusion matching. METHODS: Pigs were anaesthetised with propofol/ketamine, paralysed with doxacurium, and ventilated in either control mode (CV) or in fractal mode (FV) at baseline and then following infusion of oleic acid to result in lung injury. RESULTS: Mean RSA and mean positive RSA were nearly double with FV, both at baseline and following oleic acid. At baseline, mean RSA = 18.6 msec with CV and 36.8 msec with FV (n = 10; p = 0.043); post oleic acid, mean RSA = 11.1 msec with CV and 21.8 msec with FV (n = 9, p = 0.028); at baseline, mean positive RSA = 20.8 msec with CV and 38.1 msec with FV (p = 0.047); post oleic acid, mean positive RSA = 13.2 msec with CV and 24.4 msec with FV (p = 0.026). Heart rate variability was also greater with FV. At baseline the coefficient of variation for heart rate was 2.2% during CV and 4.0% during FV. Following oleic acid the variation was 2.1 vs. 5.6% respectively. CONCLUSION: These findings suggest FV enhances physiological entrainment between respiratory, brain stem and cardiac nonlinear oscillators, further supporting the concept that RSA itself reflects cardiorespiratory interaction. In addition, these results provide another mechanism whereby FV may be superior to conventional CV

Stimulation of skin sympathetic nerve discharge by central command. Differential control of sympathetic outflow to skin and skeletal muscle during static exercise.

Microneurographic measurements of muscle sympathetic nerve activity (SNA) have suggested that, during static exercise, central command is much less important than skeletal muscle afferents in causing sympathetic neural activation. The possibility remains, however, that the sympathetic discharge produced by central command is targeted mainly to tissues other than skeletal muscle. To examine this possibility, we recorded SNA with microelectrodes placed selectively in skin, as well as in muscle, nerve fascicles of the peroneal nerve during static handgrip maneuvers designed to separate the effects of central command from those of muscle afferents. To study the relative effects of cutaneous sympathetic activation on sudomotor versus vasomotor function, we simultaneously estimated changes in skin blood flow (laser Doppler velocimetry) and in sudomotor (electrodermal) activation in the region of skin innervated by the impaled nerve fascicle. Two minutes of static handgrip at 10%, 20%, and 30% of maximal voluntary contraction caused large and intensity-dependent increases in skin SNA. These increases in SNA immediately preceded the onset of muscle tension, accelerated progressively during sustained handgrip, and resolved promptly with the cessation of motor effort. The handgrip-induced increases in skin SNA were not maintained when handgrip was followed by arrest of the forearm circulation, a maneuver that maintains the stimulation of chemically sensitive muscle afferents while eliminating the influences of central command and mechanically sensitive muscle afferents. During normothermia, static handgrip at 30% maximal voluntary contraction caused sustained increases in skin SNA (+400 +/- 83%, mean +/- SEM, p less than 0.05) and in electrodermal activity (+276 +/- 56%, p less than 0.05) but only transient increases in estimated skin vascular resistance (+11 +/- 2%, p less than 0.05). When skin temperature was increased or decreased to a new stable baseline level, subsequent increases in skin SNA during handgrip were accompanied by sustained but directionally opposite changes in estimated skin vascular resistance, with exercise-induced vasodilation during hyperthermia but exercise-induced vasoconstriction during hypothermia. From these observations, we conclude the following: 1) static exercise markedly increases sympathetic outflow to skin as well as to skeletal muscle; 2) the increases in skin SNA, unlike muscle SNA, appear to be caused mainly by central command rather than by muscle afferent reflexes; and 3) this cutaneous sympathetic activation appears to be targeted both to sweat glands and to vascular smooth muscle, with the relative targeting being temperature dependent.(ABSTRACT TRUNCATED AT 400 WORDS