Neural drive and electromechanical alterations in the fatiguing diaphragm.
It is suggested that respiratory failure in the compromised circulation might occur as a result of respiratory muscle fatigue in the presence of adequate neural drive and muscle excitation. As the cardiac output decreases acidosis develops and ventilation increases, resulting in an increase in the work of breathing, which requires the delivery of large supplies of energy. As these demands cannot be met by the energy supply, because of low cardiac output, the diaphragm fails as a force generator and respiratory failure ensues. Diaphragmatic fatigue may occur in normal subjects if the pressure developed with each breath is greater than 40% of the maximum transdiaphragmatic pressure and hypoxia predisposes the diaphragm to fatigue. Diaphragmatic fatigue, as in other skeletal muscles, might be located either at the neuromuscular junction or distal to it and can be detected either by phrenic stimulation or by frequency analysis of the myoelectric signal. Phrenic stimulation shows that after fatigue the diaphragm develops less force at any frequency of stimulation, but the loss of force at low frequencies persists for a longer period than at high frequencies. Frequency analysis of the electromyogram reveals that the power spectrum shifts to lower frequencies. This shift occurs long before the diaphragm fails as a force generator.
D000818:Animals; D002305:Cardiac Tamponade / Q000150:complications / Q000503:physiopathology; D003964:Diaphragm / Q000503:physiopathology*; D004195:Disease Models, Animal; D004283:Dog Diseases / Q000503:physiopathology; D004285:Dogs; D004558:Electric Stimulation; D005221:Fatigue / Q000503:physiopathology*; D009119:Muscle Contraction; D009469:Neuromuscular Junction / Q000502:physiology; D010791:Phrenic Nerve / Q000502:physiology; D012131:Respiratory Insufficiency / Q000209:etiology / Q000503:physiopathology; D013997:Time Factors