Most patients with respiratory failure continue to make spontaneous efforts during mechanical ventilation unless they are under heavy sedation or neuromuscular blockade. Missing efforts and dissynchrony during assisted ventilation impair its effectiveness and increase the work of breathing. Mild hypocapnia during mechanical ventilation can reduce spontaneous respiratory drive and even totally inhibit inspiratory muscle activity. The end-tidal PCO2 at which inspiratory muscle activity returns is known as the 'recruitment threshold' (Simon 1994). The recruitment threshold depends on the tidal volume and frequency (e.g. through the influence of sensory reflexes). Sudden cessation of continuous mechanical ventilation (even in awake normocapnic patients) can result in prolonged apnea. The mechanisms are not fully understood (it may be a 'memory' phenomenon).
Mild hypercapnia during weaning seems to be a physiological response to the additional resistive load (e.g. by the tube) even in patients with normal lungs (load-induced reduction in ventilation). Thus a 'normal' PaCO2 is not strictly defended under additional load.
An increase in body temperature (e.g. fever) increases ventilation (rate as well as tidal volume) indirectly by the augmented metabolism and directly by raising the respiratory center activity. Chapter References
Bianchi, A.L., Denavit-Saubie, M., and Champagnat, J. (1995). Central control of breathing in mammals: neuronal circuitry, membrane properties and neurotransmitters. Physiological Reviews, 75, 1-45.
Nunn, J. (1993). Nunn's applied respiratory physiology (4th edn), pp. 97-109. Butterworth-Heinemann, Oxford.
Richter, D.W., Ballanyi, K., and Schwarzacher, S. (1992). Mechanisms of respiratory rhythm generation. Current Opinion in Neurobiology, 2, 788-93.
Simon, P.M. (1994). Effect of mechanical ventilation on the control of breathing. In Principles and practice of mechanical ventilation (ed. M. J. Tobin), pp. 631-45. McGraw-Hill, New York.
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