Suppression of Spontaneous Breathing

Suppressing spontaneous breathing activity during controlled mechanical ventilation can be achieved by hyperventilation, deep sedation or muscle relaxation. Hyperventilation in conjunction with respiratory alkalosis may result in a drop in cardiac output, cerebral vasoconstriction, increased oxygen consumption, bron-choconstriction and V/Q mismatch [49-51]. Analgosedation sufficient to suppress respiratory efforts is known to cause significant cardio-vascular depression. In addition, it may take longer for the patient to wake up following the long-term use of sedatives and analgesics [52]. Using muscle relaxants to facilitate adaptation to controlled mechanical ventilation is also open to question. An increasing number of reports claim that the long-term application of muscle relaxants during control-

Minute Ventilation

Fig. 7. Urine volume (Uvol), effective renal plasma flow (ERPF), and glomerular filtration rate (GFR) duringairway pressure release ventilation with and withoutspontaneous breathing. During APRV without spontaneous breathing adjusted to produce equal minute ventilation (Ve) (normocapnia) while when APRV without spontaneous breathing was administered with equal airway pressure limits (Paw) (permissive hypercapnia).

Fig. 7. Urine volume (Uvol), effective renal plasma flow (ERPF), and glomerular filtration rate (GFR) duringairway pressure release ventilation with and withoutspontaneous breathing. During APRV without spontaneous breathing adjusted to produce equal minute ventilation (Ve) (normocapnia) while when APRV without spontaneous breathing was administered with equal airway pressure limits (Paw) (permissive hypercapnia).

led mechanical ventilation in the ICU can lead to muscular atrophy, damage to the neuromuscular end-plate and other muscle function disorders and can, therefore, delay or even prevent weaning from mechanical ventilation [53-55].

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