Ventilatory pump

Impairment of the ventilatory pump can occur in conditions characterized by decreased respiratory drive, abnormal respiratory mechanics, diminished respiratory muscle performance, and impaired cardiovascular performance. 

Specific conditions such as idiopathic central alveolar hypoventilation syndrome (Ondine s curse) or central alveolar hypoventilation syndrome secondary to neurological lesions (trauma, infections, infarction. Shy Drager syndrome) can cause or contrihute to long-term ventilator dependence (40). In most ventilator-dependent patients, however, estimations of respiratory drive indicate that drive is increased and not decreased (18,41-43). 

Several lines of evidence support the likelihood that increased mechanical load contributes to LTMV dependence. First, mechanical load is greater in ventilator-dependent patients than in non-ventilator-dependent patients (41,43). Second, progression to successful weaning has been associated with improvement in work of breathing per liter of minute ventilation, which is a function of compliance, resistance, tidal volume, and minute ventilation (48). Third, the mean inspiratory flow produced for a given level of neuromuscular inspiratory drive is lower in LTMV-dependent patients than in patients who are successfully weaned after a period of PMV (Fig. 3) (41,43). Lastly, effective inspiratory impedance correlates with inspiratory pressure output (41). This correlation suggests worse load-capacity balance in patients who are dependent on LTMV than in patients who are successfully weaned after a period of PMV (41). 

Respiratory muscle weakness and respiratory muscle fatigue can decrease the capacity of these muscles to generate and sustain tension. As direct quantification of respiratory muscle tension is clinically impossible, measurements of pressure elicited by respiratory muscle contractions are used to indirectly determine their contribution to ventilator dependence. 

Detection of Respiratory Muscie Weakness in Mechanicaiiy Ventiiated Patients 

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The two principal components of the respiratory system are the lung, which participates in gas exchange, and a muscular pump, which ventilates the lungs (1,2). The ventilatory pump consists of the chest wall (rib cage and abdomen), including the muscles that displace this... 

Hypercapnic respiratory failure is due to failure of the ventilatory pump caused by acute (drug overdose, acute neuromuscular diseases) or chronic (chest wall abnormalities, chronic neuromuscular diseases) disorders. It is characterized by alveolar hypoventilation, which leads to hypercapnia with coexistent, usually mild, hypoxemia. The central drive may be globally reduced with the fall in Pa02 resulting from the increase in alveolar CO2. More commonly, the drive remains high, but the mechanical load on the respiratory systan is too great or the capacity of the muscles too low to ensure efficient CO2 elimination (Fig. 1). 

The function of the ventilatory pump is critically dependent on three factors the respiratory workload, the respiratory muscle strength, and the ventilatory drive (Fig. 1). Chronic hypercapnic respiratory failure can result from one or more of these abnormalities inadequate ventilatory drive, excessive respiratory load, and inadequate inspiratory muscle... 

From a pathophysiologic standpoint, it is usefiil to consider respiratoiy conditions that may result in LTMV, as those characterized by failure of the lungs as a gas-exchange unit and those characterized by a failure of the ventilatory pump (Fig. 2). In some ventilated patients, psychological factors may also contribute to their degree of impairment (34). 

The function of the pumping apparatus is ensure the appropriate movement of gases between the environment and the central airways and is evaluated by measuring ventilatory patterns. Ventilatory parameters must include measures of respiratory rate, tidal volume... 

Schucher B, Laier-Groeneveld G, Huettemann U, et al. Effects of intermittent self-ventilation on ventilatory drive and respiratory pump fimction. Med Klin (Munich) 1995 90(1 suppl 1) 13-16. 

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