Patofisiologia dell'insufficienza respiratoria durante esacerbazione della COPD

Translated title of the contribution: Pathophysiology of respiratory failure during exacerbation of COPD

Research output: Contribution to journalArticle

Abstract

The COPD patient during tidal breathing has to overcome an increased load: besides the "threshold" load of PEEPi and the resistive load of stenotic airways he has an increased elastic work since the overinflated lung is less distensible, being on the steeper portion of the pressure/volume curve. With respect to force, hyperinflation flattens the diaphragm and shortens the apposition zone fibers, with a consequent reduction of the diaphragm force capacity, due to a disadvantageous force/length relation. During exacerbations, the increase in respiratory rate shortens the time available for lung emptying with consequent worsening of dynamic hyperinflation (DH) and this places the diaphragm in a more disadvantageous position, reducing its forcegenerating capacity. Therefore indirect indexes of DH, like inspiratory capacity (IC), and of reduced diaphragmatic force, like maximal inspiratory pressure (Pi max) can better describe the pathophysiologic changes during exacerbations. Hypoxia is caused by worsening of ventilation/perfusion ratio, while hypercapnia is the consequence of ventilatory pump failure and alveolar hypoventilation.

Original languageItalian
Pages (from-to)103-111
Number of pages9
JournalActa Anaesthesiologica Italica / Anaesthesia and Intensive Care in Italy
Volume59
Issue number2
Publication statusPublished - 2008

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Diaphragm
Respiratory Insufficiency
Chronic Obstructive Pulmonary Disease
Ventilation-Perfusion Ratio
Inspiratory Capacity
Hypoventilation
Lung
Hypercapnia
Respiratory Rate
Respiration
Pressure

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

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N2 - The COPD patient during tidal breathing has to overcome an increased load: besides the "threshold" load of PEEPi and the resistive load of stenotic airways he has an increased elastic work since the overinflated lung is less distensible, being on the steeper portion of the pressure/volume curve. With respect to force, hyperinflation flattens the diaphragm and shortens the apposition zone fibers, with a consequent reduction of the diaphragm force capacity, due to a disadvantageous force/length relation. During exacerbations, the increase in respiratory rate shortens the time available for lung emptying with consequent worsening of dynamic hyperinflation (DH) and this places the diaphragm in a more disadvantageous position, reducing its forcegenerating capacity. Therefore indirect indexes of DH, like inspiratory capacity (IC), and of reduced diaphragmatic force, like maximal inspiratory pressure (Pi max) can better describe the pathophysiologic changes during exacerbations. Hypoxia is caused by worsening of ventilation/perfusion ratio, while hypercapnia is the consequence of ventilatory pump failure and alveolar hypoventilation.

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