Acute respiratory failure can directly alter cardiovascular function in a large number of seemingly unrelated ways. However, many of these effects are predictable from knowledge of cardiovascular function. The respiratory system and the cardiovascular systems are not separate but tightly integrated. The ultimate cardiovascular response to acute respiratory failure is dependent on the basal cardiovascular state of the subject, the type of respiratory dysfunction present, and the ventilatory pattern. Spontaneous inspiratory efforts during both acute bronchospasm and acute lung injury will induce markedly negative swings in intrathoracic pressure. Both underinflation and hyperinflation of the lung will alter pulmonary vascular resistance and heart-lung interactions, and increased work of breathing will stress the cardiovascular response to maintain and increase cardiac output to meet the increased oxygen demand ( Vo2). Furthermore, artificial ventilatory support will increase intrathoracic pressure during inspiration, in contradistinction to spontaneous ventilation which will decrease intrathoracic pressure for the same tidal breath. Heart-lung interactions involve four basic concepts

1. Inspiration increases lung volume above end-expiratory volume.

2. Spontaneous inspiration decreases intrathoracic pressure.

3. Positive-pressure ventilation increases intrathoracic pressure.

4. Ventilation is exercise: it consumes O2 and produces CO2.

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