The elevated ventilatory response in HF patients seen before lactic acidosis ensues and the carbon dioxide (CO 2) generated by the lactate is trivial relative to the rate of metabolic CO 2 production (VCO 2). Additional studies of physiological responses under stress and reconsideration of current standards are recommended.The behaviour of ventilation during exercise in heart failure (HF) and in chronic obstructive pulmonary disease (COPD) patients may differ, being characterized in the former by an out-of-proportion increase of ventilation (VE), which is greater the greater the HF severity and, in the latter, by a normal or excessive increase of ventilation in mild or moderate COPD and a blunted ventilation increase in severe COPD patients –. The mechanism for maintaining a normal carbon dioxide tension seems effective up to 2% carbon dioxide for short-term and to 1% carbon dioxide for long-term exposures. Tidal volume increases and, thereafter, breath frequency rises. Added dead space forces rebreathing of exhaled carbon dioxide which, in turn, stimulates compensatory hyperventilation to maintain a normal alveolar carbon dioxide tension. The principal physiological responses to added breathing resistance appear to be hypoventilation, reduced oxygen consumption, a "flattened" and prolonged pattern in the breathing phase to which resistance has been added, increased respiratory work, and a tendency for increased Functional Residual Lung Capacity and increased carbon dioxide retention (when compensation is incomplete). Breathing resistance and equipment dead space are two of the most important design factors contributing to this discomfort. This has been principally due to a generalized "discomfort" experienced by workers. Respirators, in general, are worn by only about 20% of workers in need of respiratory protection against hazardous substances in the workplace.
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