In the current study we observed that the HFE mutants are characterized by the lower power output generated at [VO.sub.2peak], as well as lower max minute ventilation
compared to control subjects.
The slopes of the data are calculated as the change in minute ventilation
over the change in partial pressure of carbon dioxide ([DELTA]VE/[DELTA] PCO2).
The usual initial settings were 100% minute ventilation
using the patient's ideal body weight, PEEP within the range of 2-12 cm [H.sub.2]O and the lowest Fi[O.sub.2] allowing adequate oxygenation (arterial oxygen saturation as measured by a blood gas analyser (Sa[O.sub.2]) >93% or an arterial partial pressure of oxygen (Pa[O.sub.2]) >70 mmHg) in the range of Fi[O.sub.2] 0.35-0.5 (Table 2).
during submaximal effort did not demonstrate a similar pattern to V[O.sub.2] and HR.
Variables Wald test Score HR (log rank) test VE/VC[O.sub.2] slope 0.001 0.0002 1.09 V[O.sub.2] peak/kg 0.001 0.0004 0.75 DLCO% 0.002 0.0007 0.88 Distance (meters) 0.003 0.0008 0.99 VE/VC[O.sub.2] 0.006 0.0001 1.15 ratio at AT Desaturation (%) 0.007 0.0025 1.45 Variables CI (95%) Sum-index VE/VC[O.sub.2] slope 1.04-1.15 0.0017 V[O.sub.2] peak/kg 0.60-0.95 0.0033 DLCO% 0.80-0.96 0.0035 Distance (meters) 0.98-1.00 0.0047 VE/VC[O.sub.2] 1.04-1.26 0.0074 ratio at AT Desaturation (%) 1.11-1.90 0.0102 Minute ventilation
(VE), carbon dioxide output (VC[O.sub.2]), peak oxygen consumption/kg (V[O.sub.2] peak/kg), diffusing capacity for carbon monoxide% (DLCO%), VE/VC[O.sub.2] slope at anaerobic threshold (AT), and hazard ratio (HR).
Change in cardiorespiratory function (heart rate, tidal volume, minute ventilation
, [P.sub.ET]C[O.sub.2] or Sp[O.sub.2]) from rest to the last 30 s of exercise was not different between the interventions.
In a group of patients with nocturnal desaturation, minute ventilation
fell by around 20 per cent from wakefulness to NREM, with further falls during REM sleep of almost 40 per cent, irrespective of the underlying primary disease process (2).
While the respiratory rate and vital capacity [do] not change in pregnancy, there is an increase in tidal volume, minute ventilation
(40%), and minute oxygen uptake (20%) with resultant decrease in functional residual capacity and residual volume of air as a consequence of the elevated diaphragm ...
The hypercapnia was unlikely only to have been due to lower tidal volumes (as part of the lung protective strategy), and may also have been caused by an increase in dead space (due to an increase in ventilatory frequency mandated by an attempt to maintain an acceptable minute ventilation
) and possibly intrapulmonary arterial clots (which have been shown to occur in patients with acute lung injury).1 The difference between the PeC[O.sub.2] and PaC[O.sub.2] (as a substitute for the proper Bohr equation which required average expired C[O.sub.2]) supports the contention that the patients suffered from excessive high ventilation perfusion (dead space) lung units.
Data from this system continually measured heart rate, minute ventilation
(VE), oxygen uptake (VO2) and carbon dioxide production (VCO2).
The resultant consequence of all these physiological responses is a decrease in minute ventilation
Rapid changes in these parameters will, therefore, potentially alter the minute ventilation
and work requirements for the patient.