P0.1/PIMax: An index for assessing respiratory capacity in acute respiratory failure

Fernández, Rafael; Cabrera, Judith; Calaf, Núria; Benito, S.

doi:10.1007/bf01724798

Cited by 47 publications

(23 citation statements)

References 14 publications

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“…In patients with ARF, a similar high value of P0.1/VT/tI was also observed by FERNANDEZ et al [14]. Some patients maintained a high P0.1/VT/t I when they recovered from ARF and were unable to sustain spontaneous breathing [14]. It was unclear, however, whether those patients were ready to wean, as in the present study.…”

Section: Discussionsupporting

confidence: 88%

“…Nevertheless, the increase in effective inspiratory impedance during ARF suggests that the mechanical load on the respiratory muscles is increased. In patients with ARF, a similar high value of P0.1/VT/tI was also observed by FERNANDEZ et al [14]. Some patients maintained a high P0.1/VT/t I when they recovered from ARF and were unable to sustain spontaneous breathing [14].…”

Section: Discussionsupporting

confidence: 68%

“…Because inspiratory muscle strength may affect the measurement of P0.1, P0.1/PI,max was also calculated [14].…”

Section: Methodsmentioning

confidence: 99%

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Breathing pattern during acute respiratory failure and recovery

Rosario

Sassoon²,

Chetty³

et al. 1997

Eur Respir J

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The objective of this study was to compare the breathing pattern of patients who failed to wean from mechanical ventilation to the pattern during acute respiratory failure. We hypothesized that a similar breathing pattern occurs under both conditions. Breathing pattern, mouth occlusion pressure (P0.1) and maximum inspiratory pressure (PI,max) were measured in 15 patients during acute respiratory failure, within 24 h of the institution of mechanical ventilation, and in 49 patients during recovery, when they were ready for discontinuation from mechanical ventilation. The following indices were calculated: rapid shallow breathing index (respiratory frequency/tidal volume (f R/VT)); rapid shallow breathing-occlusion pressure index (ROP = P0.1·fR/VT); P0.1/PI,max; and effective inspiratory impedance (P0.1/VT/(inspiratory time (t I)).Patients who failed to wean (n=11) had a similar ROP, fR/VT and P0.1/PI,max to those with acute respiratory failure despite a significantly reduced P0.1/VT/t I, the value of which was comparable to that of patients who weaned successfully (n=38). The PI,max of patients who failed to wean was similar to that of patients who weaned successfully.We conclude that patients who failed to wean had a breathing pattern similar to that during acute respiratory failure, despite a reduced mechanical load on the respiratory muscles and a relatively adequate inspiratory muscle strength. This suggests that strategies that enhance respiratory muscle endurance may facilitate weaning.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 68%

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Breathing pattern during acute respiratory failure and recovery

Rosario

Sassoon²,

Chetty³

et al. 1997

Eur Respir J

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“…Maximal inspiratory mouth pressure sustained for 1 s (P Imax ) was measured as described previously [21]. Respiratory capac-ity was assessed as P 0.1 /P Imax [22] to avoid underestimation of a potentially increased ventilatory drive in the presence of inspiratory muscle weakness. Maximal expiratory pressure (P Emax ) was assessed at total lung capacity according to recent guidelines [13,23].…”

Section: Methodsmentioning

confidence: 99%

Diabetic polyneuropathy is associated with respiratory muscle impairment in type 2 diabetes

et al. 2007

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Aims/hypothesis Diabetes has a major negative effect on intensive care unit outcome. This has been partly attributed to impaired respiratory neuromuscular function. However, data on respiratory neuromuscular involvement in diabetes are lacking. This study therefore aimed to assess respiratory neuromuscular function related to diabetic polyneuropathy in patients with type 2 diabetes. Methods Respiratory neuromuscular function was assessed by the use of volitional tests and twitch mouth (TwPmo) and twitch transdiaphragmatic (TwPdi) pressures during non-volitional bilateral anterior magnetic phrenic nerve stimulation in 21 male type 2 diabetic patients without pulmonary disease and in 23 healthy, well-matched controls (forced expiratory volume in 1 s 103±11 vs 103±12% predicted; p=0.9). Results Both volitionally assessed maximal inspiratory and expiratory mouth pressures, and sniff nasal and transdiaphragmatic pressures were comparable between diabetic patients and controls (p>0

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“…P 0.1 is widely accepted as an index of respiratory drive performance, 12 although it may be affected by drugs, gas exchange, respiratory muscle function, 13 or lung volume. It is important to note that variations in P aCO 2 observed with hyperoxia in subjects with COPD may be not wide enough to produce a measurable change in P 0.1 .…”

Section: See the Related Editorial On Page 473mentioning

confidence: 99%

Role of Respiratory Drive in Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With COPD

et al. 2014

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BACKGROUND: Hyperoxia-induced hypercapnia in subjects with COPD is mainly explained by alterations in the ventilation/perfusion ratio. However, it is unclear why respiratory drive does not prevent CO 2 retention. Some authors have highlighted the importance of respiratory drive in CO 2 increases during hyperoxia. The aim of the study was to examine the effects of hyperoxia on respiratory drive in subjects with COPD. METHODS: Fourteen intubated, ready-to-wean subjects with COPD were studied during normoxia and hyperoxia. A CO 2 response test was then performed with the rebreathing method to measure the hypercapnic drive response, defined as the ratio of change in airway-occlusion pressure 0.1 s after the start of inspiratory flow (⌬P 0.1 ) to change in P aCO 2 (⌬P aCO 2 ), and the hypercapnic ventilatory response, defined as the ratio of change in minute volume (⌬V E ) to ⌬P aCO 2 . RESULTS: Hyperoxia produced a significant increase in P aCO 2 (55 ؎ 9 vs 58 ؎ 10 mm Hg, P ‫؍‬ .02) and a decrease in pH (7.41 ؎ 0.05 vs 7.38 ؎ 0.05, P ‫؍‬ .01) compared with normoxia, with a non-significant decrease in V E (9.9 ؎ 2.9 vs 9.1 ؎ 2.3 L/min, P ‫؍‬ .16) and no changes in In ready-to-wean subjects with COPD exacerbations, hyperoxia is followed by an increase in P aCO 2 , but it does not significantly modify the respiratory drive or the ventilatory response to hypercapnia.

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P0.1/PIMax: An index for assessing respiratory capacity in acute respiratory failure

Cited by 47 publications

References 14 publications

Breathing pattern during acute respiratory failure and recovery

Breathing pattern during acute respiratory failure and recovery

Diabetic polyneuropathy is associated with respiratory muscle impairment in type 2 diabetes

Role of Respiratory Drive in Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With COPD

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