Automatic selection of tidal volume, respiratory frequency and minute ventilation in intubated ICU patients as startup procedure for closed-loop controlled ventilation

1994 ◽  
Vol 11 (1) ◽  
pp. 19-30 ◽  
Author(s):  
Thomas P. Laubscher ◽  
Adrian Frutiger ◽  
Sergio Fanconi ◽  
Hans Jutzi ◽  
Josef X. Brunner
Keyword(s):  
Tidal Volume ◽  
Closed Loop ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Icu Patients ◽  
Controlled Ventilation ◽  
Automatic Selection ◽  
Selection Of

scholarly journals Mechanical power at a glance: a simple surrogate for volume-controlled ventilation

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Lorenzo Giosa ◽  
Mattia Busana ◽  
Iacopo Pasticci ◽  
Matteo Bonifazi ◽  
Matteo Maria Macrì ◽  
...  
Keyword(s):  
Peak Pressure ◽  
Minute Ventilation ◽  
Clinical Intervention ◽  
Lung Parenchyma ◽  
Mechanical Power ◽  
Icu Patients ◽  
Controlled Ventilation ◽  
Volume Controlled Ventilation ◽  
New Equation ◽  
Volume Controlled

Abstract Background Mechanical power is a summary variable including all the components which can possibly cause VILI (pressures, volume, flow, respiratory rate). Since the complexity of its mathematical computation is one of the major factors that delay its clinical use, we propose here a simple and easy to remember equation to estimate mechanical power under volume-controlled ventilation: $$ \mathrm{Mechanical}\ \mathrm{Power}=\frac{\mathrm{VE}\times \left(\mathrm{Peak}\ \mathrm{Pressure}+\mathrm{PEEP}+F/6\right)}{20} $$Mechanical Power=VE×Peak Pressure+PEEP+F/620 where the mechanical power is expressed in Joules/minute, the minute ventilation (VE) in liters/minute, the inspiratory flow (F) in liters/minute, and peak pressure and positive end-expiratory pressure (PEEP) in centimeter of water. All the components of this equation are continuously displayed by any ventilator under volume-controlled ventilation without the need for clinician intervention. To test the accuracy of this new equation, we compared it with the reference formula of mechanical power that we proposed for volume-controlled ventilation in the past. The comparisons were made in a cohort of mechanically ventilated pigs (485 observations) and in a cohort of ICU patients (265 observations). Results Both in pigs and in ICU patients, the correlation between our equation and the reference one was close to the identity. Indeed, the R2 ranged from 0.97 to 0.99 and the Bland-Altman showed small biases (ranging from + 0.35 to − 0.53 J/min) and proportional errors (ranging from + 0.02 to − 0.05). Conclusions Our new equation of mechanical power for volume-controlled ventilation represents a simple and accurate alternative to the more complex ones available to date. This equation does not need any clinical intervention on the ventilator (such as an inspiratory hold) and could be easily implemented in the software of any ventilator in volume-controlled mode. This would allow the clinician to have an estimation of mechanical power at a simple glance and thus increase the clinical consciousness of this variable which is still far from being used at the bedside. Our equation carries the same limitations of all other formulas of mechanical power, the most important of which, as far as it concerns VILI prevention, are the lack of normalization and its application to the whole respiratory system (including the chest wall) and not only to the lung parenchyma.

Ventilatory response to hypoxia in unanesthetized newborn kittens

1988 ◽  
Vol 64 (6) ◽  
pp. 2544-2551 ◽  
Author(s):  
H. Rigatto ◽  
C. Wiebe ◽  
C. Rigatto ◽  
D. S. Lee ◽  
D. Cates
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Quiet Sleep ◽  
Newborn Kitten ◽  
Peripheral Mechanism ◽  
Flow Through ◽  
Ventilatory Response To Hypoxia

We studied the ventilatory response to hypoxia in 11 unanesthetized newborn kittens (n = 54) between 2 and 36 days of age by use of a flow-through system. During quiet sleep, with a decrease in inspired O2 fraction from 21 to 10%, minute ventilation increased from 0.828 +/- 0.029 to 1.166 +/- 0.047 l.min-1.kg-1 (P less than 0.001) and then decreased to 0.929 +/- 0.043 by 10 min of hypoxia. The late decrease in ventilation during hypoxia was related to a decrease in tidal volume (P less than 0.001). Respiratory frequency increased from 47 +/- 1 to 56 +/- 2 breaths/min, and integrated diaphragmatic activity increased from 14.9 +/- 0.9 to 20.2 +/- 1.4 arbitrary units; both remained elevated during hypoxia (P less than 0.001). Younger kittens (less than 10 days) had a greater decrease in ventilation than older kittens. These results suggest that the late decrease in ventilation during hypoxia in the newborn kitten is not central but is due to a peripheral mechanism located in the lungs or respiratory pump and affecting tidal volume primarily. We speculate that either pulmonary bronchoconstriction or mechanical uncoupling of diaphragm and chest wall may be involved.

scholarly journals Impact of cervical spinal cord contusion on the breathing pattern across the sleep-wake cycle in the rat

2019 ◽  
Vol 126 (1) ◽  
pp. 111-123 ◽  
Author(s):  
Kun-Ze Lee
Keyword(s):  
Spinal Cord ◽  
Tidal Volume ◽  
Spinal Injury ◽  
Cervical Spinal Cord ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Breathing Patterns ◽  
Cord Injury ◽  
Spinal Contusion ◽  
Cervical Spinal Injury

The present study was designed to investigate breathing patterns across the sleep-wake state following a high cervical spinal injury in rats. The breathing patterns (e.g., respiratory frequency, tidal volume, and minute ventilation), neck electromyogram, and electroencephalography of unanesthetized adult male rats were measured at the acute (i.e., 1 day), subchronic (i.e., 2 wk), and/or chronic (i.e., 6 wk) injured stages after unilateral contusion of the second cervical spinal cord. Cervical spinal cord injury caused a long-term reduction in the tidal volume but did not influence the sleep-wake cycle duration. The minute ventilation during sleep was usually lower than that during the wake period in uninjured animals due to a decrease in respiratory frequency. However, this sleep-induced reduction in respiratory frequency was not observed in contused animals at the acute injured stage. By contrast, the tidal volume was significantly lower during sleep in contused animals but not uninjured animals from the acute to the chronic injured stage. Moreover, the frequency of sigh and postsigh apnea was elevated in acutely contused animals. These results indicated that high cervical spinal contusion is associated with exacerbated sleep-induced attenuation of the tidal volume and higher occurrence of sleep apnea, which may be detrimental to respiratory functional recovery after cervical spinal cord injury. NEW & NOTEWORTHY Cervical spinal injury is usually associated with sleep-disordered breathing. The present study investigated breathing patterns across sleep-wake state following cervical spinal injury in the rat. Unilateral cervical spinal contusion significantly impacted sleep-induced alteration of breathing patterns, showing a blunted frequency response and exacerbated attenuated tidal volume and occurrence of sleep apnea. The result enables us to investigate effects of cervical spinal injury on the pathogenesis of sleep-disordered breathing and evaluate potential therapies to improve respiration.

Relationship between Cr and breathing pattern in mechanically ventilated patients

1994 ◽  
Vol 77 (6) ◽  
pp. 2703-2708 ◽  
Author(s):  
H. Burnet ◽  
M. Bascou-Bussac ◽  
C. Martin ◽  
Y. Jammes
Keyword(s):  
Linear Regression ◽  
Tidal Volume ◽  
Multiple Linear Regression ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Upper Airways ◽  
Mechanically Ventilated ◽  
Mechanically Ventilated Patients ◽  
Ventilated Patients

In mechanically ventilated patients the natural gas-conditioning process of the upper airways is bypassed by the use of an endotracheal tube or a tracheostomy. We hypothesized that under these conditions the breathing pattern may greatly influence the convective respiratory heat loss (Cr). Cr values were computed from minute ventilation (VE) and inspiratory and expiratory gas temperatures, which were measured in six patients under mechanical ventilation for the management of cranial trauma. In each patient the effects of 11–20 different breathing patterns were investigated. Relationships between Cr and VE and between combined tidal volume and respiratory frequency were obtained by simple and multiple linear regression methods, respectively. Comparison of the standard errors of estimate indicated that multiple linear regression gives the best fit. Thus, Cr was highly dependent on the breathing pattern and was not related only to VE. For the same VE value, Cr was higher when VE was achieved with high tidal volume and low respiratory frequency. These data are consistent with previous studies in which thermal exchanges through the upper airways were taxed by hyperventilation of frigid air.

Phonospirometry for noninvasive measurement of ventilation: methodology and preliminary results

2002 ◽  
Vol 93 (4) ◽  
pp. 1515-1526 ◽  
Author(s):  
Cheng-Li Que ◽  
Christof Kolmaga ◽  
Louis-Gilles Durand ◽  
Suzanne M. Kelly ◽  
Peter T. Macklem
Keyword(s):  
Airway Obstruction ◽  
Tidal Volume ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Flow Volume ◽  
Quiet Breathing ◽  
Neck Extension ◽  
Volume Relationship ◽  
Tracheal Sounds ◽  
Nose Clip

We measured tracheal flow from tracheal sounds to estimate tidal volume, minute ventilation (V˙i), respiratory frequency, mean inspiratory flow (Vt/Ti), and duty cycle (Ti/Ttot). In 11 normal subjects, 3 patients with unstable airway obstruction, and 3 stable asthmatic patients, we measured tracheal sounds and flow twice: first to derive flow-sound relationships and second to obtain flow-volume relationships from the sound signal. The flow-volume relationship was compared with pneumotach-derived volume. When subjects were seated, facing forward and with neck rotation, flexion, and standing, flow-volume relationship was within 15% of pneumotach-derived volume. Error increased with neck extension and while supine. We then measured ventilation without mouthpiece or nose clip from tracheal sounds during quiet breathing for up to 30 min. Normal results ± SD revealed tidal volume = 0.37 ± 0.065 liter, respiratory frequency = 19.3 ± 3.5 breaths/min, V˙i = 6.9 ± 1.2 l/min, Vt/Ti = 0.31 ± 0.06 l/s, and Ti/Ttot = 0.37 ± 0.04. Unstable airway obstruction had large V˙i due to increased Vt/Ti. With the exception of Ti/Ttot, variations in ventilatory parameters were closer to log normal than normal distributions and tended to be greater in patients. We conclude that phonospirometry measures ventilation reasonably accurately without mouthpiece, nose clip, or rigid postural constraints.

Sonomicrometric regional diaphragmatic shortening in awake sheep after thoracic surgery

1989 ◽  
Vol 67 (6) ◽  
pp. 2357-2368 ◽  
Author(s):  
A. Torres ◽  
W. R. Kimball ◽  
J. Qvist ◽  
K. Stanek ◽  
R. M. Kacmarek ◽  
...  
Keyword(s):  
Thoracic Surgery ◽  
Tidal Volume ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Quiet Breathing ◽  
Transdiaphragmatic Pressure ◽  
Right Thoracotomy ◽  
Before And After ◽  
End Tidal ◽  
End Tidal Co2

Through a right thoracotomy in seven sheep we chronically implanted sonomicrometry crystals and electromyographic electrodes in the costal and crural diaphragmatic regions. Awake sheep were studied during recovery for 4-6 wk, both during quiet breathing (QB) and during CO2 rebreathing. Tidal volume, respiratory frequency, and esophageal and gastric pressures were studied before and after surgery. Normalized resting length (LFRC) was significantly decreased for the costal segment on postoperative day 1 compared with postoperative day 28. Fractional costal shortening both during QB and at 10% end-tidal CO2 (ETCO2) increased significantly from postoperative days 1 to 28, whereas crural shortening did not change during QB but progressively increased at 10% ETCO2. Maximal costal shortening during electrophrenic stimulation was constant at 40% LFRC during recovery, although maximal crural shortening increased from 23 to 32% LFRC. Minute ventilation, tidal volume, and transdiaphragmatic pressure at 10% ETCO2 increased progressively after thoracotomy until postoperative day 28. Our results suggest there is profound diaphragmatic inhibition after thoracotomy and crystal implantation in sheep that requires at least 3-4 wk for stable recovery.

Effect of Continuous Positive Airway Pressure on the Ventilatory Response to CO2 in Preterm Infants

PEDIATRICS ◽  
1983 ◽  
Vol 71 (4) ◽  
pp. 634-638
Author(s):  
Manuel Durand ◽  
Ellen McCann ◽  
June P. Brady
Keyword(s):  
Tidal Volume ◽  
Preterm Infants ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Co2 Response ◽  
Expiratory Time ◽  
Ventilatory Response To Co2

The effect of continuous positive airway pressure (CPAP) on the ventilatory response to CO2 in newborn infants is unknown. The CO2 response to 4% CO2 in air was studied in nine preterm infants without lung disease before and during administration of CPAP (4 to 5 cm H2O) delivered by face mask. Minute ventilation, tidal volume, respiratory frequency, and end-tidal Pco2 were measured, and the slope and intercept of the CO2 response were calculated. Respiratory pattern and changes in oxygenation were also analyzed by measuring inspiratory and expiratory time, mean inspiratory flow, mean expiratory flow, effective respiratory timing, endtidal Po2, and transcutaneous Po2. CPAP significantly decreased minute ventilation from 278.7 to 197.6 mL/mm/kg (P < .001). Tidal volume and respiratory frequency were also significantly decreased. The slope of the CO2 response during CPAP was not significantly different from the slope before CPAP (36 v 33 mL/min/kg/mm Hg, P > .1), but the intercept was shifted to the right (P < .001). The decrease in respiratory frequency was primarily due to a prolongation of expiratory time (P < .05). In addition, transcutaneous Po2 increased during administration of CPAP (P < .001). These findings indicate that: (1) CPAP significantly decreases ventilation in preterm infants without lung disease, affecting both tidal volume and respiratory frequency; (2) CPAP does not appreciably alter the ventilatory response to CO2; (3) the changes in respiratory frequency are primarily accounted for by a prolongation of expiratory time; (4) CPAP improves oxygenation.

Effect of residence at altitude on the perception of breathlessness on return to sea level in normal subjects

1993 ◽  
Vol 84 (2) ◽  
pp. 159-167 ◽  
Author(s):  
Rachel C. Wilson ◽  
W. L. G. Oldfield ◽  
P. W. Jones
Keyword(s):  
Oxygen Consumption ◽  
Tidal Volume ◽  
Sea Level ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Cycle Ergometer ◽  
Respiratory Frequency ◽  
Borg Scale ◽  
Oxygen Pulse ◽  
Ventilatory Equivalent

1. The effect of residence at altitude on the perception of breathlessness after return to sea level was examined in normal subjects. Breathlessness (Borg scale), minute ventilation, respiratory frequency, tidal volume, ‘oxygen pulse’ (oxygen consumption/heart rate) and the ventilatory equivalent for oxygen (minute ventilation/oxygen consumption) were measured at exercise (cycle-ergometer) during 5 months of training before 4 weeks at 4000 m and during the 6 month period after return to sea level. 2. There was no change in the subjects' pattern of breathing (respiratory frequency and tidal volume) or ‘oxygen pulse’ after the period at altitude (P = 0.0001). The ventilatory equivalent for oxygen was increased at all work rates after the period at altitude (P = 0.02). This ratio was slightly lower after 6 weeks and had returned to normal by 6 months (P = 0.4). 3. During training there was no change in breathlessness score (P = 0.6). On return to sea level, breathlessness score relative to ventilation was reduced (P = 0.0001). This was maintained for at least 6 weeks, but not as long as 6 months. 4. This study has demonstrated that, in normal subjects, the otherwise stable and reproducible relationship between breathlessness and ventilation may be disrupted for several weeks by factors other than lung disease. 5. The mechanism responsible for this is not clear, but the observations are consistent with the hypothesis that prior experience of breathlessness may condition subsequent estimates of breathlessness.

Hypoxic respiratory responses attenuated by ablation of the cerebellum or fastigial nuclei

1995 ◽  
Vol 79 (4) ◽  
pp. 1181-1189 ◽  
Author(s):  
F. Xu ◽  
J. Owen ◽  
D. T. Frazier
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Sodium Cyanide ◽  
Respiratory Frequency ◽  
Peripheral Chemoreceptors ◽  
Before And After ◽  
Progressive Hypoxia ◽  
End Tidal ◽  
Diaphragm Activity ◽  
Respiratory Responses

The general contribution of the cerebellum to hypoxic respiratory responses and the special role of the fastigial nucleus (FN) in the hypoxic respiratory reflex mediated via peripheral chemoreceptors were investigated in anesthetized and spontaneously breathing cats. Seven cats were exposed to isocapnic progressive hypoxia before and after cerebellectomy by decreasing the fractional concentration of end-tidal O2 (FETO2) from 15 +/- 0.3% to 7% while maintaining the pressure of end-tidal CO2 at a constant level of approximately 30 mmHg. Five additional cats inhaled five breaths of pure N2 (transient hypoxia) and received sodium cyanide (50 micrograms iv) before and after thermal lesions of the bilateral FN. The results showed that cerebellectomy or FN lesions failed to alter the respiratory variables (minute ventilation, tidal volume, respiratory frequency, and the peak of integrated diaphragm activity) during eupneic breathing. However, cerebellectomy significantly attenuated minute ventilation (FETO2 < or = 13%) and the peak of integrated diaphragm activity (FETO2 < or = 10%) compared with control. During progressive hypoxia, changes in respiratory frequency were noted earlier (FETO2 < or = 13%) than changes in tidal volume (FETO2 < or = 10%). Similarly, bilateral lesions of the FN resulted in a profound reduction in these respiratory responses to transient hypoxia and sodium cyanide. We conclude that the cerebellum can facilitate the respiratory response to hypoxia and that the FN is an important region in the modulation of the hypoxic respiratory responses, presumably via its effects on inputs from peripheral chemoreceptors.

Role of the carotid bodies in chemosensory ventilatory responses in the anesthetized mouse

2004 ◽  
Vol 97 (4) ◽  
pp. 1401-1407 ◽  
Author(s):  
Masahiko Izumizaki ◽  
Mieczyslaw Pokorski ◽  
Ikuo Homma
Keyword(s):  
Tidal Volume ◽  
Carotid Body ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Whole Body ◽  
Sudden Increase ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Before And After ◽  
Carotid Body Denervation

We examined the effects of carotid body denervation on ventilatory responses to normoxia (21% O2 in N2 for 240 s), hypoxic hypoxia (10 and 15% O2 in N2 for 90 and 120 s, respectively), and hyperoxic hypercapnia (5% CO2 in O2 for 240 s) in the spontaneously breathing urethane-anesthetized mouse. Respiratory measurements were made with a whole body, single-chamber plethysmograph before and after cutting both carotid sinus nerves. Baseline measurements in air showed that carotid body denervation was accompanied by lower minute ventilation with a reduction in respiratory frequency. On the basis of measurements with an open-circuit system, no significant differences in O2 consumption or CO2 production before and after chemodenervation were found. During both levels of hypoxia, animals with intact sinus nerves had increased respiratory frequency, tidal volume, and minute ventilation; however, after chemodenervation, animals experienced a drop in respiratory frequency and ventilatory depression. Tidal volume responses during 15% hypoxia were similar before and after carotid body denervation; during 10% hypoxia in chemodenervated animals, there was a sudden increase in tidal volume with an increase in the rate of inspiration, suggesting that gasping occurred. During hyperoxic hypercapnia, ventilatory responses were lower with a smaller tidal volume after chemodenervation than before. We conclude that the carotid bodies are essential for maintaining ventilation during eupnea, hypoxia, and hypercapnia in the anesthetized mouse.

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