Effects of high-frequency breathing on pulmonary ventilation and gas exchange

1983 ◽  
Vol 55 (6) ◽  
pp. 1854-1861 ◽  
Author(s):  
C. Frostell ◽  
J. N. Pande ◽  
G. Hedenstierna

The effects of spontaneous high-frequency breathing (HFB) on lung function were evaluated in three subjects highly trained in the practice of yoga. Transpulmonary pressure was measured by an esophageal balloon catheter and gas flow by pneumotachography. The abdominal and rib cage contributions to tidal breathing were measured separately by respiratory inductive plethysmography. Gas exchange was studied by the conventional technique and by multiple inert gas elimination. During HFB, respiratory rate increased to 232 cycles/min with a tidal volume of 0.35 liter. This resulted in a more than 10-fold increase in expired minute ventilation to approximately 90 1/min. The transpulmonary pressure varied by 20 cmH2O, with the calculated elastic, resistive, and accelerative components varying by 2, 20, and 8 cmH2O, respectively. Respiratory work increased more than 200-fold in comparison with resting ventilation. A phase shift between thoracic and abdominal breathing was observed and was interpreted as a volume displacement of approximately 30 1/min between the two parts of the respiratory system. Arterial oxygen and carbon dioxide tension remained normal. Bohr dead space increased, while acetone dead space remained unaltered. A bimodal distribution of ventilation-perfusion ratios (VA/Q) was observed, with one mode in normal and another in “high” VA/Q regions.

1984 ◽  
Vol 57 (3) ◽  
pp. 881-887 ◽  
Author(s):  
G. G. Weinmann ◽  
W. Mitzner ◽  
S. Permutt

Tidal volumes used in high-frequency ventilation (HFV) may be smaller than anatomic dead space, but since gas exchange does take place, physiological dead space (VD) must be smaller than tidal volume (VT). We quantified changes in VD in three dogs at constant alveolar ventilation using the Bohr equation as VT was varied from 3 to 15 ml/kg and frequency (f) from 0.2 to 8 Hz, ranges that include normal as well as HFV. We found that VD was relatively constant at tidal volumes associated with normal ventilation (7–15 ml/kg) but fell sharply as VT was reduced further to tidal volumes associated with HFV (less than 7 ml/kg). The frequency required to maintain constant alveolar ventilation increased slowly as tidal volume was decreased from 15 to 7 ml/kg but rose sharply with attendant rapid increases in minute ventilation as tidal volumes were decreased to less than 7 ml/kg. At tidal volumes less than 7 ml/kg, the data deviated substantially from the conventional alveolar ventilation equation [f(VT - VD) = constant] but fit well a model derived previously for HFV. This model predicts that gas exchange with volumes smaller than dead space should vary approximately as the product of f and VT2.


1982 ◽  
Vol 52 (3) ◽  
pp. 683-689 ◽  
Author(s):  
H. T. Robertson ◽  
R. L. Coffey ◽  
T. A. Standaert ◽  
W. E. Truog

Pulmonary gas exchange during high-frequency low-tidal volume ventilation (HFV) (10 Hz, 4.8 ml/kg) was compared with conventional ventilation (CV) and an identical inspired fresh gas flow in pentobarbital-anesthetized dogs. Comparing respiratory and infused inert gas exchange (Wagner et al., J. Appl. Physiol. 36: 585--599, 1974) during HFV and CV, the efficiency of oxygenation was not different, but the Bohr physiological dead space ratio was greater on HFV (61.5 +/- 2.2% vs. 50.6 +/- 1.4%). However, the elimination of the most soluble inert gas (acetone) was markedly enhanced by HFV. The increased elimination of the soluble infused inert gases during HFV compared with CV may be related to the extensive intraregional gas mixing that allows the conducting airways to serve as a capacitance for the soluble inert gases. Comparing as exchange during HFV with three different density carrier gases (He, N2, and Ar), the efficiency of elimination of Co2 or the intravenously infused inert gases was greatest with He-O2. However, the alveolar-arterial partial pressure difference for O2 on He-O2 exceeded that on N2-O2 by 5.4 Torr during HFV. The finding agrees with similar observations during CV, suggesting that this aspect of gas exchange is not substantially altered by HFV.


1997 ◽  
Vol 32 (2) ◽  
pp. 203-206 ◽  
Author(s):  
Jay J Schnitzer ◽  
John E Thompson ◽  
Holly L Hedrick ◽  
Jody M Kaban ◽  
Jay M Wilson

2019 ◽  
Vol 126 (4) ◽  
pp. 863-869 ◽  
Author(s):  
Maximilian Pinkham ◽  
Russel Burgess ◽  
Toby Mündel ◽  
Stanislav Tatkov

Nasal high flow (NHF) is an emerging therapy for respiratory support, but knowledge of the mechanisms and applications is limited. It was previously observed that NHF reduces the tidal volume but does not affect the respiratory rate during sleep. The authors hypothesized that the decrease in tidal volume during NHF is due to a reduction in carbon dioxide (CO2) rebreathing from dead space. In nine healthy males, ventilation was measured during sleep using calibrated respiratory inductance plethysmography (RIP). Carbogen gas mixture was entrained into 30 l/min of NHF to obtain three levels of inspired CO2: 0.04% (room air), 1%, and 3%. NHF with room air reduced tidal volume by 81 ml, SD 25 ( P < 0.0001) from a baseline of 415 ml, SD 114, but did not change respiratory rate; tissue CO2 and O2 remained stable, indicating that gas exchange had been maintained. CO2 entrainment increased tidal volume close to baseline with 1% CO2 and greater than baseline with 3% CO2 by 155 ml, SD 79 ( P = 0.0004), without affecting the respiratory rate. It was calculated that 30 l/min of NHF reduced the rebreathing of CO2 from anatomical dead space by 45%, which is equivalent to the 20% reduction in tidal volume that was observed. The study proves that the reduction in tidal volume in response to NHF during sleep is due to the reduced rebreathing of CO2. Entrainment of CO2 into the NHF can be used to control ventilation during sleep. NEW & NOTEWORTHY The findings in healthy volunteers during sleep show that nasal high flow (NHF) with a rate of 30 l/min reduces the rebreathing of CO2 from anatomical dead space by 45%, resulting in a reduced minute ventilation, while gas exchange is maintained. Entrainment of CO2 into the NHF can be used to control ventilation during sleep.


1965 ◽  
Vol 20 (5) ◽  
pp. 816-824 ◽  
Author(s):  
J. M. Workman ◽  
R. W. B. Penman ◽  
B. Bromberger-Barnea ◽  
S. Permutt ◽  
R. L. Riley

The effect of transpulmonary pressure (Ptp) on gas exchange in the dog lung was studied in 10 open-chested dogs. Rates of pulmonary perfusion and ventilation were held constant (right heart bypass and pump respirator) while Ptp was varied. Alveolar dead space ventilation and alveolar shunt perfusion were calculated from CO2 and O2 gradients. The results are finally expressed in terms of a three-compartment lung model. It is shown that a misinterpretation is possible if alveolar dead space or alveolar shunt compartments are expressed as fractions, respectively, of all ventilated or all perfused alveoli, therefore each has been expressed as a fraction of the whole lung. It is concluded that the alveolar shunt compartment decreased as Ptp was increased, over the lower range of Ptp studied. No significant change was detected in the alveolar dead space compartment, as Ptp was varied. alveolar-arterial O2 gradient; anatomical dead space; arterial-alveolar CO2 gradient; distribution of pulmonary perfusion; distribution of pulmonary ventilation; right heart bypass preparation; ventilation/perfusion relationships Submitted on February 16, 1965


1971 ◽  
Vol 40 (4) ◽  
pp. 317-325 ◽  
Author(s):  
J. S. Guleria ◽  
J. N. Pande ◽  
M. M. Markose ◽  
R. G. Gupta ◽  
B. P. Jain

1. The process of pulmonary ventilation and gas exchange was investigated in twenty-three young patients with chronic severe anaemia, before and after its correction. 2. Various lung volumes, pulmonary mechanics, minute ventilation, oxygen consumption and carbon dioxide production were found to be normal in anaemic patients. 3. There was a mild respiratory alkalosis in anaemia. The arterial oxygen tension was lowered because of a marked widening of the alveolar-arterial oxygen tension gradient. This was mainly because of an increase in the anatomical shunt as well as ventilation/perfusion inequalities. 4. The transfer factor (pulmonary diffusing capacity) in anaemia was very much reduced. The diffusing capacity of the alveolar capillary membrane was usually decreased and volume of blood in the alveolar capillaries usually increased but these changes were not statistically significant.


1976 ◽  
Vol 41 (2) ◽  
pp. 206-210 ◽  
Author(s):  
L. D. Wood ◽  
A. C. Bryan ◽  
S. K. Bau ◽  
T. R. Weng ◽  
H. Levison

Pulmonary gas exchange was measured in seven resting supine subjects breathing air or a dense gas mixture containing 21% O2 in sulfur hexafluoride (SF6). The mean value of the alveolar-arterial oxygen difference (AaDO2) decreased from 12.4 on air to 7.0 on SF6 (P less than 0.01), and increased again to 13.4 when air breathing resumed (P less than 0.01). No differences occurred between gas mixtures for O2 consumption, respiratory quotient, minute ventilation, breathing frequency, heart rate, or blood pressure, and theimproved oxygen transfer could not be attributed to changes in cardiac output or mixed venous oxygen content in the one subject in which they were measured. These results are best explained by an altered distribution of ventilation during dense gas breathing, so that the ventilation-perfusion ratio(VA/Q) variance was reduced. Of several considered mechanisms, we favor onein which SF6 promotes cardiogenic gas mixing between peripheral parallel units having different alveolar gas concentrations. This mechanism allows forobserved increases in arterial carbon dioxide tension and dead space-to-tidal volume ratio during dense gas breathing, and suggests that intraregionalVA/Q variance accounts for at least one-half of the resting AaDO2 in healthysupine young men.


2014 ◽  
Vol 44 (4) ◽  
pp. 1023-1041 ◽  
Author(s):  
Johan Petersson ◽  
Robb W. Glenny

This review provides an overview of the relationship between ventilation/perfusion ratios and gas exchange in the lung, emphasising basic concepts and relating them to clinical scenarios. For each gas exchanging unit, the alveolar and effluent blood partial pressures of oxygen and carbon dioxide (PO2andPCO2) are determined by the ratio of alveolar ventilation to blood flow (V′A/Q′) for each unit. Shunt and lowV′A/Q′ regions are two examples ofV′A/Q′ mismatch and are the most frequent causes of hypoxaemia. Diffusion limitation, hypoventilation and low inspiredPO2cause hypoxaemia, even in the absence ofV′A/Q′ mismatch. In contrast to other causes, hypoxaemia due to shunt responds poorly to supplemental oxygen. Gas exchanging units with little or no blood flow (highV′A/Q′ regions) result in alveolar dead space and increased wasted ventilation,i.e.less efficient carbon dioxide removal. Because of the respiratory drive to maintain a normal arterialPCO2, the most frequent result of wasted ventilation is increased minute ventilation and work of breathing, not hypercapnia. Calculations of alveolar–arterial oxygen tension difference, venous admixture and wasted ventilation provide quantitative estimates of the effect ofV′A/Q′ mismatch on gas exchange. The types ofV′A/Q′ mismatch causing impaired gas exchange vary characteristically with different lung diseases.


1998 ◽  
Vol 84 (1) ◽  
pp. 327-334 ◽  
Author(s):  
Minakshi Sukumar ◽  
Mahesh Bommaraju ◽  
John E. Fisher ◽  
Frederick C. Morin ◽  
Michele C. Papo ◽  
...  

Sukumar, Minakshi, Mahesh Bommaraju, John E. Fisher, Frederick C. Morin III, Michele C. Papo, Bradley P. Fuhrman, Lynn J. Hernan, and Corinne Lowe Leach. High-frequency partial liquid ventilation in respiratory distress syndrome: hemodynamics and gas exchange. J. Appl. Physiol. 84(1): 327–334, 1998.—Partial liquid ventilation using conventional ventilatory schemes improves lung function in animal models of respiratory failure. We examined the feasibility of high-frequency partial liquid ventilation in the preterm lamb with respiratory distress syndrome and evaluated its effect on pulmonary and systemic hemodynamics. Seventeen lambs were studied in three groups: high-frequency gas ventilation (Gas group), high-frequency partial liquid ventilation (Liquid group), and high-frequency partial liquid ventilation with hypoxia-hypercarbia (Liquid-Hypoxia group). High-frequency partial liquid ventilation increased oxygenation compared with high-frequency gas ventilation over 5 h (arterial oxygen tension 253 ± 21.3 vs. 17 ± 1.8 Torr; P < 0.001). Pulmonary vascular resistance decreased 78% ( P < 0.001), pulmonary blood flow increased fivefold ( P < 0.001), and aortic pressure was maintained ( P < 0.01) in the Liquid group, in contrast to progressive hypoxemia, hypercarbia, and shock in the Gas group. Central venous pressure did not change. The Liquid-Hypoxia group was similar to the Gas group. We conclude that high-frequency partial liquid ventilation improves gas exchange and stabilizes pulmonary and systemic hemodynamics compared with high-frequency gas ventilation. The stabilization appears to be due in large part to improvement in gas exchange.


1981 ◽  
Vol 50 (2) ◽  
pp. 259-264 ◽  
Author(s):  
R. W. Patterson ◽  
A. R. Nissenson ◽  
J. Miller ◽  
R. T. Smith ◽  
R. G. Narins ◽  
...  

With measured values of arterial blood gas tensions, of expired respiratory gas fractions, and volume of the expired ventilation, the determinants of alveolar oxygen tension (PAO2) were used to evaluate their influence on the development of the arterial hypoxemia that occurs in spontaneously breathing patients undergoing hemodialysis using an acetate dialysate. Dialysis produced no significant changes in the alveolar-arterial O2 tension gradient (AaDO2). The extracorporeal dialyzer removed an average of 30 ml.m-2.min-1 of CO2. Accordingly the pulmonary gas exchange ratio (R) dropped from a mean predialysis value of 0.81 to 0.62 (P less than 0.001). The arterial CO2 tension remained constant throughout, whereas the minute ventilation, both total (P less than 0.01) and alveolar (P less than 0.01), decreased during dialysis. This decrease in ventilation accounts for more than 80% of the fall in PAO2. During dialysis there was a decrease (P less than 0.001) in arterial oxygen tension (PaO2), which varied among the individuals from 9 to 23% of control. During the postdialysis hour PaO2 returns to control values concomitant with increase in ventilation. The quantitative gas exchange relationships among R, alveolar ventilation, and AaDO2 predict the PaO2 values actually measured.


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