Dynamics of Venturi Jet Ventilation through the Operating Laryngoscope

1982 ◽  
Vol 91 (6) ◽  
pp. 615-621 ◽  
Author(s):  
Peak Woo ◽  
Stephen Eurenius

Venturi jet ventilation with the oxygen injector needle placed within the lumen of the laryngoscope was studied systematically in two dogs undergoing repeated general anesthesia suspension laryngoscopy. Using a total body plethysmograph, the effect of changes of needle angle, position and its effect on tidal volume delivery were measured. The changes of pressure regulator, flow rate and needle size were correlated with the volume delivery. Intratracheal pressure during Venturi ventilation was measured. Correlation of arterial blood gases and minute ventilation with the system was done. While ventilatory capacity is able to be achieved predictably, there are many variables. Optimal placement of the needle tip for maximum safety and efficiency appears to be at the midthird or lower third of the laryngoscope. It is important to center the needle axis to the laryngoscope axis. Other parameters subject to choice are the selection of needle size, regulator pressure setting and flow rate setting. By first selecting the correct needle size that will hyperinflate the subject, the pressure regulator can then be reduced to achieve ventilatory volumes similar to spontaneous tidal volumes. In prolonged use, the Venturi system was able to provide excellent ventilation safely and predictably.

1983 ◽  
Vol 55 (5) ◽  
pp. 1574-1581 ◽  
Author(s):  
J. P. Kiley ◽  
M. R. Fedde

To determine the importance of nonhumoral drives to exercise hyperpnea in birds, we exercised adult White Pekin ducks on a treadmill (3 degrees incline) at 1.44 km X h-1 for 15 min during unidirectional artificial ventilation. Intrapulmonary gas concentrations and arterial blood gases could be regulated with this ventilation procedure while allowing ventilatory effort to be measured during both rest and exercise. Ducks were ventilated with gases containing either 4.0 or 5.0% CO2 in 19% O2 (balance N2) at a flow rate of 12 l X min-1. At that flow rate, arterial CO2 partial pressure (PaCO2) could be maintained within +/- 2 Torr of resting values throughout exercise. Arterial O2 partial pressure did not change significantly with exercise. Heart rate, mean arterial blood pressure, and mean right ventricular pressure increased significantly during exercise. On the average, minute ventilation (used as an indicator of the output from the central nervous system) increased approximately 400% over resting levels because of an increase in both tidal volume and respiratory frequency. CO2-sensitivity curves were obtained for each bird during rest. If the CO2 sensitivity remained unchanged during exercise, then the observed 1.5 Torr increase in PaCO2 during exercise would account for only about 6% of the total increase in ventilation over resting levels. During exercise, arterial [H+] increased approximately 4 nmol X l-1; this increase could account for about 18% of the total rise in ventilation. We conclude that only a minor component of the exercise hyperpnea in birds can be accounted for by a humoral mechanism; other factors, possibly from muscle afferents, appear responsible for most of the hyperpnea observed in the running duck.


1985 ◽  
Vol 59 (6) ◽  
pp. 1955-1960 ◽  
Author(s):  
B. R. Walker ◽  
E. M. Adams ◽  
N. F. Voelkel

As a fossorial species the hamster differs in its natural habitat from the rat. Experiments were performed to determine possible differences between the ventilatory responses of awake hamsters and rats to acute exposure to hypoxic and hypercapnic environments. Ventilation was measured with the barometric method while the animals were conscious and unrestrained in a sealed plethysmograph. Tidal volume (VT), respiratory frequency (f), and inspiratory (TI) and expiratory (TE) time measurements were made while the animals breathed normoxic (30% O2), hypercapnic (5% CO2), or hypoxic (10% O2) gases. Arterial blood gases were also measured in both species while exposed to each of these atmospheric conditions. During inhalation of normoxic gas, the VT/100 g was greater and f was lower in the hamster than in the rat. Overall minute ventilation (VE/100 g) in the hamster was less than in the rat, which was reflected in the lower PO2 and higher PCO2 of the hamster arterial blood. When exposed to hypercapnia, the hamster increased VE/100 g solely through VT; however, the VE/100 g increase was significantly less than in the rat. In response to hypoxia, the hamster and rat increased VE/100 g by similar amounts; however, the hamster VE/100 g increase was through f alone, whereas the rat increased both VT/100 g and f. Mean airflow rates (VT/TI) were no different in the hamster or rat in each gas environment; therefore most of the ventilatory responses were the result of changes in TI and TE and respiratory duty cycle (TI/TT).


2016 ◽  
Vol 120 (2) ◽  
pp. 282-296 ◽  
Author(s):  
Michael M. Tymko ◽  
Ryan L. Hoiland ◽  
Tomas Kuca ◽  
Lindsey M. Boulet ◽  
Joshua C. Tremblay ◽  
...  

Our aim was to quantify the end-tidal-to-arterial gas gradients for O2 (PET-PaO2) and CO2 (Pa-PETCO2) during a CO2 reactivity test to determine their influence on the cerebrovascular (CVR) and ventilatory (HCVR) response in subjects with (PFO+, n = 8) and without (PFO−, n = 7) a patent foramen ovale (PFO). We hypothesized that 1) the Pa-PETCO2 would be greater in hypoxia compared with normoxia, 2) the Pa-PETCO2 would be similar, whereas the PET-PaO2 gradient would be greater in those with a PFO, 3) the HCVR and CVR would be underestimated when plotted against PETCO2 compared with PaCO2, and 4) previously derived prediction algorithms will accurately target PaCO2. PETCO2 was controlled by dynamic end-tidal forcing in steady-state steps of −8, −4, 0, +4, and +8 mmHg from baseline in normoxia and hypoxia. Minute ventilation (V̇E), internal carotid artery blood flow (Q̇ICA), middle cerebral artery blood velocity (MCAv), and temperature corrected end-tidal and arterial blood gases were measured throughout experimentation. HCVR and CVR were calculated using linear regression analysis by indexing V̇E and relative changes in Q̇ICA, and MCAv against PETCO2, predicted PaCO2, and measured PaCO2. The Pa-PETCO2 was similar between hypoxia and normoxia and PFO+ and PFO−. The PET-PaO2 was greater in PFO+ by 2.1 mmHg during normoxia ( P = 0.003). HCVR and CVR plotted against PETCO2 underestimated HCVR and CVR indexed against PaCO2 in normoxia and hypoxia. Our PaCO2 prediction equation modestly improved estimates of HCVR and CVR. In summary, care must be taken when indexing reactivity measures to PETCO2 compared with PaCO2.


1962 ◽  
Vol 17 (5) ◽  
pp. 771-774 ◽  
Author(s):  
Herman F. Froeb

The ventilatory stimulation arising from two different forms of passively induced body motion was chosen for study of 14 male emphysematous subjects with hypercapnia and impaired ventilatory response to carbon dioxide. Nine normal males served as controls. The object of the study was to determine whether the stimulus to ventilation from passive body motion was intact in diseased subjects and whether it could serve as a therapeutic tool by bringing about a reduction in blood carbon dioxide. The results revealed that the stimulus to ventilation was mild and comparable in both groups but was associated with two to three times more oxygen per extra liter of minute ventilation in the diseased subjects. There were no significant changes in the arterial blood gases. It was concluded that the stimulus to ventilation from passive body motion arises from weak muscle action and has no therapeutic application in emphysematous subjects as a means of lowering the PaCOCO2. Note: (With the Technical Assistance of Mabel Pearson, Roy Engstrom, Christa McReynolds, and Carol Kennedy) Submitted on March 5, 1962


1988 ◽  
Vol 64 (5) ◽  
pp. 1870-1877 ◽  
Author(s):  
M. A. Bureau ◽  
J. L. Carroll ◽  
E. Canet

This study was undertaken to measure the neonate's response to CO-induced hypoxia in the first 10 days of life. CO breathing was used to induce hypoxia because CO causes tissue hypoxia with no or minimal chemoreceptor stimulation. An inspired gas mixture of 0.25 to 0.5% CO in air was used to raise the blood carboxyhemoglobin (HbCO) progressively from 0 to 60% over approximately 20 min. The study, conducted in awake conscious lambs aged 2 and 10 days, consisted in measuring the response of ventilation and the change in arterial blood gases during the rise of HbCO. The results showed that the 2- and 10-day-old lambs tolerated very high HbCO levels without an increase in minute ventilation (VE) and without metabolic acidosis. At both ages, HbCO caused no VE change until HbCO levels rose to between 45 and 50% after which the VE change was exponential in some animals but minimal in others. The VE change was brought about by a rise in tidal volume and respiratory frequency. During the period of maturation from 2 to 10 days, there was a small shift to the right in the VE-HbCO response. In the 10-day-old lambs the VE response to high HbCO was greater than that of the 2-day-olds because of the lambs' higher respiratory frequency response. Six of the 10-day-old lambs but only two of the 2-day-old lambs showed a hypoxic tachypnea to HbCO of 55–65%. None of the lambs developed periodic breathing, dysrhythmic breathing, or recurrent apneas with an HbCO level as high as 60%.(ABSTRACT TRUNCATED AT 250 WORDS)


1975 ◽  
Vol 38 (5) ◽  
pp. 819-826 ◽  
Author(s):  
K. R. Kollmeyer ◽  
L. I. Kleinman

An extracorporeal venovenous shunt system utilizing a membrane oxygenator to alter venous blood gases was used to study the regulation of ventilation in 28 newborn and 4 adult dogs. There was no effect of the extracorporeal circuit per se (without the oxygenator in the system) on essential cardiovascular or respiratory function. When the puppies were placed on the extracorporeal circuit with the oxygenator in the system to effect changes in mixed venous blood gas composition there was a significant increase in venous P02 (Pv02), a decrease in venous Pco2 (Pvco2), a rise in venous pH (PHv), and a marked fall in minute ventilation (VE). There were no significant changes in cardiovascular function or arterial blood gases to account for the depression of ventilation. Acute changes in Pvo2 produced appropriate directional changes of VE under conditions where other arterial and venous blood gases were held constant. At a low Pvco2/Paco2 ratio, ventilation was depressed compared to those conditions with a high ratio. At any Pvc02/Paco2 ratio, ventilation could be depressed by raising the Pvo2. In adult animals ventilation could not be altered by changing venous blood gases. These experiments support the existence of a respiratory chemoreceptor sensitive to both PO2 and PCO2 in the prepulmonary or venous circulation of the newborn animal.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sophia Gutweniger ◽  
Tsogyal D. Latshang ◽  
Sayaka S. Aeschbacher ◽  
Fabienne Huber ◽  
Deborah Flueck ◽  
...  

AbstractThis trial evaluates whether nocturnal oxygen therapy (NOT) during a stay at 2048 m improves altitude-induced exercise intolerance in lowlanders with chronic obstructive pulmonary disease (COPD). 32 lowlanders with moderate to severe COPD, mean ± SD forced expiratory volume in the first second of expiration (FEV1) 54 ± 13% predicted, stayed for 2 days at 2048 m twice, once with NOT, once with placebo according to a randomized, crossover trial with a 2-week washout period at < 800 m in-between. Semi-supine, constant-load cycle exercise to exhaustion at 60% of maximal work-rate was performed at 490 m and after the first night at 2048 m. Endurance time was the primary outcome. Additional outcomes were cerebral tissue oxygenation (CTO), arterial blood gases and breath-by-breath measurements (http://www.ClinicalTrials.gov NCT02150590). Mean ± SE endurance time at 490 m was 602 ± 65 s, at 2048 m after placebo 345 ± 62 s and at 2048 m after NOT 293 ± 60 s, respectively (P < 0.001 vs. 490 m). Mean difference (95%CI) NOT versus placebo was − 52 s (− 174 to 70), P = 0.401. End-exercise pulse oximetry (SpO2), CTO and minute ventilation ($${\dot{\text{V}}}_{{\text{E}}}$$ V ˙ E ) at 490 m were: SpO2 92 ± 1%, CTO 65 ± 1%, $${\dot{\text{V}}}_{{\text{E}}}$$ V ˙ E 37.7 ± 2.0 L/min; at 2048 m with placebo: SpO2 85 ± 1%, CTO 61 ± 1%, $${\dot{\text{V}}}_{{\text{E}}}$$ V ˙ E  40.6 ± 2.0 L/min and with NOT: SpO2 84 ± 1%; CTO 61 ± 1%; $${\dot{\text{V}}}_{{\text{E}}}$$ V ˙ E  40.6 ± 2.0 L/min (P < 0.05, SpO2, CTO at 2048 m with placebo vs. 490 m; P = NS, NOT vs. placebo). Altitude-related hypoxemia and cerebral hypoxia impaired exercise endurance in patients with moderate to severe COPD and were not prevented by NOT.


1983 ◽  
Vol 54 (3) ◽  
pp. 803-808 ◽  
Author(s):  
S. Matalon ◽  
M. S. Nesarajah ◽  
J. A. Krasney ◽  
L. E. Farhi

We studied the cardiorespiratory effects of acute hypercapnia in 10 unanesthetized sheep. After a 15-min exposure to either 7.3 or 10% CO2 in air, we measured arterial blood gases, minute ventilation (VE), O2 consumption (VO2), cardiac output (Q), heart rate (HR), an index of left ventricular contractility [(dP/dt)/P], and vascular pressures. In addition, regional flows to all major organs were determined by injecting 15-microns radiolabeled microspheres into the left heart. Exposure to 7.3% CO2 (arterial CO2 partial pressure, PaCO2, 58 Torr) resulted in increased VE, (dP/dt)/P, and higher blood flows to the brain and respiratory muscles. All other variables remained unchanged. Exposure to 10% CO2 (PaCO2 75 Torr) resulted in a further augmentation of VE and a 48% increase in Q, which was associated with a tachycardia, a decrease in systemic vascular resistance, and an increase in VO2. Coronary and respiratory muscle flows increased, but all other variables remained unchanged. Thus the hemodynamic effects of hypercapnia are not related linearly to the level of PaCO2.


1990 ◽  
Vol 4 (6) ◽  
pp. 2
Author(s):  
D.R. Goldhill ◽  
A.J. Hill ◽  
R.H. Whitburn ◽  
R.O. Feneck ◽  
J. George ◽  
...  

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