scholarly journals Passive body movement and gas exchange in the frilled lizard (Chlamydosaurus kingii) and goanna (Varanus gouldii).

1998 ◽  
Vol 201 (15) ◽  
pp. 2307-2311 ◽  
Author(s):  
P B Frappell ◽  
J P Mortola
Keyword(s):  
Gas Exchange ◽  
Partial Pressure ◽  
Body Mass ◽  
Time Course ◽  
Body Movement ◽  
Blood Gases ◽  
Pulmonary Gas Exchange ◽  
Body Movements ◽  
Arterial Blood Gas ◽  
Arterial Blood

The saccular lung in lizards is large and highly compliant compared with mammalian lungs, and these properties led us to question to what extent body movements could affect pulmonary gas exchange and the partial pressure of arterial blood gases. Specimens of two species of lizards, the frilled lizard (Chlamydosaurus kingii, approximately 600 g body mass) and the goanna (Varanus gouldii, approximately 1400 mass), were anaesthetised, maintained at approximately 36 degreesC and mechanically hyperventilated to lower the arterial partial pressure of carbon dioxide (PaCO2) to below apnoeic threshold. Respiratory system compliance (Crs) averaged 0. 112 ml kg-1 Pa-1 (goanna) and 0.173 ml kg-1 Pa-1 (frilled lizard), which is approximately 7-11 times the predicted value for a mammal of similar body mass. Mechanical ventilation was interrupted, and the changes in PaCO2 and PaO2 were monitored over the following 10 min as the animal was either left immobile or subjected to imposed lateral body movements. During the post-hyperventilation apnoea, PaCO2 increased whereas PaO2 did not always fall, sometimes even increasing, suggesting a reduction in the importance of pulmonary shunts. No significant differences were detected in the time course of changes in arterial blood gas levels or heart rate between runs with or without body movement. We conclude that in these species of lizards, despite the high Crs, lateral chest wall movements neither hinder nor favour pulmonary gas exchange.

Pulmonary gas exchange during exercise in women: effects of exercise type and work increment

2000 ◽  
Vol 89 (2) ◽  
pp. 721-730 ◽  
Author(s):  
Susan R. Hopkins ◽  
Rebecca C. Barker ◽  
Tom D. Brutsaert ◽  
Timothy P. Gavin ◽  
Pauline Entin ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Gas Exchange ◽  
Blood Gases ◽  
Random Order ◽  
Pulmonary Gas Exchange ◽  
Male Athletes ◽  
Prediction Limit ◽  
Fast Running ◽  
Arterial Blood ◽  
Exercise Induced

Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial Po 2 (PaO2 ) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O2 uptake (V˙o 2 max) = 51 ml · kg−1 · min−1]. They were studied in random order (C or R), with a fastV˙o 2 max protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% ofV˙o 2 max (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in V˙o 2 maxbetween R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of V˙o 2 max. At 90% ofV˙o 2 max, PaO2 was lower during R (mean ± SE = 94 ± 2 Torr) than during C (105 ± 2 Torr, P < 0.0001), as was ventilation (85.2 ± 3.8 vs. 98.2 ± 4.4 l/min btps, P < 0.0001) and cardiac output (19.1 ± 0.6 vs. 21.1 ± 1.0 l/min, P < 0.001). Arterial Pco 2 (32.0 ± 0.5 vs. 30.0 ± 0.6 Torr, P < 0.001) and alveolar-arterial O2 difference (A-aDo 2; 22 ± 2 vs. 16 ± 2 Torr, P < 0.0001) were greater during R. PaO2 and A-aDo 2 were similar between slow and fast. Nadir PaO2 was ≤80 Torr in four women (24%) but only during fast-R. In all subjects, PaO2 atV˙o 2 max was greater than the lower 95% prediction limit calculated from available data in men ( n = 72 C and 38 R) for both R and C. These data suggest intrinsic differences in gas exchange between R and C, due to differences in ventilation and also efficiency of gas exchange. The PaO2 responses to R and C exercise in our 17 subjects do not differ significantly from those previously observed in men.

Measurement of arterial blood gases at the transition from exercise to rest

1983 ◽  
Vol 54 (5) ◽  
pp. 1340-1344 ◽  
Author(s):  
B. M. Lewis
Keyword(s):  
Partial Pressure ◽  
Blood Gases ◽  
Normal Subjects ◽  
Forced Expiratory Volume ◽  
Stair Climbing ◽  
Regulation Of Respiration ◽  
Arterial Blood Gas ◽  
Arterial Partial Pressure ◽  
Arterial Blood ◽  
Two Samples

Arterial blood gas samples obtained 5–20 s after stair-climbing exercise were compared with samples taken during the last 30 s of exercise in 137 subjects. Arterial partial pressure of CO2 (PaCO2) did not change significantly, and in 110 subjects the two samples were within the analytical variation (+/- 2 Torr), supporting the cardiodynamic hypothesis of respiratory regulation. Exceptions to this response were 10 subjects who hyperventilated (PaCO2 less than 34) during exercise and 15 with severe obstruction [forced expiratory volume in 1 s (FEV1) less than 70% forced vital capacity (FVC), and FVC less than 70% of predicted] in whom PaCO2 increased significantly. Overall, arterial partial pressure of O2 (PaO2) increased an average of 3.49 Torr (P less than 0.001). In the two groups in which PaCO2 increased, postexercise PaO2 did not rise. In addition, duration of exercise affected PaO2 response. PaO2 increased significantly more after brief (less than 2 min) periods than after longer (4–6 min) exercise, and this difference increased only when subjects with normal or borderline ventilatory function were analyzed. In 13 subjects in whom a second sample was taken 30–45 s after exercise, the increase in PaO2 was progressive and again the difference between short and long exercise was evident. Regulation of respiration to maintain PaCO2 and changes in O2-CO2 kinetics, leading to an increase in the gas exchange ratio at the exercise-rest transition, are the most likely explanations of these data which establish that the usual response to stopping exercise in normal subjects and most patients is an unchanged PaCO2 and a variable increase in PaO2.

scholarly journals The physiological basis of pulmonary gas exchange: implications for clinical interpretation of arterial blood gases

2014 ◽  
Vol 45 (1) ◽  
pp. 227-243 ◽  
Author(s):  
Peter D. Wagner
Keyword(s):  
Gas Exchange ◽  
Clinical Care ◽  
Physiological State ◽  
Pulmonary Gas Exchange ◽  
The Body ◽  
Blood Gas ◽  
Physiological Basis ◽  
Basic Principles ◽  
Arterial Blood Gas ◽  
Arterial Blood

The field of pulmonary gas exchange is mature, with the basic principles developed more than 60 years ago. Arterial blood gas measurements (tensions and concentrations of O2and CO2) constitute a mainstay of clinical care to assess the degree of pulmonary gas exchange abnormality. However, the factors that dictate arterial blood gas values are often multifactorial and complex, with six different causes of hypoxaemia (inspiratory hypoxia, hypoventilation, ventilation/perfusion inequality, diffusion limitation, shunting and reduced mixed venous oxygenation) contributing variably to the arterial O2and CO2tension in any given patient. Blood gas values are then usually further affected by the body's abilities to compensate for gas exchange disturbances by three tactics (greater O2extraction, increasing ventilation and increasing cardiac output). This article explains the basic principles of gas exchange in health, mechanisms of altered gas exchange in disease, how the body compensates for abnormal gas exchange, and based on these principles, the tools available to interpret blood gas data and, quantitatively, to best understand the physiological state of each patient. This understanding is important because therapeutic intervention to improve abnormal gas exchange in any given patient needs to be based on the particular physiological mechanisms affecting gas exchange in that patient.

Teaching pulmonary gas exchange physiology using computer modeling

2008 ◽  
Vol 32 (1) ◽  
pp. 61-64 ◽  
Author(s):  
Kent S. Kapitan
Keyword(s):  
Gas Exchange ◽  
Teaching Strategy ◽  
Pulmonary Gas Exchange ◽  
Pulmonary Medicine ◽  
Gas Composition ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
The Many ◽  
Relationship Of

Students often have difficulty understanding the relationship of O2 consumption, CO2 production, cardiac output, and distribution of ventilation-perfusion ratios in the lung to the final arterial blood gas composition. To overcome this difficulty, I have developed an interactive computer simulation of pulmonary gas exchange that is web based and allows the student to vary multiple factors simultaneously and observe the final effect on the arterial blood gas composition (available at www.siumed.edu/medicine/pulm/vqmodeling.htm ). In this article, the underlying mathematics of the computer model is presented, as is the teaching strategy. The simulation is applied to a typical clinical case drawn from the intensive care unit to demonstrate the interdependence of the above factors as well as the less-appreciated importance of the Bohr and Haldane effects in clinical pulmonary medicine. The use of a computer to vary the many interacting factors involved in the arterial blood gas composition appeals to today's students and demonstrates the importance of basic physiology to the actual practice of medicine.

Arterial Blood Gases

2014 ◽  
pp. 410-419
Author(s):  
Jeremy B. Richards ◽  
David H. Roberts
Keyword(s):  
Partial Pressure ◽  
Arterial Oxygen Saturation ◽  
Blood Gases ◽  
Altered Mental Status ◽  
Arterial Oxygen ◽  
Acid Base ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Clinical Syndromes ◽  
Acid Base Status

An arterial blood gas (ABG) provides clinically useful information about an individual's acid–base status, the partial pressure of arterial carbon dioxide, the partial pressure of arterial oxygen, and the arterial oxygen saturation. Hypoxia, dyspnea, or suspected acid–base disturbance are clear indications to check an ABG. Altered mental status, critical illness, and acute respiratory distress syndrome (ARDS) are specific clinical syndromes or presentations that warrant checking an ABG. An ABG is helpful in evaluating pulmonary pathophysiology as the presence and severity of hypoxia and/or hypercapnia can be quantified. Because an ABG can rapidly provide information about oxygenation, ventilation, and acid–base status, ABGs are particularly useful and common in the critical care setting.

Ventilation-perfusion relationships during induced normovolemic polycythemia in dogs

1988 ◽  
Vol 65 (4) ◽  
pp. 1686-1692 ◽  
Author(s):  
A. A. Balgos ◽  
D. C. Willford ◽  
J. B. West
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Base Line ◽  
Slight Improvement ◽  
Arterial Blood ◽  
The Mean ◽  
Arterial Po2

Previous studies on normal subjects and patients with polycythemia have given conflicting results of the effect of polycythemia on pulmonary gas exchange. We studied acutely induced normovolemic polycythemia in the dog and measured arterial blood gases and ventilation-perfusion (VA/Q) relationships using the multiple inert gas elimination technique. The mean base-line hematocrit of 43 +/- 5% was increased to 57 +/- 4 and 68 +/- 8%, respectively, after two exchange transfusions of packed erythrocytes. Subsequent plasma exchange transfusions returned the mean hematocrit to 44 +/- 4%. Polycythemia caused no significant arterial hypoxemia; indeed there was a slight improvement in the alveolar-arterial PO2 difference. The multiple inert gas elimination measurements showed no increase in VA/Q inhomogeneity with no increase in log SD ventilation (V) or log SD blood flow (Q). There was a shift of mean V and mean Q to high VA/Q areas because of a decrease in cardiac output, presumably caused by increased blood viscosity. This study showed no deleterious effects on pulmonary gas exchange within the hematocrit range of 36-76%.

Hypoxemia and pulmonary gas exchange during hemodialysis

1981 ◽  
Vol 50 (2) ◽  
pp. 259-264 ◽  
Author(s):  
R. W. Patterson ◽  
A. R. Nissenson ◽  
J. Miller ◽  
R. T. Smith ◽  
R. G. Narins ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Oxygen Tension ◽  
Minute Ventilation ◽  
Arterial Oxygen Tension ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Exchange Relationships ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Alveolar Oxygen

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.

Pulmonary effects of intravenous atropine induce ventilation perfusion mismatch

2014 ◽  
Vol 92 (5) ◽  
pp. 399-404 ◽  
Author(s):  
Romolo J. Gaspari ◽  
David Paydarfar
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Pulmonary Blood Flow ◽  
Gas Analysis ◽  
Pulmonary Gas Exchange ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Anticholinergic Medications ◽  
Arterial Blood ◽  
Intravenous Atropine

Atropine is used for a number of medical conditions, predominantly for its cardiovascular effects. Cholinergic nerves that innervate pulmonary smooth muscle, glands, and vasculature may be affected by anticholinergic medications. We hypothesized that atropine causes alterations in pulmonary gas exchange. We conducted a prospective interventional study with detailed physiologic recordings in anesthetized, spontaneously breathing rats (n = 8). Animals breathing a normoxic gas mixture titrated to a partial arterial pressure of oxygen of 110–120 were exposed to an escalating dose of intravenous atropine (0.001, 0.01, 0.1, 5.0, and 20.0 mg/kg body mass). Arterial blood gas measurements were recorded every 2 min (×5) at baseline, and following each of the 5 doses of atropine. In addition, the animals regional pulmonary blood flow was measured using neutron-activated microspheres. Oxygenation decreased immediately following intravenous administration of atropine, despite a small increase in the volume of inspired air with no change in respiratory rate. Arterial blood gas analysis showed an increase in pulmonary dysfunction, characterized by a widening of the alveolar–arteriole gradient (p < 0.003 all groups except for the lowest dose of atropine). The microsphere data demonstrates an abrupt and marked heterogeneity of pulmonary blood flow following atropine treatment. In conclusion, atropine was found to decrease pulmonary gas exchange in a dose-dependent fashion in this rat model.

scholarly journals Noninvasive measurement of pulmonary gas exchange: comparison with data from arterial blood gases

2019 ◽  
Vol 316 (1) ◽  
pp. L114-L118 ◽  
Author(s):  
John B. West ◽  
Daniel L. Wang ◽  
G. Kim Prisk ◽  
Janelle M. Fine ◽  
Amy Bellinghausen ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Noninvasive Method ◽  
Arterial Blood Gases ◽  
Noninvasive Technique ◽  
Arterial Blood ◽  
End Tidal

A new noninvasive method was used to measure the impairment of pulmonary gas exchange in 34 patients with lung disease, and the results were compared with the traditional ideal alveolar-arterial Po2 difference (AaDO2) calculated from arterial blood gases. The end-tidal Po2 was measured from the expired gas during steady-state breathing, the arterial Po2 was derived from a pulse oximeter if the [Formula: see text] was 95% or less, which was the case for 23 patients. The difference between the end-tidal and the calculated Po2 was defined as the oxygen deficit. Oxygen deficit was 42.7 mmHg (SE 4.0) in this group of patients, much higher than the means previously found in 20 young normal subjects measured under hypoxic conditions (2.0 mmHg, SE 0.8) and 11 older normal subjects (7.5 mmHg, SE 1.6) and emphasizes the sensitivity of the new method for detecting the presence of abnormal gas exchange. The oxygen deficit was correlated with AaDO2 ( R2 0.72). The arterial Po2 that was calculated from the noninvasive technique was correlated with the results from the arterial blood gases ( R2 0.76) and with a mean bias of +2.7 mmHg. The Pco2 was correlated with the results from the arterial blood gases (R2 0.67) with a mean bias of −3.6 mmHg. We conclude that the oxygen deficit as obtained from the noninvasive method is a very sensitive indicator of impaired pulmonary gas exchange. It has the advantage that it can be obtained within a few minutes by having the patient simply breathe through a tube.

scholarly journals Severe Hypoxemia Prevents Spontaneous and Naloxone-induced Breathing Recovery after Fentanyl Overdose in Awake and Sedated Rats

2020 ◽  
Vol 132 (5) ◽  
pp. 1138-1150
Author(s):  
Philippe Haouzi ◽  
Daniel Guck ◽  
Marissa McCann ◽  
Molly Sternick ◽  
Takashi Sonobe ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Oxygen Tension ◽  
Respiratory Rhythm ◽  
Blood Gases ◽  
Rhythmic Activity ◽  
Pulmonary Gas Exchange ◽  
High Dose ◽  
Adult Rats ◽  
Arterial Blood ◽  
Inspired Oxygen

Abstract Background As severe acute hypoxemia produces a rapid inhibition of the respiratory neuronal activity through a nonopioid mechanism, we have investigated in adult rats the effects of hypoxemia after fentanyl overdose-induced apnea on (1) autoresuscitation and (2) the antidotal effects of naloxone. Methods In nonsedated rats, the breath-by-breath ventilatory and pulmonary gas exchange response to fentanyl overdose (300 µg · kg-1 · min-1 iv in 1 min) was determined in an open flow plethysmograph. The effects of inhaling air (nine rats) or a hypoxic mixture (fractional inspired oxygen tension between 7.3 and 11.3%, eight rats) on the ability to recover a spontaneous breathing rhythm and on the effects of naloxone (2 mg · kg-1) were investigated. In addition, arterial blood gases, arterial blood pressure, ventilation, and pulmonary gas exchange were determined in spontaneously breathing tracheostomized urethane-anesthetized rats in response to (1) fentanyl-induced hypoventilation (7 rats), (2) fentanyl-induced apnea (10 rats) in air and hyperoxia, and (3) isolated anoxic exposure (4 rats). Data are expressed as median and range. Results In air-breathing nonsedated rats, fentanyl produced an apnea within 14 s (12 to 29 s). A spontaneous rhythmic activity always resumed after 85.4 s (33 to 141 s) consisting of a persistent low tidal volume and slow frequency rhythmic activity that rescued all animals. Naloxone, 10 min later, immediately restored the baseline level of ventilation. At fractional inspired oxygen tension less than 10%, fentanyl-induced apnea was irreversible despite a transient gasping pattern; the administration of naloxone had no effects. In sedated rats, when Pao2 reached 16 mmHg during fentanyl-induced apnea, no spontaneous recovery of breathing occurred and naloxone had no rescuing effect, despite circulation being maintained. Conclusions Hypoxia-induced ventilatory depression during fentanyl induced apnea (1) opposes the spontaneous emergence of a respiratory rhythm, which would have rescued the animals otherwise, and (2) prevents the effects of high dose naloxone. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

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