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.

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 d-Cystine di(m)ethyl ester reverses the deleterious effects of morphine on ventilation and arterial blood gas chemistry while promoting antinociception

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Benjamin Gaston ◽  
Santhosh M. Baby ◽  
Walter J. May ◽  
Alex P. Young ◽  
Alan Grossfield ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Intracellular Signaling ◽  
Dimethyl Ester ◽  
Diethyl Ester ◽  
Blood Gas ◽  
Negative Effects ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Gas Chemistry ◽  
Ventilatory Drive

AbstractWe have identified thiolesters that reverse the negative effects of opioids on breathing without compromising antinociception. Here we report the effects of d-cystine diethyl ester (d-cystine diEE) or d-cystine dimethyl ester (d-cystine diME) on morphine-induced changes in ventilation, arterial-blood gas chemistry, A-a gradient (index of gas-exchange in the lungs) and antinociception in freely moving rats. Injection of morphine (10 mg/kg, IV) elicited negative effects on breathing (e.g., depression of tidal volume, minute ventilation, peak inspiratory flow, and inspiratory drive). Subsequent injection of d-cystine diEE (500 μmol/kg, IV) elicited an immediate and sustained reversal of these effects of morphine. Injection of morphine (10 mg/kg, IV) also elicited pronounced decreases in arterial blood pH, pO2 and sO2 accompanied by pronounced increases in pCO2 (all indicative of a decrease in ventilatory drive) and A-a gradient (mismatch in ventilation-perfusion in the lungs). These effects of morphine were reversed in an immediate and sustained fashion by d-cystine diME (500 μmol/kg, IV). Finally, the duration of morphine (5 and 10 mg/kg, IV) antinociception was augmented by d-cystine diEE. d-cystine diEE and d-cystine diME may be clinically useful agents that can effectively reverse the negative effects of morphine on breathing and gas-exchange in the lungs while promoting antinociception. Our study suggests that the d-cystine thiolesters are able to differentially modulate the intracellular signaling cascades that mediate morphine-induced ventilatory depression as opposed to those that mediate morphine-induced antinociception and sedation.

scholarly journals The effects of lung volume reduction treatment on diffusing capacity and gas exchange

2020 ◽  
Vol 29 (158) ◽  
pp. 190171
Author(s):  
Marlies van Dijk ◽  
Karin Klooster ◽  
Nick H.T. Ten Hacken ◽  
Frank Sciurba ◽  
Huib. A.M. Kerstjens ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Lung Volume ◽  
Diagnostic Techniques ◽  
Volume Reduction ◽  
Diffusing Capacity ◽  
Blood Gas ◽  
Lung Volume Reduction ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Blood Gas Parameters

Lung volume reduction (LVR) treatment in patients with severe emphysema has been shown to have a positive effect on hyperinflation, expiratory flow, exercise capacity and quality of life. However, the effects on diffusing capacity of the lungs and gas exchange are less clear. In this review, the possible mechanisms by which LVR treatment can affect diffusing capacity of the lung for carbon monoxide (DLCO) and arterial gas parameters are discussed, the use of DLCO in LVR treatment is evaluated and other diagnostic techniques reflecting diffusing capacity and regional ventilation (V′)/perfusion (Q′) mismatch are considered.A systematic review of the literature was performed for studies reporting on DLCO and arterial blood gas parameters before and after LVR surgery or endoscopic LVR with endobronchial valves (EBV). DLCO after these LVR treatments improved (40 studies, n=1855) and the mean absolute change from baseline in % predicted DLCO was +5.7% (range −4.6% to +29%), with no real change in blood gas parameters. Improvement in V′ inhomogeneity and V′/Q′ mismatch are plausible explanations for the improvement in DLCO after LVR treatment.

Alteration in gas exchange related to body position

1990 ◽  
Vol 10 (1) ◽  
pp. 56-59 ◽  
Author(s):  
A Robichaud
Keyword(s):  
Gas Exchange ◽  
Patient Care ◽  
Body Position ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Care Plans ◽  
Arterial Blood

The diagnosis of alteration in gas exchange related to body position requires a deliberate evaluation of PaO2 responses. Body positions that improve V/Q matching and thus PaO2 need to be specified in patient care plans; individualized interventions are more useful than generic care plans that state, "turn q 2 h." Additionally, standard rotations for patients treated on mechanically rotating beds could be individualized according to gas exchange responses to the position changes. Routine documentation of patient body positions next to arterial blood gas results on flow sheets could prove valuable in the evaluation and treatment of hypoxemia in patients with pulmonary problems.

scholarly journals The effects of dobutamine and dopamine on intrapulmonary shunt and gas exchange in healthy humans

2012 ◽  
Vol 113 (4) ◽  
pp. 541-548 ◽  
Author(s):  
Tracey L. Bryan ◽  
Sean van Diepen ◽  
Mohit Bhutani ◽  
Miriam Shanks ◽  
Robert C. Welsh ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Gas Exchange ◽  
Contrast Echocardiography ◽  
Neurological Complications ◽  
Blood Gas ◽  
Intrapulmonary Shunt ◽  
Arterial Blood Gas ◽  
Healthy Humans ◽  
Arterial Blood ◽  
Present Understanding

The development of intrapulmonary shunts with increased cardiac output during exercise in healthy humans has been reported in several recent studies, but mechanisms governing their recruitment remain unclear. Dobutamine and dopamine are inotropes commonly used to augment cardiac output; however, both can increase venous admixture/shunt fraction (Qs/Qt). It is possible that, as with exercise, intrapulmonary shunts are recruited with increased cardiac output during dobutamine and/or dopamine infusion that may contribute to the observed increase in Qs/Qt. The purpose of this study was to examine how dobutamine and dopamine affect intrapulmonary shunt and gas exchange. Nine resting healthy subjects received serial infusions of dobutamine and dopamine at incremental doses under normoxic and hyperoxic (inspired O2fraction = 1.0) conditions. At each step, alveolar-to-arterial Po2difference (A-aDo2) and Qs/Qt were calculated from arterial blood gas samples, intrapulmonary shunt was evaluated using contrast echocardiography, and cardiac output was calculated by Doppler echocardiography. Both dobutamine and dopamine increased cardiac output and Qs/Qt. Intrapulmonary shunt developed in most subjects with both drugs and paralleled the increase in Qs/Qt. A-aDo2was unchanged due to a concurrent rise in mixed venous oxygen content. Hyperoxia consistently eliminated intrapulmonary shunt. These findings contribute to our present understanding of the mechanisms governing recruitment of these intrapulmonary shunts as well as their impact on gas exchange. In addition, given the deleterious effect on Qs/Qt and the risk of neurological complications with intrapulmonary shunts, these findings could have important implications for use of dobutamine and dopamine in the clinical setting.

scholarly journals D-Cystine di(m)ethyl Ester Reverses the Deleterious Effects of Morphine on Ventilation and Arterial Blood Gas Chemistry While Promoting Analgesia

2021 ◽  
Author(s):  
Ben Gaston ◽  
Santhosh M. Baby ◽  
Walter J. May ◽  
Alex P. Young ◽  
Alan Grossfield ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Minute Ventilation ◽  
Dimethyl Ester ◽  
Diethyl Ester ◽  
Blood Gas ◽  
Negative Effects ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Gas Chemistry ◽  
Ventilatory Drive

Abstract We have identified thiolesters that reverse the negative effects of opioids on breathing without compromising analgesia. Here we report the effects of D-cystine diethyl ester (D-cystine diEE) or D-cystine dimethyl ester (D-cystine diME) on morphine-induced changes in ventilation, arterial-blood gas chemistry, A-a gradient (index of gas-exchange in the lungs) and analgesia in freely moving rats. Injection of morphine (10 mg/kg, IV) elicited negative effects on breathing (e.g., depression of tidal volume, minute ventilation, peak inspiratory flow, and inspiratory drive). Subsequent injection of D-cystine diEE (500 mmol/kg, IV) elicited an immediate and sustained reversal of these effects of morphine. Injection of morphine (10 mg/kg, IV) also elicited pronounced decreases in arterial blood pH, pO2 and sO2 accompanied by pronounced increases in pCO2 (all indicative of a decrease in ventilatory drive) and A-a gradient (mismatch in ventilation-perfusion in the lungs). These effects of morphine were reversed in an immediate and sustained fashion by D-cystine diME (500 mmol/kg, IV). Finally, the duration of morphine (5 and 10 mg/kg, IV) analgesia was augmented by D-cystine diEE. D-cystine diEE and D-cystine diME may be clinically useful agents that can effectively reverse the negative effects of morphine on breathing and gas-exchange in the lungs while promoting analgesia.

Physiological Assessment of the Mechanically Ventilated Patient

2017 ◽  
Author(s):  
John W. Kreit
Keyword(s):  
Gas Exchange ◽  
Respiratory Mechanics ◽  
Volume Ratio ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Mechanically Ventilated ◽  
Arterial Blood ◽  
Physiological Assessment ◽  
Gas Measurements ◽  
Normal Ventilation

This chapter reviews the tests that can be used to determine the type and severity of respiratory failure and the extent to which one or more of the components of normal ventilation and gas exchange have been compromised by disease. Physiological Assessment of the Mechanically Ventilated Patient describes the bedside procedures, measurements, and calculations that allow the assessment of gas exchange and respiratory mechanics in mechanically ventilated patients. Topics include co-oximetry and pulse oximetry, arterial blood gas measurements, venous admixture and shunt fraction, the dead space to tidal volume ratio, time- and volume-capnography, measurement of peak and plateau pressures, and calculation of respiratory system compliance and resistance.

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.

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