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 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.

Matching and mismatching ventilation and perfusion in the lung

1996 ◽  
Vol 16 (3) ◽  
pp. 23-27 ◽  
Author(s):  
RS Misasi ◽  
JL Keyes
Keyword(s):  
Blood Flow ◽  
Regional Differences ◽  
Pulmonary Blood Flow ◽  
Healthy Adults ◽  
Gas Composition ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Different Types ◽  
Ventilation And Perfusion

Arterial blood-gas composition is determined by ventilation, pulmonary blood flow, and by how ventilation is matched to blood flow in the lungs. In healthy adults there are regional differences in both ventilation and blood flow in the lungs and the distribution of blood flow tends to parallel that of ventilation. Ventilation and blood flow can become mismatched in a variety of disease processes that affect the lungs. Mismatching of ventilation and perfusion causes decreased PaO2, may change PaCO2, and increases AaDO2 difference. Many different types of interventions are frequently necessary to treat mismatching of ventilation and perfusion.

Mechanisms of improvement in pulmonary gas exchange during isovolemic hemodilution

1999 ◽  
Vol 87 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Steven Deem ◽  
Richard G. Hedges ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Michael K. Alberts ◽  
...  
Keyword(s):  
Blood Flow ◽  
Fractal Dimension ◽  
Gas Exchange ◽  
Spatial Correlation ◽  
Pulmonary Blood Flow ◽  
Minute Ventilation ◽  
Flow Distribution ◽  
Pulmonary Gas Exchange ◽  
Normal Lung ◽  
Blood Flow Distribution

Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240–246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (V˙a/Q˙) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 ± 1.6 to 11 ± 1%. Anemia was associated with an increase in arterial [Formula: see text] in comparison with controls ( P < 0.01 between groups). The improvement in O2 exchange was associated with reducedV˙a/Q˙heterogeneity, a reduction in the fractal dimension of pulmonary blood flow ( P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow ( P = 0.04). Expired NO increased with anemia, whereas it remained stable in control animals ( P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overallV˙a/Q˙matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability.

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.

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