Dependence of phrenic motoneurone output on the oscillatory component of arterial blood gas composition.

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.

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Respiratory response of turtles (Pseudemys scripta) to changes in arterial blood gas composition

Comparative Biochemistry and Physiology ◽

10.1016/0010-406x(69)90055-3 ◽

1969 ◽

Vol 31 (4) ◽

pp. 535-546 ◽

Cited By ~ 31

Author(s):

H.M Frankel ◽

A Spitzer ◽

J Blaine ◽

E.P Schoener

Keyword(s):

Gas Composition ◽

Blood Gas ◽

Respiratory Response ◽

Arterial Blood Gas ◽

Arterial Blood ◽

Pseudemys Scripta

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Blood gas changes during and after nonspecific airway challenge in asthmatic and normal subjects

Journal of Applied Physiology ◽

10.1152/jappl.1989.67.6.2627 ◽

1989 ◽

Vol 67 (6) ◽

pp. 2627-2630 ◽

Cited By ~ 17

Author(s):

R. Dal Negro ◽

L. Allegra

Keyword(s):

Healthy Volunteers ◽

Normal Subjects ◽

Forced Expiratory Volume ◽

Base Line ◽

Gas Composition ◽

Flow Volume ◽

Blood Gas ◽

Arterial Blood Gas ◽

Arterial Blood ◽

Gas Measurements

Twenty-eight asymptomatic asthmatics and 28 healthy volunteers were challenged with ultrasonically nebulized distilled water (UNDW). Blood gas composition was monitored transcutaneously (PtCO2 and PtcCO2) over 42 min (20 min for electrode stability, 3 min base line, 5 min during UNDW, and 14 min after UNDW). Flow-volume curves were recorded before and 15 min after UNDW. Forced expiratory volume in 1 s and expiratory flows decreased in asthmatics but not in normal subjects after UNDW. Mean base-line PtCO2 and PtcCO2 were comparable in the two groups. UNDW in normal subjects produced no significant changes in mean PtcCO2 and PtCO2. In asthmatics, the UNDW-induced decrease in mean PtcCO2 was greater and longer lasting, accompanied by a prolonged decrease in mean PtCO2. PtcCO2 and PtCO2 trends showed highly significant differences compared with healthy volunteers (P less than 0.001). Arterial blood gas measurements validated these changes. UNDW in asymptomatic asthmatics gives rise to a greater and more prolonged hyperventilation than in normal subjects and to gas-exchange abnormalities presumably reflecting a ventilation-perfusion mismatching.

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Matching and mismatching ventilation and perfusion in the lung

Critical Care Nurse ◽

10.4037/ccn1996.16.3.23 ◽

1996 ◽

Vol 16 (3) ◽

pp. 23-27 ◽

Cited By ~ 6

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.

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Non-severe community-accuired pneumonia: clinic functional characteristics and diagnosing optimization

Bulletin of Siberian Medicine ◽

10.20538/1682-0363-2009-1-7-13 ◽

2009 ◽

Vol 8 (1) ◽

pp. 7-13

Author(s):

T. S. Ageyeva

Keyword(s):

Clinical Symptom ◽

Community Acquired Pneumonia ◽

Acute Stage ◽

Composition Analysis ◽

Gas Composition ◽

Blood Gas ◽

Arterial Blood Gas ◽

Arterial Blood ◽

Pulmonary Infiltration ◽

Severe Community Acquired Pneumonia

200 patients with non-severe community-acquired pneumonia (CAP) in an acute stage underwent analysis of registration frequency for main clinical symptom s and syndrome s. They were analyzed depending on type and extent of pulmonary infiltration and CAP etiology. Their value for CAP diagnosing was also studied. The value of arterial blood gas composition analysis for formation of functional component of non-severe CAP clinical diagnosis was demonstrated.

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Effects of histamine on bronchial artery blood flow and bronchomotor tone

Journal of Applied Physiology ◽

10.1152/jappl.1985.59.1.254 ◽

1985 ◽

Vol 59 (1) ◽

pp. 254-261 ◽

Cited By ~ 34

Author(s):

W. M. Long ◽

C. L. Sprung ◽

H. el Fawal ◽

L. D. Yerger ◽

P. Eyre ◽

...

Keyword(s):

Blood Flow ◽

Bronchial Artery ◽

Base Line ◽

Gas Composition ◽

Artery Blood Flow ◽

Blood Gas ◽

Pulmonary Hemodynamics ◽

Arterial Blood Gas ◽

Arterial Blood ◽

H2 Antagonist

The effects of aerosolized 5% histamine (10 breaths) on bronchial artery blood flow (Qbr), airflow resistance (RL), and pulmonary and systemic hemodynamics were studied in mechanically ventilated sheep anesthetized with pentobarbital sodium. Histamine increased mean Qbr and RL to 252 +/- 45 and 337 +/- 53% of base line, respectively. This effect was significantly different from base line for 30 min after challenge. The histamine-induced increase in RL was blocked by pretreatment with the histamine H1 receptor antagonist, chlorpheniramine, whereas the histamine-induced elevation in Qbr was prevented by the H2 antagonist, metiamide. Both responses were blocked only when both antagonists were present. Changes in Qbr were not directly associated with alterations in systemic and pulmonary hemodynamics or arterial blood gas composition. In vitro histamine caused a dose-dependent contraction of ovine bronchial artery strips that was prevented by H1 antagonist. The H2 agonist, impromidine, caused relaxation of precontracted arterial strips and was more potent and efficacious than histamine, whereas H1 agonists failed to elicit a relaxant response. Thus these findings indicate that histamine aerosol induces a vasodilation in the bronchial vascular bed; histamine has a direct effect on Qbr that is independent of alterations in RL, systemic and pulmonary hemodynamics, or arterial blood gas composition; and, histamine-induced bronchoconstriction is mediated predominantly by H1-receptors, whereas increased Qbr is controlled predominantly by H2-receptors, probably located in resistance vessels. This local effect of histamine on Qbr may have important implications in the pathophysiology of bronchial asthma and pulmonary edema.

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Influence of Bohr-Haldane effect on steady-state gas exchange

Journal of Applied Physiology ◽

10.1152/jappl.1982.52.5.1330 ◽

1982 ◽

Vol 52 (5) ◽

pp. 1330-1337 ◽

Cited By ~ 12

Author(s):

B. J. Grant

Keyword(s):

Steady State ◽

Gas Exchange ◽

Venous Blood ◽

Gas Composition ◽

Blood Gas ◽

Arterial Blood Gas ◽

Arterial Blood ◽

Venous Blood Gas ◽

Mixed Venous ◽

Haldane Effect

The influence of the Bohr-Haldane effect (BH) on steady-state gas exchange has previously been described by its effect of gas transfer from the blood when arterial and venous blood gas tensions were held constant. This report quantifies by computer analysis the effects of BH when either or both arterial and venous blood gas tensions are subject to change. When mixed venous blood gas composition is held constant, elimination of BH from a single lung unit typically reduces CO2 output by 6.5% and O2 uptake by 0.5%. Similar effects occur in a two-compartment lung model whether alveolar ventilation-perfusion (VA/Q) mismatch occurs in a parallel or series ventilatory arrangement. When arterial blood gas composition is held constant, elimination of BH increases systemic venous CO2 partial pressure, but O2 partial pressure is hardly affected in the absence of metabolic acidosis. When both mixed venous and arterial blood gas tensions vary and gas exchange is stressed by VA/Q inequality, altitude, anemia, or exercise, elimination of BH predominantly affects mixed venous rather than arterial blood gas tensions. it is concluded that BH may act primarily to reduce tissue acidosis.

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The interaction of pulmonary ventilation and the right-left shunt on arterial oxygen levels.

Journal of Experimental Biology ◽

10.1242/jeb.199.10.2121 ◽

1996 ◽

Vol 199 (10) ◽

pp. 2121-2129 ◽

Cited By ~ 14

Author(s):

T Wang ◽

J W Hicks

Keyword(s):

Blood Gases ◽

Arterial Oxygen ◽

Alternative Mechanism ◽

Relative Importance ◽

Gas Composition ◽

Blood Gas ◽

Arterial Blood Gases ◽

Arterial Blood Gas ◽

Arterial Blood ◽

Lower Vertebrates

In adult mammals, arterial blood gases closely reflect lung gas composition, and arterial blood gases can, therefore, be effectively regulated through changes in ventilation. This is not the case among most ectothermic vertebrates, where the systemic and pulmonary circulations are not completely separated, resulting in central vascular shunts. In the presence of a right-to-left shunt (R-L shunt), the O2 levels (PO2 and haemoglobin O2-saturation) of systemic arterial blood are depressed relative to those of the blood returning from the lungs. Arterial blood gas composition is, accordingly, not determined only by ventilation, but also by the magnitude of admixture as well as the blood gas composition of systemic venous blood. Changes in the central shunt patterns, therefore, represent an alternative mechanism by which to control arterial blood gas levels. The primary aim of this report is to evaluate the relative importance of the R-L shunt and ventilation in determining arterial blood gas levels. Using standard equations for gas exchange and the two-compartment model, we predicted arterial O2 levels at physiologically relevant levels of ventilation, R-L shunt and blood flows. The analyses show that the effects of changing ventilation and the size of the R-L shunt on arterial O2 levels vary with parameters such as the rate of O2 uptake, the blood O2-carrying capacity and the level of hypoxia. The relative importance of ventilation and the R-L shunt in determining arterial PO2 values is largely explained by the sigmoidal shape of the O2 dissociation curve. Thus, if lung PO2 is high relative to blood O2 affinity, a large change in ventilation may have little effect on pulmonary venous O2 content, although PO2 may have changed considerably. If an R-L shunt is taking place, this, in turn, implies that arterial O2 content is affected only marginally, with a correspondingly small effect on PO2. These predictions are discussed in the light of the limited existing experimental data on cardiac shunts in lower vertebrates; we propose that, in future experiments, the measurement of both ventilatory and cardiovascular parameters must be combined if we aim to understand the regulation of arterial blood gas levels in lower vertebrates.

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Atrial fibrillation associated with carbon monoxide poisoning

Undersea and Hyperbaric Medicine ◽

10.22462/04.06.2019.14 ◽

2019 ◽

pp. 203-206

Author(s):

Mevlut Demir ◽

◽

Muslum Sahin ◽

Ahmet Korkmaz ◽

◽

...

Keyword(s):

Atrial Fibrillation ◽

Carbon Monoxide ◽

Sinus Rhythm ◽

Partial Pressure ◽

Motor Vehicle ◽

Carbon Monoxide Poisoning ◽

Venous Blood ◽

Blood Gas ◽

Arterial Blood Gas ◽

Arterial Blood

Carbon monoxide intoxication occurs usually via inhalation of carbon monoxide that is emitted as a result of a fire, furnace, space heater, generator, motor vehicle. A 37-year-old male patient was admitted to the emergency department at about 5:00 a.m., with complaints of nausea, vomiting and headache. He was accompanied by his wife and children. His venous blood gas measures were: pH was 7.29, partial pressure of carbon dioxide (pCO2) was 42 mmHg, partial pressure of oxygen (pO2) was 28 mmHg, carboxyhemoglobin (COHb) was 12.7% (reference interval: 0.5%-2.5%) and oxygen saturation was 52.4%. Electrocardiogram (ECG) examination showed that the patient was not in sinus rhythm but had atrial fibrillation. After three hours the laboratory examination was repeated: Troponin was 1.2 pg/ml and in the arterial blood gas COHb was 3%. The examination of the findings on the monitor showed that the sinus rhythm was re-established. The repeated ECG examination confirmed the conversion to the sinus rhythm. He was monitored with the normobaric oxygen administration.

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

Scientific Reports ◽

10.1038/s41598-021-89455-2 ◽

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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