Evidence map›Paper›PMID 25085889›Full record

ArticleThe Journal of physiology2014

Increased cardiac output, not pulmonary artery systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O2.

Jonathan E Elliott, Joseph W Duke, Jerold A Hawn, John R Halliwill, Andrew T Lovering

Abstract read
In one paragraph

Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed.

  1. Trial
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  7. Hyperoxia-induced stepwise reduction in blood flow through intrapulmonary, but not intracardiac, shunt during exercise.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
  8. Oxygen uptake (Frontiers in physiology · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Jonathan E ElliottUniversity of Oregon, Department of Human Physiology, Eugene, OR, USA.
Joseph W DukeUniversity of Oregon, Department of Human Physiology, Eugene, OR, USA.
Jerold A HawnOregon Heart and Vascular Institute, Cardiology, Springfield, OR, USA.
John R HalliwillUniversity of Oregon, Department of Human Physiology, Eugene, OR, USA.
Andrew T LoveringUniversity of Oregon, Department of Human Physiology, Eugene, OR, USA lovering@uoregon.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blood flow through intrapulmonary arteriovenous anastomoses (IPAVAs) has been demonstrated to increase in healthy humans during a variety of conditions; however, whether or not this blood flow represents a source of venous admixture (Q̇ VA /Q̇T) that impairs pulmonary gas exchange efficiency (i.e. increases the alveolar-to-arterial PO2 difference (A-aDO2)) remains controversial and unknown. We hypothesized that blood flow through IPAVAs does provide a source of Q̇ VA /Q̇T. To test this, blood flow through IPAVAs was increased in healthy humans at rest breathing room air and 40% O2: (1) during intravenous adrenaline (epinephrine) infusion at 320 ng kg(-1) min(-1) (320 ADR), and (2) with vagal blockade (2 mg atropine), before and during intravenous adrenaline infusion at 80 ng kg(-1) min(-1) (ATR + 80 ADR). When breathing room air the A-aDO2 increased by 6 ± 2 mmHg during 320 ADR and by 5 ± 2 mmHg during ATR + 80 ADR, and the change in calculated Q̇ VA /Q̇T was +2% in both conditions. When breathing 40% O2, which minimizes contributions from diffusion limitation and alveolar ventilation-to-perfusion inequality, the A-aDO2 increased by 12 ± 7 mmHg during 320 ADR, and by 9 ± 6 mmHg during ATR + 80 ADR, and the change in calculated Q̇ VA /Q̇T was +2% in both conditions. During 320 ADR cardiac output (Q̇T) and pulmonary artery systolic pressure (PASP) were significantly increased; however, during ATR + 80 ADR only Q̇T was significantly increased, yet blood flow through IPAVAs as detected with saline contrast echocardiography was not different between conditions. Accordingly, we suggest that blood flow through IPAVAs provides a source of intrapulmonary shunt, and is mediated primarily by increases in Q̇T rather than PASP.

Indexed as

Blood PressureCardiac OutputAdultAirArteriovenous AnastomosisFemaleHumansMaleOxygenOxygen Inhalation TherapyPulmonary ArteryVentilation-Perfusion RatioOxygen

Identifiers

PMID25085889
PMCPMC4287743

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.