Inspiratory and expiratory resistance cause right-to-left bubble passage through the foramen ovale

Moses, Kayla L.; Seymour, McKayla; Beshish, Arij G.; Baker, Kim R.; Pegelow, David F.; Lamers, Luke; Eldridge, Marlowe W.; Bates, Melissa L.

doi:10.14814/phy2.13719

Cited by 4 publications

(3 citation statements)

References 27 publications

(58 reference statements)

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“…Intrathoracic pressure swings change rhythmically throughout the respiratory cycle and become more negative with a greater inspiratory neural drive. Thus, an increase in ventilation could, theoretically, facilitate a greater blood flow across the PFO due to greater intrathoracic pressure swings (Moses et al., 2018). In the present study, ventilation increased only ∼5 l min −1 from 21% to 10% O 2 (Table 3), which would have changed the magnitude of intrathoracic pressure swings.…”

Section: Discussionmentioning

confidence: 99%

Impaired pulmonary gas exchange efficiency, but normal pulmonary artery pressure increases, with hypoxia in men and women with a patent foramen ovale

Duke

Beasley

Speros

et al. 2020

Experimental Physiology

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New Findings What is the central question of this study?Do individuals with a patent foramen ovale (PFO+) have a larger alveolar‐to‐arterial difference in PnormalO2 (normalAnormal-normalaDO2) than those without (PFO−) and/or an exaggerated increase in pulmonary artery systolic pressure (PASP) in response to hypoxia? What is the main finding and its importance?PFO+ had a greater normalAnormal-normalaDO2 while breathing air, 16% and 14% O2, but not 12% or 10% O2. PASP increased equally in hypoxia between PFO+ and PFO−. These data suggest that PFO+ may not have an exaggerated acute increase in PASP in response to hypoxia. Abstract Patent foramen ovale (PFO) is present in 30–40% of the population and is a potential source of right‐to‐left shunt. Accordingly, those with a PFO (PFO+) may have a larger alveolar‐to‐arterial difference in PnormalO2 (normalAnormal-normalaDO2) than those without (PFO−) in normoxia and with mild hypoxia. Likewise, PFO is associated with high‐altitude pulmonary oedema, a condition known to have an exaggerated pulmonary pressure response to hypoxia. Thus, PFO+ may also have exaggerated pulmonary pressure increases in response to hypoxia. Therefore, the purposes of the present study were to systematically determine whether or not: (1) the normalAnormal-normalaDO2 was greater in PFO+ than in PFO− in normoxia and mild to severe hypoxia and (2) the increase in pulmonary artery systolic pressure (PASP) in response to hypoxia was greater in PFO+ than in PFO−. We measured arterial blood gases and PASP via ultrasound in healthy PFO+ (n = 15) and PFO− (n = 15) humans breathing air and 30 min after breathing four levels of hypoxia (16%, 14%, 12%, 10% O2, randomized and balanced order) at rest. The normalAnormal-normalaDO2 was significantly greater in PFO+ compared to PFO− while breathing air (2.1 ± 0.7 vs. 0.4 ± 0.3 Torr), 16% O2 (1.8 ± 1.2 vs. 0.7 ± 0.8 Torr) and 14% O2 (2.3 ± 1.2 vs. 0.7 ± 0.6 Torr), but not 12% or 10% O2. We found no effect of PFO on PASP at any level of hypoxia. We conclude that PFO influences pulmonary gas exchange efficiency with mild hypoxia, but not the acute increase in PASP in response to hypoxia.

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Section: Discussionmentioning

confidence: 99%

Impaired pulmonary gas exchange efficiency, but normal pulmonary artery pressure increases, with hypoxia in men and women with a patent foramen ovale

Duke

Beasley

Speros

et al. 2020

Experimental Physiology

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“…According to PFO in cryptogenic stroke study (PICSS), a PFO is considered to be present if more than one bubble appears in the LA and if >10 appear in the LA, it is considered as a large PFO [ 25 ]. Recently, it was shown that for a given PFO, the amount of right-to-left contrast shunting is a matter of expiratory pressure during the Valsalva maneuver [ 26 ].…”

Section: Pfo In Childhoodmentioning

confidence: 99%

Patent Foramen Ovale in Fetal Life, Infancy and Childhood

Das

2020

Medical Sciences

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A patent foramen ovale (PFO) is a common, incidental echocardiographic finding in otherwise healthy and asymptomatic infants and children. However, a variety of clinical conditions have been ascribed to the presence of a PFO in childhood, such as cryptogenic stroke, platypnea-orthodeoxia syndrome, decompression sickness and migraine, although the data on these are controversial and sometimes contradictory. This review discusses embryology and correlation with post-natal anatomy, anatomical variations of the atrial septum, diagnostic modalities in special circumstances of PFO associated clinical syndromes, and the role of PFO in congenital heart disease, pulmonary hypertension, dilated cardiomyopathy and heart failure in children who require an extracorporeal membrane oxygenator or ventricular assist device as life support.

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“…• The target tissue must be saturated with inert gas. [13][14][15] Although a large PFO is associated with an increased risk of DCS, testing of divers for PFO is only deemed necessary if divers have a history of cerebral, spinal, vestibular or cutaneous DCS, migraine with aura, cryptogenic stroke or a history of PFO or ASD in a first-degree relative. 16,17 The obvious risk mitigation strategy for such divers is to stop diving or to reduce the probability of post-dive venous gas bubbles by diving more conservatively.…”

Section: Introductionmentioning

confidence: 99%

The effectiveness of risk mitigation interventions in divers with persistent (patent) foramen ovale

Anderson¹,

Ebersole

Covington

et al. 2019

Diving Hyperb Med

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Introduction: Persistent (patent) foramen ovale (PFO) is a recognized risk for decompression sickness (DCS) in divers, which may be mitigated by conservative diving or by PFO closure. Our study aimed to compare the effectiveness of these two risk mitigation interventions. Methods: This was a prospective study on divers who tested positive for PFO or an atrial septal defect (ASD) and either decided to continue diving without closure ('conservative group'), or to close their PFO/ASD and continue diving ('closure group'). Divers' characteristics, medical history, history of diving and history of DCS were reported at enrollment and annually after that. The outcome measures were the incidence rate of DCS, frequency and intensity of diving activities, and adverse events of closure. Results: Divers in both groups dived less and had a lower incidence rate of confirmed DCS than before the intervention. In the closure group (n = 42) the incidence rate of confirmed DCS decreased significantly. Divers with a large PFO experienced the greatest reduction in total DCS. In the conservative group (n = 23), the post-intervention decrease in confirmed DCS incidence rate was not significant. Of note, not all divers returned to diving after closure. Seven subjects reported mild adverse events associated with closure; one subject reported a serious adverse event. Conclusions: PFO closure should be considered on an individual basis. In particular, individuals who are healthy, have a significant DCS burden, a large PFO or seek to pursue advanced diving may benefit from closure.

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Inspiratory and expiratory resistance cause right-to-left bubble passage through the foramen ovale

Cited by 4 publications

References 27 publications

Impaired pulmonary gas exchange efficiency, but normal pulmonary artery pressure increases, with hypoxia in men and women with a patent foramen ovale

Impaired pulmonary gas exchange efficiency, but normal pulmonary artery pressure increases, with hypoxia in men and women with a patent foramen ovale

Patent Foramen Ovale in Fetal Life, Infancy and Childhood

The effectiveness of risk mitigation interventions in divers with persistent (patent) foramen ovale

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