Pathophysiology of dyspnoea in acute pulmonary embolism: A cross‐sectional evaluation

Sanchez, Olivier; Caumont-Prim, Aurore; Riant, Elisabeth; Plantier, Laurent; Dres, Martin; Louis, Bruno; Collignon, Marie‐Anne; Diebold, B.; Meyer, Guy; Peiffer, Claudine; Delclaux, Christophe

doi:10.1111/resp.12961

Cited by 8 publications

(10 citation statements)

References 23 publications

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“…Seven of the 16 patients had Pa CO 2 concentrations above 39 mm Hg (range, 41-49), which, combined with Pa O 2 of less than 60 mm Hg, would be expected to induce dyspnea; we considered these patients to have probable silent hypoxemia (see above vignette for patient MD). Nine patients had Pa CO 2 concentrations below 39 mm Hg (range, [29][30][31][32][33][34][35][36][37], which can blunt the respiratory centers; we do not categorize these patients as having silent hypoxemia (see patient RM and EF vignettes).…”

Section: Dyspnea and Control Of Breathingmentioning

confidence: 99%

“…Increased thrombogenesis has been noted in patients with COVID-19 (35). Thrombi within the pulmonary vasculature can cause severe hypoxemia, and dyspnea is related to pulmonary vascular obstruction and its consequences (36). Dyspnea can also arise from the release of histamine or stimulation of juxtacapillary receptors within the pulmonary vasculature.…”

Section: Mechanism Of Silent Hypoxemiamentioning

confidence: 99%

See 1 more Smart Citation

Why COVID-19 Silent Hypoxemia Is Baffling to Physicians

Tobin

Laghi

Jubran

2020

Am J Respir Crit Care Med

518

498

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Patients with coronavirus disease (COVID-19) are described as exhibiting oxygen levels incompatible with life without dyspnea. The pairing-dubbed happy hypoxia but more precisely termed silent hypoxemia-is especially bewildering to physicians and is considered as defying basic biology. This combination has attracted extensive coverage in media but has not been discussed in medical journals. It is possible that coronavirus has an idiosyncratic action on receptors involved in chemosensitivity to oxygen, but well-established pathophysiological mechanisms can account for most, if not all, cases of silent hypoxemia. These mechanisms include the way dyspnea and the respiratory centers respond to low levels of oxygen, the way the prevailing carbon dioxide tension (Pa CO 2) blunts the brain's response to hypoxia, effects of disease and age on control of breathing, inaccuracy of pulse oximetry at low oxygen saturations, and temperature-induced shifts in the oxygen dissociation curve. Without knowledge of these mechanisms, physicians caring for patients with hypoxemia free of dyspnea are operating in the dark, placing vulnerable patients with COVID-19 at considerable risk. In conclusion, features of COVID-19 that physicians find baffling become less strange when viewed in light of long-established principles of respiratory physiology; an understanding of these mechanisms will enhance patient care if the much-anticipated second wave emerges.

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Section: Dyspnea and Control Of Breathingmentioning

confidence: 99%

Section: Mechanism Of Silent Hypoxemiamentioning

confidence: 99%

Why COVID-19 Silent Hypoxemia Is Baffling to Physicians

Tobin

Laghi

Jubran

2020

Am J Respir Crit Care Med

518

498

View full text Add to dashboard Cite

show abstract

“…However, this may well be an underestimate of the actual duration of symptoms. Since PE is generally a process whereby initially smaller clots and later larger clots embolize to the pulmonary circulation, respiratory symptoms (due to an increase in ventilatory dead space) are expected to be the initial presenting symptoms 18 . It is likely that non-surviving cardiac arrest victims may not have had the opportunity to relate whether they had experienced minor respiratory symptoms in the days preceding the major event.…”

Section: Discussionmentioning

confidence: 99%

Cardiac arrest due to pulmonary embolism

Laher

Richards

2018

Indian Heart Journal

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Pulmonary embolism (PE) is a potentially life threatening clinical condition that is fairly non-specific in presentation. Massive pulmonary embolism (PE) without cardiac arrest has been associated with a mortality rate of 30%. However, when cardiac arrest ensues, mortality may be as high as 95%. Since outcomes of cardiac arrest following PE are generally dismal, any available potentially life-saving measure must be instituted when the diagnosis of PE is suspected. Despite a lack of randomized controlled trials guiding the management of suspected PE in the cardiac arrest victim, thrombolysis and other therapies have been associated with good outcomes in the handful of published case reports and other small studies.

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“…In a prospective study of 90, non‐obese patients with PE, Sanchez et al . investigated the relationship of dyspnoea to measures of vascular obstruction and non‐vascular components such as age, anxiety levels and psychological trait . Although impact measures of dyspnoea (using the MRC scale) were related to vascular obstruction (and sequelae such as PH), the sensory component was also related to age, depression and breathing variability.…”

Section: Pulmonary Vascular Diseasementioning

confidence: 99%