Increased intrapulmonary shunt and alveolar dead space post-COVID-19, 2023, Catherine E. Farrow et al

[Mij]

NEW & NOTEWORTHY Using novel methodology quantifying intrapulmonary shunt and alveolar dead space in COVID-19 patients up to 403 days after acute illness, 37% had increased intrapulmonary shunt and 86% had elevated alveolar dead space likely due to independent pathology. Elevated shunt was partially related to severe acute illness, and increased alveolar dead space was weakly related to increasing age. Ventilation was increased in the majority of patients regardless of previous disease severity.

These results demonstrate persisting gas exchange abnormalities after recovery.

https://journals.physiology.org/doi/full/10.1152/japplphysiol.00267.2023

 

[LarsSG]

They don't seem to have any controls in this study or any pre-Covid data, so it's all based on normals for healthy people, which it's not clear these patients were (in fact, some of them were smokers, etc).

 

[SNT Gatchaman]

Abstract
Increased intrapulmonary shunt (QS/Qt) and alveolar dead space (VD/VT) are present in early recovery from 2019 Novel Coronavirus (COVID-19). We hypothesized patients recovering from severe critical acute illness (NIH category 3–5) would have greater and longer lasting increased QS /Q t and VD /V T than patients with mild-moderate acute illness (NIH 1–2).

Fifty-nine unvaccinated patients (33 males, aged 52 [38–61] yr, body mass index [BMI] 28.8 [25.3–33.6] kg/m2 ; median [IQR], 44 previous mildmoderate COVID-19, and 15 severe-critical disease) were studied 15–403 days postacute severe acute respiratory syndrome coronavirus infection. Breathing ambient air, steady-state mean alveolar PCO2, and PO2 were recorded simultaneously with arterial PO 2 /PCO 2 yielding aAPCO2 , AaPO2, and from these, QS /Qt %, VD/VT%, and relative alveolar ventilation (40 mmHg/PA CO2, VArel) were calculated.

Median PaCO2 was 39.4 [35.6–41.1] mmHg, Pa O2 92.3 [87.1–98.2] mmHg; PACO2 32.8 [28.6–35.3] mmHg, PAO2 112.9 [109.4–117.0] mmHg, AaPO2 18.8 [12.6–26.8] mmHg, aAPCO2 5.9 [4.3–8.0] mmHg, QS/Qt 4.3 [2.1–5.9]%, and VD/VT 16.6 [12.6–24.4]%. Only 14% of patients had normal QS/Q t and VD/VT; 1% increased QS/Qt but normal VD/VT; 49% normal QS/Q t and elevated VD/VT; 36% both abnormal QS/Qt and VD/VT. Previous severe critical COVID-19 predicted increased QS /Q t (2.69 [0.82–4.57]% per category severity [95% CI], P < 0.01), but not VD /VT. Increasing age weakly predicted increased VD/V T (1.6 [0.1–3.2]% per decade, P < 0.04). Time since infection, BMI, and comorbidities were not predictors (all P > 0.11). VArel was increased in most patients. In our population, recovery from COVID-19 was associated with increased QS/Qt in 37% of patients, increased VD/VT in 86%, and increased alveolar ventilation up to ~13 mo postinfection. NIH severity predicted QS/Qt but not elevated VD/VT.

Increased VD/VT suggests pulmonary microvascular pathology persists post-COVID-19 in most patients.

 

[SNT Gatchaman]

(Simply, intrapulmonary shunt represents proportion of perfused alveolar-capillary units without gas exchange due to ventilation issues, alveolar dead space represents proportion of ventilated alveoli without gas exchange due to blood flow issues. The latter appears to be the major problem post Covid as shown in fig 4D below.)

They don't seem to have any controls in this study or any pre-Covid data, so it's all based on normals for healthy people

As a validation of methodology used in the present study, we measured intrapulmonary shunt and alveolar dead space in seven healthy adults [no history of COVID-19; 3 males, age 32.9 ± 14.7 yr (means ± SD), body mass index (BMI) 24.6 ± 2.3 kg/m2].

 

[SNT Gatchaman]

(Anatomical dead space represents the conducting airways, moving air from nose to terminal bronchioles that can't be involved in gas-exchange. Total/physiological dead space = anatomical + alveolar.)

Methodological controls in this study fell within or close to published values for the 95% confidence levels for shunt (5%), and alveolar dead space (10%) in healthy adults. The advantages of this technique are that it directly measures alveolar gas, allowing accurate estimation of intrapulmonary shunt and alveolar dead space. [...] When compared to estimates of Bohr-Enghoff dead space, our measurements of alveolar dead space are less, likely as a consequence of anatomical dead space included in the Bohr-Enghoff dead space.

In a recent editorial, this methodology was described as a big step forward in gas exchange physiology which should be applied to other pulmonary conditions. Indeed, this methodology represents a simple bedside test which can be used more widely than other methods such as multiple inert gas elimination technique.

The increase in alveolar dead space implies reduced regional alveolar perfusion relative to the ventilation and may be a consequence of persistent vascular damage, redistribution of blood flow from vascular obstruction, or hypoxic pulmonary vasoconstriction in those portions of the lung. Microembolic disease is reported in the acute infection, and plasma samples in post-COVID19 patients with persistent COVID-19 symptoms 6 mo after their acute illness have increased microclots in their circulation.

They reference the recent hyperpolarised XeMRI lung perfusion studies.

It remains to be determined whether the shunt, alveolar dead space, and ventilation abnormalities observed in some post-COVID-19 patients are related to the cluster of symptoms known as “long COVID”, and whether they persist even longer or eventually resolve over time.