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

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

 

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).

 

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.

 

(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.)

 

(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.)

They reference the recent hyperpolarised XeMRI lung perfusion studies.