Tidal Volume Lowering by Instrumental Dead Space Reduction in Brain-Injured ARDS Patients: Effects on Respiratory Mechanics, Gas Exchange, and Cerebral Hemodynamics

Abstract

Background: Limiting tidal volume (V T), plateau pressure, and driving pressure is essential during the acute respiratory distress syndrome (ARDS), but may be challenging when brain injury coexists due to the risk of hypercapnia. Because lowering dead space enhances CO 2 clearance, we conducted a study to determine whether and to what extent replacing heat and moisture exchangers (HME) with heated humidifiers (HH) facilitate safe V T lowering in braininjured patients with ARDS. Methods: Brain-injured patients (head trauma or spontaneous cerebral hemorrhage with Glasgow Coma Scale at admission < 9) with mild and moderate ARDS received three ventilatory strategies in a sequential order during continuous paralysis: (1) HME with V T to obtain a PaCO 2 within 30-35 mmHg (HME1); (2) HH with V T titrated to obtain the same PaCO 2 (HH); and (3) HME1 settings resumed (HME2). Arterial blood gases, static and quasi-static respiratory mechanics, alveolar recruitment by multiple pressure-volume curves, intracranial pressure, cerebral perfusion pressure, mean arterial pressure, and mean flow velocity in the middle cerebral artery by transcranial Doppler were recorded. Dead space was measured and partitioned by volumetric capnography. Results: Eighteen brain-injured patients were studied: 7 (39%) had mild and 11 (61%) had moderate ARDS. At inclusion, median [interquartile range] PaO 2 /FiO 2 was 173 [146-213] and median PEEP was 8 cmH 2 O [5-9]. HH allowed to reduce V T by 120 ml [95% CI: 98-144], V T /kg predicted body weight by 1.8 ml/kg [95% CI: 1.5-2.1], plateau pressure and driving pressure by 3.7 cmH 2 O [2.9-4.3], without affecting PaCO 2 , alveolar recruitment, and oxygenation. This was permitted by lower airway (− 84 ml [95% CI: − 79 to − 89]) and total dead space (− 86 ml [95% CI: − 73 to − 98]). Sixteen patients (89%) showed driving pressure equal or lower than 14 cmH 2 O while on HH, as compared to 7 (39%) and 8 (44%) during HME1 and HME2 (p < 0.001). No changes in mean arterial pressure, cerebral perfusion pressure, intracranial pressure, and middle cerebral artery mean flow velocity were documented during HH.

Removal of a catheter mount and heat-and-moisture exchanger improves hypercapnia in patients with acute respiratory distress syndrome

“…In a prospective observational study of 11 ARDS patients with hypercapnia, the removal of HME (dead space of 100 mL) reduced PaCO 2 levels by 11 ± 5 mm Hg [7] . Subsequently, a prospective study of a small number of ARDS patients reported that the removal of HME significantly improved hypercapnia, confirming the usefulness of this intervention [12–14] . Moreover, in some of these studies, it was possible to achieve lung-protective ventilation by improving hypercapnia [13,14] .…”

Obesity and its implications on cerebral circulation and intracranial compliance in severe COVID‐19

“…In the present study, ICCI was significantly more present among patients with obesity. CHD prevalence was not different between groups, probably because our entire sample was composed by SARS patients, included in early stages of respiratory function depression and mechanical ventilation support, when CHD is commonly observed 31 . Survival and mechanical ventilatory support successful weaning were also significantly higher among non‐obese subjects.…”

Remote ischemic conditioning enhances oxygen supply to ischemic brain tissue in a mouse model of stroke: Role of elevated 2,3-biphosphoglycerate in erythrocytes

“…An adequate oxygen supply to the organs is essential for an organism to be able to function normally. 8,[36][37][38] It is known that interruption of the oxygen supply for just 5 min can cause irreversible brain damage in humans. 9 Blockage of blood flow by thrombosis in ischemic stroke dramatically decreases the oxygen supply to the area distal to the thrombus.…”