The effect of acute ventilation-perfusion mismatch on respiratory heat exchange in a porcine model

Background Respiratory heat exchange is an important physiological process occurring in the upper and lower respiratory tract and is usually completed when inspired gases reach the alveoli. Animal and human studies demonstrated that heat exchange can be modulated by altering pulmonary ventilation and perfusion. The purpose of this study was to examine the effect of acute ventilation-perfusion (V/Q) mismatch on respiratory heat exchange. In clinical practice, monitoring respiratory heat exchange might offer the possibility of real-time tracking of acute V/Q-mismatch. Methods In 11 anesthetized, mechanically ventilated pigs, V/Q-mismatch was established by means of four interventions: single lung ventilation, high cardiac output, occlusion of the left pulmonary artery and repeated whole-lung lavage. V/Q-distributions were determined by the multiple inert gas elimination technique (MIGET). Respiratory heat exchange was measured as respiratory enthalpy using the novel, pre-commercial VQm™ monitor (development stage, Rostrum Medical Innovations, Vancouver, CA). According to MIGET, shunt perfusion of low V/Q compartments increased during single lung ventilation, high cardiac output and whole-lung lavage, whereas dead space and ventilation of high V/Q compartments increased during occlusion of the left pulmonary artery and whole-lung lavage. Results Bohr dead space increased after pulmonary artery occlusion and whole-lung lavage, venous admixture increased during single lung ventilation and whole-lung lavage, PaO2/FiO2 was decreased during all interventions. MIGET confirmed acute V/Q-mismatch. Respiratory enthalpy did not change significantly despite significant acute V/Q-mismatch. Conclusion Clinically relevant V/Q-mismatch does not impair respiratory heat exchange in the absence of additional thermal stressors and may not have clinical utility in the detection of acute changes.

The impact of ventilation - perfusion inequality in COVID-19: a computational model

COVID-19 infection may lead to an Acute Respiratory Distress Syndrome where severe gas exchange derangements may be associated, at least in the early stages, only with minor pulmonary infiltrates. This suggests that the shunt associated to the gasless lung parenchyma is not sufficient to explain CARDS hypoxemia. We designed an algorithm (VentriQlar), based on the same conceptual grounds described by J.B West in 1969. We set 499 ventilation-perfusion (VA/Q) compartments and, after calculating their blood composition (PO2, PCO2 and pH), we randomly chose 106 combinations of five parameters controlling a bimodal distribution of blood flow. The solutions were accepted if the predicted PaO2 and PaCO2 were within 10% of the patient's values. We assumed that shunt fraction equaled the fraction of non-aerated lung tissue at the CT quantitative analysis. Five critically-ill patients later deceased were studied. The PaO2/FiO2 was 91.1±18.6 mmHg and PaCO2 69.0±16.1 mmHg. Cardiac output was 9.58±0.99 l/min. The fraction of non-aerated tissue was 0.33±0.06. The model showed that a large fraction of the blood flow was likely distributed in regions with very low VA/Q (Qmean=0.06±0.02) and a smaller fraction in regions with moderately high VA/Q. Overall LogSD, Q was 1.66 ± 0.14, suggestive of high VA/Q inequality. Data suggest that shunt alone cannot completely account for the observed hypoxemia and a significant VA/Q inequality must be present in COVID-19. The high cardiac output and the extensive microthrombosis later found in the autopsy further support the hypothesis of a pathological perfusion of non/poorly ventilated lung tissue.

P1354POSTOPERATIVE MATURATION AND CHANGES IN CARDIAC FUNCTION DIFFER BETWEEN TYPES OF VASCULAR ACCESS

Background and Aims The blood flow of vascular access can be increased about tens of times after access creation. If the flow of vascular access is too low, vascular access does not provide sufficient circulation for hemodialysis and sometimes gets thrombosed. However, if the flow of vascular access is too high, it can result in high cardiac output and trigger heart failure. Although patients receiving hemodialysis require vascular access with necessary and sufficient flow, the actual change in flow after access creation is not well known. We investigated the relationships among preoperative factors, types of vascular access, clinical courses of access maturation, and changes in cardiac function. Method This single-center retrospective observational study included patients who underwent vascular access-related surgery, except thrombectomy, in 2016. Diameters and flow volumes of the brachial artery were examined using Doppler ultrasound before surgery and 1 week, 12 months, and 24 months after surgery. Cardiac functions were assessed using sonography at the same timepoints. Patients’ background information and data related to surgery, such as anastomosis size, were extracted from medical records. The obtained data were statistically analyzed. Results Fifty-eight patients [37 arteriovenous fistula (AVF), 10 arteriovenous graft (AVG), and 11 partial replacement using grafts (PR)] participated in this study. Diameters of the brachial artery increased from 4.7 mm to 5.4 mm at 1 week after access surgery. Blood flows of the brachial artery also increased from 106 mL/min to 699 mL/min. Blood flow through AVG at 1week was significantly higher than that through AVF (940 ml/min vs. 589 ml/min). Although blood flow through AVF at 12 and 24 months after access creation was significantly increased than that at 1 week after access creation, blood flow through AVG at 12 and 24 months after access creation did not show significant changes, and blood flow through PR at 12 and 24 months after access creation was significantly decreased. AVG and PR required more catheter intervention for vascular access than AVF during this observational period. Preoperative blood flow of the brachial artery and cardiac outputs were positively correlated to postoperative blood flow through AVF. However, this relationship was not observed in AVG and PR cases. The amount of cardiac output increased from 4.2 L/min before surgery to 4.4 L/min and 4.6 L/min at 12 and 24 months, respectively, although not significantly. Cardiac output at 24 months after surgery significantly increased only in AVF cases. Conclusion The clinical maturation course after vascular access creation surgery differs between AVF and AVG cases. Because blood flow through AVF is likely to increase gradually after access creation, surgeons should consider cardiac stresses related to vascular access, especially in cases with high-flow brachial artery or high cardiac output before surgery. Blood flow through AVG is not likely to increase in the long course. However, because blood flow through AVG just after access creation is high, regardless of the brachial artery size, surgeons should consider the risk of arteriovenous access-related ischemic steal syndrome after surgery especially in cases with severe arteriosclerosis. PR is not likely to affect blood flow volume of accesses and cardiac function.