Abstract:We propose arterial pCO2 as test to discover vascular access recirculation (VAR) in bicarbonate hemodialysis (HD). We selected 30 HD patients with a ascertained well-functioning arteriovenous fistula (Control). In these patients, we artificially created VAR through the reversion of HD lines (Reversed). Results of the arterial gas analysis were collected at the start of HD (baseline) and after 5 min. At baseline, no differences of pH, pCO2 and HCO3 were found between the 2 group… Show more
“…Blood PCO 2 increases from 36 to 38 mm Hg within the first 15 minutes, and then does not change further until the end of dialysis when it returns to 36 mm Hg. These changes were not statistically significant, but the pattern of change is consistent with previous observations …”
Section: Measurement Resultssupporting
confidence: 90%
“…In either case, organic acid production causes an extra burden on the patient, because the CO 2 produced by the reaction with HCO 3 − adds to the excretory work of the lungs. This workload contributes to the small increase in blood PCO 2 that is characteristic of patients receiving hemodialysis . Finally, as noted earlier, the reaction results in an irreversible loss of alkali during hemodialysis.…”
In patients receiving hemodialysis, it has long been recognized that much more bicarbonate is delivered during treatment than ultimately appears in the blood. To gain insight into this mystery, we developed a model that allows a quantitative analysis of the patient's response to rapid alkalinization during hemodialysis. Our model is unique in that it is based on the distribution of bicarbonate in the extracellular fluid and assesses its removal from this compartment by mobilization of protons (H ) from buffers and other sources. The model was used to analyze the pattern of rise in blood bicarbonate concentration ([HCO ]), calculated from measurements of pH and PCO , in patients receiving standard bicarbonate hemodialysis. Model analysis demonstrated two striking findings: (1) 35% of the bicarbonate added during hemodialysis was due to influx and metabolism of acetate, despite its low concentration in the bath solution, because of the rapidly collapsing gradient for bicarbonate influx. (2) Almost 90% of the bicarbonate delivered to the patients was neutralized by H generation. Virtually all the new H came from intracellular sources and included both buffering and organic acid production. The small amount of added bicarbonate retained in the extracellular fluid increased blood [HCO ], on average, by 6 mEq/L in our patients. Almost all this rise occurred during the first 2 hours. Thereafter, blood [HCO ] changed minimally and always remained less than bath [HCO ]. This lack of equilibrium was due to the continued production of organic acid. Release of H from buffers is a reversible physiological response, restoring body alkali stores. By contrast, organic acid production is an irreversible process during hemodialysis and is metabolically inefficient and potentially catabolic. Our analysis underscores the need to develop new approaches for alkali repletion during hemodialysis that minimize organic acid production.
“…Blood PCO 2 increases from 36 to 38 mm Hg within the first 15 minutes, and then does not change further until the end of dialysis when it returns to 36 mm Hg. These changes were not statistically significant, but the pattern of change is consistent with previous observations …”
Section: Measurement Resultssupporting
confidence: 90%
“…In either case, organic acid production causes an extra burden on the patient, because the CO 2 produced by the reaction with HCO 3 − adds to the excretory work of the lungs. This workload contributes to the small increase in blood PCO 2 that is characteristic of patients receiving hemodialysis . Finally, as noted earlier, the reaction results in an irreversible loss of alkali during hemodialysis.…”
In patients receiving hemodialysis, it has long been recognized that much more bicarbonate is delivered during treatment than ultimately appears in the blood. To gain insight into this mystery, we developed a model that allows a quantitative analysis of the patient's response to rapid alkalinization during hemodialysis. Our model is unique in that it is based on the distribution of bicarbonate in the extracellular fluid and assesses its removal from this compartment by mobilization of protons (H ) from buffers and other sources. The model was used to analyze the pattern of rise in blood bicarbonate concentration ([HCO ]), calculated from measurements of pH and PCO , in patients receiving standard bicarbonate hemodialysis. Model analysis demonstrated two striking findings: (1) 35% of the bicarbonate added during hemodialysis was due to influx and metabolism of acetate, despite its low concentration in the bath solution, because of the rapidly collapsing gradient for bicarbonate influx. (2) Almost 90% of the bicarbonate delivered to the patients was neutralized by H generation. Virtually all the new H came from intracellular sources and included both buffering and organic acid production. The small amount of added bicarbonate retained in the extracellular fluid increased blood [HCO ], on average, by 6 mEq/L in our patients. Almost all this rise occurred during the first 2 hours. Thereafter, blood [HCO ] changed minimally and always remained less than bath [HCO ]. This lack of equilibrium was due to the continued production of organic acid. Release of H from buffers is a reversible physiological response, restoring body alkali stores. By contrast, organic acid production is an irreversible process during hemodialysis and is metabolically inefficient and potentially catabolic. Our analysis underscores the need to develop new approaches for alkali repletion during hemodialysis that minimize organic acid production.
“…If dialysis-related acidemia is found in the arterial line, then vascular access should be inspected for correct needle placement or fistula malfunction because recirculation occurs when blood exiting the filter is not flowing into systemic blood but is reentering the extracorporeal circuit [9] . A more serious problem can occur if dialysisrelated acidemia of venous line is coupled with underlying pulmonary or cardiac disease.…”
“…Moreover, when outflow tract stenosis occurs, slower blood flow and access recirculation are more likely to cause thrombus formation and cause AVF dysfunction. The ultrasound dilution technique or observations combined with measurements of the change in Kt/V and blood gas analysis are recommended to determine if access recirculation has occurred [29-31]. A reference for clinical practice based on this value needs to be established in the future.…”
<b><i>Objective:</i></b> Prepump arterial (Pa) pressure indicates the ease or difficulty with which the blood pump can draw blood from the vascular access (VA) during hemodialysis. Some studies have suggested that the absolute value of the Pa pressure to the extracorporeal blood pump flow (Qb) ratio set on the machine (|Pa/Qb|) can reflect the dysfunction of VA. This study was conducted to explore the impact of arteriovenous fistula (AVF) dysfunction and to explore the clinical reference value of |Pa/Qb|. <b><i>Methods:</i></b> We retrospectively identified adults who underwent hemodialysis at 3 hospitals. Data were acquired from electronic health records. We evaluated the pattern of the association between |Pa/Qb| and AVF dysfunction during 1 year using a Cox proportional hazards regression model with restricted cubic splines. Then, the patients were grouped based on the results, and hazard ratios were compared for different intervals of |Pa/Qb|. <b><i>Results:</i></b> A total of 490 patients were analyzed, with an average age of 55 (44, 66) years. There were a total of 85 cases of AVF dysfunction, of which 50 cases were stenosis and 35 cases were thrombosis. There was a U-shaped association between |Pa/Qb| and the risk of AVF dysfunction (<i>p</i> for nonlinearity <0.001). |Pa/Qb| values <0.30 and >0.52 increased the risk of AVF dysfunction. Compared with the group with a |Pa/Qb| value between 0.30 and 0.52, the groups with |Pa/Qb| <0.30 and |Pa/Qb| >0.52 had a 4.04-fold (<i>p</i> = 0.002) and 3.41-fold (<i>p</i> < 0.001) greater risk of AVF dysfunction, respectively. <b><i>Conclusions:</i></b> The appropriate range of |Pa/Qb| is between 0.30 and 0.52. When |Pa/Qb| is <0.30 or >0.52, the patient’s AVF function or Qb setting should be reevaluated to prevent subsequent failure.
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