INTRODUCTION. The ability of the kidney to excrete H+ ions as urinary ammonium (NH4+U) varies according to physiological needs and alterations of acid–base equilibrium [1,2]. However, the renal response to respiratory acid–base alterations has been traditionally considered as slow. OBJECTIVES. To elucidate whether a short-term period of hyper- and hypo-ventilation inducing alterations of plasmatic pH within normal ranges may lead to a rapid modification of urinary pH (pHU), and concentrations of NH4+U and others electrolytes. METHODS. We enrolled eight patients admitted to a post-operative ICU after major surgery. Patients were connected through their urinary catheter to a urinary analyzer (K.IN.G —Kidney INstant MonitorinG) [3], allowing quasi-continuous measurements of pHU, and urinary NH4+U concentration. After 30 min, an arterial blood sample was collected, and patients were randomly assigned to either a one-third reduction of their basal minute ventilation (hypo-ventilation, with arterial pH—pHa[7.40) for 2 h, or a one-third increase of their basal minute ventilation (hyper-ventilation, with pHa\7.40) for 1 h. Ventilation was then moved back to baseline ventilatory setting, and observation period lasted 4 h. Blood-gases and end-tidal CO2 (ETCO2) were monitored through the entire study period. RESULTS. In patients undergoing hypoventilation (n = 4), ETCO2 and PaCO2 progressively increased from 31 ± 3 to 41 ± 3 and from 32 ± 2 to 45 ± 5 mmHg (p\0.01) respectively, while pHa decreased from 7.45 ± 0.01 to 7.35 ± 0.01 (p\0.01). Such variations were paralleled by a slight reduction in pHU (from 5.6 ± 0.4 to 5.2 ± 0.2) and an increase in NH4+U from 4.7 ± 1.6 to 6.1 ± 2.2 mEq/L (p = ns for both). When considering the time difference to achieve the maximal variation, such increase was close to the statistical significance (up to 6.9 ± 2.2 mEq/L, p = 0.06). In patients undergoing hyperventilation (n = 4), ETCO2 and PaCO2 progressively decreased from 34 ± 2 to 29 ± 2 and from 40 ± 3 to 32 ± 4 mmHg (p\0.01) respectively, while pHa increased from 7.40 ± 0.03 to 7.47 ± 0.05 (p\0.01). Similarly, pHU rapidly increased from 5.1 ± 0.1 to 6.0 ± 0.5 (p = 0.04), and NH4+U decreased (from 10.0 ± 2.9 to 2.9 ± 2.4 mEq/L, p = 0.02). Time for achieving maximal NH4+U variation was significantly shorter in patients undergoing hyperventilation than in those undergoing hypoventilation (75 ± 10 vs. 150 ± 24 min, p = 0.03). Diuresis and hemodynamics remained stable throughout the study. CONCLUSIONS. Assessing pHU and NH4+U variations may be a non-invasive method to monitor PaCO2 variations during acid–base respiratory alterations. REFERENCES. 1. Barker ES, et al. The renal response in man to acute experimental respiratory alkalosis and acidosis. J Clin Invest. 1957;36:515–29. 2. Pitts RF. Control of renal production of ammonia. Kidney Int. 1972;1:297–305. 3. Caironi P, et al. Kidney instant monitoring (K.IN.G): a new analyzer to monitor kidney function. Minerva Anestesiol. 2010;76:316–24.

Acute variation of urinary ph and ammonium during controlled hypo- and hyper-ventilation : a preliminary report / P. Caironi, L. Zazzeron, C. Rovati, E. Scotti, M. Ferrari, D. Ottolina, M. Chiodi, C. Marenghi, L. Gattinoni. - In: INTENSIVE CARE MEDICINE. - ISSN 0342-4642. - 38:Suppl. 1(2012), pp. S192-S192. (Intervento presentato al 21. convegno European Society of Intensive Care Medicine Annual Congress tenutosi a Lisbõa nel 2012).

Acute variation of urinary ph and ammonium during controlled hypo- and hyper-ventilation : a preliminary report

P. Caironi;L. Gattinoni
2012

Abstract

INTRODUCTION. The ability of the kidney to excrete H+ ions as urinary ammonium (NH4+U) varies according to physiological needs and alterations of acid–base equilibrium [1,2]. However, the renal response to respiratory acid–base alterations has been traditionally considered as slow. OBJECTIVES. To elucidate whether a short-term period of hyper- and hypo-ventilation inducing alterations of plasmatic pH within normal ranges may lead to a rapid modification of urinary pH (pHU), and concentrations of NH4+U and others electrolytes. METHODS. We enrolled eight patients admitted to a post-operative ICU after major surgery. Patients were connected through their urinary catheter to a urinary analyzer (K.IN.G —Kidney INstant MonitorinG) [3], allowing quasi-continuous measurements of pHU, and urinary NH4+U concentration. After 30 min, an arterial blood sample was collected, and patients were randomly assigned to either a one-third reduction of their basal minute ventilation (hypo-ventilation, with arterial pH—pHa[7.40) for 2 h, or a one-third increase of their basal minute ventilation (hyper-ventilation, with pHa\7.40) for 1 h. Ventilation was then moved back to baseline ventilatory setting, and observation period lasted 4 h. Blood-gases and end-tidal CO2 (ETCO2) were monitored through the entire study period. RESULTS. In patients undergoing hypoventilation (n = 4), ETCO2 and PaCO2 progressively increased from 31 ± 3 to 41 ± 3 and from 32 ± 2 to 45 ± 5 mmHg (p\0.01) respectively, while pHa decreased from 7.45 ± 0.01 to 7.35 ± 0.01 (p\0.01). Such variations were paralleled by a slight reduction in pHU (from 5.6 ± 0.4 to 5.2 ± 0.2) and an increase in NH4+U from 4.7 ± 1.6 to 6.1 ± 2.2 mEq/L (p = ns for both). When considering the time difference to achieve the maximal variation, such increase was close to the statistical significance (up to 6.9 ± 2.2 mEq/L, p = 0.06). In patients undergoing hyperventilation (n = 4), ETCO2 and PaCO2 progressively decreased from 34 ± 2 to 29 ± 2 and from 40 ± 3 to 32 ± 4 mmHg (p\0.01) respectively, while pHa increased from 7.40 ± 0.03 to 7.47 ± 0.05 (p\0.01). Similarly, pHU rapidly increased from 5.1 ± 0.1 to 6.0 ± 0.5 (p = 0.04), and NH4+U decreased (from 10.0 ± 2.9 to 2.9 ± 2.4 mEq/L, p = 0.02). Time for achieving maximal NH4+U variation was significantly shorter in patients undergoing hyperventilation than in those undergoing hypoventilation (75 ± 10 vs. 150 ± 24 min, p = 0.03). Diuresis and hemodynamics remained stable throughout the study. CONCLUSIONS. Assessing pHU and NH4+U variations may be a non-invasive method to monitor PaCO2 variations during acid–base respiratory alterations. REFERENCES. 1. Barker ES, et al. The renal response in man to acute experimental respiratory alkalosis and acidosis. J Clin Invest. 1957;36:515–29. 2. Pitts RF. Control of renal production of ammonia. Kidney Int. 1972;1:297–305. 3. Caironi P, et al. Kidney instant monitoring (K.IN.G): a new analyzer to monitor kidney function. Minerva Anestesiol. 2010;76:316–24.
Settore MED/41 - Anestesiologia
2012
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/212715
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