Mechanical ventilation: looking for new paradigms.
Explore the source record for details and available documents.
Acute Disease↗
Biomedical subjects
Gastón Murias
Publications and source records attributed to Gastón Murias.
Effects of levosimendan in normodynamic endotoxaemia: a controlled experimental study.
OBJECTIVES: Levosimendan is an inotropic and vasodilator drug that has proved to be useful in cardiogenic shock. Pretreatment with levosimendan in experimental hypodynamic septic shock in pigs has shown valuable effects in oxygen transport. Our goal was to assess the effects of levosimendan in a normodynamic model of endotoxaemia. METHODS: Twelve sheep were anaesthetized and mechanically ventilated. After taking basal haemodynamic and oxygen transport measurements, sheep were assigned to two groups during 120 min: (1) endotoxin (5 microg/kg endotoxin); (2) levosimendan (5 microg/kg endotoxin plus levosimendan 200 microg/kg followed by 200 microg/kg/h). Both groups received hydration of 20 ml/kg/h of saline solution. RESULTS: In the endotoxin group, cardiac output, intestinal blood flow and systemic and intestinal oxygen transports and consumptions (DO(2) and VO(2)) remained unchanged. In the levosimendan group, systemic and intestinal DO(2) were significantly higher than in the endotoxin group. Because stroke volume did not change (basal versus 120': 0.9+/-0.1 ml/kg versus 0.9+/-0.2 ml/kg, p=0.3749), the elevation in cardiac output by levosimendan (145+/-17 ml/min/kg versus 198+/-16 ml/min/kg, p=0.0096) was related to an increased heart rate (159+/-32 beats l/min versus 216+/-19 beats l/min, p=0.0037). Levosimendan precluded the development of gut intramucosal acidosis at 120' (endotoxin versus levosimendan, ileal intramucosal-arterial PCO(2) difference: 19+/-4 Torr versus 10+/-4 Torr, p=0.0025). However, levosimendan decreased mean arterial blood pressure (99+/-20 Torr versus 63+/-13 Torr, p=0.0235) and increased blood lactate levels (2.4+/-0.9 mmol/l versus 4.8+/-1.5 mmol/l, p=0.0479). All p-values are differences in specific points (paired or unpaired t-test with Bonferroni correction) after two-way repeated measures ANOVA. A p-value<0.05 was considered significant. CONCLUSIONS: Levosimendan improved oxygen transport and prevented the development of intramucosal acidosis in this experimental model of endotoxaemia. However, systemic hypotension and lactic acidosis occurred. Additional studies are needed to show if different doses and timing of levosimendan administration in septic shock might improve gut perfusion without adverse effects.
Acidosis↗
Contributions of vascular flow and pulmonary capillary pressure to ventilator-induced lung injury.
OBJECTIVE: To evaluate the influence of vascular flow on ventilator-induced lung injury independent of vascular pressures. DESIGN: Laboratory study. SETTING: Hospital laboratory. SUBJECTS: Thirty-two New Zealand White rabbits. INTERVENTIONS: Thirty-two isolated perfused rabbit lungs were allocated into four groups: low flow/low pulmonary capillary pressure; high flow/high pulmonary capillary pressure; low flow/high pulmonary capillary pressure, and high flow/low pulmonary capillary pressure. All lungs were ventilated with peak airway pressure 30 cm H2O and positive end-expiratory pressure 5 cm H2O for 30 mins. MEASUREMENTS AND MAIN RESULTS: Outcome measures included frequency of gross structural failure (pulmonary rupture), pulmonary hemorrhage, edema formation, changes in lung compliance, pulmonary vascular resistance, and pulmonary ultrafiltration coefficient. Lungs exposed to high pulmonary vascular flow ruptured more frequently, displayed more hemorrhage, developed more edema, suffered larger decreases in compliance, and had larger increases in vascular resistance than lungs exposed to low vascular flows (p < .05 for each pairwise comparison between groups). CONCLUSIONS: These findings suggest that high pulmonary vascular flows might exacerbate ventilator-induced lung injury independent of their effects on pulmonary vascular pressures.
Animals↗
Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study.
INTRODUCTION: Continuous monitoring of bladder partial carbon dioxide tension (PCO2) using fibreoptic sensor technology may represent a useful means by which tissue perfusion may be monitored. In addition, its changes might parallel tonometric gut PCO2. Our hypothesis was that bladder PCO2, measured using saline tonometry, will be similar to ileal PCO2 during ischaemia and reperfusion. METHOD: Six anaesthetized and mechanically ventilated sheep were bled to a mean arterial blood pressure of 40 mmHg for 30 min (ischaemia). Then, blood was reinfused and measurements were repeated at 30 and 60 min (reperfusion). We measured systemic and gut oxygen delivery and consumption, lactate and various PCO2 gradients (urinary bladder-arterial, ileal-arterial, mixed venous-arterial and mesenteric venous-arterial). Both bladder and ileal PCO2 were measured using saline tonometry. RESULTS: After bleeding systemic and intestinal oxygen supply dependency and lactic acidosis ensued, along with elevations in PCO2 gradients when compared with baseline values (all values in mmHg; bladder DeltaPCO2 3 +/- 3 versus 12 +/- 5, ileal DeltaPCO2 9 +/- 5 versus 29 +/- 16, mixed venous-arterial PCO2 5 +/- 1 versus 13 +/- 4, and mesenteric venous-arterial PCO2 4 +/- 2 versus 14 +/- 4; P < 0.05 versus basal for all). After blood reinfusion, PCO2 gradients returned to basal values except for bladder DeltaPCO2, which remained at ischaemic levels (13 +/- 7 mmHg). CONCLUSION: Tissue and venous hypercapnia are ubiquitous events during low flow states. Tonometric bladder PCO2 might be a useful indicator of tissue hypoperfusion. In addition, the observed persistence of bladder hypercapnia after blood reinfusion may identify a territory that is more susceptible to reperfusion injury. The greatest increase in PCO2 gradients occurred in gut mucosa. Moreover, the fact that ileal DeltaPCO2 was greater than the mesenteric venous-arterial PCO2 suggests that tonometrically measured PCO2 reflects mucosal rather than transmural PCO2. Ileal DeltaPCO2 appears to be the more sensitive marker of ischaemia.
Analysis of Variance↗
Increased blood flow prevents intramucosal acidosis in sheep endotoxemia: a controlled study.
INTRODUCTION: Increased intramucosal-arterial carbon dioxide tension (PCO2) difference (DeltaPCO2) is common in experimental endotoxemia. However, its meaning remains controversial because it has been ascribed to hypoperfusion of intestinal villi or to cytopathic hypoxia. Our hypothesis was that increased blood flow could prevent the increase in DeltaPCO2. METHODS: In 19 anesthetized and mechanically ventilated sheep, we measured cardiac output, superior mesenteric blood flow, lactate, gases, hemoglobin and oxygen saturations in arterial, mixed venous and mesenteric venous blood, and ileal intramucosal PCO2 by saline tonometry. Intestinal oxygen transport and consumption were calculated. After basal measurements, sheep were assigned to the following groups, for 120 min: (1) sham (n = 6), (2) normal blood flow (n = 7) and (3) increased blood flow (n = 6). Escherichia coli lipopolysaccharide (5 microg/kg) was injected in the last two groups. Saline solution was used to maintain blood flood at basal levels in the sham and normal blood flow groups, or to increase it to about 50% of basal in the increased blood flow group. RESULTS: In the normal blood flow group, systemic and intestinal oxygen transport and consumption were preserved, but DeltaPCO2 increased (basal versus 120 min endotoxemia, 7 +/- 4 versus 19 +/- 4 mmHg; P < 0.001) and metabolic acidosis with a high anion gap ensued (arterial pH 7.39 versus 7.35; anion gap 15 +/- 3 versus 18 +/- 2 mmol/l; P < 0.001 for both). Increased blood flow prevented the elevation in DeltaPCO2 (5 +/- 7 versus 9 +/- 6 mmHg; P = not significant). However, anion-gap metabolic acidosis was deeper (7.42 versus 7.25; 16 +/- 3 versus 22 +/- 3 mmol/l; P < 0.001 for both). CONCLUSIONS: In this model of endotoxemia, intramucosal acidosis was corrected by increased blood flow and so might follow tissue hypoperfusion. In contrast, anion-gap metabolic acidosis was left uncorrected and even worsened with aggressive volume expansion. These results point to different mechanisms generating both alterations.
Acid-Base Equilibrium↗
Massive brain injury enhances lung damage in an isolated lung model of ventilator-induced lung injury.
OBJECTIVE: To assess the influence of massive brain injury on pulmonary susceptibility to injury attending subsequent mechanical or ischemia/reperfusion stress. DESIGN: Prospective experimental study. SETTING: Animal research laboratory. SUBJECTS: Twenty-four anesthetized New Zealand White rabbits randomized to control (n = 12) or induced brain injury (n = 12) group. INTERVENTIONS: After randomization, brain injury was induced by inflation of an intracranial balloon-tipped catheter, and animals were ventilated with a tidal volume of 10 mL/kg and zero end-expiratory pressure for 120 mins. Following heart-lung block extraction, isolated and perfused lungs were subjected to injurious ventilation with peak airway pressure 30 cm H2O and positive end-expiratory pressure 5 cm H2O for 30 mins. MEASUREMENTS AND MAIN RESULTS: No difference was observed between groups in gas exchange, lung mechanics, or hemodynamics during the 2-hr in vivo period following induction of brain injury. However, after 30 mins of ex vivo injurious mechanical ventilation, lungs from the brain injury group showed greater change in ultrafiltration coefficient, weight gain, and alveolar hemorrhage (all p < .05). CONCLUSIONS: Massive brain injury might increase lung vulnerability to subsequent injurious mechanical or ischemia-reperfusion insults, thereby increasing the risk of clinical posttransplant graft failure.
Animals↗
Intramucosal-arterial Pco2 gradient does not reflect intestinal dysoxia in anemic hypoxia.
BACKGROUND: An increase in intramucosal-arterial Pco2 gradient (DeltaPco2) might be caused by tissue hypoxia or by diminished blood flow. Our hypothesis was that DeltaPco2 should not be altered in anemic hypoxia with preserved blood flow. METHODS: In 18 anesthetized, mechanically ventilated sheep, oxygen transport was stepwise reduced by hemorrhage (hypovolemia, n = 9) or by hemorrhage and simultaneous dextran infusion (hemodilution, n = 9). RESULTS: Hypovolemia and hemodilution produced comparable decreases in systemic and intestinal oxygen transport and uptake. However, mixed venoarterial and mesenteric venoarterial Pco2 gradients and DeltaPco2 were significantly higher in hypovolemia than in hemodilution (25 +/- 5 vs. 10 +/- 2 mm Hg; 21 +/- 6 vs. 10 +/- 5 mm Hg; and 41 +/- 18 vs. 14 +/- 9 mm Hg, respectively; p < 0.01). CONCLUSION: DeltaPco2 did not reflect intestinal dysoxia during Vo2/Do2 dependency attributable to hemodilution. Blood flow seems to be the main determinant of DeltaPco2.
Analysis of Variance↗
Intramucosal-arterial PCO2 gap fails to reflect intestinal dysoxia in hypoxic hypoxia.
INTRODUCTION: An elevation in intramucosal-arterial PCO2 gradient (DeltaPCO2) could be determined either by tissue hypoxia or by reduced blood flow. Our hypothesis was that in hypoxic hypoxia with preserved blood flow, DeltaPCO2 should not be altered. METHODS: In 17 anesthetized and mechanically ventilated sheep, oxygen delivery was reduced by decreasing flow (ischemic hypoxia, IH) or arterial oxygen saturation (hypoxic hypoxia, HH), or no intervention was made (sham). In the IH group (n = 6), blood flow was lowered by stepwise hemorrhage; in the HH group (n = 6), hydrochloric acid was instilled intratracheally. We measured cardiac output, superior mesenteric blood flow, gases, hemoglobin, and oxygen saturations in arterial blood, mixed venous blood, and mesenteric venous blood, and ileal intramucosal PCO2 by tonometry. Systemic and intestinal oxygen transport and consumption were calculated, as was DeltaPCO2. After basal measurements, measurements were repeated at 30, 60, and 90 minutes. RESULTS: Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption. No changes occurred in the sham group. DeltaPCO2 increased in the IH group (12 +/- 10 [mean +/- SD] versus 40 +/- 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 +/- 6 versus 10 +/- 13 mmHg and 8 +/- 5 versus 9 +/- 6 mmHg; not significant). DISCUSSION: In this experimental model of hypoxic hypoxia with preserved blood flow, DeltaPCO2 was not modified during dependence of oxygen uptake on oxygen transport. These results suggest that DeltaPCO2 might be determined primarily by blood flow.
Analysis of Variance↗
Recruitment maneuvers during lung protective ventilation in acute respiratory distress syndrome.
The objective was to analyze the physiologic effects of recruitment maneuvers (RM) in 17 patients with acute respiratory distress syndrome (ARDS) ventilated with a lung protective strategy. RM consisted of 2 min of pressure-controlled ventilation at a peak pressure of 50 cm H(2)O and a positive end-expiratory pressure (PEEP) above the upper inflection point of the respiratory pressure-volume curve obtained at zero PEEP. In eight patients, RM were repeated in the late phase of ARDS. Oxygenation did not change 15 min after RM in the early and late phase of ARDS. When Pa(O(2))/fraction of inspired oxygen (FI(O(2))) increased during RM, venous admixture (Q VA/Q T) decreased. The opposite occurred in patients in whom Pa(O(2))/FI(O(2)) decreased during RM. RM-induced changes in cardiac output were not observed. A significant correlation was found between RM-induced changes in Pa(O(2))/FI(O(2)) during the RM and changes in respiratory system compliance at 15 min (r = 0.66, p < 0.01) and RM-induced changes in Q VA/Q T (r = -0.85; p < 0.01). The correlation between RM-induced changes in Pa(O(2))/FI(O(2)) in responders (improvement in Pa(O(2))/FI(O(2)) of greater than 20% during the RM) and the inspired oxygen fraction was also significant. In ARDS patients ventilated with a lung protective strategy we conclude that RM have no short-term benefit on oxygenation, and regional alveolar overdistension capable of redistributing blood flow can occur during RM.
Adult↗