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PubMed1980

Pancreatic tissue pH in experimental acidosis and alkalosis.

The pH was studied in pancreatic tissue and arterial blood in 22 dogs. Respiratory acidosis was induced by CO2 inhalations in 5 dogs, respiratory alkalosis by hyperventilation in 5 dogs, metabolic acidosis by intravenous(i.v.) infusion of 0.1 N HCl in 5 dogs, metabolic alkalosis by i.v. infusion of 4.2% Na bicarbonate in 5 dogs. The differences between the shifts of blood pH and tissue pH were not significant statistically. Infusion of Ringer's solution failed to affect the pH in blood and pancreatic tissue in two control animals. It is concluded, that with an adequate tissue blood flow the pancreatic tissue pH is uninformative unless the blood pH is known.

Acidosis↗
PubMed2004

Hypokalemic paralysis mimicking Guillain-Barré syndrome and causing acute respiratory failure.

A 33-year-old female patient admitted to the ICU with ascending muscle weakness leading to acute hypercapneic respiratory failure. She gave a 10-day history of severe diarrhea and vomiting. Laboratory work up revealed severe hypokalemia, mixed metabolic and respiratory acidosis, and renal impairment. Continuous potassium replacement produced rapid and complete recovery from quadriplegia and respiratory failure without requirement for mechanical ventilation.

Acidosis, Respiratory↗
PubMed1975

Depression of human myocardial contractility with "respiratory" and "metabolic" acidosis.

The effect of a similar degree of "respiratory" and "metabolic" acidosis was studied in seven isolated in vitro human pectinate muscles and eight ventricular muscle bundles. Either "respiratory" or "metabolic" acidosis (from 7.36 plus or minus 0.03 to 7.01 plus or minus 0.02 and 6.98 plus or minus 0.03, respectively) depressed in vitro contractility in human atrial or ventricular muscle to a similar extent. Previous contradictory responses of myocardial tissue to alterations in pH appear to be the result of species differences.

Acidosis↗
PubMed1993

Alcohol intoxication in hospitalized young teenagers.

The scientific literature concerning alcohol intoxication is enormous. However, less is known of alcohol-induced disturbances in children and adolescents and most of those reports concern cases of hypoglycemia in children under five years of age. We studied the clinical status and chemistry, especially acid-base balance, in 36 young teenagers treated at hospital for alcohol intoxication. On physical examination 6 patients were somnolent, 18 were comatose and 12 were in deep coma. The impairment of consciousness was directly proportional to the blood ethanol concentration. Acidosis was a central finding, and it was caused by a combination of respiratory and metabolic factors (a high blood PCO2 and a low base excess; r = 0.97, p < 0.001); the finding of respiratory acidosis dominated. Base excess correlated negatively with beta-hydroxybutyrate and lactate, as expected. All the metabolic products measured--acetate, beta-hydroxybutyrate and lactate--were significantly elevated compared with the control patients. No hypoglycemia was found. Prior treatment with intravenous glucose decreased vomiting and normalized the serum lactate concentration and PO2. Hypokalemia was the most common abnormality in serum electrolytes. In four patients the rate of fall of blood ethanol concentration was 2.8-3.3 mmol/h (0.13-0.15 g/l-1 h-1) and the mean acetate concentration was 0.8 mmol/l (SE 0.3). Biochemical disturbances in young teenage alcohol intoxicants resemble those previously found in adults. The severe toxicity by ethanol, manifesting in coma, occurs in lower blood alcohol concentrations in children than in adults.

Acetates↗
PubMed1991

The effect of acidosis on the interval-force relation and mechanical restitution in ferret papillary muscle.

1. The effect of a respiratory acidosis on the interval-force relation and on mechanical restitution was investigated in ferret papillary muscles. 2. Acidosis (pH 6.85) decreased developed force over a range of stimulation frequencies (1.0.06 Hz); the percentage decrease was greatest at the lowest stimulation frequencies. Qualitatively similar effects of acidosis on developed force were observed in the presence of the sarcoplasmic reticulum (SR) inhibitor ryanodine. 3. Mechanical restitution curves were constructed by interpolating extra-systoles at different test intervals following a train of steady-state beats. Mechanical restitution in ferret papillary muscle was triphasic: an initial, rapid, exponential increase in force with test intervals to 2 s, a further increase with test intervals between 60 and 90 s and then a slow decline, with a plateau at about 30 min (0.33 Hz, 30 degrees C). 4. Acidosis slowed the initial phase of mechanical restitution. The degree of slowing depended on the steady-state stimulation frequency, being greatest at low frequencies. 5. Inhibition of the SR abolished the initial phase of mechanical restitution, suggesting that this phase depends on Ca2+ release from the SR. 6. The strength of the first contraction after the extra-systole varied inversely with the size of the extra-systole under all conditions studied. 7. It is concluded that acidosis may inhibit the SR by altering the time required for Ca2+ recycling between contractions. This effect may alter Ca2+ release from the SR during acidosis, and may underlie the mechanical alternans (the alternation of small and large contractions) that can occur during acidosis.

Acidosis, Respiratory↗
PubMed1992

Ventilatory and metabolic changes during high efficiency hemodialysis.

Ventilatory and metabolic changes were measured in seven patients undergoing high efficiency hemodialysis using a cuprophane dialyzer and bicarbonate-containing dialysate. At an HCO3 concentration of 35 mEq/liter and a mean in vivo urea clearance of 3.6 ml/kg/min, hypoxemia was not detected during dialysis (PaO2 was 14.00 and 13.60 kPa before and during dialysis). The new findings, related to high efficiency bicarbonate dialysis, include a sustained rise in minute ventilation (VE, 6.1 to 6.8 liter/min, P less than 0.01), an increase in CO2 excretion (VCO2, 194 to 214 ml/min, P less than 0.05), and O2 consumption (VO2, 215 to 246 ml/min, P less than 0.05). The increment in VE and VCO2 was attributed to the high flux rate of bicarbonate while the rise in VO2 is likely the result of metabolic alkalosis. Arterial pH rose from 7.40 to 7.49 mm Hg and serum HCO3 increased from 23.8 to 29.2 mEq/liter, while pCO2 remained normal at 5.07 kPa throughout the study. The acid-base status of the blood changed from that of a metabolic acidosis to that of a respiratory acidosis across the dialyzer where the pH decreased from 7.47 to 7.41 and pCO2 rose from 5.31 to 7.72 kPa. These data indicate that a healthy ventilatory response is needed to excrete the excess CO2 generated during high efficiency bicarbonate hemodialysis. The significance and etiology of the elevated O2 consumption is undetermined.

Acid-Base Equilibrium↗
PubMed1981

Serum potassium concentration in acidemic states.

It has been generally accepted that acidosis results in hyperkalemia because of shifts of potassium from the intracellular to the extracellular compartment. There is ample clinical and experimental evidence, however, to support the conclusion that uncomplicated organic acidemias do not produce hyperkalemia. In acidosis associated with mineral acids (respiratory acidosis, end-stage uremic acidosis, NH4Cl-or CaCl2-induced acidosis), acidemia per se, results in predictable increases in serum potassium concentration. In acidosis associated with nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary to methylmalonic and isovaleric acids, and ethylene glycol, paraldehyde and salicylate intoxications), serum potassium concentration usually remains within the normal range in uncomplicated cases. A number of factors, however, may be responsible for hyperkalemia in some of these patients other than the acidemia per se. These include dehydration and renal hypoperfusion, preexisting renal disease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status of potassium balance, and therapy. The mechanism(s) of this differing effect of mineral and organic acidemias on transmembrane movement of potassium remains undefined. The prevalent hypothesis, however, favors the free penetrance of the organic anion into cells without creating a gradient for the hydrogen ions and, thus, obviating the efflux of intracellular potassium. The importance of the presence of hyperkalemia in clinical states of organic acidemias is obvious. A search for the complicating factors reviewed above should be undertaken since organic acidemias per se, should not be expected to be accompanied by elevations of serum potassium concentration. Moreover, the classical teaching that the absence of hyperkalemia during severe acidosis is indicative of severe potassium deficiency, may not be universally valid in patients with uncomplicated organic acidemias.

Acidosis↗
PubMed1988

[Arteriovenous pH- and carbon dioxide gradients during cardiopulmonary resuscitation].

During external cardiac massage and after restoration of spontaneous circulation, the arterial and central venous blood gas status of ten patients was determined. During cardiopulmonary resuscitation the median arterial pH value was 7.29 and the median central-venous pH value was 7.16. The low central-venous pH during resuscitation was probably caused by the high partial pressure of carbon dioxide, because no significant difference between arterial and central-venous base deficit was found. The arteriovenous pH and carbon dioxide gradients were significantly lower after spontaneous circulation had been restored. The arterial pH does not parallel the marked fall in central venous pH, and therefore only partly indicates acid-base changes during resuscitation. On the other hand, a central-venous blood gas status not only indicates the degree of metabolic acidosis present, but also the "respiratory" acidosis that in turn is a measure of the severity of intracellular acidosis.

Adult↗
PubMedDate not supplied

[Hemoglobin oxygen transport during experimental acute hypercapnia (author's transl)].

The effects on hemoglobin oxygen transport of acute respiratory acidosis have been studied in dogs inhaling a gaseous mixture with 12% CO2 (O2 21%) for two to five hours. In a first series of experiments, it was shown that the shape of the oxyhemoglobin dissociation curve (ODC) was not modified by severe acidosis (pH congruent to 7) lasting for two and a half hours. The Hill number (N equals 2.6) did not change significantly. The aim of the second experimental series was to stuey the Bohr effect and the hemoglobin oxygen affinity (P50). The control value for the respiratory Bohr coefficient (B) was --0.54; neither after two hours (--0.52), nor after five hours of hypercapnia (--0.55) was it significantly modified. The P50 expressed at arterial pH was much increased in acidosis (congruent to 45 torr); when expressed at standard p/ 7.4, it was slightly but significantly decreased (congruent to 1 torr) at the fifth hour. At the same time there was a decrease (p smaller than 0.05) in the erythrocyte 2,3-DPG approaching 15 p. cent; on the other hand the ATP concentration did not change significantly. No significant individual correlation was found between P50(7.4), 2,3-DPG and mean hemoglobin corpuscular concentration. These results suggest that during severe respiratory acidosis neither a change in the shape of ODC, nor a change in Bohr effect do affect the hemoglobin oxygen transport. The main characteristic remains the decrease in oxygen affinity of hemoglobin, due to the erythrocyte [H+] increase induced by hypercapnia ; this phenomenon is observed as long as the 2,3-DPG decrease stays moderate.

Acidosis, Respiratory↗
PubMed1975

The physiological assessment of acid-base balance.

Acid-base terminology including the sue of SI units is reviewed. The historical reasons why nomograms have been particularly used in acid-base work are discussed. The theoretical basis of the Henderson-Hasselbalch equation is considered. It is emphasized that the solubility of CO2 in plasma and the apparent first dissociation constant of carbonic acid are not chemical constants when applied to media of uncertain and varying composition such as blood plasma. The use of the Henderson-Hasselbalch equation in making hypothermia corrections for PCO2 is discussed. The Astrup system for the in vitro determination of blood gases and derived parameters is described and the theoretical weakness of the base excess concept stressed. A more clinically-oriented approach to the assessment of acid-base problems is presented. Measurement of blood [H+] and PCO2 are considered to be primary data which should be recorded on a chart with in vivo CO2-titration lines (see below). Clinical information and results of other laboratory investigations such as plasma bicarbonate, PO2,P50 are then to be considered together with the primary data. In order to interpret this combined information it is essential to take into account the known ventilatory response to metabolic acidosis and alkalosis, and the renal response to respiratory acidosis and alkalosis. The use is recommended of a chart showing the whole-body CO2-titration points obtained when patients with different initial levels of non-respiratory [H+] are ventilated. A number of examples are given of the use of this [H+] and PCO2 in vivo chart in the interpretation of acid-base data. The aetiology, prognosis and treatment of metabolic alkalosis is briefly reviewed. Treatment with intravenous acid is recommended for established cases. Attention is drawn to the possibility of iatrogenic production of metabolic alkalosis. Caution is expressed over the use of intravenous alkali in all but the severest cases of metabolic acidosis. The role of 2,3-diphosphoglycerate on tissue oxygenation is stressed and use of intravenous sodium phosphate as an alternative to intravenous bicarbonate is mentioned.

Acid-Base Equilibrium↗
PubMed1998

Acidosis activates complement system in vitro.

We investigated the in vitro effect of different forms of acidosis (pH 7.0) on the formation of anaphylatoxins C3a and C5a. Metabolic acidosis due to addition of hydrochloric acid (10 micromol/ml blood) or lactic acid (5.5 micromol/ml) to heparin blood (N=12) caused significant activation of C3a and C5a compared to control (both p=0.002). Respiratory acidosis activated C3a (p=0.007) and C5a (p=0.003) compared to normocapnic controls. Making blood samples with lactic acidosis hypocapnic resulted in a median pH of 7.37. In this respiratory compensated metabolic acidosis, C3a and C5a were not increased. These experiments show that acidosis itself and not lactate trigger for activation of complement components C3 and C5.

Acidosis↗
PubMed2002

[Effects of fetal anoxia and acidosis on superoxide dismutase].

OBJECTIVE: To analyze the effects of fetal anoxia, respiratory and metabolic acidosis on the activity of antioxidation in fetal distress. METHODS: Blood samples were taken from umbilical artery in 386 neonates for blood gas analysis and detection of the concentration of superoxide dismutase (SOD). Normal situation, anoxia, acidosis, respiratory acidosis, metabolic acidosis and mixed acidosis were diagnosed in all neonates according to the results of blood gas values, and the neonate asphyxia was diagnosed according to the Apgar scores (one minute). The effect of anoxia and acidosis to SOD were analyzed with multiple factor analysis of variation. RESULTS: (1) Among the all 386 cases, 317 were normal, 31 with anoxia, 17 with acidosis, and 21 with both anoxia and acidosis. Among the total cases of acidosis, 8 respiratory, 21 metabolic, and 9 mixed acidosis. (2) The plasma levels of SOD of umbilical artery blood in anoxia, acidosis, both anoxia and acidosis, and normal sitution were (118.5 +/- 7.1) mmol/L, (122.0 +/- 11.4) mmol/L, (140.0 +/- 7.0) mmol/L, and (98.5 +/- 2.6) mmol/L, respectively. The results of unvariate analysis of variance showed that anoxia: F = 4.999 (P < 0.05), acidosis: F = 7.025 (P < 0.01), and both anoxia and acidosis: F = 0.013 (P > 0.05). (3) The plasma levels of SOD with respiratory acidosis, metabolic acidosis and mixed acidosis were (127.3 +/- 18.4) mmol/L, (126.0 +/- 8.1) mmol/L, (150.0 +/- 10.4) mmol/L. The results of univariate analysis of variance showed that respiratory acidosis: F = 4.404 (P < 0.05), metabolic acidosis: F = 3.965 (P < 0.05), and mixed acidosis: F = 0.015 (P > 0.05). CONCLUSION: The superoxidation and antioxidation can be effected by factors like anoxia and acidosis, respiratory acidosis and metabolic acidosis. However, the mechanisms of these effects are different. There is additive, but not synergistic effects among them.

Acidosis↗
PubMed1975

Blood affinity for oxygen in experimental hemorrhagic shock with metabolic acidosis.

This study was designed to evaluate, in vivo, the effect of a severe non-respiratory acidosis on hemoglobin oxygen transport. Oxygen affinity of hemoglobin, Bohr effect, Hill's number and red cell 2,3-DPG were evaluated during experimental hemorrhagic shock in dogs. Three periods were considered: control, hypotension (mean arterial pressure 60 mm Hg for 2 hr 30 min) and blood replacement. There was no significant change in erythrocyte 2,3-DPG following hemorrhagic hypotension but ATP increased significantly. n, the Hill number (2.6), was not changed by in vivo acidosis (pH 7.1). Respiratory Bohr coefficient (BCO2) corresponding to pHe variations was drastically reduced (control BCO2 = 0.55, acidosis BCO2 = 0.31, blood replacement BCO2 = 0.35). P50(7.4) was not modified significantly by hemorrhagic acidosis. It is unlikely that variations of blood affinity for oxygen play a major role in oxygen delivery during early experimental hemorrhagic shock.

Acidosis↗
PubMed1992

Hypercarbia during carbon dioxide pneumoperitoneum.

Patients with cardiopulmonary insufficiency undergoing laparoscopic surgery with carbon dioxide (CO2) pneumoperitoneum may retain CO2 resulting in clinically significant respiratory acidosis. A canine model of pulmonary emphysema induced by papain inhalation was utilized to evaluate the respiratory effects of both CO2 and helium pneumoperitoneum. Prior to papain inhalation and 5 and 8 weeks after initial treatment under general anesthesia, mechanical ventilation was adjusted to maintain the end-tidal CO2 (ETCO2) at 40 mm Hg during baseline and pneumoperitoneum physiologic monitoring periods. Utilizing an analysis of variance, hemodynamic and respiratory physiologic parameters were compared. In this canine model, all dogs demonstrated consistent hypercarbia during CO2 pneumoperitoneum prior to papain treatments, but CO2 retention was significantly increased in the emphysematous state. The occurrence of hypercarbia during CO2 pneumoperitoneum may be underestimated by ETCO2 monitoring as was revealed by an increased PaCO2 (arterial carbon dioxide pressure)-ETCO2 gradient with an increasing time interval between papain exposure and period of physiologic monitoring. Irrespective of the pulmonary condition of the dog, helium pneumoperitoneum did not produce any hypercarbic or acidic changes when compared with the concomitant baseline period of dogs prior to the induction of pneumoperitoneum, thus suggesting that helium pneumoperitoneum may be a reasonable alternative in patients at risk for CO2 retention.

Acidosis, Respiratory↗
PubMed2003

Hypoxia and hypercapnia during respiration into an artificial air pocket in snow: implications for avalanche survival.

Snow avalanche case reports have documented the survival of skiers apparently without permanent hypoxic sequelae, after prolonged complete burial despite there being only a small air pocket on extrication. We investigated the underlying pathophysiological changes in a prospective, randomised 2 x 2 crossover study in 12 volunteers (28 tests) breathing into an artificial air pocket (1- or 2-l volume) in snow. Peripheral SpO(2), ETCO(2), arterialised capillary blood variables, air pocket O(2) and CO(2), snow density, and snow conditions at the inner surface of the air pocket were determined. SpO(2) decreased from a median of 99% (93-100%) to 88% (71-94%; P<0.001) within 4 min of breathing into the air pocket; the reduction was greater at 1 l, than 2 l, volume air pocket (P=0.013, intention to treat P=0.003) and correlated to snow density (r=0.50, P=0.021, partial correlation coefficient). ETCO(2) rose simultaneously from median 5.07 kPa (3.47-6.93 kPa) to 6.8 kPa (5.87-8.27 kPa; P<0.001), with consequent respiratory acidosis. Despite premature interruption due to hypoxia (SpO(2)</=75%) in 17 of 28 tests (61%), a respiratory steady state prevailed in five tests until protocol completion (30 min). We conclude that the degree of hypoxia following avalanche burial is dependent on air pocket volume, snow density and unknown individual personal characteristics, yet long-term survival is possible with only a small air pocket. Hence, the definition of an air pocket, "any space surrounding mouth and nose with the proviso of free air passages" is validated as the main criterion for triage and management of avalanche victims. Our experimental model will facilitate evaluating the interrelation between volume and inner surface area of an air pocket for survival of avalanche victims, whilst the present findings have laid the basis for future investigation of possible interactions between hypoxia, hypercapnia, and hypothermia (triple H syndrome) in snow burial.

Accidents↗
PubMed1976

Contribution of tissue acidosis to ischemic injury in the perfused rat heart.

The isolated perfused working rat heart preparation has been used to study the effects of respiratory acidosis on myocardial metabolism and contractilly. Hearts were perfused with 5 mM glucose and 10(-2) U/ml of insulin in order to enhance metabolsim of glucose relative to that of fatty acids. After perfusion with Krebs bicarbonate medium at pH 6.6, hearts rapidly ceased performing external work and peak left ventricular pressure fell by 75% after 5 minutes. Oxygen consumption, rate of ATP generation and overall glycolytic flux also declined rapidly. After about 2 minutes of perfusion, the fall of glycolytic flux showed a partial reversal, which was largely accounted for by increased lactate production, so that glucose oxidation decreased further. The reversal of glycoltic flux could be accounted for by partial release of H+ inhibition of phospho-fructokinase by increased tissue levels of adenosine 5'-diphosphate (ADP), adenosine monophosphate (AMP) and P1 and decreased levels of adenosine triphosphate (ATP) and creatine phosphate. The increased proportion of glucose uptake converted to lactate together with an increase of the tissue lactate/pyruvate ratio could be accounted for by inhibition of the malate-aspartate cycle combined with tissue hypoxia. Lactate accumulated in the tissue as a result of a decreased permeability of the plasma membrane to lactate. Decreased oxygen delivery to the myocardium was caused by secondary constriction of the coronary vessels. In further experiments, the coronary flow was regulated by an external pump which delivered fluid at a controlled rate into the aortic cannula above the coronary arteries, and the degree of tissue hypoxia was monitored by measuring changes of pyridine nucleotide reduction state by surface fluorescence techniques. The effects of acidosis uncomplicated by possible hypoxia were compared directly with those produced by ischemic hypoxia. The effects of acidosis under these conditions were similar to those described above, and to those produced by ischemia. From these and other data it is concluded that the effects of ischemia are caused by a lowering of the intracellular pH, which decreases the rate of energy production relative to the rate of energy demand. However, it is suggested that the primary cause of the decreased peak systolic pressure with either acidosis or ischemia is not a result of a defect of energy metabolism, but is due to alteration of the calcium cycle of the heart. Possible causes of irreversible heart failure after prolonged ischemia are discussed.

Acidosis, Respiratory↗
PubMed1999

Expiratory washout versus optimization of mechanical ventilation during permissive hypercapnia in patients with severe acute respiratory distress syndrome.

The aim of this study was to compare three ventilatory techniques for reducing PaCO2 in patients with severe acute respiratory distress syndrome treated with permissive hypercapnia: (1) expiratory washout alone at a flow of 15 L/min, (2) optimized mechanical ventilation defined as an increase in the respiratory frequency to the maximal rate possible without development of intrinsic positive end- expiratory pressure (PEEP) combined with a reduction of the instrumental dead space, and (3) the combination of both methods. Tidal volume was set according to the pressure-volume curve in order to obtain an inspiratory plateau airway pressure equal to the upper inflection point minus 2 cm H2O after setting the PEEP at 2 cm H2O above the lower inflection point and was kept constant throughout the study. The three modalities were compared at the same inspiratory plateau airway pressure through an adjustment of the extrinsic PEEP. During conventional mechanical ventilation using a respiratory frequency of 18 breaths/min, respiratory acidosis (PaCO2 = 84 +/- 24 mm Hg and pH = 7.21 +/- 0.12) was observed. Expiratory washout and optimized mechanical ventilation (respiratory frequency of 30 +/- 4 breaths/min) had similar effects on CO2 elimination (DeltaPaCO2 = -28 +/- 11% versus -27 +/- 12%). A further decrease in PaCO2 was observed when both methods were combined (DeltaPaCO2 = -46 +/- 7%). Extrinsic PEEP had to be reduced by 5.3 +/- 2.1 cm H2O during expiratory washout and by 7.3 +/- 1.3 cm H2O during the combination of the two modes, whereas it remained unchanged during optimized mechanical ventilation alone. In conclusion, increasing respiratory rate and reducing instrumental dead space during conventional mechanical ventilation is as efficient as expiratory washout to reduce PaCO2 in patients with severe ARDS and permissive hypercapnia. When used in combination, both techniques have additive effects and result in PaCO2 levels close to normal values.

Acidosis, Respiratory↗
PubMed2003

Mechanical effects of airway humidification devices in difficult to wean patients.

OBJECTIVE: To evaluate the influence of airway humidification devices on the efficacy of ventilation in difficult to wean patients. DESIGN: A prospective, randomized, controlled physiologic study. SETTING: A 22-bed medical intensive care unit in a university hospital. PATIENTS: Chronic respiratory failure patients. INTERVENTIONS: Performances of a heated humidifier and a heat and moisture exchanger were evaluated on diaphragmatic muscle activity, breathing pattern, gas exchange, and respiratory comfort during weaning from mechanical ventilation by using pressure support ventilation. Eleven patients with chronic respiratory failure were submitted to four pressure support ventilation sequences by using the heated humidifier and the heat and moisture exchanger at two different levels of pressure support ventilation (7 and 15 cm H(2)O). MEASUREMENT AND MAIN RESULTS: Compared with the heated humidifier and regardless of the pressure support ventilation level used, the heat and moisture exchanger significantly increased all of the inspiratory effort variables (inspiratory work of breathing expressed in J/L and J/min, pressure time product, changes in esophageal pressure, and transdiaphragmatic pressure; p <.05) and dynamic intrinsic positive end-expiratory pressure (p <.05). Similarly, the heat and moisture exchanger produced a significant increase in Paco(2) (p <.01) responsible for severe respiratory acidosis (p <.05), which was insufficiently compensated for despite a significant increase in minute ventilation (p <.05). This resulted in respiratory discomfort for all patients with the heat and moisture exchanger (p <.01). Adverse effects were partially counterbalanced by increasing the pressure support ventilation level with the heat and moisture exchanger by >or=8 cm H(2)O. CONCLUSIONS: The type of airway humidification device used may negatively influence the mechanical efficacy of ventilation and, unless the pressure support ventilation level is considerably increased, the use of a heat and moisture exchanger should not be recommended in difficult or potentially difficult to wean patients with chronic respiratory failure.

APACHE↗