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PubMed1995

[A study on erythrocyte membrane band 3 protein anion transport function in chronic respiratory failure patients].

The changes of the structure, content and anion transport function as well as the blood gases and electrolytes inside and outside the erythrocytes were investigated in 3 groups of subjects: type I respiratory failure patients (group 1, n = 40); type II respiratory failure patients (group 2, n = 40) and controls (group 3, n = 37). The results showed that (1) anion transport function impairment of erythrocyte membrane band 3 protein and HCO3-/Cl- exchange restrain may be the reasons that aggravate CO2 retention and respiratory acidosis in cor pulmonale patients with type II respiratory failure. (2) band 3 protein anion transport function impairment in patients of cor pulmonale with type II respiratory failure is reversible. Therefore, it was necessary to supply oxygen to cor pulmonale patients with hypoxemia in time, which may contribute to the recovery of anion transport function.

Aged↗
PubMed1976

Acute acid-base disorders. 2. Specific disturbances.

Evaluation of the acid-base status of the body requires measurement of bicarbonate (total carbon dioxide) concentration, pH, and partial pressure of CO2 in arterial blood. Calculation of standard bicarbonate and base excess or deficit is not necessary. The normal concentration of free hydrogen ions (H+) is approximately 40 millimoles/liter, which is equivalent to a pH of 7.4. The normal load of fixed acids is 50 to 80 millimoles in 24 hours. A steady state is maintained by excretion of an equal amount of H+ by the kidneys, which at the same time regenerate bicarbonate to replenish buffer stores. Renal excretion of H+ is in the form of titratable acid and ammonium. Synthesis of ammonia can increase severalfold under the stimulus of acidosis. This is the chief mechanism of long-term compensation. Metabolic acidosis can be due to an excessive acid load (endogenous or exogenous), impaired renal excretion of H+, or bicarbonate loss. Determination of the "anion gap" (unmeasured anions) helps to establish the mechanism of acidosis. Acidosis with a normal anion gap is due to either bicarbonate loss or ingestion of certain chloride salts. A gap larger than normal indicates the presence in the body of acids other than acidfying chloride salts. Management of metabolic acidosis requires accurate diagnosis, clear understanding of the mechansim, and individualized treatment. Metabloic alkalosis is due to loss of H+ (usually from stomach or kidneys) or ingestion of alkali. Measurement of urinary chloride helps establish the mechanism of alkalosis. In saline-responsive alkalosis, the urinary chloride level is very low. This is usually due to gastric loss of H+, and the condition responds to administration of saline solution. When the urinary chloride level is only moderately low, the alkalosis is probably not due to gastric loss of H+. This form of alkalosis (saline-resistant) does not respond well to administration of saline solution and requires use of potassium in treatment. Apprpriate compensatory responses to acidosis or alkalosis are critical to survival. Compensation for metabloic acidosis consists of hyperventilation and enhanced renal excretion of H+, chiefly as ammonium. In metabolic alkalosis, compensation is mainly renal excretion of bicarbonate. Respiratory acidosis is due to alveolar hypoventilation. In chronic situations, a compensatory rise in serum bicarbonate concentration is expected. Management consists of treatment of the cause of hypoventilation. Respiratory alkalosis is due to hyperventilation. Treatment requires identification and correction of the cause of hyperventilation.

Acid-Base Imbalance↗
PubMed1989

[Cardiopulmonary resuscitation: acid-base alterations and alkalizing therapy].

It is generally believed that metabolic acidosis prevails during cardiac arrest. However, recent experimental and clinical studies have demonstrated that respiratory acidosis in mixed venous blood and respiratory alkalosis in arterial blood with only minor increases in lactic acid characterize the early acid-base changes that follow cardiac arrest and cardiopulmonary resuscitation (CPR). While continued CO2 production with critical reduction in systemic perfusion explains the accumulation of CO2 in the venous side, the reduction of pulmonary blood flow with maintenance of constant minute ventilation explains the decreases in expired CO2 and therefore arterial PCO2. In the heart, marked increases in CO2 tension and lactic acid are associated with dramatic decreases in myocardial pH with consequent depression of contractile function. Administration of sodium bicarbonate, however, neither increases resuscitability nor improves long term outcome. Moreover, adverse effects stemming from increases in plasma osmolality, increases in hemoglobin-O2 affinity, induction of alkalemia and generation of CO2 are potentially deleterious for myocardial and cerebral function. Consequently, the American Heart Association has recently discouraged the routine administration of bicarbonate during the initial 10 minutes of CPR in which interventions with proven efficacy such as artificial ventilation, precordial compression, electric defibrillation and epinephrine administration take place. Alternative experimental buffer therapy with agents that consume CO2 have also failed to alter the outcome of cardiac arrest.

Acid-Base Imbalance↗
PubMed2006

Tissue glycogen and extracellular buffering limit the survival of red-eared slider turtles during anoxic submergence at 3 degrees C.

The goal of this study was to identify the factors that limit the survival of the red-eared slider turtle Trachemys scripta during long-term anoxic submergence at 3 degrees C. We measured blood acid-base status and tissue lactate and glycogen contents after 13, 29, and 44 d of submergence from ventricle, liver, carapace (lactate only), and four skeletal muscles. We also measured plasma Ca(2+), Mg(2+), Na(+), K(+), Cl(-), inorganic phosphate (P(i)), lactate, and glucose. After 44 d, one of the six remaining turtles died, while the other turtles were in poor condition and suffered from a severe acidemia (blood pH = 7.09 from 7.77) caused by lactic acidosis (plasma lactate 91.5 mmol L(-1)). An initial respiratory acidosis attenuated after 28 d. Lactate rose to similar concentrations in ventricle and skeletal muscle (39.3-46.1 micromol g(-1)). Liver accumulated the least lactate (21.8 micromol g(-1)), and carapace accumulated the most lactate (68.9 micromol g(-1)). Plasma Ca(2+) and Mg(2+) increased significantly throughout submergence to levels comparable to painted turtles at a similar estimated lactate load. Glycogen depletion was extensive in all tissues tested: by 83% in liver, by 90% in ventricle, and by 62%-88% in muscle. We estimate that the shell buffered 69.1% of the total lactate load, which is comparable to painted turtles. Compared with painted turtles, predive tissue glycogen contents and plasma HCO(-)(3) concentrations were low. We believe these differences contribute to the poorer tolerance to long-term anoxic submergence in red-eared slider turtles compared with painted turtles.

Acid-Base Equilibrium↗
PubMed1992

Blood gas and catecholamine levels in capture stressed desert bighorn sheep.

Forty-seven bighorn sheep (Ovis canadensis nelsoni) were captured within a 3-day period in December, 1989 as part of a California Department of Fish and Game effort to repopulate historic ranges in California. They were captured on the Mojave Desert in the Kelso Mountains near Old Dad Peak, San Bernardino County, California. Venous blood gases measured at the site of capture demonstrated a severe metabolic acidosis (base deficit, 23 mEq/liter), with no evidence of respiratory acidosis. There were moderately elevated plasma epinephrine (1.25 ng/ml), norepinephrine (2.60 ng/ml), and dopamine (114 pg/ml) levels. These data appear to reflect animals that have been moderately stressed. These acid-base-catecholamine values differ from values in resting domestic sheep, and are similar to those reported in greyhounds after brief strenuous exercise.

Acid-Base Equilibrium↗
PubMedDate not supplied

[CO2 mass transfer and acid-base balance under conditions of muscular activity at sea level and in the mountains].

The state of the blood acid-base balance and dynamics of carbonic acid gas mass transfer were studied in sportsmen at the sea level and in mountains. It is shown that at the sea level due to an intensive muscular activity large amounts of CO2 are formed and excreted; the mass transfer of this gas is multiply accelerated, simultaneously, a pronounced decompensated metabolic acidosis is observed which in some cases is complicated respiratory acidosis. The similar exercises in mountains are followed by a more pronounced disturbance in the acid-base balance and a more intensified mass-transfer of CO2. After 12-day acclimatization and training in mountains the buffer blood capacity increases, the metabolic acidosis under conditions of muscular activity is less pronounced.

Acclimatization↗
PubMed1983

Lactic acidosis in severe asthma.

Twelve patients with severe asthma in whom lactic acidosis developed are presented. All had an arterial blood pH level lower than that expected for the measured partial pressure of arterial carbon dioxide, all had an abnormally large anion gap, and the blood lactate level exceeded 2.8 mmol/liter. Respiratory acidosis subsequently developed in eight patients, and six required intubation. Lactic acidosis can develop in patients with severe asthma. Such patients are in danger of the development of respiratory failure and must be treated vigorously and observed closely.

Acidosis↗
PubMedDate not supplied

[Gasometric studies and lactic acid determinations in arterial blood and cerebrospinal fluid in brain infarction].

In 54 cases of brain infarction and 17 control cases the gasometric parameters and lactic acid level were determined in arterial blood and cerebrospinal fluid. Metabolic acidosis was demonstrated in the arterial blood and cerebrospinal fluid. Respiratory acidosis compensated partly metabolic acidosis. Changes in the cerebrospinal fluid were more frequent and more pronounced, especially in cases with fatal outcome. Deep disturbances of acid-base balance complicated with hypoxia may have prosnostic significance while moderate rise in lactic acid level is without this significance.

Aged↗
PubMed1981

Effects of brief and intermediate exposures to sulfate submicron aerosols and sulfate injections and cardiopulmonary function of dogs and tracheal mucous velocity of sheep.

Pulmonary mechanics of anesthetized dogs were not changed or were minimally altered by breathing the following compounds as submicron aerosols in concentrations up to 17.3 mg/m3 for 7.5 min: (1) sodium chloride (as a control), (2) sodium sulfate, (3) ammonium sulfate, (4) zinc sulfate, (5) zinc ammonium sulfate, (6) ammonium bisulfate, (7) aluminum sulfate, (8) manganese sulfate, (9) nickel sulfate, (10) copper sulfate, (11) ferrous sulfate, and (12) ferric sulfate. Submicron aerosols of these compounds in concentrations of 4.1-8.8 mg/m3, administered for 4 h to anesthetized dogs, did not affect mechanics of breathing, hemodynamics, and arterial blood gases. In conscious sheep, tracheal mucous velocity was not altered by exposure to the submicron aerosols of the sulfate compounds. None of these compounds, injected iv in a dose of 1 mg, had adverse effects on mechanics of breathing, pulmonary and systemic hemodynamics, or arterial blood gases. In 100-mg injections, zinc sulfate and zinc ammonium sulfate produced a fall in cardiac output, systemic hypotension, hypoxemia, and metabolic acidosis. Copper sulfate at this dose produced pulmonary hypertension, a fall in cardiac output, hypoxemia, respiratory acidosis, and a decrease of specific total respiratory conductance. It is concluded that submicron aerosols of sulfate salts do not have adverse cardiopulmonary effects when administered in high concentrations for up to 4 h. However, prolonged exposure to high concentrations of zinc sulfate, zinc ammonium sulfate, and copper sulfate aerosols should be carefully monitored because of the possibility that lower levels of these compounds in the bloodstream for long time period might have adverse cardiopulmonary effects.

Aerosols↗
PubMed1975

Respiratory care following open heart surgery.

Respiratory care of patients undergoing open heart surgery should begin in the preoperative period. Patients must stop smoking, and if obese they are encouraged to lose weight. Pulmonary infection is treated and secretions must be eliminated. Postoperative hypoxemia, which is an expected event following anesthesia and surgery, is aggravated by circulatory instability and pulmonary complications. Following open heart surgery pulmonary complications such as atelectasis, congestion, edema, postperfusion lung, pneumothorax, pleural effusion, and hemothorax are common. Respiratory care should be planned to avoid these complications and to treat them promptly should they occur. Routinely every patient is mechanically ventilated for at least 12 to 18 hours following surgery. The type of ventilator used and its parameters are adjusted according to the clinical condition of the patient to maintain adequate oxygenation and to prevent any respiratory acidosis. When indicated, PEEP is applied to improve arterial oxygenation. Respiratory care is extended for at least 5 days after termination of artificial ventilation. Oxygen therapy is given with either a nasal catheter or a mask, according to the patient's need. IPPB and physiotherapy are continued until the patient shows no signs of pulmonary infection and is capable of effectively eliminating secretions. This routine management and extended postoperative respiratory care definitely contribute to the successful outcome of open heart surgery.

Breathing Exercises↗
PubMed1995

Intracellular pH in vascular smooth muscle: regulation by sodium-hydrogen exchange and multiple sodium dependent HCO3- mechanisms.

OBJECTIVES: The aim was to determine the mechanisms, particularly bicarbonate dependent mechanisms, of intracellular pH (pHi) recovery from various acidoses in vascular smooth muscle and to explore the ATP dependency of the respective mechanisms. METHODS: Experiments were conducted in rat aortic smooth muscle cells grown in primary culture and synchronised in a non-growing state by serum deprivation. pHi was measured in cells loaded with the pH sensitive fluorescent dye, 2',7'-bis-(2-carboxyethyl)-5-(and 6)-carboxyfluorescein (BCECF). Chloride efflux was studied by determination of the rate of efflux of 36Cl over 5 min. Cells were ATP depleted by substitution of glucose in the medium by 2-deoxyglucose. Acidoses were induced by CO2 influx and NH3 efflux techniques. RESULTS: In the absence of HCO3-, the 5-(N-ethyl-N-isopropyl) amiloride (EIPA) sensitive Na+/H+ exchange accounted for the recovery from intracellular acidosis. In the presence of HCO3- ions the response to respiratory acidosis (CO2 influx) was predominantly via activation of Na+/H+ exchange and an EIPA sensitive Na+ and HCO3- dependent mechanism. A 4-acetamido-4'-isothiocyanostilbene-2',2'-sulphonic acids (SITS) sensitive Na+ dependent Cl-/HCO3- mechanism which is also sensitive to EIPA makes a small contribution during severe intracellular acidosis. Under such conditions HCO3- dependent mechanisms contributed about 40% to the overall pHi regulating capacity of vascular smooth muscle cells. However, under conditions which deplete cellular ATP these pHi regulating mechanisms account for virtually all of theses cells' ability to regulate pHi. The inability of Na+/H+ exchange to participate in pHi recovery under these circumstances, reduces the ability of vascular smooth muscle cells to recover pHi by approximately 50-60%. Chloride efflux was approximately linear over 5 min and was increased by 36% in the presence of extracellular HCO3-. Efflux in the presence of HCO3- was inhibited similarly by both SITS and EIPA. CONCLUSIONS: At least three transporters contribute to recovery from acidosis in vascular smooth muscle: Na+/H+ exchange, an Na(+)-HCO3- cotransporter which is sensitive to EIPA, and an Na+ dependent HCO3-/Cl- exchange sensitive to both SITS and EIPA. The Na(+)-HCO3- cotransporter appears to be similar to that described in human vascular smooth muscle. When the Na+/H+ exchanger is attenuated by cellular ATP depletion, the alternative pathways, particularly the Na(+)-HCO3- cotransporter, ensure that substantial pHi regulatory capacity is maintained.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1997

Noninvasive mechanical ventilation and acute respiratory failure: indications and limitations.

Noninvasive mechanical ventilation (NMV) now represents the first step in the management of acute on chronic respiratory failure (A/CRF). During the last 5 yrs, many studies have confirmed the feasibility of NMV in an acute setting, either by facial or nasal interface, used in addition to volumetric or barometric respirators, to manage A/CRF. The best indications for NMV are slowly progressive A/CRF, frequently represented by chronic obstructive pulmonary disease (COPD), or restrictive pulmonary disease. The criteria to initiate NMV in such patients are worsening of respiratory status and arterial blood gas (ABG) values, with increased hypoxia, hypercapnia and respiratory acidosis, despite optimal management with medication, physiotherapy and oxygen therapy. Respiratory encephalopathy is not an absolute contraindication; however, bronchial hypersecretion indicates that care is needed under NMV. Invasive mechanical ventilation with endotracheal (ET) intubation is discussed in the case of failure of NMV, when clinical status and ABG values worsen in spite of it. The signal for ET intubation is then obvious, represented by severe dyspnoea leading to respiratory pauses or arrest, severe cyanosis, and signs of haemodynamic instability. Despite immediate evidence of ominous cardiorespiratory inefficiency, ET intubation may be delayed and often avoided with the help of NMV. Criteria should be studied to identify guidelines for cessation of NMV, in order not to continue with the technique too long considering the safety of the patient. Indications for NMV in other kinds of ARF have received less study and are more controversial.

Acute Disease↗
PubMed1997

Effect of extreme metabolic acidosis on oxygen delivery capacity of the blood--an in vitro investigation of changes in the oxyhemoglobin dissociation curve in blood with pH values of approximately 6.30.

OBJECTIVES: To determine the oxyhemoglobin dissociation curve in blood with pH of approximately 6.3 due to metabolic and superimposed respiratory acidosis, and to evaluate the oxygen delivery capacity of the blood under these circumstances. DESIGN: In vitro study. SETTING: A blood gas laboratory in a university institute for respiratory physiology. SUBJECTS: Heparinized normal human blood. INTERVENTIONS: The oxyhemoglobin dissociation curve was determined by measuring PO2, pH, PCO2, and hemoglobin oxygen saturation at 37 degrees C in mixtures of blood from two reservoirs, both prepared by titration with lactic acid to a pH of 6.3 during tonometry with gases containing 4.2% CO2 and high and low oxygen percentages, respectively. For determination of the effect of additional increases in PCO2, the reservoir blood thus produced was prepared by further tonometry with gases containing 12.8% CO2 and the same oxygen percentages. MEASUREMENTS AND MAIN RESULTS: With the same degree of lactic acidosis (blood lactate concentration of 52 mmol/L), the position of the oxyhemoglobin dissociation curve was the same for blood with PCO2 of 30 torr (4 kPa) and pH of 6.295 and for blood with PCO2 of 90 torr (12 kPa) and pH of 6.165. During tonometry with a gas with PCO2 of 30 torr (4 kPa) and PO2 of 20 torr (2.7 kPa) and addition of increasing amounts of lactic acid, leading to a stepwise change in pH from 6.7 to 6.0, hemoglobin oxygen saturation decreased with decreasing pH from 6.7 to 6.4, but remained the same at a pH of between 6.4 and 6.0. The measured rightward shift of the oxyhemoglobin dissociation curve at such a low pH was clearly less pronounced than that calculated using commonly applied equations, in particular, at the lowest pH. The beneficial effects of the rightward shift of the oxyhemoglobin dissociation curve on the estimates of extractable oxygen at a given venous PO2 decrease with decreasing pH, and disappear rapidly when the Pao2 is reduced below normal. CONCLUSIONS: The acidemia-induced rightward shift of the oxyhemoglobin dissociation curve does not increase further at a pH < 6.4, and is, at such extreme acidemia, less pronounced than calculated by the commonly used equations. To obtain optimal tissue oxygenation in patients with severe circulatory failure and extreme metabolic acidosis, Pao2 should be > 250 torr (> 33.3 kPa).

Acidosis, Lactic↗
PubMed1980

Carotid bodies and ventilatory control dynamics in man.

The normal role of the carotid bodies in ventilatory dynamics in man has been inferred from studies comparing the responses of a group of control subjects to: a) hypoxic-hyperoxic transitions, b) steady-state hypercapnia, c) constant-load and incremental exercise, and d) breath holding with various inspired O2 levels, with the responses of subjects who had had both carotid bodies surgically resected (CBR). Ventilation, metabolic rate, and alveolar gas tensions were computed breath by breath and blood was sampled from a brachial artery catheter. With eucapnia, hypoxic ventilatory drive is subserved entirely by the carotid bodies, both at rest and during exercise, whereas only approximatly equal to 30% of the hyercapnic response in euoxia is attributable to these structures. CBR resulted in appreciable slowing of the ventilatory dynamics during exercise, causing a transient respiratory acidosis. In the steady state of moderate exercise, ventilation was normal in the CBR group, as other receptors provide the approximately equal to 15% of the drive attributable to the carotid bodies. The respiratory compensation for the acute metabolic acidosis of exercise appears to be exclusively mediated by the carotid bodies. Breath-holding time is significantly prolonged following CBR, especially under hypoxic conditions. The carotid bodies therefore provide important information to respiratory control in man, most notably under hypoxia, metabolic acidosis, and dynamic states of muscular exercise.

Acid-Base Equilibrium↗
PubMed1983

Oxygen therapy and oxygen toxicity.

When oxygen therapy is warranted, the minimum effective dose generally should be given. Hypoxemic patients who have normal baseline ABG may be treated initially with an intermediate to high FiO2 in the range of 35% to 100%, depending on the severity of the respiratory distress. The majority of patients with exacerbations of COPD who are not in extremis may be given an initial FiO2 of 28%, especially if their previous response to oxygen is known. When treating patients who have chronic severe hypercapnia (eg, those requiring chronic home oxygen), the initial FiO2 should be 24% even though renal compensation of the respiratory acidosis has occurred. Further mild elevation of the PaCO2, due mainly to the V/Q mismatch that oxygen therapy induces, may be sufficient to precipitate unacceptable hypercapnia. Patients with exacerbations of COPD who are obviously in extremis, with severe hypoxemia and acidosis, should start with an FiO2 of 24% unless they are being mechanically ventilated. The severity of the hypoxemia and acidosis is more predictive for the development of CO2 narcosis and respiratory failure than is the degree of hypercapnia in these patients. The FiO2 can be increased to 28% and incrementally higher if low FiO2 is tolerated. The use of a high FiO2 is subject to the following guidelines for prevention of clinically significant oxygen toxicity: 100% oxygen at atmospheric pressure is safe if given for less than six hours; 70% oxygen is probably safe for 24 hours; and after this time, 45% should be the approximate upper limit to the FiO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Carbon Dioxide↗
PubMed1981

Filtered bicarbonate and plasma pH as determinants of renal bicarbonate reabsorption.

To examine if bicarbonate reabsorption varies with filtered bicarbonate and plasma pH, we infused anesthetized dogs i.v. with sodium chloride and sodium bicarbonate to alter plasma bicarbonate concentration (PHCO3) without changing hematocrit. Examinations in five dogs over a wide range of glomerular filtration rates (GFR) during ethacrynic acid infusion showed that bicarbonate reabsorption at equal filtered load and equal plasma pH of 7.5 was not significantly changed by increasing PHCO3 from 30.2 +/- 0.4 to 55.2 +/- 0.6 mM and PCO2 from 33.8 +/- 0.7 to 74.1 +/- 2.1 mm Hg. Examinations during respiratory and metabolic alkalosis in five dogs at plasma pH of 7.8 showed that bicarbonate reabsorption at equal filtered load was not significantly different at a PCO2 of 20.2 +/- 0.8 and 36.8 +/- 0.8 mm Hg. Finally, in five dogs that did not receive ethacrynic acid, plasma pH was lowered by inducing respiratory acidosis at a PHCO3 of 30 mM and raised during progressive respiratory and metabolic alkalosis, Bicarbonate reabsorption was linearly related to plasma pH within the range 7.1 to 7.85 (r = 0.92). By altering plasma pH by 0.1 unit, bicarbonate reabsorption was altered by 10 +/- 1%. Thus, filtered bicarbonate rather than GFR and plasma pH rather than PCO2 are important acute regulators of bicarbonate reabsorption. This regulation may be achieved by determining pH and bicarbonate concentration in the luminal fluid along the proximal tubules.

Alkalosis↗
PubMed1978

Mechanism of the effect of varying PCO2 on gluconeogenesis from lactate in the perfused rat liver.

1. The effects of varying PCO2 on glucose output and the intracellular concentrations of lactate, pyruvate, phosphoenolpyruvate, 2-phosphoglycerate and 3-phosphoglycerate were studied in the isolated rat liver perfused with differing concentrations of lactate. 2. When the perfusate lactate concentration is above 1.5 mmol/l respiratory acidosis (simulated by high perfusate PCO2) inhibits gluconeogenesis from lactate, whereas respiratory alkalosis stimulates gluconeogenesis. 3. In general there were significant positive correlations between intracellular pH (pHi) and hepatocyte phosphoenolpyruvate, 2-phosphoglycerate and 3-phosphoglycerate concentrations, and negative correlations between pHi and lactate and pyruvate concentrations; there were usually significant correlations in the opposite sense between these metabolites and log PCO2. 4. The results suggest that CO2 exerts an inhibitory effect on gluconeogenesis at a step between pyruvate and phosphoenolypruvate; however, this is not the only effect of CO2 on the gluconeogenic sequence. CO2 probably acts by changing pHi, but direct effects of CO2 and HCO-3 cannot be excluded. 5. Except at low lactate concentrations, nonionic diffusion probably does not play a major role in the entry of lactate into the hepatocyte.

Animals↗
PubMed2004

Effects of end-inspiratory and end-expiratory pressures on alveolar recruitment and derecruitment in saline-washout-induced lung injury -- a computed tomography study.

BACKGROUND: Lung protective ventilation using low end-inspiratory pressures and tidal volumes (VT) has been shown to impair alveolar recruitment and to promote derecruitment in acute lung injury. The aim of the present study was to compare the effects of two different end-inspiratory pressure levels on alveolar recruitment, alveolar derecruitment and potential overdistention at incremental levels of positive end-expiratory pressure. METHODS: Sixteen adult sheep were randomized to be ventilated with a peak inspiratory pressure of either 35 cm H2O (P35, low VT) or 45 cm H2O (P45, high VT) after saline washout-induced lung injury. Positive end-expiratory pressure (PEEP) was increased in a stepwise manner from zero (ZEEP) to 7, 14 and 21 cm of H2O in hourly intervals. Tidal volume, initially set to 12 ml kg(-1), was reduced according to the pressure limits. Computed tomographic scans during end-expiratory and end-inspiratory hold were performed along with hemodynamic and respiratory measurements at each level of PEEP. RESULTS: Tidal volumes for the two groups (P35/P45) were: 7.7 +/- 0.9/11.2 +/- 1.3 ml kg(-1) (ZEEP), 7.9 +/- 2.1/11.3 +/- 1.3 ml kg(-1) (PEEP 7 cm H2O), 8.3 +/- 2.5/11.6 +/- 1.4 ml kg(-1) (PEEP 14 cm H2O) and 6.5 +/- 1.7/11.0 +/- 1.6 ml kg(-1) (PEEP 21 cm H2O); P < 0.001 for differences between the two groups. Absolute nonaerated lung volumes during end-expiration and end-inspiration showed no difference between the two groups for given levels of PEEP, while tidal-induced changes in nonaerated lung volume (termed cyclic alveolar instability, CAI) were larger in the P45 group at low levels of PEEP. The decrease in nonaerated lung volume was significant for PEEP 14 and 21 cm H2O in both groups compared with ZEEP (P < 0.005). Over-inflated lung volumes, although small, were significantly higher in the P45 group. Significant respiratory acidosis was noted in the P35 group despite increases in the respiratory rate. CONCLUSION: Limiting peak inspiratory pressure and VT does not impair alveolar recruitment or promote derecruitment when using sufficient levels of PEEP.

Animals↗