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At least 667 records · Page 37Linked to original sources
PubMed1993

Comparative cardiopulmonary effects of carbon dioxide versus helium pneumoperitoneum.

The recent surge in enthusiasm for laparoscopic surgery has created concern that abdominal insufflation with carbon dioxide produces a respiratory acidosis. This may be because of both transperitoneal gas absorption and impaired ventilation with increased dead space from elevated intraabdominal pressure. To examine the relative contributions of these factors, we developed an animal model of surgical pneumoperitoneum that evaluated the cardiorespiratory effects of abdominal insufflation. Helium was chosen as an alternative to CO2 because it is both chemically and biologically inert. Carbon dioxide absorption during CO2 pneumoperitoneum caused arterial PCO2 to increase from 41.3 +/- 3.0 to a maximum of 58.3 +/- 4.0 mm Hg, with pH descending from 7.46 +/- 0.02 to a nadir of 7.31 +/- 0.02 (p < 0.05). Pulmonary artery pressure increased to twice baseline levels during CO2 insufflation (p < 0.05). Helium did not cause hypercarbia, acidemia, or pulmonary hypertension despite insufflation under identical conditions. These results indicate that transperitoneal absorption of CO2, not increased dead space, is responsible for the respiratory acidosis observed. Helium merits further study as an agent to induce pneumoperitoneum, especially when concerns of underlying acidosis or impaired gas exchange are present.

Acidosis, Respiratory↗
PubMed1999

Oxygen therapy during exacerbations of chronic obstructive pulmonary disease.

Venturi masks (VMs) and nasal prongs (NPs) are widely used to treat acute respiratory failure (ARF) in chronic obstructive pulmonary disease (COPD). In this study, these devices were compared in terms of their potentiality to worsen respiratory acidosis and their capacity to maintain adequate (> 90%) arterial oxygenation (Sa,O2) through time (approximately 24 h). In a randomized cross-over study, 18 consecutive COPD patients who required hospitalization because of ARF were studied. After determining baseline arterial blood gas levels (on room air), patients were randomized to receive oxygen therapy through a VM or NPs at the lowest possible inspiratory oxygen fraction that resulted in an initial Sa,O2 of > or = 90%. Arterial blood gas levels were measured again 30 min later (on O2), and Sa,O2 recorded using a computer during the subsequent approximately 24 h. Patients were then crossed-over to receive O2 therapy by means of the alternative device (NPs or VM), and the same measurements obtained again in the same order. It was observed that both the VM and NPs improved arterial oxygen tension (p<0.0001) to the same extent (p=NS), without any significant effect upon arterial carbon dioxide tension or pH. However, despite this adequate initial oxygenation, Sa,O2 was < 90% for 3.7+/-3.8 h using the VM and for 5.4+/-5.9 h using NPs (p<0.05). Regression analysis showed that the degree of arterial hypoxaemia (p<0.05) and arterial hypercapnia (p<0.05) present before starting O2 therapy and, particularly, the initial Sa,O2 achieved after initiation of O2 therapy (p<0.0001) enabled the time (in h) that patients would be poorly oxygenated (Sa,O2 < 90%) on follow-up to be predicted. These findings suggest that, in order to maintain an adequate (> 90%) level of arterial oxygenation in patients with chronic obstructive pulmonary disease and moderate acute respiratory failure: 1) the initial arterial oxygen saturation on oxygen should be maximized whenever possible by increasing the inspiratory oxygen fraction; 2) this strategy seems feasible because neither the VM nor NPs worsen respiratory acidosis significantly; and 3) the Venturi mask (better than nasal prongs) should be recommended.

Acidosis, Respiratory↗
PubMed2004

Acidosis in a patient with cholera: a need to redefine concepts.

A patient presented with cholera and a severe degree of ECF volume contraction. Despite large losses of bicarbonate (HCO3-)-containing diarrhoeal fluid, laboratory acid-base values were remarkably close to normal. A detailed analysis emphasizing principles of physiology and a quantitative approach provided new insights and eventually better definitions of metabolic and respiratory acidosis. A shift in focus from HCO3- concentration to HCO3- content in the extracellular fluid (ECF) compartment revealed the presence of metabolic acidosis. Central to this analysis was an emphasis on the haematocrit to enable a more accurate estimate of the degree of ECF volume contraction. The latter also revealed 'contraction' metabolic alkalosis, which masked the underlying metabolic acidosis. The presence of a respiratory acidosis of the tissue type was evident from the raised venous PCO2, which was not surprising once the magnitude of the ECF contraction had been appreciated. 'Bad buffering', as defined by Professor McCance, was the immediate danger and prompted swift action to restore an effective circulation. The haematocrit and the venous PCO2 also contribute valuable information to monitor the response to therapy. Nevertheless, there were still dangers to be discovered when an in-depth analysis suggested that the administration of isotonic saline would introduce an unanticipated danger for the patient.

Acidosis↗
PubMed2004

Acid-base balance during hypoxic hypometabolism: selected vertebrate strategies.

An important functional advantage of hypoxic hypometabolism is that it blunts the acid-base consequences of hypoxia. Hypoxia can lead to anaerobiosis and metabolic acidosis and, in animals that are apneic, to respiratory acidosis. A fall in blood and tissue pH is a major limiting factor in hypoxic tolerance and a variety of strategies occur in vertebrates, in concert with hypometabolism, to respond to this acid-base challenge. These include sequestering of lactic acid away from the circulating blood during the hypoxic exposure, either in underperfused tissues or in mineralized tissues, supplementing extracellular buffering by releasing bone mineral into the circulation, and utilizing alternative metabolic pathways for anaerobiosis to produce ethanol rather than lactate as the principal end-product. For submerged air-breathing ectotherms, effective cutaneous O2 and CO2 exchange can also allow an animal to avoid or minimize both anaerobiosis and respiratory acidosis. These responses serve to maintain a viable acid-base state in the body and to extend the time that the hypoxic stress can be endured.

Acclimatization↗
PubMed1965

HOMEOSTATIC PROBLEMS IN GENERAL SURGERY.

For electrolyte problems that arise during surgical procedures, the surgeon must be versed in the physiologic function of the organs that play vital roles in homeostasis. Pulmonary and renal evaluation before operation can give forewarning of potential dangers. Hyperaldosteronism, a disease entity influencing electrolytic changes and causing other pathophysiological effects, should be understood by the surgeon. Not only should he understand the causes of dehydration, hyperhydration, metabolic and respiratory acidosis and metabolic and respiratory alkalosis, he should also be able to recognize their deleterious effects clinically, know how to make use of adequate laboratory procedures to substantiate a diagnosis and determine the effect of treatment. The effect of water deficit and water excess, and of deficits and excesses of such ions as sodium, potassium, calcium, carbon dioxide and bicarbonate on the renal, cardiac, pulmonary and neuromuscular systems must be considered.Tetany before or after operation challenges a surgeon's diagnostic acuity. Relying on laboratory tests only, without correlating the results with history and clinical features, may lead to errors in the administration of electrolytic fluids.

Acidosis, Respiratory↗
PubMedDate not supplied

Acid-base disorders in hyperglycemia of insulin-dependent diabetic patients on chronic dialysis.

The authors studied hyperglycemia occurring in insulin-dependent diabetic patients on chronic dialysis to determine the types of associated acid-base disorders, their treatment, and any differences from hyperglycemia in diabetic patients with intact renal function. Eighty-eight episodes of serum glucose greater than 25 mmol/L were observed, 23 in hemodialysis patients and 65 in patients on continuous peritoneal dialysis. Treatment consisted of low-dose insulin in 77 episodes and low-dose insulin plus saline in 11; no base was administered. Seventeen episodes (19%) presented with ketoacidosis. Arterial blood gas determinations were carried out at presentation in 37 of the episodes without ketoacidosis. Of these, 12 had respiratory alkalosis, six had respiratory acidosis and severe pulmonary edema, 14 had other single or mixed acid-base disorders, and only five had normal acid-base status. Insulin corrected the ketoacidosis in all instances and both pulmonary edema and respiratory acidosis in five of six instances. In eight cases metabolic alkalosis developed during treatment, without external acid loss. At the completion of treatment respiratory alkalosis was present in half the cases. No difference was noted between patients treated with hemodialysis or peritoneal dialysis. Insulin alone is sufficient for the management of hyperglycemia in dialysis patients. Certain acid-base disorders persist, but do not need further treatment. Hyperglycemia in patients on dialysis is characterized by infrequent development of metabolic acidosis and frequent presentation with respiratory alkalosis, by respiratory acidosis that is corrected by insulin, and by metabolic alkalosis developing during treatment without external cause.

Acid-Base Imbalance↗
PubMed1993

Respiratory muscle acidosis stimulates endogenous opioids during inspiratory loading.

Activation of endogenous opioid pathways during intense inspiratory flow-resistive loading (IRL) results in greater inhibition of EMG activity in the external oblique (EMGeo) relative to the diaphragm (EMGdi). Dichloroacetate (DCA) abolishes opioid-mediated inhibitory influences upon these muscles, suggesting a causal relationship between respiratory muscle lactic acidosis and activation of endogenous opioid pathways, during IRL. We tested the hypothesis that a more intense acidosis of the external oblique relative to the diaphragm may be the signal that determines the differential inhibitory opioid-mediated effect upon the respiratory muscles during IRL. Unanesthetized goats were exposed to IRL (50 cm H2O/1/s) for 120 min, before and after intravenous pretreatment with DCA (50 mg/kg) or saline. We measured peak phasic EMGdi and EMGeo, and respective muscle interstitial pH (pHdi, pHeo) using flexible pH probes. After 120 min IRL with saline, pHdi, and pHeo declined by -0.12 +/- 0.03 (mean +/- SEM) and -0.20 +/- 0.04 units, respectively (p < 0.05, pHdi versus pHeo). Naloxone (NLX), 0.3 mg/kg given intravenously at this time, increased EMGdi by 26.5 +/- 6.1%, but EMGeo by 81.9 +/- 13.3% (p < 0.05, EMGdi versus EMGeo). DCA blunted both the change in pHdi and pHeo during IRL (to -0.01 +/- 0.01 and -0.08 +/- 0.03 units, respectively) (p < 0.05, DCA versus saline) and the increase in EMGdi and EMGeo with NLX (to -1.0 +/- 2.6% and 5.7 +/- 5.8%, respectively) (p < 0.05, DCA versus saline).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Lactic↗
PubMed1991

Effects of extracellular pH, PCO2 and HCO3- on intracellular pH in isolated type-I cells of the neonatal rat carotid body.

1. The effects of changing PCO2 extracellular pH (pHo) and HCO3- on intracellular pH (pHi) were studied in isolated neonatal rat type-I carotid body cells using the pH-sensitive fluoroprobe, carboxy-SNARF-1. 2. Simulated respiratory acidosis and alkalosis (i.e. changes in PCO2 at constant HCO3-) led to rapid (half-time t0.5 = 3 s) monotonic changes in pHi. The relationship between pHi and pHo under these conditions was linear, steep (0.63 pHi/pHo) and remarkably similar to the response predicted from a passive cell model (i.e. a cell lacking pHi regulation). 3. In order to model the above pHi changes (point 2), it was necessary to determine beta i (intrinsic intracellular buffering power). By using small incremental acid loads in the cell (progressive [NH4+]o removal), beta i was determined as a function of pHi to be: beta i = 127.6-16.04 pHi. 4. Changes in PCO2 at constant pHo (i.e. simultaneously changing HCO3-) caused rapid transient changes in pHi but did not significantly affect steady-state pHi over the range 1-10% CO2. 5. When PCO2 was held constant (5%), changing HCO3- and thus pHo (i.e. a simulated metabolic acidosis/alkalosis) led to much slower changes in pHi (t0.5 approximately 1 min). Steady-state pHi showed an almost identical dependence on pHo (slope 0.68) to that found for simulated respiratory acidosis/alkalosis. Therefore, over the range of pHo, PCO2 and [HCO3-]o tested, steady-state pHi appeared to be a unique function of pHo and independent of PCO2 and [HCO3-]o. 6. The effects on pHi of respiratory acidosis, metabolic acidosis and increases of PCO2 at constant pHo (present work) were compared with previously published work on the ability of similar manoeuvres to increase the carotid sinus nerve (CSN) discharge rate. The two sets of data showed several striking similarities: (i) in both cases, the response to a respiratory acidosis was rapid in onset, maintained and reversible; (ii) in both cases, the speed of response to a metabolic acidosis was significantly slower than in (i) but, again, it was maintained and reversible; (iii) in both cases, increases in PCO2 at constant pHo elicited a rapid response but one which was only transient with no change in the steady-state value. 7. The close correlation between the effects of changing pHo, PCO2 and [HCO3-]o on pHi and on CSN discharge suggests that a change in type-I cell pHi is the first step in the chemoreception of blood pH by the carotid body.(ABSTRACT TRUNCATED AT 400 WORDS)

Acidosis↗
PubMed1976

Acid-base changes in milk and blood of rats in acidosis and alkalosis.

Lactating white rats (Rattus norvegicus) were subjected to metabolic and respiratory acidosis and metabolic alkalosis. Before and during the various treatments, the acid-base status of heart blood and milk was determined. Acute metabolic acidosis lowered the pH of plasma and milk; Pco(2) and bicarbonate concentrations in plasma were lowered, and in milk Pco(2) was raised and the bicarbonate concentration remained unchanged. Respiratory acidosis and acetazolamide caused a drop in blood pH and in blood and milk bicarbonate concentrations; milk pH remained unchanged, but Pco(2) was raised in both plasma and milk. Acute metabolic alkalosis raised the blood pH and milk Pco(2); plasma Pco(2) and bicarbonate concentrations in blood and milk remained unchanged. The data show that greater changes occur in acid-base parameters of blood than milk when animals are exposed to acidifying and alkalinizing stimuli.

Acid-Base Equilibrium↗
PubMed1979

Carbonic anhydrase isoenzyme B in erythrocytes of subjects with chronic acidosis.

A specific and quantitative immunological method for determination of human erythrocyte carbonic anhydrase isoenzyme B has been used to ascertain the contents of this enzyme in the erythrocytes of healthy persons and of subjects with chronic metabolic and respiratory acidosis. The investigations have shown significant increase of carbonic anhydrase type B in the erythrocytes of patients suffering from renal failure with chronic acidosis, and in patients with chronic obstructive lung disease and chronic respiratory acidosis. The erythrocytes of acidotic uremic patients have a significantly higher content of erythrocyte carbonic anhydrase isoenzyme B than do the erythrocytes of uremic subjects without chronic acidosis. In chronic obstructive lung disease, the content of this enzyme in erythrocytes was significantly higher in the hypercapnic patients than in the normocapnic ones. In renal failure, significant correlation was found between carbonic anhydrase isoenzyme B and standard bicarbonate. In chronic obstructive lung disease no significant correlation was found between carbonic anhydrase and pCO2.

Acidosis↗
PubMed2003

Effects of helium-oxygen on respiratory mechanics, gas exchange, and ventilation-perfusion relationships in a porcine model of stable methacholine-induced bronchospasm.

OBJECTIVE: To explore the consequences of helium/oxygen (He/O(2)) inhalation on respiratory mechanics, gas exchange, and ventilation-perfusion (VA/Q) relationships in an animal model of severe induced bronchospasm during mechanical ventilation. DESIGN: Prospective, interventional study. SETTING: Experimental animal laboratory, university hospital. INTERVENTIONS: Seven piglets were anesthetized, paralyzed, and mechanically ventilated, with all ventilator settings remaining constant throughout the protocol. Acute stable bronchospasm was obtained through continuous aerosolization of methacholine. Once steady-state was achieved, the animals successively breathed air/O(2) and He/O(2) (FIO(2) 0.3), or inversely, in random order. Measurements were taken at baseline, during bronchospasm, and after 30 min of He/O(2) inhalation. RESULTS: Bronchospasm increased lung peak inspiratory pressure (49+/-6.9 vs 18+/-1 cm H(2)O, P<0.001), lung resistance (22.7+/-1.5 vs 6.8+/-1.5 cm H(2)O x l(-1).s, P<0.001), dynamic elastance (76+/-11.2 vs 22.8+/-4.1 cm H(2)O x l(-1), P<0.001), and work of breathing (1.51+/-0.26 vs 0.47+/-0.08, P<0.001). Arterial pH decreased (7.47+/-0.06 vs 7.32+/-0.06, P<0.001), PaCO(2) increased, and PaO(2) decreased. Multiple inert gas elimination showed an absence of shunt, substantial increases in perfusion to low VA/Q regions, and dispersion of VA/Q distribution. He/O(2) reduced lung resistance and work of breathing, and worsened hypercapnia and respiratory acidosis. CONCLUSIONS: In this model, while He/O(2) improved respiratory mechanics and reduced work of breathing, hypercapnia and respiratory acidosis increased. Close attention should be paid to monitoring arterial blood gases when He/O(2) is used in mechanically ventilated acute severe asthma.

Acute Disease↗
PubMed1984

Effects of acidosis and carbonic anhydrase inhibition in the elasmobranch rectal gland.

We studied the effects of acidosis and carbonic anhydrase inhibition on rectal gland fluid secretion. In the anesthetized dogfish shark, Squalus acanthias, volume expanded by a constant infusion of Ringer solution, fluid formation was halved by severe systemic metabolic and respiratory acidosis (pH approximately 7.10) and carbonic anhydrase inhibition. Mild respiratory acidosis (pH approximately 7.6) equivalent to the measured systemic pH during carbonic anhydrase inhibition was without effect. Inhibition of rectal gland enzyme produced severe glandular acidosis, which is indicated by an increase in gland fluid PCO2 (from 7 to 26 mmHg) and HCO3- (from 1.2 to 2.4 mM) and a decrease in pH (from 6.7 to 6.4). Gland tissue total CO2 dropped from 18 to 11 mmol/kg. These changes occurred despite nearly 50% reduction in fluid formation, O2 consumption, and CO2 output. We propose that carbonic anhydrase facilitates CO2 transfer from sites of metabolism to capillary blood by its conversion to HCO3-. This maintains a tolerable intracellular acid-base milieu during stimulated fluid secretion.

Acidosis↗
PubMed1989

[Respiratory insufficiency in mucoviscidosis. Pathophysiologic aspects of conservative drug therapy].

The compensated chronic respiratory acidosis in a girl with cystic fibrosis changed into a mixed respiratory acidosis and metabolic alkalosis under the influence of therapeutic measures. As a consequence respiratory insufficiency worsened. Conservative management of the alkalosis alone both improved hypoxemia and hypercapnia without needing artificial ventilation.

Acid-Base Equilibrium↗
PubMed1997

Developmental changes in the effect of acidosis on contraction, intracellular pH, and calcium in the rabbit mesenteric small artery.

The purpose of the present study was to determine developmental changes in the effect of respiratory acidosis on vascular smooth muscle contraction. Vessel diameter, intracellular pH (pHi), and calcium concentration ([Ca]i) were measured in a cannulated preparation of the small mesenteric artery of newborn and adult rabbits. In the artery precontracted by high KCl, acidosis caused a vasorelaxation both in the newborn and the adult; the vasorelaxation was greater in the newborn than in the adult. The fura-2 fluorescence ratio, an indicator of [Ca]i, decreased transiently during acidosis and the decrease was similar in the two age groups. In the artery precontracted by norepinephrine, acidosis caused a transient vasoconstriction in the adult and a vasorelaxation in the newborn. In these vessels, the fura-2 fluorescence ratio increased transiently during acidosis; the increase was similar in the two groups. Upon induction of acidosis, pHi fell rapidly in the artery precontracted by norepinephrine or high KCl, and the depression of pHi was similar in the two groups. In the skinned smooth muscle preparation, a tension-[Ca] relationship curve at pH 7.1 was not significantly different from that at pH 6.8 in the adult. In the newborn, the tension-[Ca] curve at pH 6.8 was shifted to the right, compared with that at pH 7.1. These data suggest that the vasorelaxant effect of respiratory acidosis in the premature vessel is greater than in the adult. The greater vasorelaxation in the newborn cannot be explained by the age-related difference in pHi or [Ca]i during acidosis. The greater sensitivity of myofibrils to low pHi in the newborn may, at least in part, be responsible for the greater vasorelaxation in this age group.

Acidosis, Respiratory↗
PubMed1983

Effects of pH on maximal power output and fatigue during short-term dynamic exercise.

Six healthy subjects performed four exercise studies in random order on separate days: a control study, metabolic acidosis induced by ammonium chloride, metabolic alkalosis induced by sodium bicarbonate, and respiratory acidosis induced by 5% CO2 inhalation. The subjects exerted maximal force on the pedals of a constant-velocity cycle ergometer at 100 rpm for 30 s; torque was measured and power calculated. Arterialized venous blood was sampled, and plasma lactate concentrations was measured immediately after and at 2-min intervals for 10 min following exercise. Although maximal peak power and total work, for the 30-s test, were lower in the two acidosis conditions, this effect was not statistically significant. Plasma lactate 30-s postexercise was lower in metabolic acidosis (2.8 +/- 1.6 mmol X 1(-1) (mean +/- SD) and respiratory acidosis (1.5 +/- 0.8 mmol X 1(-1) than in placebo conditions (5.9 +/- 3.3 mmol X 1(-1) and metabolic alkalosis 7.8 +/- 4.2 mmol X 1(-1). These differences were maintained but lessened during 10 min of recovery. In contrast to previous studies, which showed a marked reduction in endurance time during sustained heavy exercise, reductions in blood pH are associated with only small reductions in the total work performed in 30 s of maximal exercise. A delayed and smaller accumulation of lactate in plasma was observed following exercise during acidosis.

Acid-Base Equilibrium↗
PubMed1997

Effect of acidosis on contraction, intracellular pH, and calcium in the newborn and adult rabbit aorta.

This study investigated the effect of acidosis on intracellular pH (pHi), intracellular calcium concentration ([Ca]i), and vascular contraction in the aorta of the newborn and adult rabbit. Isometric tension, pHi, and [Ca]i were measured in an isolated ring preparation. After the vascular contraction was induced with 50mM KC1, the effect of respiratory acidosis produced by elevation of PCO2 was studied. Respiratory acidosis caused a transient depression followed by a recovery of contractile tension. The decrease in developed tension was greater in the newborn than in the adult. The decrease in pHi during acidosis was similar in the two age groups. [Ca]i increased during acidosis and the increase was greater in the newborn than in the adult. These data show that the vasorelaxant effect of acidosis in the newborn aorta is greater than that in the adult aorta. The greater vasodilation in the newborn cannot be explained by the difference in pHi or [Ca]i.

Acidosis, Respiratory↗
PubMed1993

Effects of a continuous infusion of tris(hydroxymethyl)aminomethane on acidosis, oxygen affinity, and serum osmolality.

The effects of a continuous infusion of tris(hydroxymethyl)aminomethane (THAM) on pH, base excess, p50, serum osmolality, and plasma drug concentration during respiratory acidosis were studied in newborn piglets. Measurements were made during three experimental periods: (1) control period with normal blood gases; (2) hypercapnia period, and (3) hypercapnia plus THAM period (THAM infusion: 1.65 mmol/kg/h). pH decreased and paCO2 increased between control period (7.40 +/- 0.05 and 45 +/- 3 mm Hg) and hypercapnia period (7.24 +/- 0.06 and 59 +/- 2 mm Hg; p < 0.001; mean +/- SD). pH returned to baseline (7.37 +/- 0.04) during the hypercapnia plus THAM period, while paCO2 remained elevated (63 +/- 4 mm Hg). p50 increased from 30.7 +/- 5.9 to 38.3 +/- 4.7 (p < 0.05) during hypercapnia and decreased with hypercapnia plus THAM. THAM concentration and base excess increased with time and were linearly related. Serum osmolality was unchanged during the THAM infusion. We conclude that continuous infusion of THAM is effective in normalizing pH during respiratory acidosis in the piglet.

Acidosis, Respiratory↗