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PubMed1988

Assessment of collecting tubule hydrogen ion secretion in acute respiratory alkalosis using the urinary pCO2.

The use of the urine-blood (U-B) pCO2 difference as a marker of collecting tubule H+ secretion (CTH+S) faces serious interpretative pitfalls when applied to animals with respiratory acidosis. The present study was aimed to examine the use of this parameter in rats with acute respiratory alkalosis. During infusion of sodium bicarbonate, the U-B pCO2 was only slightly lower in hypocapnic than in eucapnic rats (30 +/- 2.2 and 39 +/- 3.3 mmHg, p less than 0.05) and this difference was no longer significant when this parameter was examined as a function of urine bicarbonate concentration. In contrast, the increment in urine pCO2 elicited by bicarbonate loading (i.e. the delta pCO2) was markedly reduced in hypocapnic as compared to eucapnic rats (22 +/- 3.0 and 38 +/- 4.5 mmHg, respectively, p less than 0.01). The infusion of carbonic anhydrase while the urine was highly alkaline and the blood pCO2 kept constant resulted in a decrement in urine pCO2 which was less in hypocapnic than in eucapnic rats (-23.9 +/- 1.9 vs -33 +/- 2.8 mmHg, p less than 0.02). These findings indicate that pCO2 generation from CTH+S and titration of bicarbonate is reduced in hypocapnic rats. The data are in accord with our proposal that the delta pCO2 is a better index of CTH+S than the U-B pCO2 is the assessment of respiratory acid-base disorders.

Alkalosis, Respiratory↗
PubMed2006

Acidosis in models of cardiac ventricular myocytes.

The effects of acidosis on cardiac electrophysiology and excitation-contraction coupling have been studied extensively. Acidosis decreases the strength of contraction and leads to altered calcium transients as a net result of complex interactions between protons and a variety of intracellular processes. The relative contributions of each of the changes under acidosis are difficult to establish experimentally, however, and significant uncertainties remain about the key mechanisms of impaired cardiac function. In this paper, we review the experimental findings concerning the effects of acidosis on the action potential and calcium handling in the cardiac ventricular myocyte, and we present a modelling study that establishes the contribution of the different effects to altered Ca2+ transients during acidosis. These interactions are incorporated into a dynamical model of pH regulation in the myocyte to simulate respiratory acidosis in the heart.

Acidosis↗
PubMed1989

Neurologic manifestations of pulmonary disease.

Respiratory insufficiency of any cause has significant effects on the nervous system. Headache, mental status changes, papilledema, and numerous motor abnormalities including asterixis are commonly seen. Abnormalities in ventilation and gas exchange result in hypoxia, hypercapnia, and respiratory acidosis, and these, in turn, interfere with cerebral metabolism, increase CBF, and may raise intracranial pressure. Chronic respiratory insufficiency can persist for many months with minimal neurologic symptoms, as numerous compensatory mechanisms, particularly renal, may take effect. Treatment includes restoring adequate ventilation and improving gas exchange and may require tracheal intubation and assisted ventilation. Supplemental oxygen therapy should be carefully monitored, as high rates of flow may suppress the hypoxic drive for respiration and lead to significant carbon dioxide retention. The sleep apnea syndromes are a group of disorders in which abnormal respiratory patterns during sleep result in hypercapnia and hypoxemia. Intermittent obstruction of the upper airway and abnormalities of brainstem respiratory centers cause frequent nocturnal awakenings and apneas in these patients. Treatments vary and include weight loss in obese subjects, respiratory stimulants, tracheostomy, and diaphragmatic pacing. Rapid ascent to high altitudes may result in headache, changes in mental status, papilledema, and other neurologic symptoms in certain individuals: a syndrome known as high-altitude sickness. Hypoxia leading to cerebral edema, nocturnal periodic breathing, and hypobaria produces neurologic symptoms in these individuals. Acetazolamide and dexamethasone may be effective in minimizing symptoms of this disorder. Sustained hyperventilation produces acral and circumoral paresthesias and lightheadedness in anxious individuals and can be maintained by relatively normal ventilatory patterns once established. These symptoms are due to hypophosphatemia and respiratory alkalosis, the latter reducing CBF and causing localized tissue hypoxia. Rebreathing into a paper bag at the first awareness of symptoms is the most effective form of treatment.

Brain Diseases↗
PubMed1988

Bilateral diaphragmatic paralysis: clinical spectrum, prognosis, and diagnostic approach.

In a retrospective review of the clinical course of five patients with nontrauma-related bilateral diaphragmatic paralysis, we found that the diagnosis is generally delayed (median delay: two years) in the presence of moderate to severe respiratory insufficiencies. Orthopnea out of proportion to the underlying cardiopulmonary status and thoracoabdominal paradoxus in the supine position are the clues to the diagnosis. Pulmonary function tests showed a typical restrictive ventilatory defect, and arterial blood gas showed chronic respiratory acidosis. Failure to recognize the diaphragmatic impairment led to cardiopulmonary decompensations such as cor pulmonale and acute respiratory failure. However, with the institution of appropriate therapy, adverse effects resolved and all five patients are alive and continue to lead independent lives. We conclude that nontrauma-related bilateral diaphragmatic paralysis is an underrecognized and underdiagnosed condition. The results also indicate that early diagnosis and treatment can minimize morbidity and mortality, and that excellent long-term, good-quality survival can be expected.

Aged↗
PubMed1998

Non-invasive continuous positive airway pressure in acute hypoxaemic respiratory failure--experience of an emergency department.

Non-invasive continuous positive airway pressure (CPAP) seems to decrease the need for intubation in patients with severe cardiogenic pulmonary oedema (CPO) in the intensive care unit. The goals of our study were to delineate indications for CPAP in the emergency department, and to confirm its usefulness in such a setting. We retrospectively assess the evolution of all patients ventilated under CPAP for an acute hypoxaemic respiratory failure over a 1-year period (n = 64 patients). Hypercarbia and respiratory acidosis were present in most patients with CPO (PaCO2 = 54.4+/-22.3 mmHg; pH = 7.27+/-0.13), according to respiratory exhaustion, although initial PaCO2 was low in the pneumonia group. There was a significant improvement of arterial blood gases after 1 hour of ventilation in the CPO group (PaO2 = 254.1+/-121.0 mmHg; PaCO2 = 44.0+/-12.6 mmHg; pH = 7.34+/-0.08; p < 0.0001 for both parameters). In the pneumonia group, oxygenation was also improved but with the persistence of a significant shunt (PaO2 = 157.6+/-84.4 mmHg). Fifty-four patients (84%) were considered as successfully ventilated under CPAP, with no need for intubation and a favourable evolution, mainly in the CPO group. No side effects were reported. In conclusion, CPAP is a useful and easy-to-use ventilatory device in the emergency department. It is now one of our first line treatments during prehospital and emergency care of patients with CPO.

Acute Disease↗
PubMed2001

Acute respiratory and metabolic acidosis induced by excessive muscle contraction during spinal evoked stimulation.

Spinal somatosensory evoked potentials (SSEPs) have been used to monitor spinal cord function during corrective scoliosis surgery. We report three cases in which direct epidural stimulation for measurement of SSEPs produced paraspinal muscle contraction, resulting in respiratory and metabolic acidosis. In two of the cases, SSEP-induced acidosis was observed even when only the first twitch of the train-of-four response was detectable after a second dose of muscle relaxant. In one of these two cases, the acidosis was abolished after a sufficient dose of vecuronium to ablate the twitch response. To prevent SSEP-induced respiratory and metabolic acidosis, we recommend that SSEPs should be measured only when profound neuromuscular blockade has been obtained.

Acidosis↗
PubMed1982

[Alcohol-induced lactic acidosis in thiamine deficiency].

Thiamine deficiency leads to a moderate hyperlactacidemia. As a result of an acute alcohol exposure the hyperlactacidemia is increased. In addition metabolic and respiratory acidosis with a distinct low pH value occurs. These changes constitute vital risks and may be considered as basic arguments for the explanation of sudden death in chronic alcoholics.

Acidosis↗
PubMedDate not supplied

An assessment of central-peripheral ventilatory chemoreflex interaction in humans.

The independence of the central and peripheral chemoreflexes has been tested in humans. Acute metabolic acidosis generated by a prior bout of brief, hard exercise was used to stimulate primarily the peripheral chemoreceptors, and respiratory acidosis generated by inhaled CO2 was used to stimulate both central and peripheral chemoreceptors. Seven healthy young men were studied. Ventilation and arterial pH, PCO2 and PO2 were recorded. Peripheral chemoreflex sensitivity to hypoxia during acute metabolic acidosis was repeatedly determined by measuring ventilation in euoxia (PETO2 = 100 Torr) and hypoxia (PETO2 = 50 Torr) as the subject recovered from exercise-induced acidosis. Peripheral chemoreflex sensitivity to hypoxia during CO2 inhalation was repeatedly determined by measuring ventilation in euoxia and hypoxia at two levels of hypercapnia (PETCO2 = 45 Torr and PETCO2 = 50 Torr). The ventilatory sensitivity to hypoxia at matched arterial pH values was not significantly different between conditions of high (CO2 inhalation) and low (metabolic acidosis) central chemoreceptor activity. We therefore conclude that interaction between central and peripheral chemoreflexes was non-significant in all subjects.

Adolescent↗
PubMed1986

Effects of medium pH on duodenal and ileal calcium active transport in the rat.

To study the effect of pH on Ca active transport in vitro pH was varied from 7.1 to 7.7, and bidirectional transmural Ca fluxes were measured under short-circuited conditions across duodenum or ileum from rats fed either normal chow (NCD, 1.2% Ca) or low Ca (LCD, 0.002% Ca). Duodenum and ileum from rats fed LCD actively absorbed calcium at medium pH 7.4. Reduction in mucosal and serosal medium bicarbonate from 25 to 10 mM (pH 7.4 to 7.1) decreased duodenal net Ca absorption (Jnet) from 121 +/- 32 to 39 +/- 9 nmol X cm-2 X h-1 (P less than 0.02) and ileal Jnet from 74 +/- 13 to 22 +/- 6 (P less than 0.01). The decline in duodenal and ileal Ca Jnet was due to a decrease in the mucosal-to-serosal flux (Jm----s). Raising medium pH from 7.4 to 7.7 by increasing bicarbonate from 25 to 50 mM did not alter Ca Jm----s, serosal-to-mucosal flux (Js----m), or Jnet X Ca fluxes across ileum from rats fed NCD demonstrated net secretion. LCD ileal Jm----s was unaltered when pH was reduced from 7.4 to 7.1 by increasing the PCO2 content of the buffer from 30 to 81 mmHg while maintaining bicarbonate at 24 mM. The results indicate that in vitro conditions that simulate metabolic acidosis (low bicarbonate and pH, normal PCO2) inhibit 1,25D-mediate calcium Jm----s, whereas conditions that simulate respiratory acidosis have no effect on Ca fluxes. The present studies suggest that decreases in calcium Jm----s is by a primary alteration in transport of other ions rather than direct effect on Ca transport.

Animals↗
PubMed1985

[Acid-base equilibrium and spinal fluid enzyme activity in newborn infants with pathology of the nervous system].

The acid-base balance of the blood and cerebrospinal fluid was studied in 90 babies born in asphyxia in order to use these data in assessing the damage to the nervous system. Analysis revealed the hypoxic nature of the cerebral affection which was manifested by anaerobic glycolysis of the cerebral tissue and arterial hypoxemia. The degree of acidosis detected in the cerebrospinal fluid correlated with the severity of the nervous system damage. Children with the lethal outcome presented deeompensated respiratory acidosis, in the cerebrospinal fluid whereas children with severe neurological pathology had alkalosis. It is concluded that alkolosis is induced by an intensified catabolism of the nervous system proteins which leads to the accumulation of ammoniac compounds. The same children showed pulmonary hyperventilation leading to respiratory acidocis which was not related to pulmonary pathology. The latter points to the hypoxic impairment of the respiratory centre. At the same time, a considerable increase in the activity of the glycolytic enzymes was observed; the activity of glutamate oxalacetate transaminase increased 5-fold, the activity of lactate dehydrogenase rose two-fold.

Aspartate Aminotransferases↗
PubMed1995

Hypertonic saline-dextran resuscitation from hemorrhagic shock induces transient mixed acidosis.

OBJECTIVE: To evaluate the magnitude and mechanism of potential metabolic acidosis after resuscitation with 7.5% sodium chloride/6% dextran-70. DESIGN: Blinded, randomized, control trial. SETTING: Laboratory setting. SUBJECTS: Sixteen healthy Yorkshire swine. INTERVENTIONS: Anesthetized, mechanically ventilated swine underwent 90 mins of hemorrhagic hypotension (mean arterial pressure of 50 to 55 mm Hg), and a lactic acid infusion (1.5 to 2.4 mmol/kg) was given during the last 60 mins of hemorrhage to produce pretreatment acidosis. The pigs were then given either 4 mL/kg of intravenous normal saline (n = 8) or 7.5% sodium chloride/6% dextran-70 (n = 8). Groups then received isotonic lactated Ringer's solution to restore and maintain cardiac output for 120 mins. MEASUREMENTS AND MAIN RESULTS: There was no difference between groups during baseline or shock for any parameter. At the end of shock, arterial pH and base balance were below baseline values. During resuscitation, cardiac output was reached and maintained in both groups. One minute after infusion of hypertonic saline/dextran, there was a significant but transient decrease in arterial pH (from 7.407 +/- 0.015 to 7.339 +/- 0.025) and base balance (from -6.5 +/- 0.7 to -9.9 +/- 1.0 mmol/L). These changes returned to shock levels by 10 mins and then normalized to baseline levels. Hypertonic saline dextran resulted in an immediate hypernatremia, hyperchloremia, and hypokalemia, a decrease in inorganic strong ion difference (calculated as sodium plus potassium minus chloride concentrations), and no immediate change in anion gap. The normal saline group did not show an initial transient decrease in pH and base balance during resuscitation. Plasma lactate, total protein, and hemoglobin concentrations decreased equally in both groups, although they decreased more quickly with hypertonic saline/dextran. CO2 temporarily and insignificantly increased in arterial blood slightly more after the administration of hypertonic saline/dextran. By 120 mins, acid-base, electrolyte and protein changes were normalizing with hypertonic saline/dextran, while pH, base balance, and protein were decreasing below shock values in animals initially treated with normal saline. CONCLUSIONS: Hypertonic saline/dextran caused an immediate, transient acidemia, which was primarily due to a hyperchloremic, hypokalemic, metabolic acidosis with normal anion gap and decreased inorganic strong ion difference, but which was partially due to a mild transient respiratory acidosis. The acidemia was transient because of the offsetting alkalotic effects of decreasing serum protein, normalization of electrolytes, and transient nature of the increase in CO2. Lactic acidosis was not the cause of the acidemia. Over time, the acid-base status appeared to be improved more effectively with hypertonic saline/dextran than with isotonic saline resuscitation.

Acid-Base Equilibrium↗
PubMed1996

Cardio-pulmonary function during acute unilateral occlusion of the pulmonary artery in broilers fed diets containing normal or high levels of arginine-HCl.

Cardio-pulmonary function was measured in male broilers reared on diets formulated to contain 1.5% arginine (NORMAL group) or 2.5% arginine (ARGININE group). A snare placed around the right pulmonary artery permitted acute shunting of the entire cardiac output (CO) through the left pulmonary artery, resulting in sustained increases in blood flow (BF) through the left lung in both groups. The unilateral increase in BF was accompanied by sustained increases in pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) in the NORMAL group. However, following initial transient increases in PAP and PVR in the ARGININE group, subsequent pulmonary vasodilation gradually reduced PVR, and thus PAP, in spite of the ongoing elevation of BF through the left lung. The capacity of the pulmonary vasculature in the ARGININE group to accommodate an increased BF at a normal PAP accounts for the previously reported lower incidence of pulmonary hypertension syndrome (PHS, ascites) in cold-stressed broilers fed supplemental dietary arginine. Hypoxemia and respiratory acidosis ensued rapidly in both groups after tightening the pulmonary artery snare, in spite of a compensatory increase in the respiratory rate. The gradual return of PVR and PAP to presnare levels in the ARGININE group did not eliminate the concurrent ventilation-perfusion mismatch caused by the increased rate of BF through the left lung. Tightening the pulmonary artery snare caused mean systemic arterial pressure (MAP) to drop from control levels of approximately 98 mm Hg to sustained hypotensive levels of approximately 65 mm Hg in both groups. This systemic hypotension was caused by decreases in CO and total peripheral resistance (TPR). The reduction in CO were caused by reduction in stroke volume (SV) rather than heart rate (HR), suggesting that acutely tightening the pulmonary artery snare increased PVR sufficiently to impede left ventricular filling. Accordingly, the maximum increment in PAP attainable by the right ventricle during acute increases in PVR apparently was inadequate to propel the entire CO through the pulmonary vasculature, setting the stage for the congestive right-sided pooling of blood routinely associated with PHS in broilers.

Animal Feed↗
PubMed1976

[Responses of small intestine tissue chemoreceptors to change in the pCO2, pH and (HCO3-) in perfusion solutions].

Perfusion of the small intestine of anesthetized cats with a solution having excessive CO2 and H+ concentration (pCO2 60 mm Hg; pH; 7.2; [HCO3-] 25 MM) produced a threshold reflex increase in the blood pressure. The subsequent increase of pCO2 to 380 mm Hg and decrease of pH to 6.4 evoked a gradual raise of the blood pressure (8.0+/-0.6 mm Hg) followed by the sharp increase of pressor reflexes amplitude within the range of pH 6.4--6.1. Tissue receptors were found to be essentially sensitive to solutions imitating metabolic acidosis (decrease of [HCO3-] within the physiological range of pH changes (pH 7.1--6.8). Solutions with pH 6.4--6.1 imitating respiratory acidosis (increase of pCO2) were more effective than those imitating metabolic acidosis. The possible role of interstitial pH changes in responses of the tissue chemoreceptors to CO2, is discussed.

Animals↗
PubMed1998

[Respiratory failure based on pulmonary tuberculosis sequelae and its management].

According to the complexity of pathological change of pulmonary tuberculosis sequelae (TB seq), on which respiratory failure based shows the higher incidence of marked degree of hypoxemia and hypercapnia than that based on chronic pulmonary emphysema (CPE). In TB seq, pulmonary artery mean pressure is higher, nocturnal oxyhemoglobin desaturation is much lower than in CPE. Also hypoxemia on exercise is lower, and oxygen inhalation for this hypoxemia is more effective than in CPE. The most effective therapy is continuous oxygen therapy. Home oxygen therapy has improved the prognosis and quality of life (QOL) of patients with respiratory failure based on TB seq. Artificial positive pressure ventilation (TIPPV) with intubation or tracheotomy is carried out for patients with severe hypercapnia and respiratory acidosis. Recently, early application of nasal mask ventilation (NPPV) on patients with TB seq has prohibited acute exacerbation of chronic respiratory failure. And also for patients with severe hypercapnia, NPPV with BIPAP method is effective for their QOL. Comprehensive respiratory rehabilitation is also successfully applied for their management.

Humans↗
PubMed1998

Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease.

BACKGROUND: Variation of the arterial carbon dioxide partial pressure (PaCO2) is not uncommon in anesthetic practice. However, little is known about the myocardial consequences of respiratory alkalosis and acidosis, particularly in patients with coronary artery disease. The aim of the current study was to investigate the effects of variation in PaCO2 on myocardial blood flow (MBF), metabolism, and systemic hemodynamics in patients before elective coronary artery bypass graft surgery. METHODS: In 10 male anesthetized patients, measurements of MBF, myocardial contractility, metabolism, and systemic hemodynamics were made in a randomized sequence at PaCO2 levels of 30, 40, and 50 mmHg, respectively. The MBF was measured using the Kety-Schmidt technique with argon as a tracer. End-diastolic left ventricular pressure and the maximal increase of left ventricular pressure were assessed using a manometer-tipped catheter. RESULTS: The cardiac index significantly changed with varying PaCO2 levels (hypocapnia, - 9%; hypercapnia, 13%). This reaction was associated with inverse changes in systemic vascular resistance index levels. The MBF significantly increased by 15% during hypercapnia, whereas no change was found during hypocapnia. Myocardial oxygen and glucose uptake and the maximal increase of left ventricular pressure were not affected by varying PaCO2 levels. CONCLUSIONS: In anesthetized patients with coronary artery disease, short-term variations in PaCO2 have significant effects on MBF but do not influence global myocardial oxygen and glucose uptake. Changes in systemic hemodynamics associated with respiratory alkalosis and acidosis are caused by changes in systemic vascular resistance rather than by alterations in myocardial contractility.

Acidosis, Respiratory↗
PubMed1992

Neonatal complications and risk of intraventricular-periventricular hemorrhage.

We have prospectively studied 117 premature infants < or = 1500 gm (VLBW) to assess the relationship between maternal, obstetric, fetal and newborn complications and the grade of periventricular-intraventricular hemorrhage (PVH-IVH). PVH-IVH was documented by cranial ultrasonography in 41% of surviving neonates. 83% of infants with PVH-IVH grade I-II survived as compared to the 39% of infants with PVH-IVH grade III-IV (p < .001). Maternal and obstetric complications were not associated with PVH-IVH (NS). Newborn respiratory complications (p < .004) and major infections (p < .02) are independent variables associated with PVH-IVH. Immaturity at delivery, metabolic acidosis, respiratory distress syndrome and recurrent apnea are important mechanisms of cerebral injury contributing to severity of PVH-IVH.

Acid-Base Equilibrium↗
PubMed1966

The respiratory response of the new-born lamb to inhaled CO-2 with and without accompanying hypoxia.

1. The respiratory response to inhaled CO(2) was measured in twenty unanaesthetized new-born lambs aged 4 hr-10 days. Measurement of resting arterial pH, P(CO2) and plasma bicarbonate showed a non-respiratory acidosis immediately after birth which was corrected in the first 24-28 hr: thereafter, the acid-base pattern was of a compensated respiratory alkalosis.2. When CO(2) was added to the inspired gases and resting arterial oxygen tension (P(a), (O2)) was controlled, the average increase in minute ventilation (V) was 0.075 l.min(-1).kg(-1).mm Hg, P(a), (CO2) (-1) and duplicate responses in the same lamb differed by 6-22.5%.3. The slope of the V/P(a), (CO2) line (S) varied inversely with P(a), (O2). In one lamb, severe hypoxia (P(a), (O2) = 21 mm Hg) caused a marked depression of the slope.4. Neither the slope S nor the horizontal intercept B of the lines was related to the age of the lamb. B was not related to pH(a) and only slightly affected by acute hypoxia. B was related to arterial [HCO(3) (-)] and values for both were reduced with the acid-base disturbances seen in the first 10 days after birth. Evidence was given which suggested that the response of the new-born lamb to inhaled CO(2) was similar to that of man acclimatized to a P(a), (O2) of 70-75 mm Hg.5. In the lightly anaesthetized lamb, bilateral section of the sinus nerves caused a small reduction in the sensitivity to inhaled 5% CO(2) in air, an increase in the respiratory lag and a reduction in the rate at which V increased.6. It was concluded that, in the new-born lamb, the carotid chemo-receptors are involved in the response to inhaled CO(2) and that hypoxia potentiates this response.

Acidosis↗
PubMed1983

Cerebral vascular resistance in premature infants.

The cerebral vascular bed is a low-resistance system in which continuous forward or advancing diastolic blood flow can be demonstrated. This advancing flow increases progressively with vasodilation and decreases or is absent when vessels are constricted. By using the Doppler technique, an indirect assessment of vascular resistance can be made by comparing systolic and diastolic flow amplitudes. We examined nine premature infants and found that respiratory acidosis alone, or hypoxia and acidosis in combination, resulted in significant vasodilation. This effect was reversible when arterial blood gas tensions returned to normal. The results indicate that within a physiologic range of BPs, premature infants with acute respiratory distress can alter their cerebral vascular resistance in response to spontaneous changes in blood gas tensions.

Acidosis↗