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PubMedDate not supplied

[Semi-automatic determination of blood lactate in the newborn infant of the insulin-dependent diabetic mother].

Blood lactate levels were determined by Lactate Analyzer 640 Kontron in 5 infants of diabetic mothers with pregestational insulin-dependent-diabetes, class B-C-D White, BPSP negative, in strict glycemic control all along the pregnancy. In the mothers blood lactate was found in a normal range after-delivery. In the absence of complications, the neonate of diabetic mother did not show blood lactate changes above the normal range. As well as in the neonate of non diabetic mother, blood lactate increases were found only in concomitance with respiratory acidosis. In the cases with favourable course, lactate values above 2 mmol/l were normalized in the first 24 hours after the birth. The semiautomatic determination of blood lactate supplies a good prognostic evaluation of the association between metabolic and respiratory acidosis in the neonate and should therefore be routinely used in centers for management of diabetic pregnancy.

Acidosis↗
PubMed1986

Amelioration of hypoxia-induced lactic acidosis by superimposed hypercapnea or hydrochloric acid infusion.

Recent studies have shown that ketoacid production is exquisitely sensitive to changes in systemic pH, with a decrease inhibiting and an increase stimulating the production rate. To determine whether inhibition of net endogenous acid production is a widely applicable mechanism for the defense of acid-base homeostasis, we examined the effect of superimposed acidosis on lactic acid production by hypoxic rats. Anesthetized paralyzed mechanically ventilated rats with normocapnia increased blood lactate progressively in response to a fractional inspired O2 (FIO2) of 8% (PaO2, 35-38 mmHg) and achieved a level of 7.0 +/- 1.2 mM at 3 h. Superimposition of either mild respiratory acidosis (PCO2, 59 mmHg) or exogenous inorganic metabolic acidosis (intra-arterial HCl sufficient to decrease pH from 7.33 to 7.23) after 1 h of hypoxia dramatically diminished the rise in blood lactate. At the end of the third hour, blood lactate levels averaged 1.7 +/- 0.6 mM with superimposed respiratory acidosis and 2.7 +/- 0.4 mM with superimposed metabolic acidosis, both values being significantly less than the hypoxic controls. Termination of the superimposed respiratory acidosis resulted in a rapid increase in blood lactate levels, demonstrating the reversibility of the pH modulation of lactic acid production. Thus systemic acidosis appears to feed back in a protective fashion to inhibit net lactic acid production in rats with hypoxia-induced lactic acidosis. These findings suggest that finely tuned feedback control mechanisms that keep systemic pH within a narrow range operate under both major conditions of enhanced endogenous acid production (i.e., keto- and lactic acidosis).

Acidosis↗
PubMed2006

Laparoscopic surgery during pregnancy.

PURPOSE OF REVIEW: In the past decade, laparoscopic procedures have become increasingly popular owing to decreased morbidity and convalescence compared with open procedures. The purpose of this review is to evaluate recent literature on laparoscopic surgery in pregnancy and make recommendations for anesthesia based on understanding of physiology of carbon dioxide pneumoperitoneum. RECENT FINDINGS: Increasing numbers of successful cases of laparoscopic surgery are being reported. For reasons unknown, the results obtained in sheep studies do not match the observations in humans. Maternal respiratory acidosis, a common finding in sheep studies during CO2 pneumoperitoneum has not been observed in pregnant women undergoing laparoscopic surgery. A recent finding of persisting fetal sheep hypoxia beyond the duration of CO2 pneumoperitoneum calls for further investigation to determine if this finding is limited to sheep akin to sheep maternal respiratory acidosis. SUMMARY: Present evidence suggests laparoscopic surgery in pregnancy is a safe option. Left uterine displacement, maintaining end-tidal carbon dioxide between 32-34 mmHg and maternal blood pressures within 20% of baseline, and limiting abdominal insufflation pressure of carbon dioxide to 12-15 mmHg are essential hallmarks of anesthesia procedure. Although no apparent long time consequences have been reported, further studies are necessary to confirm the validity of sheep fetal hypoxia studies.

Acidosis, Respiratory↗
PubMed1997

Intratracheal pulmonary ventilation and continuous positive airway pressure in a sheep model of severe acute respiratory failure.

STUDY OBJECTIVES: Previously we have shown that optimal pulmonary gas exchange can be sustained at normal airway pressures in a model of severe acute respiratory failure (ARF), using intratracheal pulmonary ventilation (ITPV), with weaning to room air. In an identical model of ARF, we have now explored whether ITPV, combined with continuous positive airway pressure (CPAP), can sustain adequate ventilation, with weaning to room air. DESIGN: Randomized study in sheep. SETTING: Animal research laboratory at the National Institutes of Health. INTERVENTIONS: ARF was induced in 12 sheep, using mechanical ventilation at peak inspiratory pressure of 50 cm H2O, but excluding 5 to 8% of lungs. Sheep were then randomized into two groups: the CPAP-ITPV group (n=6), in which ITPV was combined with a novel CPAP system; and a control group (n=6) in which the same CPAP circuit was used, but without ITPV. MEASUREMENTS AND RESULTS: All sheep in the CPAP-ITPV group were weaned to room air in 38.7+/-14 h. PaO2/fraction of inspired oxygen (FIO2) progressively increased from 108.8+/-43 to 355.7+/-93.1; PaCO2 remained within normal range; respiratory rate (RR) ranged from 18 to 120 breaths/min, and tidal volume (VT) was as low as 1.1 mL/kg. All sheep in the control group (CPAP alone) developed severe respiratory acidosis and hypoxemia after 4.8+/-4 h. PaO2/FIO2 decreased from 126.6+/-58.2 to 107.2+/-52.5 mm Hg, with a final PaCO2 of 166.8+/-73.3 mm Hg. CONCLUSIONS: All sheep treated with CPAP-ITPV maintained good gas exchange without hypercapnia at high RR and at low VT, with weaning to room air. All control animals treated with CPAP alone developed severe hypercapnia, respiratory acidosis, and severe hypoxemia, and were killed.

Acidosis, Respiratory↗
PubMed2001

Hypokalemic metabolic acidosis attributed to cough mixture abuse.

This report describes a patient with mixed normal anion gap hyperchloremic metabolic and respiratory acidosis associated with hypokalemia attributed to cough mixture abuse. Metabolic acidosis was likely related to an overdose of ammonium chloride, whereas respiratory acidosis was probably related to the effect of hypokalemia on respiratory muscles, causing hypoventilation. Hypokalemia was caused by a transcellular shift of potassium induced by ephedrine and pseudoephedrine. Both ammonium chloride and ephedrine were probably present in the cough mixture obtained by our patient as an over-the-counter medication. Physicians should be aware of the potential for cough mixture abuse to cause major electrolyte disturbances that may carry the risk for major cardiac arrhythmias, particularly in youth.

Acidosis↗
PubMed1989

Does acidosis contribute to stress-induced ulceration in rat stomachs?

The present study examines the involvement of acidosis in stress ulceration in rat stomachs. Cold restraint stress for 2 hr did not affect the blood lactate level; however, it produced respiratory acidosis, as reflected by the depressed respiratory rate which was associated with increased CO2 tension and a lowered blood pH. Severe hemorrhagic ulceration was found in the glandular mucosa. The effects of stress on blood pH and the stomach were reversed by IV infusion of NaHCO3. Infusion of HCl IV decreased the blood pH and HCO-3 level and produced gastric ulceration. It is concluded that respiratory acidosis could be involved in stress ulceration. The metabolic acidosis evoked by HCl also induced gastric damage, but the effect was much less.

Acidosis, Respiratory↗
PubMed1976

Acid-base determinations in normal and asphyxiated term infants during the first 24 hours of life.

Vigorous term infants who are born normally initially have a moderate metabolic and respiratory acidosis which is corrected by the time the infant is 6 hours old. Asphyxiated infants consistently show a greater degree of acidosis, both metabolic and respiratory. Caesarean section results in higher pCO2 values, especially when 'diffusion apnoea' occurs. Indications for the correction of acidosis in asphyxia are proposed.

Acid-Base Equilibrium↗
PubMed1988

Incomplete global myocardial ischemia during cardiac arrest and resuscitation.

During cardiac arrest (no flow) and CPR (low flow), the onset of myocardial ischemia is followed by myocardial respiratory acidosis. Myocardial contractility is more decreased by respiratory than by metabolic acidosis. We demonstrated in a porcine model of cardiac arrest and in human patients increases in mixed venous PCO2 during CPR, whereas PaCO2 was decreased. Consequently, there was a striking increase in the venoarterial gradients for both [H+] and CO2. Both cardiac output (pulmonary blood flow) and the concentration of expired CO2 were simultaneously decreased. In great cardiac vein blood, even more profound respiratory acidosis with only minor decreases in bicarbonate and only moderate increases in lactate were observed. Intramyocardial pH was profoundly decreased. The severity of respiratory acidosis as a determinant of resuscitability and survival should be further investigated.

Animals↗
PubMed1993

Effects of acute and chronic acetazolamide on resting ventilation and ventilatory responses in men.

The effects of acetazolamide (ACTZ) on ventilatory control are thought to be mediated by metabolic acidosis. However, carbonic anhydrase (CA) inhibition within brain and chemoreceptors and tissue respiratory acidosis may also be important. We compared the acute effects of ACTZ (tissue respiratory acidosis and tissue CA inhibition without metabolic acidosis) on ventilation and ventilatory control with chronic ACTZ (acute effects plus metabolic acidosis). Five men were studied 1 h after 500 mg iv ACTZ or 0.9% saline (acute effects) and also after three doses of ACTZ (500 mg po every 6 h; chronic effects). Minute ventilation (VE), steady-state hypercapnic ventilatory response (HCVR), and hypoxic ventilatory response (HVR) were measured with respiratory inductance plethysmography. Resting VE was increased equally by acute and chronic ACTZ. HCVR increased with chronic ACTZ in hyperoxia and even further in hypoxia. In contrast, acute ACTZ had no effect on the HCVR slope in hyperoxia and suppressed its augmentation by hypoxia. HVR was fully suppressed by acute ACTZ but unchanged with chronic ACTZ. ACTZ also slowed the rate of full ventilatory response to CO2. These findings show that CA inhibitors affect ventilatory control in a complex fashion, not only through changes in systemic acid-base balance but also by central and peripheral chemoreceptor inhibition.

Acetazolamide↗
PubMed2006

Bridge to lung transplantation with the novel pumpless interventional lung assist device NovaLung.

BACKGROUND: Worsening of lung failure in patients awaiting a lung transplantation might lead to ventilation-refractory hypercapnia and respiratory acidosis. Most transplant centers consider pretransplantation extracorporeal membrane oxygenation as a contraindication for lung transplantation because of the poor outcome. We have, for the first time, applied the novel pumpless interventional lung assist NovaLung for bridge to lung transplantation in patients with severe ventilation-refractory hypercapnia. We report on our initial experience. METHODS: Between March 2003 and March 2005, 176 lung transplantations were performed, of which 60% were high-urgency lung transplantations. Twelve of the high-urgency recipients had severe ventilation-refractory hypercapnia and respiratory acidosis. These patients were connected to the novel pumpless interventional lung assist NovaLung for bridge to lung transplantation. RESULTS: The length of interventional lung assist NovaLung support was 15 +/- 8 days (4-32 days). PaO2, pH, and PaCO2 levels in arterial blood prior to interventional lung assist NovaLung implantation were 71 +/- 27 mm Hg, 7.121 +/- 0.1, and 128 +/- 42 mm Hg, respectively. Six hours after interventional lung assist NovaLung implantation, PaO2, pH, and PaCO2 levels had changed to 83 +/- 17 mm Hg (ns), 7.344 +/- 0.1 (P < .05), and 52 +/- 5 mm Hg (P < .05), respectively. Four patients died of multiorgan failure, 2 patients before and 2 after lung transplantation. Thus, 10 out of 12 patients were successfully bridged to lung transplantation, and 8 are still alive (1-year survival, 80%). CONCLUSIONS: This report suggests that interventional lung assist NovaLung implantation is an effective bridge to lung transplantation strategy in patients with ventilation-refractory hypercapnia.

Acidosis, Respiratory↗
PubMed1993

Brainstem bilirubin toxicity in the newborn primate may be promoted and reversed by modulating PCO2.

The auditory brainstem response (ABR) was monitored during infusion of bilirubin in six ventilated newborn rhesus monkeys (138-145 d gestation) while acute changes in pH were produced by varying inspired CO2. Prolonged respiratory acidosis without bilirubin infusion produced minimal changes in the ABR (one animal). CO2 exposure, usually initiated when the bilirubin level reached approximately 20 mg/dL, decreased arterial pH to values ranging from 6.85 to 7.10. ABR changes, including prolongation of the wave II-IV peak to peak intervals and decreased wave amplitudes, first developed 2-4 h after initial exposure to CO2. Total and unbound bilirubin levels at this time ranged from 376 to 564 mumol/L (22-33 mg/dL) and 38 to 65 nmol/L (2.5-3.8 micrograms/dL), respectively. Correction of respiratory acidosis produced partial to complete reversal of ABR changes within 3 to 20 min. Reexposure to CO2 immediately reproduced the ABR abnormality. Production and reversal of the abnormal ABR was obtained through two to three cycles in three animals. Thus, when the brainstem bilirubin level was near the threshold for toxicity, the effect of changes in PCO2 on the ABR were immediate, suggesting that auditory pathway toxicity is initially mediated by a reversible pH-dependent bilirubin-membrane complex. In contrast to humans, in monkeys auditory toxicity appeared to be a late manifestation of bilirubin toxicity, inasmuch as all monkeys were obtunded and apneic 30-70 min before ABR abnormalities appeared. Notwithstanding these limitations, the results support the hypothesis that bilirubin toxicity can be both promoted and reversed by modulating brain pH.

Acidosis, Respiratory↗
PubMedDate not supplied

The diagnosis of potentially fatal asthma.

The concept of life-threatening asthma is not new. Reviews of fatal asthma often describe retrospectively identified factors that were associated with or contributed to the patient's demise. We report 55 patients considered to have the diagnosis of potentially fatal asthma who were managed for 4.8 +/- 4.3 years per patient. The diagnostic criteria of potentially fatal asthma included at least one of the following four potentially fatal asthma events: 1) mechanical ventilation for respiratory arrest or failure, 2) acute respiratory acidosis that did not necessitate mechanical ventilation, 3) two episodes of acute pneumomediastinum or pneumothorax associated with status asthmaticus, 4) two or more hospitalizations for status asthmaticus in spite of long term oral corticosteroids. The mean age of patients with potentially fatal asthma was 39.6 +/- 19.1 (range 8.5-79.5 years). During 262 patient-years of management, one 79 year old demented patient died from disseminated cryptococcal infection. Two patients died from asthma after leaving our service, one patient having left the hospital against medical advice with arterial blood gases demonstrating acute respiratory acidosis during status asthmaticus. Fifty-two patients are alive and ambulatory. Long-term corticosteroids have been essential in 43 of 45 patients in this series currently managed by full-time faculty of the Northwestern University Allergy Service. Complicating psychosocial factors of some patients with potentially fatal asthma include schizophrenia, bipolar disorders, denial of disease, adolescent non-compliance, and parental interference with essential medications for children. We believe that the diagnosis of potentially fatal asthma should be made following occurrence of major asthma events that place the patient at high risk for a death from asthma.

Acidosis, Respiratory↗
PubMed1970

Acidosis and hypercalciuria: renal mechanisms affecting calcium, magnesium and sodium excretion in the sheep.

1. Observations were made on the excretion of calcium and magnesium by the sheep's kidney following manipulation of the acid-base status.2. Intravascular administration of a synthetic solution resembling saliva abolished the naturally occurring acidosis in sheep during feeding, and it also prevented the normal onset of post-prandial hypercalciuria and hypermagnesiuria.3. Non-respiratory acidosis (induced by infusion of hydrochloric acid) and respiratory acidosis arising from inhalation of 6% (v/v) CO(2) in air both caused an acute increase in calcium excretion.4. Measurement of filtered loads showed that feeding exerted an effect on the functional characteristics of the sheep's kidney. The renal clearances of calcium and magnesium increased, whereas sodium clearance decreased.5. Experimental conditions were arranged so that variations in acid-base status could be imposed at a time when the filtered load of calcium was declining.6. With hydrochloric acid-acidosis the renal excretion of calcium increased, despite a steady fall in the filtered load. With sodium bicarbonate alkalosis, the filtered load and the renal excretion of calcium decreased in unison.7. These variations in calcium excretion were not accompanied by corresponding changes in the excretion of sodium.8. It is concluded that the renal tubules in the sheep are sensitive to acid-base status and that they respond to a lowering of the blood pH by decreasing the tubular reabsorption of filtered calcium.

Acid-Base Equilibrium↗
PubMed2005

Parkinsonism following bilateral lesions of the globus pallidus: performance on a variety of motor tasks shows similarities with Parkinson's disease.

OBJECTIVES: The authors report the results of detailed investigations into the motor function of a patient who, after a heavy drinking binge and subsequent unconsciousness, respiratory acidosis, and initial recovery, developed parkinsonism characterised by hypophonic speech and palilalia, "fast micrographia", impaired postural reflexes, and brady/akinesia in proximal (but not distal) alternating upper limb movements. METHODS: In addition to brain magnetic resonance imaging (MRI), different aspects of motor function were investigated using reaction time (RT) tasks, pegboard and finger tapping tasks, flex and squeeze tasks, movement related cortical potentials (MRCPs), and contingent negative variation (CNV). Cognitive function was also assessed. The results were compared to those previously reported in patients with Parkinson's disease (PD). RESULTS: Brain MRI showed isolated and bilateral globus pallidus (GP) lesions covering mainly the external parts (GPe). These lesions were most probably secondary to respiratory acidosis, as other investigations failed to reveal an alternative cause. The results of the RT tasks showed that the patient had difficulties in preparing and maintaining preparation for a forthcoming movement. MRCP and CNV studies were in line with this, as the early component of the MRCP and CNV were absent prior to movement. The patient's performance on pegboard and finger tapping, and flex and squeeze tasks was normal when performed with one hand, but clearly deteriorated when using both hands simultaneously or sequentially. CONCLUSIONS: In general, the present results were similar to those reported previously in patients with PD. This provides further indirect evidence that the output of globus pallidus is of major importance in abnormal motor function in PD. The possible similarities of the functional status of GP in PD and our case are discussed.

Acidosis, Respiratory↗
PubMed1999

Development of chemosensitivity of rat medullary raphe neurons.

In many neonatal mammals, including humans and rats, there is a developmental increase in the ventilatory response to elevated pCO2. This maturation of central respiratory chemoreception may result from maturation of intrinsic chemosensitivity of brainstem neurons. We have examined age-related changes in chemosensitivity of neurons from the rat medullary raphe, a putative site for central chemoreception, using perforated patch-clamp recordings in vitro. In brain slices from rats younger than 12 days old, firing rate increased in 3% of neurons and decreased in 17% of neurons in response to respiratory acidosis (n = 36). In contrast, in slices from rats 12 days and older, firing rate increased in 18% of neurons and decreased in 15% of neurons in response to the same stimulus (n = 40). A tissue culture preparation of medullary raphe neurons was used to examine changes in chemosensitivity with age from three to 74 days in vitro. In cultured neurons younger than 12 days in vitro, firing rate increased in 4% of neurons and decreased in 44% of neurons in response to respiratory acidosis (n = 54). In contrast, in neurons 12 days in vitro and older, firing rate increased in 30% of neurons and decreased in 24% of neurons in response to respiratory acidosis (n = 105). In both types of chemosensitive neuron ("stimulated" and "inhibited"), the magnitudes of the changes in firing rate were greater in older neurons than in young neurons. These results indicate that the incidence and the degree of chemosensitivity of medullary raphe neurons increase with age in brain slices and in culture. This age-related increase in cellular chemosensitivity may underlie the development of respiratory chemoreception in vivo. Delays in this maturation process may contribute to developmental abnormalities of breathing, such as sudden infant death syndrome.

Aging↗
PubMed1990

Effect of acute hypercapnia on limb muscle contractility in humans.

The effect of acute hypercapnia on skeletal muscle contractility and relaxation rate was investigated. The contractile force of fresh and fatigued quadriceps femoris (QF) and adductor pollicis (AP) was studied in normal humans by use of electrical stimulation. Maximum relaxation rate from stimulated contractions was measured for both muscles. Acute hypercapnia led to a rapid substantial reduction of contraction force. The respiratory acidosis after 9% CO2 was breathed for 20 min [mean venous blood pH 7.26 and end-tidal PCO2 (PETCO2) 65.1 Torr] reduced 20- and 100-Hz stimulated contractions of QF to 72.8 +/- 4.4 and 80.0 +/- 5.1% of control values, respectively. After 8 and 9% CO2 were breathed for 12 min, AP forces at 20- and 50-Hz stimulation were also reduced. Twitch tension of AP was reduced by a mean of 25.5% when subjects breathed 9% CO2 for 12 min [mean arterialized venous blood pH (pHav) 7.25 and PETCO2 66 Torr]. Over the range of 5% (pHav 7.38 and PETCO2 47 Torr) to 9% CO2, there was a linear relationship between twitch tension loss and pHav, arterialized venous blood PCO2, and PETCO2. Acute respiratory acidosis (mean PETCO2 61 Torr) increased the severity of low-frequency fatigue after intermittent voluntary contractions of AP. At 20 min of recovery, twitch tension was 63.2 +/- 13.4 and 46.8 +/- 16.4% of control value after exercise breathing air and 8% CO2, respectively. Acute hypercapnia (mean PETCO2 65.1 and 60.5 Torr) did not alter the maximum relaxation rate from tetanic contractions of fresh QF and from twitch tensions of AP.

Acidosis, Respiratory↗
PubMed1994

Transesophageal echocardiographic assessment of left ventricular function during apnea testing for brain death.

The effects of apnea testing-induced respiratory acidosis on left ventricular function (LVF) are still controversial. The aim of the study was to assess LVF during apnea testing using transesophageal echocardiography (TEE). Twenty consecutive patients suspected of brain death, hemodynamically stable, and considered as potential organ donors were prospectively studied. A 20-min apnea test was performed after obtaining a PaCO2 > 35 mmHg and 20 min of FIO2 1 ventilation. LVF was assessed using TEE with a CFM 750 (Diasonic) connected to a 5 MHz probe. Heart rate (HR), mean arterial pressure (MAP), left ventricle end-diastolic and systolic area (LVEDA, LVESA), and LVF assessed by fractional area changes (FAC), systolic wall motion (SWM) scores, and blood gases were recorded at baseline, and after 5, 10, 15, and 20 min of apnea testing. In 19 patients, no spontaneous respiratory movement occurred during the standard 20-min period. In one patient (No. 15), the apnea test had to be stopped after 10 min because of hypoxia. HR, LVEDA, LVESA, and SWM were not significantly modified during the study. There was a progressive statistically significant decrease in MAP during apnea (from 77 +/- 10 to 63 +/- 11 mmHg), associated with a statistically significant increase in FAC at 20 min (from 48 +/- 13 to 56 +/- 8%). PaCO2 progressively rose (from 40 +/- 3 to 95 +/- 11 mmHg), associated with a decrease in pH (from 7.42 +/- 0.06 to 7.09 +/- 0.08). At the same time, PaO2 decreased slightly in all patients, but values remained well above hypoxic levels, except for one patient. Despite severe respiratory acidosis the increase in FAC suggests that apnea testing is well tolerated for brain death assessment.

Acidosis, Respiratory↗
PubMed1989

Hypophosphatemia induced by mechanical ventilation in patients with chronic obstructive pulmonary disease.

The aim of this study was to assess prospectively the variations of serum phosphorus concentration (P) after onset of mechanical ventilation (MV) in patients with chronic obstructive pulmonary disease (COPD) and acute respiratory acidosis. In 14 COPD patients, we measured P, PaCO2, and pH, immediately before MV (H0), then one hour (H1), 4 (H4), 7 (H7), 12 (H12), and 24 h (H24) after starting MV. P at H0 was in or above the normal range in ten patients and below normal range in four patients. P decreased significantly (p less than .001) after MV at H1, H4, H7, H12, and H24. Hypophosphatemia was present in all patients after MV, but was severe (p less than .3 mmol/L) in only two patients. There was a significant correlation (r = .56 p less than .01) between the decrease of P and the increase of pH after MV. Hypophosphatemia was a constant and early finding after institution of MV in COPD patients and was presumably related to an intracellular shift of P secondary to the correction of respiratory acidosis.

Acidosis, Respiratory↗