Respiratory Compensation For Metabolic Acidosis Research Articles

The Two-Digit Rule and Winter’s Formula

No abstract available. Article truncated after 150 words. I recently wondered, “How does the “Two-digit rule” for determining the adequacy of respiratory compensation for metabolic acidosis relate to Winter’s formula?” Many clinicians were taught this rule-of-thumb: the last two digits of the pH (those visible if you hold your thumb over the “7”) should provide an approximation of pCO2 (in mm Hg) in the presence of normal respiratory compensation. Although Winter’s formula is easy to remember and perform, the Two-digit rule is even easier. Winter’s formula and the Two-digit rule have both been derived empirically from clinical data (1,2). But the reason the Two-digit rule should work has never, to our knowledge, been adequately explained. We wondered how the two rules were related. We began with serum HCO3 values ranging from 4 -18 mmol/L and used them to calculate the corresponding predicted pCO2 values using Winter’s formula (3). Next, we used the Henderson-Hasselbalch equation to calculate the corresponding …

Характеристика стійкого стану функцій спортсменів у видах спорту з варіативними умовами змагальної діяльності

The purpose of the study was to develop generalized and specific characteristics of the steady state of the highly qualified athletes, who specialize in the standard program of sports dance and boxing. Materials and methods. Twenty sportsmen-dancers and twenty boxers of high qualification took part in the research. Gas analysis. Measurements of О2 consumption reaction, СО2 emissions, minute volume of breathing were carried out using the MetaMax 3B analyzer. Ergometry. Modeling of standard conditions of measurement was carried out on the basis of bicycle ergometer Monark. Standard conditions are associated with the use of a given ergometric load power of 50 W. The composition of Cardiorespiratory Intermittent endurance test included eight accelerated 10-second intervals, eight 20-second rest intervals. The duration of the task is four minutes. Mathematic statistics. Descriptive statistics suggested determining the arithmetic mean – x ̅, standard deviation – S, as well as median – Me, maximum (max) and minimum (min) indices, 25% and 75% indices. Steady state is a period of competitive activity, in the process of which sportsmen demonstrate high level of technical and tactical skills and physical performance. Steady state diagnostics is an essential reserve for managing the functional support of special performance of athletes in sports with variable conditions of competitive activity. Results and discussion. An increase in the response of pulmonary ventilation indicates its role as a response to respiratory compensation of metabolic acidosis. Differences in the breathing response in standard measurement conditions are related to the specificity of the breathing response of athletes-dancers. To some extent, “artificial” management of the breathing response causes a decrease in the intensity of breathing cycles. Empirical knowledge indicates that this refers to the “aesthetic” component of the judges' assessment of the performance of the sports dance program. To some extent, this is related to the specifics of the formation of programs of special physical training, correction of certain structural components of functional maintenance of working capacity, in this case, the respiratory system. Another obvious fact is related to the structure of the load, when the intensity of the work of boxers causes more significant acidemic shifts and, as a result, predicts an increase in the reaction of pulmonary ventilation as a mechanism for removing excess CO2 during work. The increase (maintenance) of the O2 consumption response of athletes-dancers is associated with the formation of excess CO2 within the RER – 1.03–1.05 and excessive pulmonary ventilation in the range of 37.2–39.1. Boxers, respectively, with the formation of excess CO2 within the limits of RER – 1.07–1.09 and excessive pulmonary ventilation in the range of 40.0–44.1. The increase in excess ventilation in the third-fifth of dancers was 4.9%, 9.9% – in boxers, provided that the O2 consumption reaction remained stable. Conclusion. The steady state of the functional support of the special performance of athletes in sports with variable conditions of competitive activity ensures the stable development of cardio-respiratory system and aerobic energy supply in the middle of intense motor activity

Organic Acidemias.

Organic Acidemias.

SPECIFIC CHARACTERISTICS OF STABILITY OF FUNCTIONAL PROVISION OF SPECIAL WORKING CAPACITY OF DANCE ATHLETES

Introduction. The relevance of research is due to the search for new opportunities to improve the functionality of dancers based on the study of specific characteristics of the cardiorespiratory system and energy supply. One of the ways to solve the problem is to improve the stability of the functional provision of special ability to work as a leading factor in demonstrating the skills of dancers in the standard program. The basis for the implementation of this area of ​​research is the formation of the regulatory framework of stability, its quantitative and qualitative characteristics that form a specialized direction of special physical training. The aim of the study is to identify specific characteristics of the stability of the functional support of the special ability of qualified athletes in sport dances. Material and methods: gas analysis, biochemical research methods, monitoring of competitive activity. Results. Characteristics of stability of functional support of special working capacity of dancers: at male partners VO2 max, VE, La in semifinals and finals of the standard program accordingly: 53.2 ± 0.5 ml · min-1 · kg-1 and 54.0 ± 0.4 ml · min-1 · kg-1; 116.3 ± 1.6 l · min-1 and 123.5 ± 1.5 l · min-1; 8.0 ± 0.4 mmol · l-1 and 13.0 ± 0.3 mmol · l-1. Differences in the specific performance of EqO2 during the quickstep and Viennese waltz were 3.0% in the semifinals and 4.2% in the final, respectively; EqCO2 - 4.4% in the semifinals and 5.2% in the finals; VO2 quickstep / VO2 in / waltz - 0.3% and 0.2%. The female partners VO2 max, VE, La in the semifinals and finals of the standard program, respectively: 48.8 ± 0.4 ml · min-1 · kg-1 and 49.1 ± 0.4 ml · min-1 · kg-1; 88.7 ± 1.6 l · min-1 and 111.0 ± 1.6 l · min-1; 6.7 ± 0.3 mmol · l-1 and 9.7 ± 0.4 mmol · l-1. Differences in the specific performance of EqO2 during the quickstep and Viennese waltz were 1.8% in the semifinals and 3.3% in the finals, respectively; EqCO2 - 3.1% in the semifinals and 4.0% in the finals; VO2 quickstep / VO2 in / waltz - 0.7% and 0.7%. Conclusions. The high level of power and stability of aerobic and anaerobic energy supply, the severity of the reaction of respiratory compensation of metabolic acidosis form the conditions for the implementation of the stability of functional support of special performance, which are presented to dancers in the middle and final part of competitive activities.

Spironolactone-furosemide combination therapy and acid-base disorders in liver cirrhosis patients .

Respiratory alkalosis (RA) and dilutional hyperchloremic acidosis (DHA) are the most common acid-base balance (ABB) disorders in patients with liver cirrhosis. The aims of this study were to clarify whether RA develops in relation to DHA via respiratory compensation of metabolic acidosis and whether spironolactone in combination with low-dose furosemide - diuretics known to ameliorate DHA - positively affects RA in liver cirrhosis patients. 59 patients with advanced cirrhosis were divided into two groups. Group D consisted of individuals (urine sodium concentration (UNa+) > 20 mmol/L) who responded to combination therapy consisting of spironolactone and low-dose furosemide. The non-D group consisted of individuals (UNa+ ≤ 20 mmol/L) who either did not respond to the treatment or who were not administered it. In both groups, we examined serum and urine concentrations of electrolytes and ABB parameters, including SNa+-SCl- and SNa+/SCl- values. In group D, we found a statistically significant relationship between pCO2 and SHCO3-: r = 0.756 (p < 0.001) and between pCO2 and SNa+-SCl-: r = 0.522 (p = 0.001). Neither Salb nor the corrected anion gap were associated with changes in SHCO3- or pCO2 values. Although SHCO3- values were normal, abnormal pCO2 values were observed in one third of group D patients. Based on multivariable analysis, SHCO3- proved to be a statistically significant influencing factor on pCO2 values. DHA contributes to the development of RA in individuals with liver cirrhosis. Reducing DHA by means of effective diuretic therapy comprising spironolactone and furosemide has a beneficial effect on RA in such patients.

Survey On Methanol Poisoning Epidemic in Rafsanjan City in Year 2013

Background: Examination and early detection of the methanol toxicity epidemic are very important, so identification and initiation of appropriate therapy can significantly reduce morbidity and mortality. Therefore, this study was aimed to investigation methanol poisoning epidemic in Rafsanjan city.Methods: This case series study was conducted in 252 patients with methanol poisoning in 2013 in the Ali-ibn-Abi-Talib hospital of Rafsanjan. Data were through interviews and records that were collected at hospital admission. Due to the large number of patients and the possible lack of ability of rapid measurement of serum levels of methanol and need of rapid intervention, treatment to reduce any further complications, early diagnosis and treatment were carried out by clinical history and interpretation of arterial blood gas test results. Data record on provided checklists and then analyzed using SPSS version 19.Results: The mean pH was 0.13±7.27. The most frequent clinical features were visual disturbances (39.7%), dyspnea (1.2%), and gastrointestinal symptoms (7.1%). There was a trend towards decreasing PCO2 with decreasing pH amongst the patients surviving. The opposite trend was demonstrated in the dying; the difference was highly significant by linear regression analyses (P&lt; 0.001).Conclusions: Methanol poisoning still has a high morbidity and mortality, mainly because of late diagnosis and treatment. Respiratory arrest, coma and severe metabolic acidosis upon admission were strong predictors of poor outcome. Early admission and ability of respiratory compensation of metabolic acidosis were associated with survival.

The global peripheral chemoreflex drive in patients with systemic sclerosis: a rebreathing and exercise study.

Exercise intolerance (EI) in systemic sclerosis (SSc) is difficult to manage by the clinician. The peripheral chemoreflex drive compensates for metabolic acidosis during exercise and may be related to EI. To assess the global peripheral chemoreflex drive (GPCD) in patients with SSc at rest and during exercise. Consecutively tested SSc patients (n = 49) were evaluated by pulmonary function tests, carbon dioxide (CO2) rebreathing studies and non-invasive cardiopulmonary exercise testing (CPET). Results of their CO2 rebreathing tests were compared with those of controls (n = 32). Respiratory compensation for metabolic acidosis during CPET was defined by the occurrence of a sharp increase in minute ventilation (VdotE) and the ventilatory equivalent for CO2 (V'E and V'CO2) at the end of the isocapnic buffer phase. Euoxic (eVHR) and hyperoxic (hVHR) ventilatory responses to hypercapnia were measured and its difference (eVHR - hVHR) was considered to reflect the GPCD. In 45 patients with SSc, CPET results showed respiratory compensation at the occurrence of metabolic acidosis. eVHR - hVHR in patients with diffuse cutaneous SSc (dcSSc) differed significantly from that in patients with limited cutaneous SSc (lcSSc) and from that in controls (0.47 ± 0.38 (dcSSc) vs. 0.90 ± 0.77 (lcSSc) and 0.90 ± 0.49 (controls) l/min/mmHg; P = 0.04 and P = 0.03, respectively). Respiratory compensation for metabolic acidosis occurred in all patients. However, the GPCD was diminished in dcSSc patients, suggesting an altered control of breathing. Its assessment may help the clinician to better understand reported EI and exertional dyspnea in dcSSc patients.

845

Introduction: Pancreatitis usually presents as a self limiting disease. In its severe form is complicated by multi system failure and has a high mortality. On the other hand, APACHE II score provides an objective assessment of severity of illness and Ranson criteria are used as an indicator assessing the systematic affects. Hypothesis: The aim of our study was to test the hypothesis that there is a difference among severity indexes like APACHE II score values, Ranson score, Glasgow Coma Scale (GCS) as well as length of stay (LOS) and vendilation days (VD) between patients with acute pancreatitis who died and patients with acute pancreatitis who survived ICU. Methods: From November 2005 to April 2012, 406 patients admitted to our ICU. From these, 11 (2.7 %) were indicated with the diagnosis of acute pancreatitis. The patients separated in two groups. In Group A involved 4 patients who survived ICU and in group B involved 7 patients who died. We looked for statistical significant difference (p value two tailed) between the medians values of two groups, using the unpaired Mann - Whithney test or the unpaired t test Welch corrected according to the normality test. Results: We detected no statistical difference between the two groups according: age (p=0.11), APACHE II score (p=0.65), Ranson score (p=0.93), GCS (p=0.96), LOS (p=0.21), VD (p=0.58), temperature (p=0.72), MAP (p=0.49), HR (p=0.68), Na (p=0.69), k (p=0.16), BUN (p=0.40), Cr (p=0.39), WBC (p=0.77), Ht (p=0.86), PaO2 (p=0.62), PH (p=0.36), albumine (p=0.95), glucose (p=0.99), Bilirubin (p=0.08), Ca (p=0.43), amylase (p=0.55). We detected statistical significant higher group B value according, PaCO2 (p=0.04), Conclusions: According to our data, there was no statistical difference detected between the two groups according to the severity indexes as well as to the allocating parameters. The only difference detected was that the patients who died (Group B), had a significant higher PaCO2 value (p=0.04). Our data suggest that patient who survived, had a better ability for respiratory compensation of metabolic acidosis, limiting the PH changes and perhaps, limiting the later multiple organ failure.

Respiratory Manifestations of Malaria

Respiratory distress develops in up to 25% of adults and 40% of children with severe falciparum malaria. Its diverse causes include respiratory compensation of metabolic acidosis, noncardiogenic pulmonary edema, concomitant pneumonia, and severe anemia. Patients with severe falciparum, vivax, and knowlesi malaria may develop acute lung injury (ALI) and ARDS, often several days after antimalarial drug treatment. ARDS rates, best characterized for severe Plasmodium falciparum, are 5% to 25% in adults and up to 29% in pregnant women; ARDS is rare in young children. ARDS pathophysiology centers on inflammatory-mediated increased capillary permeability or endothelial damage leading to diffuse alveolar damage that can continue after parasite clearance. The role of parasite sequestration in the pulmonary microvasculature is unclear, because sequestration occurs intensely in P falciparum, less so in P knowlesi, and has not been shown convincingly in P vivax. Because early markers of ALI/ARDS are lacking, fluid resuscitation in severe malaria should follow the old adage to "keep them dry." Bacteremia and hospital-acquired pneumonia can complicate severe malaria and may contribute to ALI/ARDS. Mechanical ventilation can save life in ALI/ARDS. Basic critical care facilities are increasingly available in tropical countries. The use of lung-protective ventilation has helped to reduce mortality from malaria-induced ALI/ARDS, but permissive hypercapnia in unconscious patients is not recommended because increased intracranial pressure and cerebral swelling may occur in cerebral malaria. The best antimalarial treatment of severe malaria is IV artesunate.

Three cases of severe metformin-related lactic acidosis

The American Diabetes Association and the European Association for the Study of Diabetes published a consensus statement on the approach to hyperglycaemia in individuals with type 2 diabetes.1 In accordance with this statement, metformin is widely prescribed, as it is the first-line drug for type 2 diabetes treatment. Lactic acidosis incidence during metformin therapy is estimated to be two to nine cases per 100 000 patients per year, an incidence not too different from that reported in patients with type 2 diabetes who do not take metformin.2 In fact, there is some controversy concerning the association between metformin and lactic acidosis. Metformin does not seem to be the initial cause of lactic acidosis but could, possibly, precipitate the acid–base imbalance and contribute to the severity of the acidosis.3 The risk factors for metformin-related lactic acidosis include decreased renal, cardiac and hepatic functions and/or suspected tissue hypoxia. On the contrary, in recent years, several cases of severe lactic acidosis have been reported in the literature, even in the absence of these risk factors. Medical therapy for metformin-associated lactic acidosis includes management of concurrent diseases; mechanical ventilation to prevent muscle fatigue, to help to maintain respiratory compensation for metabolic acidosis and to optimize oxygenation; bicarbonate haemodialysis or continuous veno-venous haemofiltration (CVVH) to decrease the metformin level and correct acidosis; and intensive vasoactive support with norepinephrine or epinephrine. The use of bicarbonate is known to worsen intracellular acidosis and hyperlactacidaemia and remains controversial. In the last 14 months, three patients undergoing chronic metformin therapy have been admitted to our critical care unit for severe lactic acidosis (Table 1).Table 1: Patient characteristicsAll patients we saw were hypothermic with a high Simplified Acute Physiology Score II (SAPS II) score at admission. Two patients required high doses of epinephrine due to hypotension refractory to norepinephrine–dobutamine association. Liver function was never affected. Patient 1 and patient 2 had risk factors for lactic acidosis, as they had mild and moderate previous elevation of creatinine level, respectively; in these cases, metformin should be withdrawn. Patient 3 had no contraindication to metformin use.4 Two out of three had a mild infection before admission (patients 1 and 3). Diabetic nephropathy often develops insidiously. Moreover, infection or dehydration can rapidly lead to renal function impairment. Cohen and Woods divided lactic acidosis into two categories. Type A is lactic acidosis occurring in association with clinical evidence of poor tissue perfusion or oxygenation, whereas type B occurs when no clinical evidence of poor tissue perfusion or oxygenation exists. All three patients had developed acute renal failure, a known cause of type B lactic acidosis. Two patients had infections, which may also have contributed to tissue hypoxia and type A lactic acidosis. Regardless of the type of lactic acidosis in our patients, the incidence of metformin toxicity can be reduced with close monitoring of renal function. Serum creatinine should be checked at least annually, and probably more often in patients with exposure to risk factors for renal impairment.5 These cases suggest a high index of suspicion for metformin-associated lactic acidosis in older patients, a prompt metformin withdrawal during periods of suspected tissue hypoxia or impaired renal function and the importance of giving patients full information about this side-effect. We have outlined the importance of taking into account risk factors for lactic acidosis and contraindications in prescribing metformin. We also would like to emphasize that, despite the severity of clinical presentation, two patients had an excellent recovery.

Hypoglycemia and Hyperlactatemia Associated with Lymphoma in an Angus Cow

Hypoglycemia and Hyperlactatemia Associated with Lymphoma in an Angus Cow

Exercise test mode dependency for ventilatory efficiency in women but not men

Ventilatory efficiency is commonly defined as the level of ventilation V(E) at a given carbon dioxide output (V(CO(2) )). The slope of the V(E) versus V(CO(2) ) relationship and the lowest V(E)/V(CO(2) ) are two ventilatory efficiency indices that can be measured during cardiopulmonary exercise testing (CPET). A possible CPET mode dependency for these indices was evaluated in healthy men and women. Also evaluated was the relationship between these two indices as, in theory, V(E)/V(CO(2) ) falls hyperbolically towards an asymptote that numerically equals the V(E) versus V(CO(2) ) slope at exercise levels below the ones that cause respiratory compensation for metabolic acidosis. Twenty-eight healthy subjects (14 men) underwent treadmill and cycle ergometer CPET on different days. Ventilation and the gas fractions for oxygen and CO(2) were measured with a vacumed metabolic cart. In men, paired t-test analysis failed to find a mode difference for either ventilatory efficiency index but the opposite was true in the women as each woman had higher values for both indices on the treadmill. For men, the lowest V(E)/V(CO(2) ) was larger than the V(E) versus V(CO(2) ) slope by 1.3 on the treadmill and 0.8 on the cycle ergometer. The corresponding values for women were 1.7 and 1.4. We conclude that in healthy subjects, women, but not men, demonstrate a mode dependency for the two ventilatory efficiency indices investigated in this study. Furthermore, our results are consistent with the theoretical expectation that the lowest V(E)/V(CO(2) ) has a numerical value just above the asymptote of the V(E)/V(CO(2) ) versus V(CO(2) ) relationship.

Methanol outbreak in Norway 2002–2004: epidemiology, clinical features and prognostic signs

Knowledge on methanol poisoning does mainly come from clinical studies. We therefore report epidemiological, clinical and prognostic features from the large methanol outbreak in Norway in 2002-2004 where the new antidote fomepizole was the primary antidote in use. Combined prospective and retrospective case series study of 51 hospitalized patients who were confirmed poisoned with methanol, of whom nine died. In addition, eight patients died outside hospital. Most patients were admitted in a late stage and because of symptoms. Treatment consisted of alkali, fomepizole (71%) and haemodialysis (73%). The median serum methanol was 25.0 mmol L-1 (80 mg dL-1) (range 3.1-147.0 mmol L-1), median pH was 7.20 (6.50-7.50), and median base deficit 22 mmol L-1 (range 0-31). The most frequent clinical features reported were visual disturbances (55%), dyspnoea (41%), and gastrointestinal symptoms (43%). Twenty-four per cent were comatose on admission, of whom 67% died. There was a trend towards decreasing pCO2 with decreasing pH amongst the patients surviving. The opposite trend was demonstrated in the dying; the difference was highly significant by linear regression analyses (P<0.001). Methanol poisoning still has a high morbidity and mortality, mainly because of late diagnosis and treatment. Respiratory arrest, coma and severe metabolic acidosis (pH<6.90, base deficit>28 mmol L-1) upon admission were strong predictors of poor outcome. Early admission and ability of respiratory compensation of metabolic acidosis was associated with survival.

Arginine in burn injury improves cardiac performance and prevents bacterial translocation

This study examined the effects of arginine supplement of fluid resuscitation from burn injury on cardiac contractile performance and bacterial translocation after a third-degree burn comprising 43% of the total body surface area in adult rats. Before burn injury, rats were instrumented to measure blood pressure; after burn (or sham injury), paired groups of sham-burned and burned rats were given vehicle (saline), L-arginine, D-arginine, or N-methyl-L-arginine (300 mg/kg in 0.3 ml of saline 30 min, 6 h, and 23 h postburn) plus fluid resuscitation; sham-burned rats received drug only. Twenty-four hours after burn trauma, hemodynamics were measured; the animals were then killed and randomly assigned to Langendorff heart studies or to studies examining translocation of gut bacteria. Burn rats treated with vehicle, D-arginine, or N-methyl-L-arginine had well-defined cardiocirculatory responses that included hypotension, tachycardia, respiratory compensation for metabolic acidosis, hypocalcemia, cardiac contractile depression, and significant bacterial translocation. Compared with values measured in vehicle-treated burn rats, L-arginine given after burn improved blood pressure, prevented tachycardia, reduced serum lactate levels, improved cardiac performance, and significantly reduced bacteria translocation, confirming that L-arginine administration after burn injury provided significant cardiac and gastrointestinal protection. Circulating neutrophil counts fell after burn trauma and serum glucagon levels rose, but these changes were not altered by pharmacological intervention. Our finding of significantly higher coronary perfusate guanosine 3',5'-cyclic monophosphate concentration in L-arginine-treated burn rats suggests that the beneficial effects of L-arginine were mediated by nitric oxide production.

Respiratory acidosis in carbonic anhydrase II-deficient mice.

To investigate the role of carbonic anhydrase (CA) II on pulmonary CO2 exchange, we analyzed arterial blood gases from CA II-deficient and normal control mice. CA II-deficient mice had a low arterial blood pH (7.18 +/- 0.06) and HCO3- concentration ([HCO3-]; 17.5 +/- 1.9 meq/l) and a high Pco2 (47.4 +/- 5.3 mmHg), consistent with mixed respiratory and metabolic acidosis. To eliminate the influence of metabolic acidosis on arterial blood gases, NaHCO3 (4 mmol/kg body weight) was given intraperitoneally, and arterial blood gases were analyzed 4 h later. Normal mice had a small increase in pH and were able to maintain Pco2 and [HCO3-]. The metabolic acidosis in CA II-deficient mice was corrected ([HCO3-], 22.9 +/- 2.4 meq/l), and respiratory acidosis became more profound (Pco2, 50.4 +/- 2.4 mmHg). These results indicate that CA II-deficient mice have a partial respiratory compensation for metabolic acidosis. We conclude that CA II-deficient mice have a mixed respiratory and metabolic acidosis. It is most likely that CO2 retention in these animals is due to CA II deficiency in both red blood cells and type II pneumocytes.

Reproducibility of VO2-VCO2 relationship during incremental exercise protocol.

We examined the effect of two different slope protocols to the reproducibility of the VO2-VCO2 relationship and the lactic acidosis threshold (LAT) during incremental exercise. Two adult male subjects performed a cycle ergometer exercise 2 to 4 times repeatedly in which the increase of work rate was 25 W every 1 or 2 min according to experimental design method. Gas exchange parameters during each exercise was measured every 10 s. The V-slope method was applied to the data which remained after the deletion of the data during the transient phase with the onset of exercise and above respiratory compensation of metabolic acidosis (RCMA), for detecting LAT and summarizing the VO2-VCO2 relationship below and above LAT. LAT had a high reproducibility whichever slope protocol was used. The confidential limit of LAT estimated by a statistical method was about +/- 0.1 l/min in terms of VO2. There were stable and reasonable responses of VO2-VCO2 during incremental exercise in which the work rate increased 25 W every 1 min.

Comment on ‘Ventilation and blood lactate increase exponentially during incremental exercise’

A recent paper in this journal has examined the ventilatory compensation for metabolic acidosis with increasing oxygen uptake, making extensive use of mathematical and statistical techniques. The authors conclude that '...respiratory compensation for metabolic acidosis during incremental exercise is a continuous process...'. While this may indeed be so, the following major aspects of the paper render the evidence at best dubious, surely inconclusive and perhaps even worthless: (1) The mathematical and statistical methodology is sloppy, incomplete and, at times, flawed. (2) No discontinuous model is presented for comparative purposes, only three continuous ones. (3) The authors ignore the fact that some threshold models produce smooth continuous data, and as a consequence, a good fit of a smooth continuous model cannot exclude the presence of a threshold. (4) The data in Table 5 show the amplitude parameter A of the preferred model to be not significantly different from zero. This paper draws these matters to the attention of readers of this journal, reviewers of manuscripts and other researchers, with comment and suggestion. This is done in the hope that all those concerned with mathematical and statistical methodologies will become more aware of their proper use.

Acid-base status in paediatric &lt;italic&gt;Plasmodium falciparum&lt;/italic&gt; malaria

We measured the acid-base status of children with falciparum malaria in order to determine the prognostic significance and rate of resolution of acidaemia in patients with severe disease. We prospectively studied 141 Malawian children who were admitted to Hospital, with falciparum malaria, 60 of whom had cerebral malaria (unrousable coma, unable to localize a painful stimulus). Of the 60 patients with cerebral malaria 25 (42%) were acidaemic (capillary blood pH < 7.3); of 81 children with uncomplicated malaria 4 (5%) were acidaemic (p < 0.0001). Eleven patients died; of these, eight presented with cerebral malaria, eight with acidaemia and seven with both. The strong association of altered acid-base status with disease severity and mortality was independent of other previously identified predictors of illness and death in malaria. Acidaemia was not associated with shock, bacteraemia or hypoxaemia. Acidaemic patients had a slower mean respiratory rate and a higher incidence of respiratory rhythm abnormalities than other patients, suggesting that acidaemia is in part the result of inadequate respiratory compensation for metabolic acidosis. Although acidaemia is quickly corrected by fluids and antimalarial drugs, specific therapy to correct acidaemia needs evaluation in children with severe malaria.

Endurance training regimen based upon arterial blood lactate: effects on anaerobic threshold.

The purpose of this investigation was to assess the effect of endurance training based upon the intensity as determined by the arterial blood lactate concentration (LA). Seven healthy male college students performed endurance training on a Monark bicycle ergometer for 15 min on 3 days/week for 8 weeks, at an intensity corresponding to 4 mmol X l-1 arterial blood LA determined during an incremental exercise test (25 watts increment every minute on a bicycle at 50 rpm). Another six male students served as the control group. To assess the training effect, both an incremental exercise test and a submaximal exercise test were performed before and after the endurance training. In the incremental exercise test, VO2max, VE at VO2max, anaerobic threshold (AT), and the onset of respiratory compensation for metabolic acidosis (RCMA) were measured. AT was determined as the point at which arterial LA rose above the resting value, and RCMA was determined as the point at which Paco2 decreased during the incremental exercise test. After training, AT increased significantly (37% increment expressed in VO2, p less than 0.05). There was a significant increase (p less than 0.05) in RCMA (17%) and VO2max (14%). This training decreased VO2 (4%), VE (15%), heart rate (10%), respiratory exchange ratio (5%), and LA (23%) significantly (p less than 0.05) during the submaximal exercise test after training. On the other hand, there were no significant changes in the control group through the period when the training group performed their training. These results showed that the endurance training intensity corresponding to 4 mmol X l-1 arterial blood LA was effective for the improvement in AT as well as VO2max. It is suggested that the present training regimen could delay the onset of anaerobic glycolysis, thus shifting AT to the higher workload and decreasing LA at a given submaximal exercise after training.

EFFICIENCY OF RESPIRATORY COMPENSATION FOR METABOLIC ACIDOSIS IN PREMATURE INFANTS.

EFFICIENCY OF RESPIRATORY COMPENSATION FOR METABOLIC ACIDOSIS IN PREMATURE INFANTS.