Degree Of Acidemia Research Articles

Acidemia Detected on Venous Blood Gas After Out-of-Hospital Cardiac Arrest Predicts Likelihood to Survive to Hospital Discharge.

Sudden cardiac arrest is the most common cause of death worldwide, and prognostication after survival remains challenging. Decisions regarding prognosis can be fraught with error in the immediate postarrest period, with guidelines recommending the use of various tests, including blood gas pH, to determine which interventions to perform. Despite these recommendations, the prognostic utility of blood gas pH remains unclear. In this retrospective cohort study, we aimed to demonstrate the prognostic utility of emergency department blood gas pH after return of spontaneous circulation (ROSC) in out-of-hospital cardiac arrest. A retrospective cohort study was performed, including all adult survivors of out-of-hospital cardiac arrest (n=79). Primary disease-oriented outcome was venous blood pH after ROSC and survival to hospital discharge. In patients with out-of-hospital cardiac arrest, pH<7.2 was associated with decreased likelihood of survival to hospital discharge (odds ratio 0.06), with every 0.1-unit increase in pH being associated with an increased likelihood of survival (1.98). Based on the area under the receiver curve, the pH that optimizes sensitivity and specificity for predicting survival was 7.04. Both presence and degree of acidemia on initial blood gas after ROSC was associated with a decreased likelihood of survival to hospital discharge. The optimal cutoff for prediction in this cohort of patients was 7.04. Using a higher pH cutoff would result in fewer patients receiving intervention that would otherwise have survived.

A Global View of Neonatal Asphyxia and Resuscitation.

Birth asphyxia (BA), assumed to be related to intrapartum related hypoxia-ischemia, accounts for one million neonatal deaths annually. In the low resource setting BA is usually defined as a failure to initiate or sustain spontaneous breathing at birth. In the resource replete setting BA is a biochemical definition related to impaired gas exchange, due to interruption of placental blood flow (PBF). An umbilical arterial pH <7.00 referred to as severe fetal acidemia, reflects a degree of acidosis, where potential risk of adverse neurologic sequelae is increased. However, even with this degree of acidemia, the likelihood of mortality or adverse neurologic sequelae remains low. The aim is to focus on the definition of BA in the low resource setting, and compare it to the diagnosis in the resource replete setting, highlighting the importance of interruption of placental blood flow as it relates to morbidity and mortality. With asphyxia, the fetus aims to redistribute cardiac output to protect more vital organs e.g., brain, myocardium, and adrenal gland at the expense of decreased flow to organs such as kidney or intestine. In an experimental newborn model, animals subjected to asphyxia immediately develop primary apnea with bradycardia sustained blood pressure and normal pH. Recovery of respirations follows basic interventions, i.e. stimulation coupled with reversal of asphyxia. However, if asphyxia is sustained, secondary apnea manifests with bradycardia, hypotension, and pH <7.00. More intensive resuscitation including bag mask ventilation ± intubation ± cardio-pulmonary resuscitation may be necessary for correction upon reversal of asphyxia. Identification of a severely acidemic state (cord arterial pH < 7.00) in the newborn, may help to differentiate the truly asphyxiated intrapartum related cases that result in mortality, from those cases where mortality is related to delay in or ineffective basic resuscitation.

Acute Renal Failure Following Near-Drowning

IntroductionAcute kidney injury associated with near-drowning (ND-AKI) has rarely been reported and its incidence among survivors is unknown. A patient with AKI and urine biomarkers indicating tubular injury led us to assess the occurrence and clinical characteristics of ND-AKI and to evaluate possible causative mechanisms.MethodsWe evaluated medical records of patients rescued from near-drowning in the Mediterranean Sea and treated in a tertiary-level medical center during 2000 to 2017.ResultsNinety-five patients with the diagnosis of near-drowning in seawater were treated. Forty-two of these patients (43%) developed ND-AKI and 17 (18%) were classified as AKI Kidney Disease: Improving Global Outcomes stages 2 to 3. ND-AKI was associated with the need for resuscitation and mechanical ventilation, with the calculated seawater volume ingestion (extrapolated from rising plasma sodium) and with the degree of acidemia, lactemia, and ventilatory failure. This series and 28 additional published cases of ND-AKI in the literature showed an overall male predisposition.ConclusionAKI is a common complication of near-drowning and is associated with increased in-hospital mortality. Data analysis suggests a predominant role of hypoxic tubular injury due to systemic hypoxemia in ND-AKI, combined with intense sympathetic activity (reflected by tachyarrhythmias, hyperglycemia, and relative hypokalemia) and increased oxygen expenditure for intensified distal tubular sodium transport. Androgen-related reduced renal vasodilatory capacity may explain male gender predominance.

Intermittent versus continuous renal replacement therapy in acute methanol poisoning: comparison of clinical effectiveness in mass poisoning outbreaks

BackgroundIntermittent hemodialysis (IHD) is the modality of choice in the extracorporeal treatment (ECTR) of acute methanol poisoning. However, the comparative clinical effectiveness of intermittent versus continuous modalities (CRRT) is unknown. During an outbreak of mass methanol poisoning, we therefore studied the effect of IHD versus CRRT on mortality and the prevalence of visual/central nervous system (CNS) sequelae in survivors.MethodsThe study was designed as prospective observational cohort study. Patients hospitalized with a diagnosis of acute methanol poisoning were identified for the study. Exploratory factor analysis and multivariate logistic regression were applied to determine the effect of ECTR modality on the outcome.ResultsData were obtained from 41 patients treated with IHD and 40 patients with CRRT. The follow-up time in survivors was two years. Both groups of patients were comparable by age, time to presentation, laboratory data, clinical features, and other treatment applied. The CRRT group was more acidemic (arterial blood pH 6.96 ± 0.08 vs. 7.17 ± 0.07; p < 0.001) and more severely poisoned (25/40 vs. 9/41 patients with Glasgow Coma Scale (GCS) ≤ 8; p < 0.001). The median intensive care unit length of stay (4 (range 1–16) days vs. 4 (1–22) days; p = 0.703) and the number of patients with complications during the treatment (11/41 vs. 13/40 patients; p = 0.576) did not differ between the groups. The mortality was higher in the CRRT group (15/40 vs. 5/41; p = 0.008). The number of survivors without sequelae of poisoning was higher in the IHD group (23/41 vs. 10/40; p = 0.004). There was a significant association of ECTR modality with both mortality and the number of survivors with visual and CNS sequelae of poisoning, but this association was not present after adjustment for arterial blood pH and GCS on admission (all p > 0.05).ConclusionsIn spite of the faster correction of the acidosis and the quicker removal of the toxic metabolite in intermittent dialysis, we did not find significant differences in the treatment outcomes between the two groups after adjusting for the degree of acidemia and the severity of poisoning on admission. These findings support the strategy of “use what you have” in situations with large outbreaks and limited dialysis capacity.

Le pH eucapnique néonatal à la naissance : application à une cohorte de 5392 nouveau-nés

ObjectiveTo apply a newly concept of neonatal eucapnic pH at birth [pH euc (n)] and compare its contribution towards conventional criteria of severe metabolic acidosis. MethodsAnalysis of a cohort of 5392 neonates from 2010 to 2014 in a level 1 maternity. clinical data (birth weight, gestational age, mode of delivery, APGAR score) were collected from archived files. Biological data were collected from umbilical cord blood, consisting of pH, PCO2, Base deficit, lactate. Eucapnic pH and eucapnic base deficit were calculated from pH and PCO2 with the Henderson-Hasselbalch equation applied in the Charles-Racinet diagram and/or with an Excel spreadsheet. ResultsData set the prevalence of neonatal acidemia<7.00 to 0.62 %. The current cohort shows 32 cases of severe neonatal metabolic acidosis according to ACOG-AAP (2014) criteria and 26/29 cases according to McLennan (2015) criteria, of which 80 % were born by cesarean section or instrumental delivery. In 55 % of cases, calculated eucapnic pH at birth did not confirm the severity of metabolic acidosis based on a threshold set at 7.11. Five cases were transferred in neonatalogy only on clinical considerations of poor neonatal adaptation but not on biological consideration (pH euc<7.11 was equally distributed between transferred and non-transferred neonates, P=0.76; the same distribution was observed with the pH, P=0.20) and followed normal outcome. Discussion and conclusionThe pH determination provides information only on the degree of acidemia and not on respiratory and/or metabolic components. Moreover, hypercapnia always present at birth is not included in the instructions to determine a metabolic acidosis (The American College of Obstetricians and Gynecologists, 2014; MacLennan et al., 2015). The new concept of neonatal eucapnic pH at birth accounts for only the metabolic component. We feel it should fine tune indications for cerebral hypothermia and thus improve its effectiveness. From a medicolegal perspective, for cases of cerebral palsy, it often allows to refute metabolic acidosis in perpartum events, often wrongfully being linked to generate cerebral injuries.

Secondary renal tubular acidosis in a Hereford calf

A 3-month-old Hereford heifer calf was presented for lethargy. Blood gas analysis and plasma biochemical testing revealed severe metabolic acidosis, azotemia, hyponatremia, hyperchloremia, and normal anion gap. Results of a urinalysis were consistent with acute tubular necrosis with inadequate acidification of urine based on the degree of acidemia. Salmonella enterica serovar agona was cultured from both urine and feces. The calf was treated with intravenous polyionic fluids, bicarbonate, and antimicrobials. Acidosis and azotemia resolved, and 4 months following initial presentation the heifer was clinically normal.

Uncovering the basis of a severe degree of acidemia in a patient with diabetic ketoacidosis

In this teaching exercise, the goal is to demonstrate how an application of principles of physiology can reveal the basis for a severe degree of acidaemia (pH 6.81, bicarbonate <3 mmol/l (P(HCO(3))), PCO(2) 8 mmHg), why it was tolerated for a long period of time, and the issues for its therapy in an 8-year-old female with diabetic ketoacidosis. The relatively low value for the anion gap in plasma (19 mEq/l) suggested that its cause was both a direct and an indirect loss of NaHCO(3). Professor McCance suggested that ileus due to hypokalaemia might cause this direct loss of NaHCO(3), and that an excessive excretion of ketoacid anions without NH(4)(+) in the urine accounted for the indirect loss of NaHCO(3). In addition, he suspected that another factor also contributing to the severity of the acidaemia was a low input of alkali. He was also able to explain why there was a 16-h delay before there was a rise in the P(HCO(3)) once therapy began. The missing links in this interesting story, including a possible basis for the hypokalaemia, emerge during the discussion between the medical team and Professor McCance.

Tissue oxygen monitoring in rodent models of shock

Tissue Po(2) (tPo(2)) reflects the balance between local O(2) supply and demand and, thus, could be a useful monitoring modality. However, the consistency and amplitude of the tPo(2) response in different organs during different cardiorespiratory insults is unknown. Therefore, we investigated the effects of endotoxemia, hemorrhage, and hypoxemia on tPo(2) measured in deep and peripheral organ beds. We compared arterial pressure, blood gas and lactate levels, descending aortic and renal blood flow, and tPo(2) in skeletal muscle, bladder epithelium, liver, and renal cortex during 1) LPS infusion (10 mg/kg), 2) sequential removal of 10% of circulating blood volume, and 3) reductions in inspired O(2) concentration in an anesthetized Wistar rat model with values measured in sham-operated animals. Different patterns were seen in each of the shock states, with condition-specific variations in the degree of acidemia, lactatemia, and tissue O(2) responses between organs. Endotoxemia resulted in a rise in bladder tPo(2) and an early fall in liver tPo(2) but no significant change in muscle and renal cortical tPo(2). Progressive hemorrhage, however, produced proportional declines in liver, muscle, and bladder tPo(2), but renal cortical tPo(2) was maintained until profound blood loss had occurred. By contrast, progressive hypoxemia resulted in proportional decreases in tPo(2) in all organ beds. This study highlights the heterogeneity of responses in different organ beds during different shock states that are likely related to local changes in O(2) supply and utilization. Whole body monitoring is not generally reflective of these changes.

Relationship between middle cerebral artery velocimetry, computer fetal heart rate assessment and degree of acidemia at birth in intrauterine growth restricted fetuses

Relationship between middle cerebral artery velocimetry, computer fetal heart rate assessment and degree of acidemia at birth in intrauterine growth restricted fetuses

Umbilical venous pressure in normal, growth-retarded, and anemic fetuses

OBJECTIVE: Our purpose was to establish a reference range with gestation for umbilical venous blood pressure and to examine possible changes in intrauterine growth retardation and red blood cell isoimmunization. STUDY DESIGN: Umbilical venous pressure was measured at cordocentesis in pregnancies complicated by intrauterine growth retardation (n = 20) and red blood cell isoimmunization (n = 61) both before and after intravascular fetal blood transfusion. The values were compared with a reference range that was constructed from the study of 111 pregnancies undergoing prenatal diagnosis at 18 to 40 weeks' gestation. RESULTS: In the control group the mean umbilical venous pressure increased significantly with gestation. In the growth-retarded fetuses umbilical venous pressure was higher, normal, or decreased, and there was no significant association between umbilical venous pressure and either fetal size or degree of acidemia. In the pregnancies complicated by red blood cell isoimmunization umbilical venous pressure increased with anemia but decreased to normal in the most severely anemic and hydropic fetuses. After intravascular blood transfusion umbilical venous pressure increased in proportion to the improvement in fetal hemoglobin concentration. CONCLUSION: Umbilical venous pressure is not the equivalent of central venous pressure but reflects both left and right heart function and placental resistance. (AM J OBSTET GYNECOL 1994;170:487-94.)

Vanadate causes hypokalemic distal renal tubular acidosis.

Considerable evidence supports the presence of an H(+)-K(+)-ATPase along the mammalian nephron. Inhibition of this enzyme might be expected to reduce acid excretion while increasing potassium excretion, thus causing hypokalemic distal renal tubular acidosis (RTA). In this study we administered vanadate at a dose of 5 mg/kg ip for 10 days to rats. These animals developed hypokalemic distal RTA with a blood pH of 7.22 +/- 0.01, a plasma bicarbonate of 15.2 +/- 0.6 meq/l, and a plasma potassium of 3.28 +/- 0.06 meq/l. The vanadate-treated animals had a urine pH of 6.70 +/- 0.09, a value significantly higher than NH4Cl-treated animals with the same degree of acidemia (urine pH = 5.25 +/- 0.04). When cortical collecting tubules (CCT) from these animals were microdissected and H(+)-K(+)-ATPase was measured, it was decreased by approximately 75% (P less than 0.001); but H(+)-ATPase was no different from control. In medullary collecting tubule, H(+)-K(+)-ATPase was also decreased but less than in CCT. Muscle potassium concentration in the vanadate-treated animals was significantly lower than in controls. These results demonstrate that vanadate causes hypokalemic distal RTA in association with inhibition of collecting tubule H(+)-K(+)-ATPase activity.

Analytic Reviews : Acid-Base Abnormalities in Cardiopulmonary Arrest: Varying Patterns in Different Locations Within the Hospital

Arterial blood gas analysis performed in 67 episodes who suffered cardiopulmonary arrest revealed that the degree of acidemia correlated with the location of the patient within the hospital: emergency department (ED), general hospital bed (HB), or intensive care unit (ICU). Acidemia was most severe in patients who pre sented either in the ED (pH = 7.15) or in a HB (pH = 7.10) as a result of combined metabolic (bicarbonate ion [HCO 3-] = 20 ± 16 and 15 ± 10 mEq/L) and respiratory acidosis (arterial carbon dioxide tension [PaCO2] = 59 ± 30 and 50 ± 24 mm Hg). In contrast, patients in the ICU had only mild acidemia or even alkalemia (pH = 7.28); respiratory acidosis was un common in this setting (PaCO2 = 36 ± 18 mm Hg), and patients exhibited a degree of metabolic acidosis ([HCO3 - ] = 18 ± 8 mEq/L) similar to that seen in patients in EDS or HBS. This relative hypocarbia seen in patients in the ICU was attributed to the fact that most (14 of 22, 64% ) were already receiving mechanical ven tilation at the time of the cardiopulmonary arrest. Pa tients who were successfully resuscitated (20, 30% ) did not differ from those in whom resuscitation failed (47, 70% ) in degree of acidemia or location of arrest. Serum potassium levels obtained in 29 patients at the time of arrest revealed that serum potassium levels were greater than 5.2 mEq/L only 8 times; there was only one mea surement greater than 6.0 mEq/L, which did not corre late with the degree of acidemia.

Diabetic ketoacidosis during long-term treatment with continuous subcutaneous insulin infusion.

During 1880 patient-months of treatment with continuous subcutaneous insulin infusion in 101 patients with IDDM, 36 episodes of acute, severe loss of glycemic control, including 29 with significant ketoacidosis, occurred in 20 patients. Fifteen episodes were attributable to failure of insulin delivery to the patient while 13 were precipitated by infection. Insufficiently frequent blood glucose monitoring, failure by patients to detect mechanical and technical problems with infusion systems, failure to adhere to "sick day" regimens, and delay in seeking medical help all contributed to the progression of a number of episodes. Thirst, nausea, and vomiting were the common clinical manifestations of decompensation; and the degree of acidemia was often mild in relation to the degree of hyperglycemia. Response to conventional management was usually prompt.

The Use of Corticosteroids in the Treatment of Acute Asthma

A study of 23 patients admitted to hospital with severe acute asthma is reported in which plasma cortisol level on admission was significantly correlated with the degree of acidaemia and pulse rate. Patients who had not previously received treatment with corticosteroids responded satisfactorily to repeated daily injections of tetracosactrin depot, the rate of improvement being comparable to that observed in other patients treated with intravenous hydrocortisone hemisuccinate. A prompt and sustained rise in plasma cortisol was also seen following tetracosactrin. The total daily dose of hydrocortisone required to achieve plasma cortisol levels above 100 mug/100 ml was less when given by continuous intravenous infusion compared with intermittent injections, and a regime of 3 mg/kg body weight every six hours by infusion appeared satisfactory. Most patients reported subjective improvement by about four hours after starting treatment but objective evidence did not appear until about six hours from the start. Measurements of FEV1 and FVC proved to be the most reliable indices of the beginning of improvement although pulse rate was the first index to show maximum improvement. Previous maintenance treatment with corticosteroids in patients with asthma did not appear materially to affect the plasma half-life of intravenous hydrocortisone (4 mgm/kg body weight) when compared with healthy subjects or other patients with asthma who had not previously been treated with corticosteroids.

Metabolic acidosis--diabetic.

METABOLIC ACIDOSIS is a clinical state characterized by an excess of hydrogen ions, the source of which are acids other than carbonic. In diabetic acidosis, the source of the excessive hydrogen ion is ketoacids formed during the process of intermediary metabolism in the absence of insulin. The degree of acidemia, ie, lowering of arterial blood pH, will depend on the severity of the metabolic disturbance on the one hand and the efficiency of the compensating mechanisms on the other. Reductions in arterial blood acid-base parameters, pH, [HCO 3 —], and P co 2 , define the pattern of the metabolic acidosis. Reduction in P co 2 is a reflection of the compensatory hyperventilation (Kussmaul respiration) occurring presumably in response to the lowered pH. If untreated, diabetic acidosis is fatal. History1 Stadelmann 2 in 1883 was the first to recognize that the symptom complex of diabetic coma was similar to the acid intoxication produced in rabbits by Walter. 3