COVID-19 myocarditis and postinfection Bell's palsy.

Here we present the case of a 37-year-old previously healthy man who developed fever, headache and a unilateral, painful neck swelling while working offshore. He had no known contact with anyone with COVID-19; however, due to the ongoing pandemic, a nasopharyngeal swab was performed, which was positive for the virus. After transfer to hospital for assessment his condition rapidly deteriorated, requiring admission to intensive care for COVID-19 myocarditis. One week after discharge he re-presented with unilateral facial nerve palsy. Our case highlights an atypical presentation of COVID-19 and the multifaceted clinical course of this still poorly understood disease.

Hyperventilation Syndrome and Sustained Hyperchloremia After Kidney Transplant: Time-Sequence Swing of Acid-Base Interpretation.

An interaction between regained renal function in a transplanted kidney and hyperventilation syndrome may interfere with correct diagnosis of acid-base status in patients with preoperative nongap acidosis. Here, we present a patient with glomerular nephritis and hyperchloremia who underwent kidney transplant. Progressively increasing bicarbonate reabsorption by the renal graft, which thereby changed the arterial carbon dioxide tension-to-bicarbonate ratio, resulted in a time-sequence swing of an acid-base interpretation despite persistent mixed respiratory alkalosis due to hyperventilation syndrome and nongap metabolic acidosis due to preexisting hyperchloremia. Specifically, the sequence was mixed primary metabolic acidosis and primary respiratory acidosis immediately after surgery, primary metabolic acidosis and secondary respiratory alkalosis on postoperative days 1 and 2, mixed primary hyperchloremic metabolic acidosis and primary respiratory alkalosis on postoperative day 3, and finally primary respiratory alkalosis and secondary hyperchloremic metabolic acidosis on postoperative day 7. This swing in the acid-base interpretation indicates that the acid-base imbalance described here does not fit the empirical relationship for calculating the expected bicarbonate or carbon dioxide tension value, suggesting that "correct" interpretation of acid-base status may not lead to "correct" diagnosis of acid-base status. It should be remembered that not every acid-base imbalance fits the empirical relationship.

Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low Plasma Bicarbonate Using the Urine Anion Gap.

Hypobicarbonatemia, or a reduced bicarbonate concentration in plasma, is a finding seen in 3 acid-base disorders: metabolic acidosis, chronic respiratory alkalosis and mixed metabolic acidosis and chronic respiratory alkalosis. Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy. Proper diagnosis of the cause of hypobicarbonatemia requires integration of the laboratory values, arterial blood gas, and clinical history. The information derived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of urine anion gap, as a surrogate marker of urine ammonium excretion, in the evaluation of a patient with low plasma bicarbonate concentration to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of urine acid-base indexes at bedside (urine pH, urine bicarbonate, and urine anion gap) to evaluate urine acidification are discussed.

[Prehospital arterial blood gas analysis after collapse connected to triathlon participation].

Long-distance athletes are at risk of serious fluid and electrolyte disturbances, such as hypernatraemia (dehydration). Recently, cases of serious morbidity have been reported, due to acute exercise-associated hyponatraemia, which can advance to encephalopathy. An arterial blood gas analysis (ABG) was drawn from collapsed athletes at the championship of full-distance triathlon 2015, and different electrolyte imbalances were found. Our findings show that prehospital ABG can assist in differentiating the cause of collapse, and presumably, targeted treatment can be initiated already on scene.

Hyperchloremia - Why and how.

Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance.

Effect of Acetazolamide vs Placebo on Duration of Invasive Mechanical Ventilation Among Patients With Chronic Obstructive Pulmonary Disease: A Randomized Clinical Trial.

IMPORTANCE: Acetazolamide has been used for decades as a respiratory stimulant for patients with chronic obstructive pulmonary disease (COPD) and metabolic alkalosis, but no large randomized placebo-controlled trial is available to confirm this approach. OBJECTIVE: To determine whether acetazolamide reduces mechanical ventilation duration in critically ill patients with COPD and metabolic alkalosis. DESIGN, SETTING, AND PARTICIPANTS: The DIABOLO study, a randomized, double-blind, multicenter trial, was conducted from October 2011 through July 2014 in 15 intensive care units (ICUs) in France. A total of 382 patients with COPD who were expected to receive mechanical ventilation for more 24 hours were randomized to the acetazolamide or placebo group and 380 were included in an intention-to treat analysis. INTERVENTIONS: Acetazolamide (500-1000 mg, twice daily) vs placebo administered intravenously in cases of pure or mixed metabolic alkalosis, initiated within 48 hours of ICU admission and continued during the ICU stay for a maximum of 28 days. MAIN OUTCOMES AND MEASURES: The primary outcome was the duration of invasive mechanical ventilation via endotracheal intubation or tracheotomy. Secondary outcomes included changes in arterial blood gas and respiratory parameters, weaning duration, adverse events, use of noninvasive ventilation after extubation, successful weaning, the duration of ICU stay, and in-ICU mortality. RESULTS: Among 382 randomized patients, 380 (mean age, 69 years; 272 men [71.6%]; 379 [99.7%] with endotracheal intubation) completed the study. For the acetazolamide group (n = 187), compared with the placebo group (n = 193), no significant between-group differences were found for median duration of mechanical ventilation (-16.0 hours; 95% CI, -36.5 to 4.0 hours; P = .17), duration of weaning off mechanical ventilation (-0.9 hours; 95% CI, -4.3 to 1.3 hours; P = .36), daily changes of minute-ventilation (-0.0 L/min; 95% CI, -0.2 to 0.2 L/min; P = .72), or partial carbon-dioxide pressure in arterial blood (-0.3 mm Hg; 95% CI, -0.8 to 0.2 mm Hg; P = .25), although daily changes of serum bicarbonate (between-group difference, -0.8 mEq/L; 95% CI, -1.2 to -0.5 mEq/L; P < .001) and number of days with metabolic alkalosis (between-group difference, -1; 95% CI, -2 to -1 days; P < .001) decreased significantly more in the acetazolamide group. Other secondary outcomes also did not differ significantly between groups. CONCLUSIONS AND RELEVANCE: Among patients with COPD receiving invasive mechanical ventilation, the use of acetazolamide, compared with placebo, did not result in a statistically significant reduction in the duration of invasive mechanical ventilation. However, the magnitude of the difference was clinically important, and it is possible that the study was underpowered to establish statistical significance. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01627639.

Enhancement on Wingate Anaerobic Test Performance With Hyperventilation.

UNLABELLED: Relatively long-lasting metabolic alkalizing procedures such as bicarbonate ingestion have potential for improving performance in long-sprint to middle-distance events. Within a few minutes, hyperventilation can induce respiratory alkalosis. However, corresponding performance effects are missing or equivocal at best. PURPOSE: To test a potential performance-enhancing effect of respiratory alkalosis in a 30-s Wingate Anaerobic Test (WAnT). METHODS: 10 men (mean ± SD age 26.6 ± 4.9 y, height 184.4 ± 6.1 cm, body-mass test 1 80.7 ± 7.7 kg, body-mass test 2 80.4 ± 7.2 kg, peak oxygen uptake 3.95 ± 0.43 L/min) performed 2 WAnTs, 1 with and 1 without a standardized 15-min hyperventilation program pre-WAnT in randomized order separated by 1 wk. RESULTS: Compared with the control condition, hyperventilation reduced (all P < .01) pCO2 (40.5 ± 2.8 vs 22.5 ± 1.6 mm Hg) and HCO3 - (25.5 ± 1.7 vs 22.7 ± 1.6 mmol/L) and increased (all P < .01) pH (7.41 ± 0.01 vs 7.61 ± 0.03) and actual base excess (1.4 ± 1.4 vs 3.2 ± 1.6 mmol/L) pre-WAnT with an ergogenic effect on WAnT average power (681 ± 41 vs 714 ± 44 W) and total metabolic energy (138 ± 12 vs. 144 ± 13 kJ) based on an increase in glycolytic energy (81 ± 13 vs 88 ± 13 kJ). CONCLUSION: Hyperventilation-induced respiratory alkalosis can enhance WAnT cycling sprint performance well in the magnitude of what is seen after successful bicarbonate ingestion.

Acid-base disturbance in patients with cirrhosis: relation to hemodynamic dysfunction.

PURPOSE: Acid-base disturbances were investigated in patients with cirrhosis in relation to hemodynamic derangement to analyze the hyperventilatory effects and the metabolic compensation. METHODS: A total of 66 patients with cirrhosis and 44 controls were investigated during a hemodynamic study. RESULTS: Hyperventilatory hypocapnia was present in all patients with cirrhosis and progressed from Child class A to C (P<0.01). Arterial pH increased significantly from class A to C (P<0.001) and was correlated inversely to the mean arterial blood pressure (r=-0.30, P<0.02), systemic vascular resistance (r=-0.25, P<0.05), indocyanine green clearance (r=-0.37, P<0.005), and serum sodium (r=-0.38, P<0.002). Metabolic compensation was shown by a reduced standard base excess in all patients (P<0.001). Standard base excess contained elements related to changes in serum albumin, water dilution, and effects of unidentified ions (all P<0.001). A significant hepatic component in the acid-base disturbances could not be identified. CONCLUSION: Hypocapnic alkalosis is related to disease severity and hyperdynamic systemic circulation in patients with cirrhosis. The metabolic compensation includes alterations in serum albumin and water retention that may result in a delicate acid-base balance in these patients.

Hepatopulmonary syndrome: the role of intra-abdominal hypertension and a novel mouse model.

OBJECTIVE: Hepatopulmonary syndrome (HPS) is considered as a triad of chronic liver disease, pulmonary vascular ectasia and severe hypoxemia. The study aims to investigate the pathological mechanism of intra-abdominal pressure (IAP) in HPS and establish a novel mouse model. METHODS: Fifty male ICR mice were randomly divided into experimental and control group, receiving subcutaneous injection of carbon tetrachloride and water, respectively. Mice in experimental group were then divided into 4 sub-groups with the intraperitoneal injection of different volume of albumin to form different IAP (0, 5, 10 and 20 cmH2O). All the mice were then sacrificed 24 hours later and blood gas analysis was conducted. In addition, liver and lung histopathology was also examined. RESULTS: Blood gas analysis in different IAP suggested the respiratory alkalosis. Arterial partial pressure of oxygen significantly decreased in the IAP=10 cmH2O (68.13 ± 3.56, P<0.01) and 20 cmH2O (66.00 ± 3.78, P<0.01). Alveolar-arterial oxygen pressure difference increased markedly in the IAP=10 cmH2O (54.60 ± 6.80, P<0.001) and 20 cmH2O (57.04 ± 5.60, P<0.001). According to lung histopathology, macrophages were found to accumulate in the alveolar spaces and the widened alveolar walls were detected. In addition, there was visible blood stasis in the alveolar walls and numerous red blood cells extravasated into air space in the IAP=10 and 20 cmH2O. CONCLUSIONS: Our study suggested that intra-abdominal hypertension was a significant pathological mechanism of HPS. Meanwhile, we have established a novel mouse model that will now be optimized with further investigation of the mechanism and therapeutic targets of HPS.

Simple acid-base tutorial.

The nutrition support practitioner is confronted with numerous metabolic abnormalities in the daily care of patients. An understanding of the basic principles of acid-base balance, along with the ability to recognize common causes of the various disorders, enhances the clinician's ability to provide specialized nutrition support. The basic metabolic and respiratory disorders, along with common causes, are reviewed in this tutorial.

Methylphenidate actively induces emergence from general anesthesia.

BACKGROUND: Although accumulating evidence suggests that arousal pathways in the brain play important roles in emergence from general anesthesia, the roles of monoaminergic arousal circuits are unclear. In this study, the authors tested the hypothesis that methylphenidate (an inhibitor of dopamine and norepinephrine transporters) induces emergence from isoflurane general anesthesia. METHODS: Using adult rats, the authors tested the effect of intravenous methylphenidate on time to emergence from isoflurane general anesthesia. They then performed experiments to test separately for methylphenidate-induced changes in arousal and changes in minute ventilation. A dose-response study was performed to test for methylphenidate-induced restoration of righting during continuous isoflurane general anesthesia. Surface electroencephalogram recordings were performed to observe neurophysiological changes. Plethysmography recordings and arterial blood gas analysis were performed to assess methylphenidate-induced changes in respiratory function. Intravenous droperidol was administered to test for inhibition of methylphenidate's actions. RESULTS: Methylphenidate decreased median time to emergence from 280 to 91 s. The median difference in time to emergence without methylphenidate compared with administration of methylphenidate was 200 [155-331] s (median, [95% CI]). During continuous inhalation of isoflurane, methylphenidate induced return of righting in a dose-dependent manner, induced a shift in electroencephalogram power from delta (less than 4 Hz) to theta (4-8 Hz), and induced an increase in minute ventilation. Administration of intravenous droperidol (0.5 mg/kg) before intravenous methylphenidate (5 mg/kg) largely inhibited methylphenidate-induced emergence behavior, electroencephalogram changes, and changes in minute ventilation. CONCLUSIONS: Methylphenidate actively induces emergence from isoflurane general anesthesia by increasing arousal and respiratory drive, possibly through activation of dopaminergic and adrenergic arousal circuits. The authors' findings suggest that methylphenidate may be useful clinically as an agent to reverse general anesthetic-induced unconsciousness and respiratory depression at the end of surgery.

A mathematical model of tumour and blood pHe regulation: The HCO3-/CO2 buffering system.

Malignant tumours are characterised by a low, acidic extracellular pH (pHe) which facilitates invasion and metastasis. Previous research has proposed the potential benefits of manipulating systemic pHe, and recent experiments have highlighted the potential for buffer therapy to raise tumour pHe, prevent metastases, and prolong survival in laboratory mice. To examine the physiological regulation of tumour buffering and investigate how perturbations of the buffering system (via metabolic/respiratory disorders or changes in parameters) can alter tumour and blood pHe, we develop a simple compartmentalised ordinary differential equation model of pHe regulation by the HCO3-/CO2 buffering system. An approximate analytical solution is constructed and used to carry out a sensitivity analysis, where we identify key parameters that regulate tumour pHe in both humans and mice. From this analysis, we suggest promising alternative and combination therapies, and identify specific patient groups which may show an enhanced response to buffer therapy. In addition, numerical simulations are performed, validating the model against well-known metabolic/respiratory disorders and predicting how these disorders could change tumour pHe.

A 19-month-old boy with recurrent respiratory distress.

We present a 19-month-old boy with a history of asthma who presented to the pediatric emergency department with noisy breathing and tachypnea partially responsive to albuterol. He was discharged to routine care at home. His parents brought him back the next day for persistent respiratory distress despite routine home albuterol. A check of electrolytes showed a low bicarbonate level.

Hyperventilation and finger exercise increase venous-arterial Pco2 and pH differences.

INTRODUCTION: Since the invention of the pulse oximeter, physicians often or even routinely perform venous blood gas analysis (VBGA). However, it has not been generally agreed that the application of VBGA is practically meaningful in routine clinical situations such as in an ED. METHODS: We measured venous-arterial Pco(2) difference ((v-a)Pco(2)) and arterial-venous pH difference ((a-v)pH), and analyzed the physiological factors that affect these differences in healthy volunteers and hyperventilation patients. RESULTS: In healthy volunteers, both (v-a)Pco(2) and (a-v)pH increased during finger exercise or hyperventilation in an intensity-dependent manner. Doppler echography indicated that increases in (v-a)Pco(2) and (a-v)pH during hyperventilation are induced by reduction of peripheral blood flow. Approximately 40% of patients with untreated respiratory alkalosis were found to be incorrectly diagnosed if based only on VBGA. CONCLUSIONS: It must be noted that VBGA may lead to overestimation of acidosis and to underestimation of respiratory alkalosis when extremities muscles are active or patients are hyperventilating. Physicians should keep these limitations in mind when conducting VBGA.

Central lactic acidosis, hyperventilation, and respiratory alkalosis: leading clinical features in a 3-year-old boy with malignant meningeal melanoma.

Meningeal tumors are extremely rare in children and are diagnostically as well as therapeutically challenging. Among the least common types of malignancies in childhood is malignant melanoma, counting for less than 1% of pediatric tumors. Due to the rarity and the wide spectrum of appearance, initial clinical features may be misleading. A 3-year-old boy was referred to our hospital with symptoms of hyperventilation, dyspnoea, tachycardia, respiratory alkalosis, inarticulate speech, and fatigue. Measurement of pH in cerebrospinal fluid (CSF) yielded central lactic acidosis despite alkalosis in peripheral blood. Diagnostic imaging procedures as well as histology and immunohistochemistry revealed the diagnosis of a malignant meningeal melanoma. We hypothesize that central lactate production of the tumor nests might have induced central acidification, thus inducing hyperventilation by stimulation of central chemoreceptors. This case is a model example of the key role of central pH as an inducer/suppressor of ventilation in humans and illustrates the critical importance of central pH for regulating both ventilation and acid-base homeostasis. Thus, pH of CSF should be measured whenever a malignant brain tumor is suspected.

A guide to regulation of blood gases: part three.

In the third and final part of this series looking at blood gas analysis, Liz Allibone and Nicola Nation provide three examples of how arterial blood gas results assist in the diagnosis and management of illness.

Control of rectal gland secretion by blood acid-base status in the intact dogfish shark (Squalus acanthias).

In order to address the possible role of blood acid-base status in controlling the rectal gland, dogfish were fitted with indwelling arterial catheters for blood sampling and rectal gland catheters for secretion collection. In intact, unanaesthetized animals, isosmotic volume loading with 500 mmol L-1 NaCl at a rate of 15 mL kg-1 h-1 produced a brisk, stable rectal gland secretion flow of about 4 mL kg-1 h-1. Secretion composition (500 mmol L-1 Na+ and Cl-; 5 mmol L-1 K+; <1 mmol L-1 Ca2+, Mg2+, SO(4)2-, or phosphate) was almost identical to that of the infusate with a pH of about 7.2, HCO3- mmol L-1<1 mmol L-1 and a PCO2 (1 Torr) close to PaCO2. Experimental treatments superimposed on the infusion caused the expected disturbances in systemic acid-base status: respiratory acidosis by exposure to high environmental PCO2, metabolic acidosis by infusion of HCl, and metabolic alkalosis by infusion of NaHCO3. Secretion flow decreased markedly with acidosis and increased with alkalosis, in a linear relationship with extracellular pH. Secretion composition did not change, apart from alterations in its acid-base status, and made negligible contribution to overall acid-base balance. An adaptive control of rectal gland secretion by systemic acid-base status is postulated-stimulation by the "alkaline tide" accompanying the volume load of feeding and inhibition by the metabolic acidosis accompanying the volume contraction of exercise.

Uncompensated metabolic acidosis: an underrecognized risk factor for subsequent intubation requirement.

BACKGROUND: There are no published reports identifying an inadequate ventilatory response to metabolic acidosis as a predictor of impending respiratory failure. Metabolic acidosis should induce a respiratory alkalosis in which the partial pressure of carbon dioxide (Paco2) is (1.5 [HCO3-] + 8) +/- 2. This study examined the relation between inadequate ventilatory compensation and intubation among trauma patients. METHODS: A retrospective chart review was performed for trauma patients admitted between January 1999 and December 2000. Age, gender, Injury Severity Score and combined Trauma and Injury Severity Score, chest injury, history of cardiac or pulmonary disease, partial pressure of oxygen (Pao2), Paco2, Glasgow Coma Score, respiratory rate, systolic blood pressure, base deficit, and ability to compensate were analyzed with respect to intubation and need for ventilator support. RESULTS: Of 140 patients with metabolic acidosis, 45 ultimately were intubated. The mean Paco2 for the unintubated patients was 34 +/- 7 mm Hg, as compared with 41 +/- 11 mm Hg for the intubated patients (p < 0.001). Only injury severity and ability to compensate for metabolic acidosis were independent predictors of intubation. Patients with inadequate compensation were 4.2 times more likely to require intubation when control was used for the Injury Severity Score (95% confidence interval, 1.8-9.7; p < 0.001). CONCLUSIONS: Inability to mount an adequate hyperventilatory response to metabolic acidosis is associated with an increased likelihood of respiratory failure and a need for ventilatory support. Recognition of this relation should lead to closer monitoring of patients with this condition, and could help to avert unforeseen crisis intubations. This observation needs to be validated in a prospective study.