Management of Neurogenic Respiratory Alkalosis and Concomitant Lactatemia After Resection of a Posterior Fossa Meningioma: A Case Report.

Central neurogenic hyperventilation (CNH) is a rare disease, caused by chemical or mechanical disturbance of respiratory centers. It is characterized by the absence of extracerebral respiratory stimuli. A woman developed severe respiratory alkalosis and lactatemia after resection of a posterior fossa meningioma despite lack of cardio-respiratory or metabolic alterations. Cerebral computed tomography (cCT) revealed edema of the pontomedullary area. Treatment with mannitol and dexamethasone reestablished normal breathing patterns. Lactatemia was likely due to reduced splanchnic lactate utilization. Intracranial pathologies should be suspected in case of hyperventilation without overt reasons. cCT to confirm edema or ischemia and prompt treatment is suggested.

Respiratory Acidosis and Respiratory Alkalosis: Core Curriculum 2023.

The respiratory system plays an integral part in maintaining acid-base homeostasis. Normal ventilation participates in the maintenance of an open buffer system, allowing for excretion of CO2 produced from the interaction of nonvolatile acids and bicarbonate. Quantitatively of much greater importance is the excretion of CO2 derived from volatile acids produced from the complete oxidation of fat and carbohydrate. A primary increase in CO2 tension of body fluids is the cause of respiratory acidosis and develops most commonly from one or more of the following: (1) disorders affecting gas exchange across the pulmonary capillary, (2) disorders of the chest wall and the respiratory muscles, and/or (3) inhibition of the medullary respiratory center. Respiratory alkalosis or primary hypocapnia is most commonly caused by disorders that increase alveolar ventilation and is defined by an arterial partial pressure of CO2 <35 mm Hg with subsequent alkalization of body fluids. Both disorders can lead to life-threatening complications, making it of paramount importance for the clinician to have a thorough understanding of the cause and treatment of these acid-base disturbances.

Critical Hypophosphatemia in a Special Operations Combat Dive Candidate: A Case Report.

In contrast to shallow water (hypoxic) blackout and swimming-induced pulmonary edema (SIPE), acute electrolyte disturbance secondary to acute respiratory alkalosis is not considered a common Combat Swimmer injury but has the potential to be life-threatening. We present the case of a 28-year-old Special Operations Dive Candidate who presented to the Emergency Department after a near-drowning incident with altered mental status, generalized weakness, respiratory distress, and tetany. He was found to have severe symptomatic hypophosphatemia (1.00mg/dL) and mild hypocalcemia secondary to intentional hyperventilation between subsurface "cross-overs," causing subsequent acute respiratory alkalosis. This is a unique presentation of a common electrolyte abnormality in a highly specialized population that is self-limiting when caused by acute respiratory alkalosis but poses a significant danger to Combat Swimmers if rescue personnel are not able to respond quickly.

Extreme alkalaemia with mixed alkalosis due to suspected acute-on-chronic respiratory alkalosis.

Herein we present a case of severe alkalaemia (pH 7.81) due to suspected acute-on-chronic respiratory alkalosis in a patient with chronic anxiety and metabolic alkalosis secondary to emesis. The patient was managed in the intensive care unit with significant improvement and discharged in stable condition. The case report emphasises considering a broad differential of aetiologies that can cause acid-base status derangements and identifying the appropriate therapeutic approach.

[Severe respiratory alkalosis due to psychogenic hyperventilation. Report of one case]. / Alcalosis respiratoria grave, la transformación de un cuadro funcional en orgánico. Caso clínico.

Severe respiratory alkalosis is a life-threatening condition, as it induces hypo- calcaemia and extreme adrenergic sensitivity leading to cerebral and myocardial vasoconstriction. We report a 37-year-old woman with previous consultations for a conversion disorder. While she was infected with SARS-CoV-2 (without pulmonary involvement), she consulted in the emergency room due to panic attacks. On admission, she developed a new conversion crisis with progressive clinical deterioration, hyperventilation, and severe respiratory alkalosis (pH 7.68, Bicarbonate 11.8 mEq/L and PaCO2 10 mmHg). Clinically, she was in a coma, with respiratory and heart rates 55 and 180 per min, a blood pressure of 140/90 mmHg, impaired perfusion (generalized lividity, distal coldness, and severe skin mottling) and tetany. She also had electrocardiographic changes and high troponin levels suggestive of ischemia, and hyperlactatemia. She was managed in the hospital with intravenous benzodiazepines. The clinical and laboratory manifestations resolved quickly, without the need for invasive measures and without systemic repercussions.

Alcalosis respiratoria grave, la transformación de un cuadro funcional en orgánico. Caso clínico / Severe respiratory alkalosis due to psychogenic hyperventilation. Report of one case

Severe respiratory alkalosis is a life-threatening condition, as it induces hypo- calcaemia and extreme adrenergic sensitivity leading to cerebral and myocardial vasoconstriction. We report a 37-year-old woman with previous consultations for a conversion disorder. While she was infected with SARS-CoV-2 (without pulmonary involvement), she consulted in the emergency room due to panic attacks. On admission, she developed a new conversion crisis with progressive clinical deterioration, hyperventilation, and severe respiratory alkalosis (pH 7.68, Bicarbonate 11.8 mEq/L and PaCO2 10 mmHg). Clinically, she was in a coma, with respiratory and heart rates 55 and 180 per min, a blood pressure of 140/90 mmHg, impaired perfusion (generalized lividity, distal coldness, and severe skin mottling) and tetany. She also had electrocardiographic changes and high troponin levels suggestive of ischemia, and hyperlactatemia. She was managed in the hospital with intravenous benzodiazepines. The clinical and laboratory manifestations resolved quickly, without the need for invasive measures and without systemic repercussions.

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.

Cardiogenic Auto-Triggering as a Consequence of Hemoperitoneum.

A 70-year-old woman presented with hemorrhagic shock secondary to hemoperitoneum following a paracentesis. On hospital day 3, she developed respiratory alkalosis and increased respiratory rates observed on the ventilator despite no spontaneous inspiratory effort. Converting to pressure support mode uncovered a cardiogenic oscillatory flow that had been auto-triggering the ventilator. This cardiogenic auto-triggering resolved with large-volume paracentesis. Cardiogenic auto-triggering leads to patient-ventilator dyssynchrony, respiratory alkalosis, lung distension, and difficulty with weaning from the ventilator, and it may be unrecognized in ICUs.

Lessons of the month 2: A forgotten cause of transient T-wave inversion.

A 19-year-old patient presented with severe chest pain, which is not typical for cardiac angina. However, his smoking history and the strong family history of ischaemic heart disease coupled with evidence of progressive T-wave changes on his electrocardiogram (ECG) caused dilemma in deciding further management. His blood tests were normal apart from hypophosphataemia, and he had two negative troponin results. His arterial blood gases showed respiratory alkalosis. He was given analgesia for a diagnosis of musculoskeletal chest pain and the next morning his ECG, arterial blood gases and phosphate levels all normalised. He had a normal echocardiogram and was reviewed by the cardiologist who diagnosed musculoskeletal chest pain which led to distress and hyperventilation causing hypophosphataemia and transient T-wave inversion. This case is a reminder of an under-recognised physiological phenomenon involving the cardiac conduction during hyperventilation.

Unilateral recurrent laryngeal nerve palsy post-thyroidectomy: Looking for hyperventilation syndrome.

AIMS: Unilateral Recurrent Laryngeal Nerve (RLN) palsy is responsible for dysphonia and difficulties in swallowing. The role of unilateral RLN palsy on dyspnea is not fully elucidated. Our hypothesis is that air leak could be responsible for development of hyperventilation syndrome (HVS). OBJECTIVE: The objective of this study was to determine in patients with unilateral RLN palsy if dyspnea could be associated with HVS. MATERIAL AND METHODS: Over a 12-month period, all patients with permanent unilateral RLN palsy after thyroidectomy complaining from the onset of unexplained dyspnea were tested. Measurement of Nijmegen score, an hyperventilation test, an arterial blood gas, lung function and cardiac tests were performed. The diagnosis of HVS was defined if at least two criteria were present among: Nijmegen score>23; reproduction of at least 2 usual symptoms during hyperventilation test; an expirated pressure of CO2 (EpCO2)<30mmHg or<90% of the initial EpCO2 after a 5minutes recovery period following a 3minutes voluntary hyperventilation. RESULTS: Ten out of 366 patients with thyroidectomy for benign disease had permanent unilateral RLN palsy and dyspnea. Among 10 patients included, 8 were diagnosed having HVS on the hyperventilation test without cardiac/lung dysfunction. CONCLUSION: In summary, this study is a proof of concept that HVS might be involved in dyspnea associated with unilateral RLN palsy.

Spontaneous Hyperventilation in Severe Traumatic Brain Injury: Incidence and Association with Poor Neurological Outcome.

BACKGROUND: Hypocapnia induces cerebral vasoconstriction leading to a decrease in cerebral blood flow, which might precipitate cerebral ischemia. Hypocapnia can be intentional to treat intracranial hypertension or unintentional due to a spontaneous hyperventilation (SHV). SHV is frequent after subarachnoid hemorrhage. However, it is understudied in patients with severe traumatic brain injury (TBI). The objective of this study was to describe the incidence and consequences on outcome of SHV after severe TBI. METHODS: We conducted a retrospective, observational study including all intubated TBI patients admitted in the trauma center and still comatose 24 h after the withdrawal of sedation. SHV was defined by the presence of at least one arterial blood gas (ABG) with both PaCO2 < 35 mmHg and pH > 7.45. Patient characteristics and outcome were extracted from a prospective registry of all intubated TBI admitted in the intensive care unit. ABG results were retrieved from patient files. A multivariable logistic regression model was developed to determine factors independently associated with unfavorable outcome (defined as a Glasgow Outcome Scale between 1 and 3) at 6-month follow-up. RESULTS: During 7 years, 110 patients fully respecting inclusion criteria were included. The overall incidence of SHV was 69.1% (95% CI [59.9-77]). Patients with SHV were more severely injured (median head AIS score (5 [4-5] vs. 4 [4-5]; p = 0.016)) and exhibited an elevated morbidity during their stay. The proportion of patients with an unfavorable functional neurologic outcome was significantly higher in patients with SHV: 40 (52.6%) versus 6 (17.6%), p = 0.0006. After adjusting for confounders, SHV remains an independent factor associated with unfavorable outcome at the 6-month follow-up (OR 4.1; 95% CI [1.2-14.4]). CONCLUSIONS: SHV is common in patients with a persistent coma after a severe TBI (overall rate: 69%) and was independently associated with unfavorable outcome at 6-month follow-up.

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.

Respiratory alkalosis may impair the production of vitamin D and lead to significant morbidity, including the fibromyalgia syndrome.

Hyperventilation caused by physical and/or psychological stress may lead to significant respiratory alkalosis and an elevated systemic pH. The alkalotic pH may in turn suppress the normal renal release of phosphate into the urine, thereby interrupting the endogenous production of 1,25-dihydroxyvitamin D (calcitriol). This could cause a shortfall in its normal production, leading to a variety of adverse consequences. It might partially explain the pathogenesis of acute mountain sickness, a treatable disease characterized by severe hyperventilation secondary to the hypoxia of high altitude exposure. Milder degrees of hyperventilation due to different forms of stress may produce other conditions which share characteristics with acute mountain sickness. One of these may be the fibromyalgia syndrome, a chronic painful disorder for which no satisfactory treatment exists. Should fibromyalgia and acute mountain sickness have a common etiology, may they also share a common form of treatment? Evidence is presented to support this hypothesis.

A Quick Reference on Respiratory Alkalosis.

Respiratory alkalosis, or primary hypocapnia, occurs when alveolar ventilation exceeds that required to eliminate the carbon dioxide produced by tissues. Concurrent decreases in Paco2, increases in pH, and compensatory decreases in blood HCO3- levels are associated with respiratory alkalosis. Respiratory alkalosis can be acute or chronic, with metabolic compensation initially consisting of cellular uptake of HCO3- and buffering by intracellular phosphates and proteins. Chronic respiratory alkalosis results in longer-lasting decreases in renal reabsorption of HCO3-; the arterial pH can approach near-normal values.

Respiratory Acid-Base Disorders in the Critical Care Unit.

The incidence of respiratory acid-base abnormalities in the critical care unit (CCU) is unknown, although respiratory alkalosis is suspected to be common in this population. Abnormal carbon dioxide tension can have many physiologic effects, and changes in Pco2 may have a significant impact on outcome. Monitoring Pco2 in CCU patients is an important aspect of critical patient assessment, and identification of respiratory acid-base abnormalities can be valuable as a diagnostic tool. Treatment of respiratory acid-base disorders is largely focused on resolution of the primary disease, although mechanical ventilation may be indicated in cases with severe respiratory acidosis.

A Case of Neuro-Behcet's Disease Presenting with Central Neurogenic Hyperventilation.

BACKGROUND: Behcet's disease is a chronic inflammatory disorder usually characterized by the triad of oral ulcers, genital ulcers, and uveitis. Central to the pathogenesis of Behcet's disease is an autoimmune vasculitis. Neurological involvement, so called "Neuro-Behcet's disease", occurs in 10-20% of patients, usually from a meningoencephalitis or venous thrombosis. CASE REPORT: We report the case of a 46-year-old patient with Neuro-Behcet's disease who presented with central neurogenic hyperventilation as a result of brainstem involvement from venulitis. CONCLUSIONS: To the best of our knowledge, central neurogenic hyperventilation has not previously been described in a patient with Neuro-Behcet's disease.