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Background: The perioperative management of patients with chronic cough or cough hypersensitivity syndrome and its sometimes severe effects is currently under-researched and under-reported. Case presentation: A 46-year-old female patient with a history of chronic cough and Cough Hypersensitivity Syndrome. After laparoscopic hiatoplasty and anterior fundoplication under general anesthesia, experienced a pronounced exacerbation of coughing symptoms. Despite prompt and extensive treatment involving antitussives, inhalants, anxiolytics, and sedatives, the symptoms remained uncontrollable. Within a few hours, the patient developed a respiratory alkalosis with severe and life-threatening electrolyte shift (pH 7.705, pCO2 1.72 kPa, K+ 2.1 mmol/l). Lactatemia lasted for more than 12 hours with values up to 6.6 mmol/l. Acute bleeding, pneumothorax, and an acute cardiac event were ruled out. Deep analgosedation and inhalation of high-percentage local anesthetics were necessary to manage the clinical symptoms. Conclusions: This case highlights the challenging nature of chronic cough and hypersensitivity syndrome perioperatively. A tailored anesthesiologic approach, exclusion of other provoking medical problems, and knowledge of possible management and treatment options are key. [ABSTRACT FROM AUTHOR]

Extreme heat caused by climate change is increasing the transmission of infectious diseases, resulting in a sharp rise in heat-related illness and mortality. Understanding the mechanistic link between heat, inflammation, and disease is thus important for public health. Thermal hyperpnea, and consequent respiratory alkalosis, is crucial in febrile seizures and convulsions induced by heat stress in humans. Here, we address what causes thermal hyperpnea in neonates and how it is affected by inflammation. Transient receptor potential cation channel subfamily V member 1 (TRPV1), a heat-activated channel, is sensitized by inflammation and modulates breathing and thus may play a key role. To investigate whether inflammatory sensitization of TRPV1 modifies neonatal ventilatory responses to heat stress, leading to respiratory alkalosis and an increased susceptibility to hyperthermic seizures, we treated neonatal rats with bacterial LPS, and breathing, arterial pH, in vitro vagus nerve activity, and seizure susceptibility were assessed during heat stress in the presence or absence of a TRPV1 antagonist (AMG-9810) or shRNA-mediated TRPV1 suppression. LPS-induced inflammatory preconditioning lowered the threshold temperature and latency of hyperthermic seizures. This was accompanied by increased tidal volume, minute ventilation, expired CO2, and arterial pH (alkalosis). LPS exposure also elevated vagal spiking and intracellular calcium concentrations in response to hyperthermia. TRPV1 inhibition with AMG-9810 or shRNA reduced the LPS-induced susceptibility to hyperthermic seizures and altered the breathing pattern to fast shallow breaths (tachypnea), making each breath less efficient and restoring arterial pH. These results indicate that inflammation exacerbates thermal hyperpnea-induced respiratory alkalosis associated with increased susceptibility to hyperthermic seizures, primarily mediated by TRPV1 localized to vagus neurons. [ABSTRACT FROM AUTHOR]

Abstract Background The perioperative management of patients with chronic cough or cough hypersensitivity syndrome and its sometimes severe effects is currently under-researched and under-reported. Case presentation A 46-year-old female patient with a history of chronic cough and Cough Hypersensitivity Syndrome. After laparoscopic hiatoplasty and anterior fundoplication under general anesthesia, experienced a pronounced exacerbation of coughing symptoms. Despite prompt and extensive treatment involving antitussives, inhalants, anxiolytics, and sedatives, the symptoms remained uncontrollable. Within a few hours, the patient developed a respiratory alkalosis with severe and life-threatening electrolyte shift (pH 7.705, pCO2 1.72 kPa, K+ 2.1 mmol/l). Lactatemia lasted for more than 12 hours with values up to 6.6 mmol/l. Acute bleeding, pneumothorax, and an acute cardiac event were ruled out. Deep analgosedation and inhalation of high-percentage local anesthetics were necessary to manage the clinical symptoms. Conclusions This case highlights the challenging nature of chronic cough and hypersensitivity syndrome perioperatively. A tailored anesthesiologic approach, exclusion of other provoking medical problems, and knowledge of possible management and treatment options are key.

Chilaiditi syndrome is defined as the interposition of the colon between the liver and the diaphragm or abdominal wall and is known as Chilaiditi's sign on X-rays. Although rare, this procedure can lead to serious complications. Due to its infrequency and propensity for severe complications, diagnosing and differentiating this syndrome from other acute abdominal emergencies are very important for preventing unnecessary treatment or surgical procedures. We present a 72-year-old male with a history of chronic obstructive pulmonary disease (COPD) who presented to the emergency department with persistent shortness of breath, abdominal discomfort, and vomiting. Physical examination revealed chest crepitation, tenderness in the left iliac fossa, and high blood pressure. Laboratory tests revealed a positive COVID-19 status, elevated C-reactive protein level, and respiratory alkalosis. Imaging, including a chest X-ray and CT scan, confirmed the presence of bowel loops under the diaphragm, confirming the diagnosis of Chilaiditi syndrome. Collaborative management by surgical and medical teams was essential in navigating this complex condition. This case highlights the complexity of chilaiditi syndrome, which can be episodic and intermittent, in addition to the importance of recognizing Chilaiditi's sign on imaging, particularly on CT scans, to differentiate it from pneumoperitoneum. Vigilance is crucial in identifying potential complications and guiding appropriate treatment to prevent adverse outcomes.

Hypoxia during supramaximal exercise reduces aerobic metabolism with a compensatory increase in anaerobic metabolism without affecting exercise performance. A similar response is elicited by preexercise voluntary hypocapnic hyperventilation, but it remains unclear whether hypocapnic hyperventilation and hypoxia additively reduce aerobic metabolism and increase anaerobic metabolism during supramaximal exercise. To address that issue, 12 healthy subjects (8 males and 4 females) performed the 30-second Wingate anaerobic test (WAnT) after (1) spontaneous breathing in normoxia (control, ∼21% fraction of inspired O2 [FiO2]), (2) voluntary hypocapnic hyperventilation in normoxia (hypocapnia, ∼21% FiO2), (3) spontaneous breathing in hypoxia (hypoxia, ∼11% FiO2), or (4) voluntary hypocapnic hyperventilation in hypoxia (combined, ∼11% FiO2). Mean power output during the 30-second WAnT was similar among the control (561 [133] W), hypocapnia (563 [140] W), hypoxia (558 [131] W), and combined (560 [133] W) trials (P =.778). Oxygen uptake during the 30-second WAnT was lower in the hypocapnia (1523 [318] mL/min), hypoxia (1567 [300] mL/min), and combined (1203 [318] mL/min) trials than in the control (1935 [250] mL/min) trial, and the uptake in the combined trial was lower than in the hypocapnia or hypoxia trial (all P <.001). Oxygen deficit, an index of anaerobic metabolism, was higher in the hypocapnia (38.4 [7.3] mL/kg), hypoxia (37.8 [6.8] mL/kg), and combined (40.7 [6.9] mL/kg) trials than in the control (35.0 [6.8] mL/kg) trial, and the debt was greater in the combined trial than in the hypocapnia or hypoxia trial (all P <.003). Our results suggest that voluntary hypocapnic hyperventilation and hypoxia additively reduce aerobic metabolism and increase anaerobic metabolism without affecting exercise performance during the 30-second WAnT. [ABSTRACT FROM AUTHOR]

This article provides a step-by-step guide for nurses to interpret arterial blood gas (ABG) results, focusing on five key components: SaO2, PaO2, pH, PaCO2, and HCO3-. It explains how to assess a patient's oxygenation status, compensation levels, and determine if there is an acid-base disturbance and if that disturbance is respiratory or metabolic. [ABSTRACT FROM AUTHOR]

Passive hyperthermia causes cerebral hypoperfusion primarily from heat‐induced respiratory alkalosis. However, despite the cerebral hypoperfusion, it is possible that the mild alkalosis might help to attenuate cerebral inflammation. In this study, the cerebral exchange of extracellular vesicles (microvesicles), which are known to elicit pro‐inflammatory responses when released in conditions of stress, were examined in hyperthermia with and without respiratory alkalosis. Ten healthy male adults were heated passively, using a warm water‐perfused suit, up to core temperature + 2°C. Blood samples were taken from the radial artery and internal jugular bulb. Microvesicle concentrations were determined in platelet‐poor plasma via cells expressing CD62E (activated endothelial cells), CD31+/CD42b− (apoptotic endothelial cells), CD14 (monocytes) and CD45 (pan‐leucocytes). Cerebral blood flow was measured via duplex ultrasound of the internal carotid and vertebral arteries to determine cerebral exchange kinetics. From baseline to poikilocapnic (alkalotic) hyperthermia, there was no change in microvesicle concentration from any cell origin measured (P‐values all >0.05). However, when blood CO2 tension was normalized to baseline levels in hyperthermia, there was a marked increase in cerebral uptake of microvesicles expressing CD62E (P = 0.028), CD31+/CD42b− (P = 0.003) and CD14 (P = 0.031) compared with baseline, corresponding to large increases in arterial but not jugular venous concentrations. In a subset of seven participants who underwent hypercapnia and hypocapnia in the absence of heating, there was no change in microvesicle concentrations or cerebral exchange, suggesting that hyperthermia potentiated the CO2/pH‐mediated cerebral uptake of microvesicles. These data provide insight into a potential beneficial role of respiratory alkalosis in heat stress. Key points: The hyperthermia‐induced hyperventilatory response is observed in most humans, despite causing potentially harmful reductions in cerebral blood flow.We tested the hypothesis that the respiratory‐induced alkalosis is associated with lower circulating microvesicle concentrations, specifically in the brain, despite the reductions in blood flow.At core temperature + 2°C with respiratory alkalosis, microvesicles derived from endothelial cells, monocytes and leucocytes were at concentrations similar to baseline in the arterial and cerebral venous circulation, with no changes in cross‐brain microvesicle kinetics.However, when core temperature was increased by 2°C with CO2/pH normalized to resting levels, there was a marked cerebral uptake of microvesicles derived from endothelial cells and monocytes. The CO2/pH‐mediated alteration in cerebral microvesicle uptake occurred only in hyperthermia.These new findings suggest that the heat‐induced hyperventilatory response might serve a beneficial role by preventing potentially inflammatory microvesicle uptake in the brain. [ABSTRACT FROM AUTHOR]

Purpose: We investigated the effects of pre-exercise voluntary hyperventilation and the resultant hypocapnia on metabolic and cardiovascular responses during and after high-intensity exercise. Methods: Ten healthy participants performed a 60-s cycling exercise at a workload of 120% peak oxygen uptake in control (spontaneous breathing), hypocapnia and normocapnia trials. Hypocapnia was induced through 20-min pre-exercise voluntary hyperventilation. In the normocapnia trial, voluntary hyperpnea was performed with CO2 inhalation to prevent hypocapnia. Results: Pre-exercise end-tidal CO2 partial pressure was lower in the hypocapnia trial than the control or normocapnia trial, with similar levels in the control and normocapnia trials. Average VO2 during the entire exercise was lower in both the hypocapnia and normocapnia trials than in the control trial (1491 ± 252vs.1662 ± 169vs.1806 ± 149 mL min-1), with the hypocapnia trial exhibiting a greater reduction than the normocapnia trial. Minute ventilation during exercise was lower in the hypocapnia trial than the normocapnia trial. In addition, minute ventilation during the first 10s of the exercise was lower in the normocapnia than the control trial. Pre-exercise hypocapnia also reduced heart rates and arterial blood pressures during the exercise relative to the normocapnia trial, a response that lasted through the subsequent early recovery periods, though end-tidal CO2 partial pressure was similar in the two trials. Conclusions: Our results suggest that preexercise hyperpnea and the resultant hypocapnia reduce VO2 during high-intensity exercise. Moreover, hypocapnia may contribute to voluntary hyperventilation-mediated cardiovascular responses during the exercise, and this response can persist into the subsequent recovery period, despite the return of arterial CO2 pressure to the normocapnic level. [ABSTRACT FROM AUTHOR]

Respiratory alkalosis is one of the four basic disturbances to the acid-base equilibrium. Persistent primary respiratory alkalosis during non-invasive mechanical ventilation in patients with hypoxemic respiratory failure could be a risk factor for NIV failure. A 69-year-old man with acute hypoxemic respiratory failure caused by severe COVID-19 pneumonia demonstrated progressive worsening of gas exchange and clinical conditions. Despite a positive response to noninvasive mechanical ventilation, a therapeutic increase in respiratory support was required. [ABSTRACT FROM AUTHOR]

Respiratory alkalosis during hemodialysis session is a rare complication. We managed two patients with severe respiratory alkalosis, a woman who developed this 75 min after the beginning of the session and a man who developed it about 1 h before the end of the session. In both, the cause was a hypotensive episode, and both hypotension and alkalosis were successfully treated. [ABSTRACT FROM AUTHOR]

The neuromuscular blocking potency of rocuronium varies with respiratory pH changes, increasing at lower pH and decreasing at higher pH; thus, hyperventilation-induced respiratory alkalosis is expected to decrease the potency of rocuronium. We report a case of anesthetic management of modified electroconvulsive therapy (m-ECT) for a patient monitored with electromyography-based neuromuscular monitoring during two patterns of ventilation to elucidate their relationship and propose the possible mechanisms underlying the effects by computational simulations. Case presentation: The patient was a 25-year-old man with schizophrenia. In m-ECT, hyperventilation may be used to produce longer seizures. We compared the neuromuscular monitoring data recorded during hyperventilation and during normal ventilation while receiving the same dose of rocuronium. Despite receiving the same dose of rocuronium, the time required for the first twitch to decrease to 80% of the control value was delayed in hyperventilation compared to normal ventilation. Conclusions: This case report and computational simulation suggest that respiratory alkalosis might delay the action of rocuronium. It is necessary to consider the delayed action of rocuronium when hyperventilation is performed. [ABSTRACT FROM AUTHOR]

The article focuses on the respiratory system and its role in maintaining acid-base balance in the body. It discusses three main topics: the physiology of respiratory acid-base regulation, common respiratory disorders that can lead to acid-base imbalances, and diagnostic approaches and treatment options for managing acid-base disorders associated with respiratory dysfunction.

Background: The current paradigms in arterial blood gas analysis are based on mathematical or physicochemical models that require complex algorithms for interpretation. This leads to avoidance or dislike from health care professionals. Purpose: To formulate a new approach to the analysis and classification of acid base disturbances. Methodology: we conducted a systematic review of the related literature and a paradigm shift for data interpretation. Results: Acid-base disorders can be grouped and managed according to the underlying biochemical processes. Conclusions: This proposal represents a new classification, which groups acid base disorders according to the underlying causal biochemical process. Disorders with an elevated anion gap relate to alterations in cellular respiration (energy/ATP production)- All disturbances with normal anion gap relate to transmembrane ion exchange.

The most common causes of tetany are hypocalcemia, hypomagnesemia, hypokalemia, and alkalosis. Most case reports of tetany in the literature include some combination of the above metabolic derangements leading to non-life-threatening symptoms. We present a unique case of severe life-threatening tetany in a 38-year-old female with a history of Crohn's disease. She was previously dependent on total parenteral nutrition (TPN) but discontinued TPN two weeks prior to presentation due to the improvement of her Crohn's symptoms with a new medication regimen. We propose that malabsorption led to multiple electrolyte abnormalities, resulting in acute tetany that subsequently caused rhabdomyolysis. This case reviews the most common causes of acute tetany and highlights the interaction between electrolytes implicated in both tetany and rhabdomyolysis. It also emphasizes the importance of considering tetany as a diagnosis in a patient with unstable vital signs and diffuse muscle spasms.

Background: Acid-base status in full-term pregnant women is characterised by hypocapnic alkalosis. Whether this respiratory alkalosis is primary or consequent to changes in CSF electrolytes is not clear.Methods: We enrolled third-trimester pregnant women (pregnant group) and healthy, non-pregnant women of childbearing age (controls) undergoing spinal anaesthesia for Caesarean delivery and elective surgery, respectively. Electrolytes, strong ion difference (SID), partial pressure of carbon dioxide ( [Formula: see text] ), and pH were measured in simultaneously collected CSF and arterial blood samples.Results: All pregnant women (20) were hypocapnic, whilst only four (30%) of the controls (13) had an arterial [Formula: see text] <4.7 kPa (P<0.001). The incidence of hypocapnic alkalosis was higher in the pregnant group (65% vs 8%; P=0.001). The CSF-to-plasma Pco2 difference was significantly higher in pregnant women (1.5 [0.3] vs 1.0 [0.4] kPa; P<0.001), mainly because of a decrease in arterial Pco2 (3.9 [0.3] vs 4.9 [0.5] kPa; P<0.001). Similarly, the CSF-to-plasma difference in SID was less negative in pregnant women (-7.8 [1.4] vs -11.4 [2.3] mM; P<0.001), mainly because of a decreased arterial SID (31.5 [1.2] vs 36.1 [1.9] mM; P<0.001). The major determinant of the reduced plasma SID of pregnant women was a relative increase in plasma chloride compared with sodium.Conclusions: Primary hypocapnic alkalosis characterises third-trimester pregnant women leading to chronic acid-base adaptations of CSF and plasma. The compensatory SID reduction, mainly sustained by an increase in chloride concentration, is more pronounced in plasma than in CSF, as the decrease in Pco2 is more marked in this compartment.Clinical Trial Registration: NCT03496311. [ABSTRACT FROM AUTHOR]

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Background: Postoperative hypoxia (POH) is a complication that often occurs in patients after Coronary Artery Bypass Grafting (CABG). Breathing exercises are considered effective in overcoming POH after CABG. However, this intervention has not been implemented using the dynamic nurse-patient relationship model from Ida Jean Orlando. The dynamic nurse-patient relationship model is expected to improve the quality of nursing care after cardiac surgery. Purpose: This study aimed to describe the application of breathing exercises in postoperative hypoxia after CABG using the dynamic nurse-patient relationship model. Methods: This study was the summary of the case presentation along with the interventions on three patients after CABG through the dynamic nurse-patient relationship model approach with the main intervention focusing on breathing exercises. Results: After three days of implementing the intervention, most patients showed improvement in POH. Background: Postoperative hypoxia (POH) is a complication that often occurs in patients after Coronary Artery Bypass Grafting (CABG). Breathing exercises are considered effective in overcoming POH after CABG. However, this intervention has not been implemented using the dynamic nurse-patient relationship model from Ida Jean Orlando. The dynamic nurse-patient relationship model is expected to improve the quality of nursing care after cardiac surgery. Purpose: This study aimed to describe the application of breathing exercises in postoperative hypoxia after CABG using the dynamic nurse-patient relationship model. Methods: This study was the summary of the case presentation along with the interventions on three patients after CABG through the dynamic nurse-patient relationship model approach with the main intervention focusing on breathing exercises. Results: After three days of implementing the intervention, most patients showed improvement in POH. This condition was evidenced by an increase in the PaO2/FiO2 ratio from less than 200 to above 200, with an average increase of 89.3. The blood gas analysis results supported the results from a respiratory alkalosis condition to a normal PH and a PaCO2 value from <35 mmHg to the normal range (35-45 mmHg). Also, X-rays of the patients showed pulmonary atelectasis improvement. Conclusion: Applying breathing exercises in postoperative hypoxia after CABG using the dynamic nurse-patient relationship model can improve POH in post-cardiac surgery patients. We recommend using the model theory approach because this theory can see patients' psychological and physical changes dynamically in post- CABG patients. [ABSTRACT FROM AUTHOR]

Physiological hyperventilation and dyspnoea in pregnancy are well-established phenomena and commonly lead to a chronic respiratory alkalosis with compensatory renal excretion of bicarbonate. However, the underlying mechanism of dyspnoea during normal pregnancy remains largely undefined. Increasing progesterone levels are a primary factor leading to increased respiratory drive to ensure the rising metabolic demands of the pregnancy are met. Dyspnoea symptoms typically begin in the first or second trimester, are mild, and do not interfere with activities of daily living. We report the case of a 35-year-old female with severe physiological hyperventilation of pregnancy presenting with profound dyspnoea, tachypnoea, and presyncope from 18 weeks of gestation until delivery. Subsequent investigations revealed no identifiable underlying pathology. There remain limited reports of such severe physiological hyperventilation of pregnancy. This case highlights interesting questions regarding the respiratory physiology of pregnancy and underlying mechanisms. [ABSTRACT FROM AUTHOR]

Dyspnea, shortness of breath, and chest pain are frequent symptoms of post-COVID syndrome (PCS). These symptoms are unrelated to organ damage in most patients after mild acute COVID infection. Hyperventilation has been identified as a cause of exercise-induced dyspnea in PCS. Since there is a broad overlap in symptomatology with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), causes for dyspnea and potential consequences can be deduced by a stringent application of assumptions made for ME/CFS in our recent review papers. One of the first stimuli of respiration in exercise is caused by metabolic feedback via skeletal muscle afferents. Hyperventilation in PCS, which occurs early on during exercise, can arise from a combined disturbance of a poor skeletal muscle energetic situation and autonomic dysfunction (overshooting respiratory response), both found in ME/CFS. The exaggerated respiratory response aggravating dyspnea does not only limit the ability to exercise but further impairs the muscular energetic situation: one of the buffering mechanisms to respiratory alkalosis is a proton shift from intracellular to extracellular space via the sodium–proton-exchanger subtype 1 (NHE1), thereby loading cells with sodium. This adds to two other sodium loading mechanisms already operative, namely glycolytic metabolism (intracellular acidosis) and impaired Na+/K+ATPase activity. High intracellular sodium has unfavorable effects on mitochondrial calcium and metabolism via sodium–calcium-exchangers (NCX). Mitochondrial calcium overload by high intracellular sodium reversing the transport mode of NCX to import calcium is a key driver for fatigue and chronification. Prevention of hyperventilation has a therapeutic potential by keeping intracellular sodium below the threshold where calcium overload occurs. [ABSTRACT FROM AUTHOR]

Respiratory illnesses and failure are common in pediatric population compared to adults due to anatomical and physiological differences in respiratory system. Respiratory acidosis is commonly seen in intensive care settings and needs immediate attention. Treatment depends on underlying pathology and mechanical ventilation. Respiratory alkalosis is least common only mainly iatrogenic or child is hyperventilating.

Background: Previous studies reported a slow neuromuscular response with the currently recommended dose of cisatracurium in critically ill patients. Pharmacokinetic and pharmacodynamic studies of cisatracurium in critically ill patients are still limited. To our knowledge, this is the first study performed to better understand the pharmacokinetics (PKs) and pharmacodynamics (PDs) of a loading dose of cisatracurium and to identify factors that affect PK and PD changes in critically ill patients. Methods: A prospective PKs and PDs study was designed. Arterial blood samples of 10 critically ill patients with respiratory failure were collected after administering a loading dose of 0.2 mg/kg of cisatracurium. Plasma cisatracurium and laudanosine concentrations were determined using liquid chromatography-tandem mass spectrometry. The achievement of the desired pharmacodynamic response was evaluated by both 1) clinical assessment and 2) train-of-four monitoring. The PK/PD indices were analyzed for their correlation with patient'characteristics and other factors. Results: The one-compartment model best described the plasma pharmacokinetic parameters of cisatracurium. The volume of distribution at steady state and total clearance were 0.11 ± 0.04 L/kg and 2.74 ± 0.87 ml/minute/kg, respectively. The mean time to train-of-four 0/4 was 6 ± 3.86 minutes. A time to the desired pharmacodynamic response of less than 5 minutes was found in 10% of the patients. A positive correlation was found between cisatracurium concentration and albumin levels and between pharmacokinetics data and patient factors [partial pressure of carbon dioxide and respiratory alkalosis]. Conclusion: The currently recommended loading dose of cisatracurium might not lead to the desired pharmacodynamic response in critically ill patients with respiratory failure. Trial registration: ClinicalTrials.gov, NCT03337373. Registered on 9 November 2017 [ABSTRACT FROM AUTHOR]

A pregnant mother undergoes significant changes in acid-base status as well as sodium and calcium metabolism to combat her physiological needs of pregnancy. Pregnant patients experience mild respiratory alkalosis due to the stimulation of the respiratory center by progesterone. This is associated with a corresponding increase in bicarbonate excretion by kidneys; as a result, the pH remains slightly high (7.40-7.45) but within the normal range. Pregnant women are predisposed to starvation ketosis as compared to nonpregnant states due to relative insulin resistance and increased production of the counter-regulatory hormone. Physiological mild hyponatremia occurs during pregnancy due to increased AVP secretion caused by resetting of osmoreceptors in the hypothalamus at a lower osmolality, but values below 130 mEq/L require a diagnostic workup and intervention. Gestational diabetes insipidus can occur due to increased production or decreased destruction of enzyme vasopressinase. Secretion of parathyroid hormone-related peptide by the placenta and breasts and two- to three-fold increased calcium and phosphate absorption in the maternal gut are the key changes in calcium metabolism during pregnancy. Though rare, both hypo- and hypercalcemia in pregnancy are associated with significant maternofetal morbidity and mortality. [ABSTRACT FROM AUTHOR]

Bidirectional ventricular tachycardia (BVT) is a rare arrhythmia that is generally observed in patients with catecholaminergic ventricular tachycardia or digoxin overdose. Herein, we present a case of BVT and electrical storm (ES) in an acute ischemic heart failure patient that is typically induced by hypokalemia. The patient was in invasive mechanical ventilator (MV) support and hypokalemia was related to acute respiratory alkalosis and that caused refractory hypokalemia despite intravenous (IV) potassium replacement. We also discuss our approach to solve refractory hypokalemia caused by respiratory alkalosis. [ABSTRACT FROM AUTHOR]

We present a case of a 46-year-old male with a history of biopsy-proven pulmonary Langerhans cell histiocytosis (LCH) who presented with shortness of breath and progressive neurologic decline. Neurologic examination suggested both posterior fossa and bilateral supratentorial dysfunction without papilledema and arterial blood gas revealed a respiratory alkalosis. Magnetic resonance imaging of the brain was suggestive of central nervous system (CNS)-LCH. The patient was diagnosed with central neurogenic hyperventilation (CNH) secondary to CNS-LCH. He was treated with intravenous morphine and lorazepam without improvement in his respiratory alkalosis. He received two doses of immunoglobulin and empiric chemotherapy with vinblastine and prednisone for the LCH. This case illustrates one of a few reported cases of CNH due to suspected CNS LCH.

Chilaiditi syndrome is defined as the interposition of the colon between the liver and the diaphragm or abdominal wall and is known as Chilaiditi's sign on X-rays. Although rare, this procedure can lead to serious complications. Due to its infrequency and propensity for severe complications, diagnosing and differentiating this syndrome from other acute abdominal emergencies are very important for preventing unnecessary treatment or surgical procedures. We present a 72-year-old male with a history of chronic obstructive pulmonary disease (COPD) who presented to the emergency department with persistent shortness of breath, abdominal discomfort, and vomiting. Physical examination revealed chest crepitation, tenderness in the left iliac fossa, and high blood pressure. Laboratory tests revealed a positive COVID-19 status, elevated C-reactive protein level, and respiratory alkalosis. Imaging, including a chest X-ray and CT scan, confirmed the presence of bowel loops under the diaphragm, confirming the diagnosis of Chilaiditi syndrome. Collaborative management by surgical and medical teams was essential in navigating this complex condition. This case highlights the complexity of chilaiditi syndrome, which can be episodic and intermittent, in addition to the importance of recognizing Chilaiditi's sign on imaging, particularly on CT scans, to differentiate it from pneumoperitoneum. Vigilance is crucial in identifying potential complications and guiding appropriate treatment to prevent adverse outcomes., (© 2024 The Authors.)

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. [ABSTRACT FROM AUTHOR]

Objectives: During the COVID-19 pandemic, healthcare professionals are recommended to use PPE to prevent the transmission of disease. Healthcare workers who use N95 FFR, which has an important place, experience complaints such as headache and dizziness. In this study, we plan to find the cause of these complaints and aim to clarify whether they are associated with the use of N95 mask. Method: Healthcare workers first put on a surgical mask for at least 1 h and a maximum of 4 h, this process was then repeated on another day with the same workers wearing N95 masks. After removing the mask, capillary blood gases were taken and a questionnaire was given. Results: Thirty-four participants over the age of 18 were included in the study; 19 participants were female (56%) and 15 male (44%). The results of the capillary blood gas analysis after the use of surgical mask and N95 mask, respectively: pH: 7.43 ± 0.03; 7.48 ± 0.04 (p < 0.001); pCO2: 37.33 ± 8.81; 28.46 ± 7.77 mmHg (p < 0.001); HCO3: 24.92 ± 2.86; 23.73 ± 3.29 mmol/L (p = 0.131); Base excess (BE): 1.40 (− 3.90–3.10); − 2.68 (− 4.50–1.20) [median (Q1−Q3)] (p = 0.039); lactate: 1.74 ± 0.68; 1.91 ± 0.61 (p = 0314). Headache, attention deficit and difficulty in concentrating were significantly higher after using N95 mask. Conclusion: Respiratory alkalosis and hypocarbia were detected after the use of N95. Acute respiratory alkalosis can cause headache, anxiety, tremor, muscle cramps. In this study, it was quantitatively shown that the participants' symptoms were due to respiratory alkalosis and hypocarbia. [ABSTRACT FROM AUTHOR]

Twenty minutes of voluntary hypocapnic hyperventilation prior to exercise reduces the aerobic metabolic rate with a compensatory increase in the anaerobic metabolic rate without affecting exercise performance during the Wingate anaerobic test (WAnT). Thus, pre-exercise hypocapnic hyperventilation may be a useful means of stressing the anaerobic energy system during training, ultimately improving anaerobic exercise performance. However, it remains unclear whether a shorter (e.g., 5 min) pre-exercise hypocapnic hyperventilation is sufficient to reduce the aerobic metabolic rate during high-intensity exercise. We therefore compared the effects of 5-min and 20-min pre-exercise hypocapnic hyperventilation on aerobic metabolism during the 30-s WAnT. Ten healthy young males and one female performed the WAnT following 20 min of spontaneous breathing (control trial) or 5 or 20 min of voluntary hypocapnic hyperventilation. Both the 5-min and 20-min hyperventilation reduced end-tidal CO2 partial pressure (an index of arterial CO2 partial pressure) to ∼23 mmHg, whereas it remained unchanged during the spontaneous breathing. The peak, mean and minimum power outputs during the WAnT did not differ among the three trials. Oxygen uptake during the WAnT was lower in both the 5-min (1493 ± 257 mL min−1) and 20-min (1397 ± 447 mL min−1) hyperventilation trials than during the control trial (1847 ± 286 mL min−1), and was similar in the two hyperventilation trials. These results suggest that 5 min of pre-exercise hypocapnic hyperventilation reduces aerobic metabolism during the 30-s WAnT to a level similar to that seen with the 20-min hyperventilation. Moreover, exercise performance was unaffected, which implies anaerobic metabolism was enhanced. [ABSTRACT FROM AUTHOR]

The high metabolic demand of cerebral tissue requires that local perfusion is tightly coupled with local metabolic rate (neurovascular coupling; NVC). During chronic altitude exposure, where individuals are exposed to the antagonistic cerebrovascular effects of hypoxia and hypocapnia, pH is maintained through renal compensation and NVC remains stable. However, the potential independent effect of acute hypocapnia and respiratory alkalosis on NVC remains to be determined. We hypothesized that acute steady‐state hypocapnia via voluntary hyperventilation would attenuate the magnitude of NVC. We recruited 17 healthy participants and insonated the posterior cerebral artery (PCA) with transcranial Doppler ultrasound. NVC was elicited using a standardized strobe light stimulus (6 Hz; 5 × 30 s on/off) where absolute delta responses from baseline (BL) in peak, mean, and total area under the curve (tAUC) were quantified. From a BL end‐tidal (PET)CO2 level of 36.7 ± 3.2 Torr, participants were coached to hyperventilate to reach steady‐state hypocapnic steps of Δ‐5 Torr (31.6 ± 3.9) and Δ‐10 Torr (26.0 ± 4.0; p < 0.001), which were maintained during the presentation of the visual stimuli. We observed a small but significant reduction in NVC peak (ΔPCAv) from BL during controlled hypocapnia at both Δ‐5 (−1.58 cm/s) and Δ‐10 (−1.37 cm/s), but no significant decrease in mean or tAUC NVC response was observed. These data demonstrate that acute respiratory alkalosis attenuates peak NVC magnitude at Δ‐5 and Δ‐10 Torr PETCO2, equally. Although peak NVC magnitude was mildly attenuated, our data illustrate that mean and tAUC NVC are remarkably stable during acute respiratory alkalosis, suggesting multiple mechanisms underlying NVC. [ABSTRACT FROM AUTHOR]

Abstract The high metabolic demand of cerebral tissue requires that local perfusion is tightly coupled with local metabolic rate (neurovascular coupling; NVC). During chronic altitude exposure, where individuals are exposed to the antagonistic cerebrovascular effects of hypoxia and hypocapnia, pH is maintained through renal compensation and NVC remains stable. However, the potential independent effect of acute hypocapnia and respiratory alkalosis on NVC remains to be determined. We hypothesized that acute steady‐state hypocapnia via voluntary hyperventilation would attenuate the magnitude of NVC. We recruited 17 healthy participants and insonated the posterior cerebral artery (PCA) with transcranial Doppler ultrasound. NVC was elicited using a standardized strobe light stimulus (6 Hz; 5 × 30 s on/off) where absolute delta responses from baseline (BL) in peak, mean, and total area under the curve (tAUC) were quantified. From a BL end‐tidal (PET)CO2 level of 36.7 ± 3.2 Torr, participants were coached to hyperventilate to reach steady‐state hypocapnic steps of Δ‐5 Torr (31.6 ± 3.9) and Δ‐10 Torr (26.0 ± 4.0; p