Chilaiditi syndrome in COPD patient: A case report.

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.

Hyperventilation Syndrome and Hypocalcemia: A Unique Case in Autism Spectrum Disorder.

This case report delves into the rare occurrence of hyperventilation syndrome (HVS) with hypocalcemia in an 18-year-old female diagnosed with autism spectrum disorder (ASD). The rare occurrence highlights the importance of recognizing the potential association between HVS, hypocalcemia, and ASD, emphasizing the need for comprehensive evaluation and management strategies in individuals with ASD presenting with unusual symptoms. Despite ongoing psychotherapeutic treatment, the patient's clinical examination revealed ASD-related communication anomalies. Treatment with Escitalopram resolved panic attacks but left residual anxiety. During an emergency room visit for menstrual-related abdominal pain, a hyperventilation crisis ensued, leading to respiratory alkalosis and hypocalcemia. Swift intervention, including closed mask ventilation and electrolyte infusion, successfully alleviated symptoms. Follow-up assessments indicated normal thyroid function and vitamin D levels. The case highlights the necessity for clinicians to consider electrolyte imbalances in anxiety attacks among ASD patients, emphasizing the importance of timely management for patient safety. The intricate interplay between hyperventilation syndrome, anxiety, and hypocalcemia in ASD patients is explored, offering valuable insights for the nuanced understanding and comprehensive assessment of such cases.

Severe Respiratory Alkalosis during Hemodialysis.

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.

The Impact of Inflammation on Thermal Hyperpnea: Relevance for Heat Stress and Febrile Seizures.

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.

Cerebral uptake of microvesicles occurs in normocapnic but not hypocapnic passive hyperthermia in young healthy male adults.

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.

Respiratory Acid-Base Disorders.

Respiratory acid-base disorders are often not thought of as frequently as their metabolic cousins, which occur more frequently in the emergency department. Although most respiratory and acid-base disturbances are driven by lung pathology, central nervous system and other organ systems can and do play a role as well. Although managing the airway and appropriate mechanical ventilation may be necessary, it is akin to placing a band-aid on a large wound. It is crucial for the emergency clinician to discover the etiology of the disturbance as management depends on treating the underlying etiology to prevent worsening acid-base status.

Acid Base Disorders in Cirrhosis.

Metabolic and respiratory acid-base disorders are common in individuals with liver disease and cirrhosis. The most common disorder is respiratory alkalosis, which may be related to dyspnea or respiratory stimulation. Primary metabolic disorders are less common. Although the liver plays a role in metabolism of amino acids and generation of acid from dietary sources, it does not play a role in the regulation of pH. Instead, metabolic disorders may arise from alterations in normal metabolism or from medications, particularly diuretics and osmotic laxatives, used in the treatment of these complex patients. Understanding the mechanistic underpinnings of these disorders can aid in the management of individuals with liver disease in the hospital and in outpatient settings.

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.

Rocuronium action can be affected by hyperventilation: a case report and computational simulation.

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.

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.

An efficient transition metal chalcogenide sensor for monitoring respiratory alkalosis.

For many biomedical applications, high-precision CO2 detection with a rapid response is essential. Due to the superior surface-active characteristics, 2D materials are particularly crucial for electrochemical sensors. The liquid phase exfoliation method of 2D Co2Te3 production is used to achieve the electrochemical sensing of CO2. The Co2Te3 electrode performs better than other CO2 detectors in terms of linearity, low detection limit, and high sensitivity. The outstanding physical characteristics of the electrocatalyst, including its large specific surface area, quick electron transport, and presence of a surface charge, can be credited for its extraordinary electrocatalytic activity. More importantly, the suggested electrochemical sensor has great repeatability, strong stability, and outstanding selectivity. Additionally, the electrochemical sensor based on Co2Te3 could be used to monitor respiratory alkalosis. Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-023-03497-z.

Urinary Ammonium in Clinical Medicine: Direct Measurement and the Urine Anion Gap as a Surrogate Marker During Metabolic Acidosis.

Ammonium is the most important component of urinary acid excretion, normally accounting for about two-third of net acid excretion. In this article, we discuss urine ammonium not only in the evaluation of metabolic acidosis but also in other clinical conditions such as chronic kidney disease. Different methods to measure urine NH4+ that have been employed over the years are discussed. The enzymatic method used by clinical laboratories in the United States to measure plasma ammonia via the glutamate dehydrogenase can be used for urine ammonium. The urine anion gap calculation can be used as a rough marker of urine ammonium in the initial bedside evaluation of metabolic acidosis such as in distal renal tubular acidosis. Urine ammonium measurements, however, should be made more available in clinical medicine for a precise evaluation of this important component of urinary acid excretion.

Urine anion gap can differentiate respiratory alkalosis from metabolic acidosis in the absence of blood gas results.

INTRODUCTION: Low plasma bicarbonate concentration due to chronic respiratory alkalosis may be misdiagnosed as metabolic acidosis and mistreated with administration of alkali therapy, particularly when arterial blood gas is not available. METHODS: We measured urine anion gap [urine (Na+ + K+ ) - (Cl- )], as a surrogate of renal ammonium excretion in 15 patients presenting with hyperventilation and low serum bicarbonate concentration to distinguish chronic respiratory alkalosis (CRA) from metabolic acidosis (MA) when blood gas was unavailable. RESULTS: Hyperventilation and low serum bicarbonate concentrations were associated with urine pH above 5.5 and positive urine anion gap in all, suggesting CRA. The diagnosis was later confirmed by obtaining capillary blood gas, which showed a decrease in PCO2 and high normal pH values. CONCLUSION: The use of urine anion gap can help to differentiate between chronic respiratory alkalosis and metabolic acidosis, especially when arterial blood gas is not obtained.

Combined Effects of Hypocapnic Hyperventilation and Hypoxia on Exercise Performance and Metabolic Responses During the Wingate Anaerobic Test.

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.

Effects of Pre-Exercise Voluntary Hyperventilation on Metabolic and Cardiovascular Responses During and After Intense Exercise.

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 V˙O2 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 pre-exercise hyperpnea and the resultant hypocapnia reduce V˙O2 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.

Cerebrospinal fluid and arterial acid-base equilibria in spontaneously breathing third-trimester pregnant women.

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.

Study of Arterial Blood Gas Analysis in Moderate-to-Severe COVID-19 Patients.

Background The high prevalence of pneumonia and renal involvement in coronavirus disease 2019 (COVID-19) leads to frequent acid-base abnormalities in serious patients and affects prognosis. In this study, we aimed to assess the arterial blood gas (ABG) and acid-base patterns in COVID-19 patients admitted to a tertiary care hospital. Methodology A retrospective observational study was conducted in a designated COVID-19 hospital involving 267 reverse transcription-polymerasechain reaction-positive COVID-19 patients. Demographic and laboratory data including ABG data within the first day after admission and in patients with multiple ABG analyses, only the first measurement was collected and analyzed statistically, including its association with comorbidities. Results The most common age group of the patients was 51-60 years (30.8%), with a male predominance (male:female = 2.7:1). The most common comorbidities were hypertension, diabetes mellitus, and chronic obstructive pulmonary disease found in 147 (55%) COVID-19 patients. Alkalosis and acidosis were observed in 145 (54.3%) and 50 (18.7%) patients, respectively. The most common ABG abnormality observed was primary respiratory alkalosis with secondary metabolic acidosis in 67 (25.1%) patients, followed by primary respiratory alkalosis with secondary metabolic alkalosis in 54 (20.2%) patients. Statistically significant negative correlation was found with PaCO2 and pH (r = -0.530, p < 0.0001), statistically significant positive correlation was found between pH and base (r = 0.533, p < 0.0001), pH and TCO2 (r = 0.260, p < 0.0001), and pH and HCO3 (r = 0.354, p < 0.0001). Conclusions Acid-base abnormalities are commonly encountered in COVID-19 patients. Respiratory alkalosis as a part of a single or mixed pattern on ABG was the most common pattern found in critically ill COVID-19 patients. ABG on admission in moderate-to-severe COVID-19 patients can help in the early correction of metabolic abnormalities leading to improved patient outcomes.

Cardiac Pacing a Rare Cause of Ventilator Auto Triggering.

Ventilator auto triggering is an avoidable complication in ventilators, if left unnoticed can lead to deleterious effects. There are various causes for ventilator auto triggering. Though rare, there are some cardiac causes for inadvertent ventilator triggering. We report a case of 44-years-old male paced with atrial epicardial wires postcoronary artery bypass. The wires were close to the right phrenic nerve, causing the right diaphragm to contract in synchronization with the heartbeat. This caused ventilator auto triggering and ended up delivering inadvertent breaths. The pacemaker output was immediately reduced to the required minimum to continue pacing the heart and decrease phrenic nerve stimulation. This caused immediate changes in ventilator waveform and auto triggering was completely stopped and the patient could be successfully weaned off the ventilator. This case report emphasizes he need for timely recognition of alteration in ventilator waveforms and early intervention to avert any untoward events. How to cite this article: Mukunthan MN, Bhardwaj V. Cardiac Pacing a Rare Cause of Ventilator Auto Triggering. Indian J Crit Care Med 2022;26(5):643-645.

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.