A sizable fraction of dyspneic patients with only mild to moderate COPD exhibit a heightened ventilatory response to exercise relative to metabolic demands, i.e. a high ventilation (V.E)/CO2 output (V.CO2). The lack of continuous assessment of gas exchange efficiency and estimates of arterial CO2 partial pressure has hindered our understanding of the physiological underpinnings of this dynamic phenomenon. We compared key indices of gas exchange efficiency relative to the intra-breath CO2 profile as a function of expired volume using breath-by-breath volumetric capnography in 30 patients (FEV1 = 76 ± 17%) and 30 sex- and age-matched controls during incremental cycle ergometry. Wasted ventilation in the physiological dead space (VDphys) was calculated as the sum of airway and alveolar (alv) dead space divided by tidal volume (VT). Transcutaneous (tc) readings provided estimates of arterialised PCO2. Patients exhibited lower exercise tolerance, reporting higher dyspnoea throughout exercise (p < 0.05). Higher V.E/V.CO2 was associated with higher absolute (L) alveolar dead space (VDalv), but similar VT; thus, both VDphys/VT and VDalv/VT were consistently higher in patients (p < 0.05). V.E/V.CO2 was elevated (≥34) in normocapnic patients (PtcCO2≥35 mmHg) who had a high VDphys/VT (≥0.3); conversely, high V.E/V.CO2 coexisted with a lower VDphys/VT only in hypocapnic subjects (p < 0.05). Higher VDalv and lower PtcCO2 were independently associated with a high V.E/V.CO2 nadir and iso-work rate dyspnoea (p < 0.001). Based on this innovative, high-density data-acquisition approach, we conclude that both wasted ventilation and alveolar hyperventilation, in a highly variable combination, contribute to excessive ventilation in dyspneic patients with mild-to-moderate COPD.

An automated method is presented to derive the logistic curve model (LCM), to express the simultaneous effects of partial pressure of arterial CO2 (PaCO2) on cerebral blood flow (CBF) and cerebral autoregulation, without the need for operator assistance. Measurements of middle cerebral artery blood velocity (MCAv, transcranial Doppler), arterial blood pressure (Finometer) and end-tidal CO2 (EtCO2, capnography) were performed in 106 healthy subjects. Hypercapnia was induced with breathing 5% CO2 and hypocapnia was induced with hyperventilation. Dynamic autoregulation was expressed by the Autoregulation Index (ARI). Confidence limits for the fitting error were obtained with a surrogate bootstrap approach for both MCAv and ARI. An algorithm for the gradual removal of outlier values was implemented to identify optimal number of samples that minimises the fitting error. Induction of hyper- and hypocapnia was demonstrated by the range of EtCO2 values achieved (28.4 ± 6.0 to 47.7 ± 5.8 mmHg, p < 0.001). LCMs meeting confidence limit requirements were obtained for MCAv (n = 98/106) and ARI (104/106). Females showed an upwards shift of their LCM for MCAv (p = 0.001) compared to males and their ARI model was shifted laterally towards lower values of EtCO2 (p = 0.0053). Automated identification of the LCM for MCAv and ARI, with rigorous confidence limits of the fitting error is feasible and can identify differences due to biological sex.

Fructose-1,6-bisphosphatase (FBP1) deficiency is characterized by episodic acute crises of lactic acidosis and ketotic hypoglycemia, manifesting as hyperventilation, apneic spells, seizures, and/or coma. Acute crises are most common in early childhood; nearly half of affected children have hypoglycemia in the neonatal period (especially the first 4 days) resulting from deficient glycogen stores. Factors known to trigger episodes include fever, fasting, decreased oral intake, vomiting, infections, and ingestion of large amounts of fructose. In untreated individuals, symptoms worsen progressively as continued catabolism leads to multiorgan failure (especially liver, brain, and later heart). Morbidity and mortality are high. Sepsis, blindness, and Reye syndrome-like presentation have been reported. In between acute episodes, children are asymptomatic. While the majority of affected children have normal growth and psychomotor development, a few have intellectual disability, presumably due to early and prolonged hypoglycemia.

Functional disorders affecting the cardiorespiratory system are common. Non-cardiac chest pain affects more than 10% of the population. It can result from gastro-oesophageal reflux or chest wall disorders but is also very often associated with anxiodepressive disorders, particularly panic disorder. Postural orthostatic tachycardia syndrome (POTS), a rarer entity, is characterized by a sharp increase in heart rate without orthostatic hypotension when standing. The pathophysiological mechanisms of POTS include 'partial' autonomic neuropathy, hypovolaemia and noradrenergic dysregulation, but it is also closely linked to anxiety disorders and deconditioning to exertion. Functional respiratory disorders, particularly hyperventilation syndrome, are accompanied by various manifestations ranging from tetany to gastrointestinal symptoms. They are highly prevalent, especially among women and people suffering from anxiety, and particularly in the case of associated respiratory disease such as asthma. The diagnosis of hyperventilation syndrome is based on the Nijmegen questionnaire. The pathophysiology does not necessarily involve hypocapnia but is related to cerebral conditioning phenomena and vicious circles linked to anticipatory anxiety. Cardiorespiratory functional disorders are often linked to each other and to other functional somatic disorders and have in common a dysregulation of the autonomic nervous system. Psychological, cognitive and behavioural factors play a central role in their persistence. While each has its specificities, all have a complex circular causality. Their management currently relies primarily on physical rehabilitation, often associated with symptomatic treatments such as beta-blockers. The place of cognitive and behavioral therapies would be well worth exploring in these disorders.

Malignant hyperthermia (MH) is a rare but life-threatening pharmacogenetic disorder triggered by volatile anesthetics and/or depolarizing muscle relaxants, resulting in a hypermetabolic crisis. We report a case of postoperative fulminant MH in a 26-year-old man who underwent general anesthesia with desflurane and rocuronium for mandibular fracture repair. Despite a history of multiple uneventful anesthetics, the patient developed acute hypercapnia, tachycardia, muscle rigidity, and rapid hyperthermia during emergence, following sugammadex administration. Initial treatment for presumed bronchospasm and postoperative shivering-including sevoflurane sedation, hyperventilation, and inhaled bronchodilators-proved ineffective. A clinical diagnosis of MH was made based on the progression of clinical findings, and treatment with intravenous dantrolene 100 mg, active cooling, and antipyretics was initiated. The patient responded well to intervention and recovered without sequelae. This case highlights the importance of considering MH even in the postoperative phase, particularly with the use of desflurane and potentially contributory agents such as sugammadex and ondansetron. Early clinical suspicion, rapid administration of dantrolene, and supportive measures are critical for favorable outcomes. Anesthesia providers must remain vigilant for MH at all perioperative stages and ensure that emergency protocols, appropriate drug stock, and staff readiness are in place.

The 2025 Korean pediatric advanced life support guideline update introduces clinically important revisions emphasizing airway strategy, physiologic resuscitation targets, post-cardiac arrest hemodynamics, neuroprotection, and extracorporeal support. In out-of-hospital pediatric cardiac arrest, bag-mask ventilation is now suggested over endotracheal intubation or supraglottic airway placement. In in-hospital arrest, evidence is insufficient to favor bag-mask ventilation versus advanced airways; however, endotracheal intubation or supraglottic airway insertion is reasonable when performed with minimal interruption or when bag-mask ventilation is ineffective. For patients with an advanced airway in place, age-adjusted ventilation rates are proposed to avoid hypoventilation and hyperventilation: 30/min (<1 yr), 20-30/min (1-8 yr), and 10-20/min (8-18 yr in healthcare settings). When invasive arterial monitoring is available during in-hospital cardiac arrest, target diastolic blood pressure is ≥25 mmHg in infants and ≥30 mmHg in children ≥1 year. After return of spontaneous circulation, systolic blood pressure during the first 6 hours should be maintained above the age-specific 10th percentile. Neuroprognostication should be multimodal, incorporating serial examinations, electroencephalography (up to 72 hours), early computed tomography (<24 hours), magnetic resonance imaging (72 hours to 2 weeks), lactate trends, and pupillary reflexes. Extracorporeal cardiopulmonary resuscitation (CPR) is limited to appropriately resourced hospitals and may be considered for selected in-hospital arrests (e.g., cardiac disease) unresponsive to conventional CPR; evidence remains insufficient for out-of-hospital use. These revisions shift pediatric resuscitation toward physiology-guided, resource-stratified, and neuroprotective care.

Studies involving breath-hold dives as deep as 60 m have identified a spike in arterial Po2 ([Formula: see text]) and Pco2 ([Formula: see text]) apparently associated with lung compression by water pressure as depth increases. Competitive breath-hold dives may exceed 100 m, raising the possibility that a spike in [Formula: see text] might contribute to narcosis-like symptoms sometimes experienced. To predict the magnitude of this spike, three elite breath-hold divers were instrumented with radial artery catheters and had arterial blood specimens taken at the bottom on separate dives to 20, 40, 60, and 80 m with another specimen either after beginning apnea but before leaving the surface (one participant) or on arrival back at the surface while still apneic (two participants). Contrary to previous expectations, the greatest spike in [Formula: see text] was at 40 m (mean: 29.3 kPa, 220 mmHg) and the trajectory of rise in [Formula: see text] also plateaued at 40 m [mean: 5.61 kPa, 42.1 mmHg (from a mean baseline of 2.53 kPa after predive hyperventilation) and 5.54 kPa, 41.6 mmHg at 60 m] before rising again after 60 m (80 m mean: 6.9 kPa, 51.5 mmHg). This suggests that a spike in arterial gases associated with lung compression was detectable until the greatest proportional changes in lung volume with increasing pressure had occurred. Thereafter, [Formula: see text] decreased through metabolism, and [Formula: see text] increased through simple metabolic accumulation. The compression effect seemed maximal at 40 m (five atmospheres absolute pressure) which may relate to the simple Boyle's law prediction that the lung may be compressed to close to residual volume (20%-30% of total lung capacity) at this pressure.NEW & NOTEWORTHY In descending deep breath-hold divers, spikes in [Formula: see text] and [Formula: see text] associated with compression of the lungs by increasing water pressure have been reported. This study, which reports the deepest arterial blood gas specimens taken to date, raises the possibility that these spikes are detectable until the greatest proportional changes in lung volume with increasing pressure have occurred, after which [Formula: see text] will decrease through metabolism and [Formula: see text] will increase through simple metabolic accumulation.

Background/Objectives: This report is an assessment of the characteristics associated with cardiovascular dysautonomia (CVD) in the context of long Coronavirus disease (COVID), which is currently inadequately characterized. Material and Methods: A retrospective cross-sectional study was performed involving 106 patients with long COVID, including 34 individuals diagnosed with CVD, among whom eight met the criteria for Postural Tachycardia Syndrome (PoTS). The variables assessed encompassed individual characteristics (e.g., age, sex, comorbidities), immunization parameters (e.g., vaccination/viral status, timing, frequency), cellular and humoral anti-Spike and anti-Nucleocapsid (Nuc) immune responses, inflammatory and allergic biomarkers, as well as an extensive panel of common autoantibodies comprising anti-nuclear antibodies, anti-central nervous system antibodies (cerebellum, brain), and anti-peripheral nervous system antibodies (gangliosides). Results: An age < 45 years, body mass index, hyperventilation syndrome as well as a higher cumulative number of antigenic contacts (vaccinations plus infections ≥ 3) and an elevated basophil count (≥0.06 G/L) were independently associated with CVD. There was no association between CVD and inflammatory markers or common autoantibodies. Patients with PoTS criteria had a strong anti-Spike cellular immune response and increased IgG anti-Nuc humoral immunity when compared with CVD and non-CVD long COVID counterparts. Conclusions: Compared to other long COVID patients, patients with long COVID-associated CVD have distinctive clinical and immunovirological features. Our results suggest the potential role of the immune response against Spike and of allergic pathways rather than humoral autoimmunity against common autoantibodies in long COVID CVD.