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BackgroundHVP testing has been used for > 25 years within a service to investigate a patients breathing pattern. The protocol utilises a 3-minute resting phase, then if resting values are within the normal range voluntary hyperventilation (VH) is commenced for 3 minutes followed by recovery monitoring for 3 minutes. Low PETCO2 may cause cardiac arrhythmias, coronary artery spasm and seizures (Kane et al, Seizure.2014) in susceptible patients and therefore if a shorter period of VH could be utilised within the test then this may be safer for patients. Other Services have used a 1 min VH within their protocol.AimCan the VH stage of the HVPT be reduced from 3 minutes to 1 minute (in keeping with other Services protocol) and still elicit the required reduction in PETCO2?MethodPatients that attended for HVPT over 3 months were identified, demographics and clinical details recorded. PETCO2 at 1, 2 and 3 minutes were noted in those patients who progressed to the VH stage and compared using a one-way Anova and post Hoc Tukey analysis.Results73 patients were identified, 3 were excluded.70 patients were included: 22 being classified as experiencing chronic hyperventilation, 22 acute and 26 showing normal PETCO2 responses. 4 patients with normal PETCO2 had evidence of a breathing pattern disorder (BPD). 48 patients went on to perform VH.A one-way Anova was used to assess whether there was a statistical difference between PETCO2 at 1 minute, 2 minutes, 3 minutes and combinations of all 3.P between all 3= 0.006P between 1 and 2 minutes= 0.002P between 2 and 3 minutes= 0.285P between 1 and 3 minutes= 0.016(Figure 1)Abstract P18 Figure 1[Image Omitted. See PDF.]ConclusionData suggests that VH could be reduced from 3 minutes to 2 minutes. ETCO2 at 1 minute is significantly higher than at 2 minutes suggesting that either a change in protocol may be required to reduce ETCO2 to desired level or that 2 minutes of VH is required to reach ‘target’ ETCO2. A standardised protocol for HVPT by the ARTP that offers guidance on protocol and target ETCO2 range would be desirable.

IntroductionEucapnic voluntary hyperpnoea (EVH) is a validated surrogate for exercise in the objective diagnosis of exercise-induced bronchoconstriction (EIB) (figure 1) 1. However, its validity traditionally depends on achieving a minimum hyperventilation target, defined as ventilation (VE) ≥80% of maximum voluntary ventilation (MVV)2.This strict threshold can lead to invalid tests for individuals unable to meet it due to physiological or technical limitations. This case series explores the use of a novel validity criterion (VE ≥60% of MVV) in three diverse participants, demonstrating its ability to preserve diagnostic integrity.MethodsThree participants (M:2, F:1; aged 17–27 years) underwent EVH testing at using a Jaeger CPX system. Hyperventilation breath by breath data was captured continual for six minutes. Entrained directly into the circuit was a gas mix consisting of 21% O2 5% CO2 and 74% Nitrogen.Baseline and post-EVH FEV1 values were recorded at 3,5,7,10,15,20 minutes. Post 20-minute time a 2.5 mg Salbutamol nebuliser was administered.VE as a percentage of MVV was calculated, with test validity determined using traditional (≥80%) and novel (≥60%) thresholds.ResultsSubject 1 (M, 27 years): VE = 54.54% MVV, 7.6% FEV1 reduction (normal response).Subject 2 (M, 17 years): VE = 76.20% MVV, 8.9% FEV1 reduction (normal response).Subject 3 (F, 19 years): VE = 65.15% MVV, 13% FEV1 reduction (mild airway hyperresponsiveness).Abstract P64 Figure 1[Image Omitted. See PDF.]ConclusionFor participants with suboptimal ventilatory performance, such as those with lower fitness levels achieving 80% of MVV may not be feasible, leading to the invalidation of their tests. Subject 1, for instance, achieved only 54.54% of MVV yet demonstrated a normal post-test FEV1 reduction of 7.6%, indicative of a valid negative response. Similarly, Subject 3 achieved 65.15% of MVV, with a 13% FEV1 reduction consistent with mild airway hyperresponsiveness. Both cases would have been excluded under the traditional criteria, potentially delaying or misdirecting clinical care.Expanding test validity criteria balances methodological rigour with practical applicability. These findings emphasise the need for further research to evaluate the impact of ventilatory thresholds on EVH outcomes across diverse populations and settings. Additional studies are warranted to confirm broader applicability.

At a point during the latter third of an incremental exercise protocol, ventilation begins to exceed the rate of clearance of carbon dioxide (CO 2 ) at the lungs ( V ˙ CO 2 ). The onset of this hyperventilation, which is confirmed by a fall from a period of stability in end-tidal and arterial CO 2 tensions (PCO 2 ), is referred to as the respiratory compensation point (RCP). The mechanisms that contribute to the RCP remain debated as does its surrogacy for the maximal metabolic steady state of constant-power exercise (i.e., the highest work rate associated with maintenance of physiological steady state). The objective of this current opinion is to summarize the original research contributions that support and refute the hypotheses that: (i) the RCP represents a rapid, peripheral chemoreceptor-mediated reflex response engaged when the metabolic rate at which the buffering systems can no longer constrain the rise in hydrogen ions ([H + ]) associated with rising lactate concentration and metabolic CO 2 production is surpassed; and (ii) the metabolic rate at which this occurs is equivalent to the maximal metabolic steady state of constant power exercise. In doing so, we will shed light on potential mechanisms contributing to the RCP, attempt to reconcile disparate findings, make a case for its adoption for exercise intensity stratification and propose strategies for the use of RCP in aerobic exercise prescription.

BackgroundEarly diagnosis of shock is a pre-determining factor for a good prognosis in intensive care. An elevated central venous to arterial PCO2 difference (ΔPCO2) over 0.8 kPa (6 mmHg) is indicative of low blood flow states. Disturbances around the time of blood sampling could result in inaccurate calculations of ΔPCO2, thereby misrepresenting the patient status. This study aimed to determine the influences of acute changes in ventilation on the ΔPCO2.MethodsEight pigs without cardiovascular or respiratory disease were studied. Arterial and central venous catheters were inserted following anaesthetization. Baseline ventilator settings were titrated to achieve an EtCO2 of 5 ± 0.5 kPa (VT = 8 ml/kg, Freq = 14±2 breaths per minute). Blood was sampled simultaneously from both catheters at baseline and 30, 60, 90, 120, 180 and 240 seconds after a change in ventilation. Pigs were subjected to both hyperventilation and hypoventilation, wherein the respiratory frequency was doubled or halved from baseline. ΔPCO2 changes from baseline were analysed using Repeated Measures ANOVA with post-hoc analysis using Bonferroni’s correction.ResultsResponse of ΔPCO2 to acute changes in ventilation are illustrated in figure 1. ΔPCO2 at baseline was 0.76 ± 0.29 kPa (5.7 ± 2.2 mmHg). Following hyperventilation there was a rapid increase in the ΔPCO2, plateauing at 1.31 ± 0.24 kPa (9.75 ± 1.80 mmHg). There was a corresponding decrease in the ΔPCO2 following hypoventilation, reaching a maximum at 0.23 ± 0.31 (1.73 ± 2.33 mmHg). These changes were statistically significant from baseline 30 seconds after the change in ventilation.Abstract P249 Figure 1Change in APCO, in response to acute changes in ventilationChanges in APCO, (kPa) in response to hyperventilation (black) and hypoventilation (grey), presented as mean (SD; one sided). N=8.*statistically significant when compared to baseline using a Repeated Measures ANOVA and a post-hoc analysis with Bonferroni’s correction (P<0.05)†analysis done with n=7 due to an erroneous blood sample.ConclusionDisturbances around the time of blood sampling can rapidly affect the PCO2, represented here by the changes in ventilation. This leads to inaccurate calculations of the ΔPCO2 resulting in misinterpretation of patient status, possibly affecting patient management decisions. We, therefore, advocate mindfulness when interpreting blood gases and caution with the use of these parameters while assessing patient status, especially if there is doubt as to the presence of a transient change in the patient’s ventilation status.

IntroductionHypoxic challenge tests (HCT) are recommended by the British Thoracic Society to assess the requirement for in flight supplemental O2. During an HCT, the FiO2 is reduced to 15% replicating the PiO2 experienced during air travel. Various HCT methods exist, potentially affecting clinical outcomes. In the UK, two main techniques are used, the ‘Venturi mask method’ (V-HCT), which employs 100% N2 via a 40% O2 venturi barrel, and the ‘Mouthpiece method’ (M-HCT), which uses pre-mixed 15% O2 via a mouthpiece. We compared these methods in elderly individuals with airflow obstruction, hypothesising that the M-HCT would induce hyperventilation (assessed via transcutaneous CO2 – tCO2) and potentially yield false-negative results.MethodsParticipants with self-reported COPD or asthma, aged over 60 and naïve to HCT, attended the University of Winchester for a screening visit followed by two experimental visits. Spirometry during the screening visit confirmed airflow obstruction. During the experimental visits, participants completed both V-HCT and M-HCT in a random order, with continuous measurements of tCO2, SpO2, and HR. They also reported any claustrophobia and answered, ‘If asked to perform a HCT by your clinician, what test would you rather perform?’.ResultsTwelve participants completed both HCT methods (see table 1 for demographics). Five found the M-HCT claustrophobic, while none did for the V-HCT, and all preferred the V-HCT. In contrast to our hypothesis, tCO2 levels were similar between methods, with no significant difference from baseline to the final three minutes (M-HCT: 5.1 to 5.0 kPa; V-HCT: 5.1 to 5.1 kPa). Furthermore, ten participants had lower SpO2 nadirs during the M-HCT. Statistical analysis on the grouped data was not feasible as two participants’ SpO2 dropped <83% during the M-HCT, necessitating an FiO2 increase as per ethical guidelines.Abstract P19 Table 1Participant demographicsConclusionPatients preferred the V-HCT, reporting less claustrophobia than the M-HCT, but no evidence of hyperventilation during either method was shown. The reason for lower SpO2 with the V-HCT in ten participants remains unclear, although room air entrainment through the mask’s expiratory ports, raising the FiO2 is a possible explanation. Future studies are required to accurately measure the true FiO2 inhaled during the Venturi technique.

Measurement of ventilatory efficiency, defined as minute ventilation per unit carbon dioxide production (VE/VCO2), by cardiopulmonary exercise testing (CPET) has been proposed as a screen for hyperventilation syndrome (HVS). However, increased VE/VCO2 may be associated with other disorders which need to be distinguished from HVS. A more specific marker of HVS by CPET would be clinically useful. We hypothesized ventilatory control during exercise is abnormal in patients with HVS. Patients who underwent CPET from years 2015 through 2017 were retrospectively identified and formed the study group. HVS was defined as dyspnea with respiratory alkalosis (pH >7.45) at peak exercise with absence of acute or chronic respiratory, heart or psychiatric disease. Healthy patients were selected as controls. For comparison the Student t-test or Mann-Whitney U test were used. Data are summarized as mean ± SD or median (IQR); p<0.05 was considered significant. Twenty-nine patients with HVS were identified and 29 control subjects were selected. At rest, end-tidal carbon dioxide (PETCO2) was 27 mmHg (25-30) for HVS patients vs. 30 mmHg (28-32); in controls (p = 0.05). At peak exercise PETCO2 was also significantly lower (27 ± 4 mmHg vs. 35 ± 4 mmHg; p<0.01) and VE/VCO2 higher ((38 (35-43) vs. 31 (27-34); p<0.01)) in patients with HVS. In contrast to controls, there were minimal changes of PETCO2 (0.50 ± 5.26 mmHg vs. 6.2 ± 4.6 mmHg; p<0.01) and VE/VCO2 ((0.17 (-4.24-6.02) vs. -6.6 (-11.4-(-2.8)); p<0.01)) during exercise in patients with HVS. The absence of VE/VCO2 and PETCO2 change during exercise was specific for HVS (83% and 93%, respectively). Absence of VE/VCO2 and PETCO2 change during exercise may identify patients with HVS.

We performed this study to investigate whether real-time tidal volume feedback increases optimal ventilation and decreases hyperventilation during manikin-simulated cardiopulmonary resuscitation (CPR). We developed a new real-time tidal volume monitoring device (TVD) which estimated tidal volume in real time using a magnetic flowmeter. The TVD was validated with a volume-controlled mechanical ventilator with various tidal volumes. We conducted a randomized, crossover, manikin-simulation study in which 14 participants were randomly divided into a control (without tidal volume feedback, n = 7) and a TVD group (with real-time tidal volume feedback, n = 7) and underwent manikin simulation. The optimal ventilation was defined as 420-490 mL of tidal volumes for a 70-kg adult manikin. After 2 weeks of the washout period, the simulation was repeated via the participants' crossover. In the validation study, 97.6% and 100% of the difference ratios in tidal volumes between the mechanical ventilator and TVD were within ±1.5% and ±2.5%, respectively. During manikin-simulated CPR, TVD use increased the proportion of optimal ventilation per person. Its median values (range) of the control group and the TVD group were 37.5% (0.0-65.0) and 87.5% (65.0-100.0), respectively, P < .001). TVD use also decreased hyperventilation. The proportions of hyperventilation in the control group and the TVD group were 25.0% vs 8.9%, respectively (P < .001). Real-time tidal volume feedback using the new TVD guided the rescuers to provide optimal ventilation and to avoid hyperventilation during manikin-simulated CPR.