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OBJECTIVE: To compare the portion of tidal volume (VT) ventilating dead space volumes in nonbrachycephalic cats and dogs with small body mass receiving volume-controlled ventilation (VCV) with a fixed VT. STUDY DESIGN: Prospective, experimental study. ANIMALS: A group of eight healthy adult cats and dogs [ideal body weight (IBW): 3.0 ± 0.5 and 3.8 ± 1.1 kg, respectively]. METHODS: Anesthetized cats and dogs received VCV with a 12 mL kg-1 VT (inspiratory pause ≥ 0.5 seconds). Respiratory rate (fR) was adjusted to maintain normocapnia. Airway dead space (VDaw) and alveolar tidal volume (VTalv) were measured by volumetric capnography. Physiological dead space (VDphys) and VDphys/VT ratio were calculated using the Bohr-Enghoff method. Data recorded before surgery were compared by an unpaired t-test or Mann-Whitney U test (p < 0.05 considered significant). RESULTS: The IBW (p = 0.07), PaCO2 (p = 0.40) and expired VT [VT(exp)] (p = 0.77) did not differ significantly between species. The VDaw (mL kg-1) was lower in cats (3.7 ± 0.4) than in dogs (7.7 ± 0.9) (p < 0.0001). The VTalv (mL kg-1) was larger in cats (8.3 ± 0.7) than in dogs (4.3 ± 0.7) (p < 0.0001). Cats presented a smaller VDphys/VT ratio (0.33 ± 0.03) and VDphys (4.0 ± 0.3 mL kg-1) than dogs (VDphys/VT: 0.60 ± 0.09; VDphys: 7.2 ± 1.4 mL kg-1) (p < 0.0001). The fR and minute ventilation (VT(exp) × fR) were lower in cats than in dogs (p = 0.048 and p = 0.038, respectively). CONCLUSIONS AND CLINICAL RELEVANCE: A fixed VT results in more effective ventilation in cats than in dogs with small body mass because of species-specific differences in and VDaw and VDphys. Because of the smaller VDaw and VDphys in cats than in dogs, a lower fR is required to maintain normocapnia in cats.

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OBJECTIVE: To evaluate the impact of a 30% end-inspiratory pause (EIP) on alveolar tidal volume (VTalv), airway (VDaw) and physiological (VDphys) dead spaces in mechanically ventilated horses using volumetric capnography, and to evaluate the effect of EIP on carbon dioxide (CO2) elimination per breath (Vco2br-1), PaCO2, and the ratio of PaO2-to-fractional inspired oxygen (PaO2:FiO2). STUDY DESIGN: Prospective research study. ANIMALS: A group of eight healthy research horses undergoing laparotomy. METHODS: Anesthetized horses were mechanically ventilated as follows: 6 breaths minute-1, tidal volume (VT) 13 mL kg-1, inspiratory-to-expiratory time ratio 1:2, positive end-expiratory pressure 5 cmH2O and EIP 0%. Vco2br-1 and expired tidal volume (VTE) of 10 consecutive breaths were recorded 30 minutes after induction, after adding 30% EIP and upon EIP removal to construct volumetric capnograms. A stabilization period of 15 minutes was allowed between phases. Data were analyzed using a mixed-effect linear model. Significance was set at p < 0.05. RESULTS: The EIP decreased VDaw from 6.6 (6.1-6.7) to 5.5 (5.3-6.1) mL kg-1 (p < 0.001) and increased VTalv from 7.7 ± 0.7 to 8.6 ± 0.6 mL kg-1 (p = 0.002) without changing the VTE. The VDphys to VTE ratio decreased from 51.0% to 45.5% (p < 0.001) with EIP. The EIP also increased PaO2:FiO2 from 393.3 ± 160.7 to 450.5 ± 182.5 mmHg (52.5 ± 21.4 to 60.0 ± 24.3 kPa; p < 0.001) and Vco2br-1 from 0.49 (0.45-0.50) to 0.59 (0.45-0.61) mL kg-1 (p = 0.008) without reducing PaCO2. CONCLUSIONS AND CLINICAL RELEVANCE: The EIP improved oxygenation and reduced VDaw and VDphys, without reductions in PaCO2. Future studies should evaluate the impact of different EIP in healthy and pathological equine populations under anesthesia.

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Cumulative evidence has demonstrated that the ventilatory ratio closely correlates with mortality in acute respiratory distress syndrome (ARDS), and a primary feature in coronavirus disease 2019 (COVID-19)-ARDS is increased dead space that has been reported recently. Thus, new attention has been given to this group of dead space ventilation-related indices, such as physiological dead space fraction, ventilatory ratio, and end-tidal-to-arterial PCO2 ratio, which, albeit distinctive, are all global indices with which to assess the relationship between ventilation and perfusion. These parameters have already been applied to positive end expiratory pressure titration, prediction of responses to the prone position and the field of extracorporeal life support for patients suffering from ARDS. Dead space ventilation-related indices remain hampered by several deflects; notwithstanding, for this catastrophic syndrome, they may facilitate better stratifications and identifications of subphenotypes, thereby providing therapy tailored to individual needs.

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Patients with heart failure with preserved ejection fraction (HFpEF) exhibit cardiopulmonary abnormalities that could affect the predictability of exercise [Formula: see text] from the Jones corrected partial pressure of end-tidal CO2 (PJCO2) equation (PJCO2 = 5.5 + 0.9 × [Formula: see text] - 2.1 × VT). Since the dead space to tidal volume (VD/VT) calculation also includes [Formula: see text] measurements, estimates of VD/VT from PJCO2 may also be affected. Because using noninvasive estimates of [Formula: see text] and VD/VT could save patient discomfort, time, and cost, we examined whether partial pressure of end-tidal CO2 ([Formula: see text]) and PJCO2 can be used to estimate [Formula: see text] and VD/VT in 13 patients with HFpEF. [Formula: see text] was measured from expired gases measured simultaneously with radial arterial blood gases at rest, constant-load (20 W), and peak exercise. VD/VT[art] was calculated using the Enghoff modification of the Bohr equation, and estimates of VD/VT were calculated using [Formula: see text] (VD/VT[ET]) and PJCO2 (VD/VT[J]) in place of [Formula: see text]. [Formula: see text] was similar to [Formula: see text] at rest (-1.46 ± 2.63, P = 0.112) and peak exercise (0.66 ± 2.56, P = 0.392), but overestimated [Formula: see text] at 20 W (-2.09 ± 2.55, P = 0.020). PJCO2 was similar to [Formula: see text] at rest (-1.29 ± 2.57, P = 0.119) and 20 W (-1.06 ± 2.29, P = 0.154), but underestimated [Formula: see text] at peak exercise (1.90 ± 2.13, P = 0.009). VD/VT[ET] was similar to VD/VT[art] at rest (-0.01 ± 0.03, P = 0.127) and peak exercise (0.01 ± 0.04, P = 0.210), but overestimated VD/VT[art] at 20 W (-0.02 ± 0.03, P = 0.025). Although VD/VT[J] was similar to VD/VT[art] at rest (-0.01 ± 0.03, P = 0.156) and 20 W (-0.01 ± 0.03, P = 0.133), VD/VT[J] underestimated VD/VT[art] at peak exercise (0.03 ± 0.04, P = 0.013). Exercise [Formula: see text] and VD/VT[ET] provides better estimates of [Formula: see text] and VD/VT[art] than PJCO2 and VD/VT[J] does at peak exercise. Thus, estimates of [Formula: see text] and VD/VT should only be used if sampling arterial blood during CPET is not feasible.NEW & NOTEWORTHY [Formula: see text] provides a better estimate of [Formula: see text] than PJCO2 at peak exercise, and VD/VT[ET] provides a better estimate of VD/VT[art] than VD/VT[J] at peak exercise. Although we reported significant correlations, we did not find an identity between [Formula: see text] and estimates of [Formula: see text], nor did we find an identity between VD/VT[art] and estimates of VD/VT[art]. Thus, caution should be taken and estimates of [Formula: see text] and VD/VT should only be used if sampling arterial blood during CPET is not feasible.

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Hypercapnia occurs in ventilated infants even if tidal volume (VT) and minute ventilation (VE) are maintained. We hypothesised that increased physiological dead space (Vd,phys) caused decreased minute alveolar ventilation (VA; alveolar ventilation (VA) × respiratory rate) in well-ventilated infants with hypercapnia. We investigated the relationship between dead space and partial pressure of carbon dioxide (PaCO2) and assessed VA. Intubated infants (n = 33; mean birth weight, 2257 ± 641 g; mean gestational age, 35.0 ± 3.3 weeks) were enrolled. We performed volumetric capnography (Vcap), and calculated Vd,phys and VA when arterial blood sampling was necessary. PaCO2 was positively correlated with alveolar dead space (Vd,alv) (r = 0.54, p < 0.001) and Vd,phys (r = 0.48, p < 0.001), but not Fowler dead space (r = 0.14, p = 0.12). Normocapnia (82 measurements; 35 mmHg ≤ PaCO2 < 45 mmHg) and hypercapnia groups (57 measurements; 45 mmHg ≤ PaCO2) were classified. The hypercapnia group had higher Vd,phys (median 0.57 (IQR, 0.44-0.67)) than the normocapnia group (median Vd,phys/VT = 0.46 (IQR, 0.37-0.58)], with no difference in VT. The hypercapnia group had lower VA (123 (IQR, 87-166) ml/kg/min) than the normocapnia group (151 (IQR, 115-180) ml/kg/min), with no difference in VE.Conclusion: Reduction of VA in well-ventilated neonates induces hypercapnia, caused by an increase in Vd,phys. What is Known: • Volumetric capnography based on ventilator graphics and capnograms is a useful tool in determining physiological dead space of ventilated infants and investigating the cause of hypercapnia. What is New: • This study adds evidence that reduction in minute alveolar ventilation causes hypercapnia in ventilated neonates.

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RATIONALE: COVID-19 ARDS could differ from typical forms of the syndrome. OBJECTIVE: Pulmonary microvascular injury and thrombosis are increasingly reported as constitutive features of COVID-19 respiratory failure. Our aim was to study pulmonary mechanics and gas exchanges in COVID-2019 ARDS patients studied early after initiating protective invasive mechanical ventilation, seeking after corresponding pathophysiological and biological characteristics. METHODS: Between March 22 and March 30, 2020 respiratory mechanics, gas exchanges, circulating endothelial cells (CEC) as markers of endothelial damage, and D-dimers were studied in 22 moderate-to-severe COVID-19 ARDS patients, 1 [1-4] day after intubation (median [IQR]). MEASUREMENTS AND MAIN RESULTS: Thirteen moderate and 9 severe COVID-19 ARDS patients were studied after initiation of high PEEP protective mechanical ventilation. We observed moderately decreased respiratory system compliance: 39.5 [33.1-44.7] mL/cmH2O and end-expiratory lung volume: 2100 [1721-2434] mL. Gas exchanges were characterized by hypercapnia 55 [44-62] mmHg, high physiological dead-space (VD/VT): 75 [69-85.5] % and ventilatory ratio (VR): 2.9 [2.2-3.4]. VD/VT and VR were significantly correlated: r2 = 0.24, p = 0.014. No pulmonary embolism was suspected at the time of measurements. CECs and D-dimers were elevated as compared to normal values: 24 [12-46] cells per mL and 1483 [999-2217] ng/mL, respectively. CONCLUSIONS: We observed early in the course of COVID-19 ARDS high VD/VT in association with biological markers of endothelial damage and thrombosis. High VD/VT can be explained by high PEEP settings and added instrumental dead space, with a possible associated role of COVID-19-triggered pulmonary microvascular endothelial damage and microthrombotic process.

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OBJECTIVES: To compare the anatomical (VD-Ana ) and alveolar dead space (VD-Alv ) in term and prematurely born infants and identify the clinical determinants of those indices. WORKING HYPOTHESIS: VD-Ana and VD-Alv will be higher in prematurely born compared to term born infants. STUDY DESIGN: Retrospective analysis of data collected at King's College Hospital NHS Foundation Trust, London, UK. PATIENT SELECTION: Fifty-six infants (11 term, 45 preterm) were studied at a median age of 8 (IQR 2-33) days. METHODOLOGY: VD-Ana was determined using Fowler's method of volumetric capnography. VD-Alv was determined by subtracting VD-Ana from the physiological dead space which was determined by the Bohr-Enghoff equation. VD-Ana and VD-Alv were related to body weight at the time of study. RESULTS: The median VD-Ana /kg was higher in prematurely born infants [3.7 (IQR: 3.0-4.5) mL/kg] compared to term infants [2.4 (IQR: 1.9-2.9) mL/kg, adjusted P = 0.001]. The median VD-Alv /kg was not higher in prematurely born infants [0.3 (IQR: 0.1-0.5)] compared to term infants [0.1 (IQR: 0.0-0.2) mL/kg] after adjusting for differences in respiratory rate and days of ventilation (P = 0.482). VD-Ana /kg was related to postmenstrual age (r = -0.388, P < 0.001), birth weight (r = -0.397, P < 0.001), and weight at measurement (r = -0.476, P < 0.001). VD-Alv /kg was related to postmenstrual age (r = -0.254, P < 0.001), birth weight (r = -0.291, P = 0.002), and weight at measurement (r = -0.281, P = 0.003) and related to days of ventilation (r = 0.194, P = 0.044). CONCLUSIONS: VD-Ana /kg and VD-Alv /kg increased with decreasing weight and gestation. VD-Alv was higher in infants that have undergone prolonged mechanical ventilation.

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We hypothesized that exercise ventilation and arterial H(+) ([H(+)]a) are mutually interactive, [H(+)]a stimulating V(E) and V(E) regulating [H(+)]a increase. Fifty-five patients were studied, 10 normal and 45 with cardio-respiratory disorders. Each patient underwent cardiopulmonary exercise testing with simultaneous serial arterial blood gas and pH measurements. Subsequently, they were classified into one of 7 clinical groups: (1) normal, (2) exercise-induced hypoxemia (PaO2<50mmHg), (3) exercise-induced myocardial ischemia, (4) heart failure, (5) COPD, (6) interstitial lung disease, and (7) pulmonary vasculopathy. The average resting pHa was 7.42 or 7.43 for each group. At anaerobic (lactic acidosis) threshold (AT), [H(+)]a increased due to PaCO2 increase (+2mmHg), primarily. At peak exercise, [H(+)]a increased further due to arterial HCO3(-) decrease. In summary, [H(+)]a appears to be closely regulated at rest to AT and further to peak exercise by CO2 elimination from the venous return. No evidence was observed for over-ventilation of CO2, causing the arterial blood to become more alkaline during exercise in the patient groups studied.

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