China
Africa
Explore chapters and articles related to this topic
Introduction to the clinical stations
Published in Sukhpreet Singh Dubb, Core Surgical Training Interviews, 2020
I would examine the result of the arterial blood gas and look for favourable PaO2 and PaCO2 values, or more specifically, an alveolar-arterial gradient less than 20 mmHg. I would examine the ECG recording and look for signs of a pulmonary embolism such as tachycardia, new presentations of right axis deviation and right bundle branch block. There may also be the characteristic finding of an S-wave in lead 1 and Q-waves with T-wave inversion in lead 3. I would combine these investigations along with my clinical suspicion to produce a risk score, using a suitable scoring system such as the Wells score, PERC score or the Geneva score. A chest radiograph would also be helpful for the primary diagnosis and a pulmonary embolism.
Unusual Inherited Pulmonary Diseases Which Provide Clues to Pulmonary Physiology and Function
Published in Stephen D. Litwin, Genetic Determinants of Pulmonary Disease, 2020
Thomas Κ. C. King, Robert A. Norum
Although the resting may be normal in early cases, it has been shown that the alveolar-arterial gradient for pO2 is nearly always abnormal [30]. An even more sensitive test is the on exercise, since it is well known that arterial hypoxemia is enhanced by this maneuver.
Respiratory Medicine
Published in Paul Bentley, Ben Lovell, Memorizing Medicine, 2019
ABG: pH/HCO3: Determines chronicity and whether renal compensation has occurred: Alveolar–arterial gradient (PAO2 – PaO2)PAO2 (Alveolar O2) = 20 –(PaCO2 × 1.25)Normal A–a gradient = 2 kPa (50-y-old, at sea-level, room air)Raised A–a gradient indicates diffusion failure or V/Q mismatch
Anti-IL-8 antibody potentiates the effect of exogenous surfactant in respiratory failure caused by meconium aspiration
Published in Experimental Lung Research, 2018
Pavol Mikolka, Jana Kopincova, Petra Kosutova, Maros Kolomaznik, Andrea Calkovska, Daniela Mokra
Parameter PaO2/FiO2 was calculated as a ratio between arterial oxygen partial pressure (PaO2) and fraction of inspired oxygen (FiO2), in our case 1.0. Alveolar–arterial gradient (AaG) was calculated as AaG = [FiO2 (Patm – PH2O) – PaCO2 /0.8] – PaO2, where Patm is barometric pressure and PH2O is pressure of water vapor. Cdyn was calculated as a ratio between the tidal volume adjusted per kg b.w. and the airway pressure gradient (PIP – PEEP). Mean airway pressure (MAP) was calculated as: MAP = (PIP + PEEP)/2; oxygenation index (OI) as: OI = (MAP × FiO2)/PaO2) and ventilation efficiency index (VEI) as VEI = 3800/[(PIP−PEEP) × frequency × PaCO2].
Disease staging and sub setting of interstitial lung disease associated with systemic sclerosis: impact on therapy
Published in Expert Review of Clinical Immunology, 2018
Peter M. George, Athol U. Wells
Immediate treatment is not required in asymptomatic SSc-ILD when HRCT involvement is limited and pulmonary function testing demonstrates minimal physiological impairment. Therapeutic intervention in such a group can be harmful as side effects outweigh any marginal benefits. If there is any doubt as to the clinical relevance of limited HRCT appearances, a maximal cardiopulmonary exercise test with near-normal peak oxygen consumption (VO2 max) and no widening of the alveolar–arterial gradient can provide reassurance that disease is genuinely subclinical.
Pharmacotherapy options in pulmonary alveolar proteinosis
Published in Expert Opinion on Pharmacotherapy, 2020
Sabina Antonela Antoniu, Ruxandra Rajnoveanu, Mihaela Grigore, Ileana Antohe
A phase II study performed in Japan by the same author enrolled patients with autoimmune PAP who showed no improvement in their alveolar arterial gradient after a 12-week observation period. A total of 39 patients received high-dose sargramostim therapy (250 µg twice daily every other week for 12 weeks), followed by (in 35 patients only) a low-dose regimen (125 µg twice daily every other week for 12 weeks), and then a 52-week follow up period. The primary endpoint was a change in alveolar-arterial gradient between successive periods. Secondary endpoints were represented by similar changes in lung function and serum biomarkers and by safety. A therapeutic response was defined as a decrease of at least 10 mmHg of baseline alveolar-arterial gradient at the end of the low-dose regimen. The change in alveolar arterial gradient from baseline at the end of the high-dose therapy was 8.3 mmHg (p < 0.001) and 12.3 mmHg at the end of the low-dose regimen (p < 0.0001). Thus, the improvement was greater after the high dose than after the low dose therapy (p = 0.026). The overall response rate was 62%, and occurred early in 17 patients (i.e. during the high-dose period) and later (during the low-dose period) in 7 patients. The overall gradient improvement in responders was −18.2 mmHg (p < 0.001), and was higher (−13.3 mmHg p < 0.001) in early responders compared to late responders (−4.9 mmHg p = 0.009). Inhaled GM-CSF therapy was also associated with significant improvements in dyspnea, exercise capacity, lung function testing variables, imaging (HRCT) abnormalities, and serum biomarkers such as LDH, SP-A, and SP-D. A significant decrease in the need for supplemental oxygen was also reported. Gradient dynamics were found to correlate well with diffusion capacity and with an extension of lung imaging abnormalities. No side effects were detected, and all 35 patients who completed the low-dose regimen remained stable for the entire 52-week observation period [22].