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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
Current management strategies and the potential of inhaled GM-CSF for the treatment of autoimmune pulmonary alveolar proteinosis
Published in Expert Opinion on Orphan Drugs, 2019
The same group conducted a national, multicenter, phase II trial at nine pulmonary centers in Japan. They enrolled fifty patients with severe autoimmune PAP; during the first 12 weeks of the observation period, 11 patients were excluded from the treatment due to spontaneous remission or consent withdrawal. Thirty-nine patients with progressive/unremitting disease entered the treatment phase of the study. Treatments included high-dose GM-CSF (sargramostim) administration (125 μg twice daily on Days 1–8, none on Days 9–14) for six 2-week cycles, then low-dose administration (125 μg once daily on Days 1–4, none on Days 5–14) for six 2-week cycles. Four patients did not finish the low-dose treatment. Of 35 patients completing the high- and low-dose therapy, 24 improved, resulting in an overall response rate of 62% during the 6-month treatment period and reduction in alveolar-arterial gradient of oxygen of 12.3 mm Hg, compared to baseline. No serious adverse events occurred during this trial. Twenty-nine of 35 patients remained stable without further therapy for 1 year [48].
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].
Sleep disordered breathing in pregnant women: maternal and fetal risk, treatment considerations, and future perspectives
Published in Expert Review of Respiratory Medicine, 2018
Kimberly Kay Truong, Christian Guilleminault
Several physiologic changes during pregnancy make it a period of increased risk for OSA (Table 1). Upper airway dimensions based on acoustic reflectance are significantly more narrow during the third trimester when compared to repeat measures postpartum and to nonpregnant controls [16]. There are several reasons for increased upper airway resistance and reduction of the cross-sectional area of upper airway. First, estrogen production is 1000 times premenopausal ovulatory levels [17]. Increased levels of estrogen cause upper airway mucosal edema, hypersecretion, gestational rhinitis, and overall increase in nasal and oropharyngeal resistance [18]. Second, women gain approximately 25–35 pounds routinely during pregnancy [19]. The excess fat deposition has been observed under the mandible, within the tongue, soft palate, uvula, and pharyngeal soft tissue, thereby contributing to airway compression [20]. In addition, obesity and a gravid uterus results in reduced functional residual capacity (FRC) by 20%, which further decreases in supine position and during sleep. Reduction in FRC results in decreased oxygenation in the mother from an increase in alveolar-arterial gradient and increase in ventilation-perfusion mismatch [21], resulting in more severe oxygen desaturation for any given apneic length [22]. Lastly, there is an increased respiratory drive associated with increased levels of circulating progesterone [23], which may increase negative intraluminal pressure of upper airway and promote upper airway instability and collapse. These physiologic changes of pregnancy may exacerbate or unmask preexisting SDB in women.