Cardiovascular effects of exercise induced dynamic hyperinflation in COPD patients-Dynamically hyperinflated and non-hyperinflated subgroups.

INTRODUCTION: An increase in respiratory rate and expiratory flow limitation can facilitate dynamic hyperinflation (DH), which may cause an element of the intrathoracic pressure in connection with the worsening of venous return, with negative effect on stroke volume (SV) and cardiac output (CO). It has been unclassified, whether poor circulatory adaptation to exercise can be attributed to DH or poor cardio-vascular performance itself in COPD. Only a subset of COPD patients exhibit dynamic hyperinflation during exercise. PATIENTS AND METHODS: We designed a study to show how lung mechanical and cardiovascular parameters change in hyperinflated and non-hyperinflated COPD patients during exercise with a new experimental set-up. Thirty-three COPD patients with similar severity of COPD and left ventricular performance (20 men, 13 women, mean±SD age: 65,36±6,95 years) participated. We measured the cardiovascular parameters with a non-invasive device (Finometer-pro) including the left ventricular ejection time index (LVETi) and estimated the change of DH with inspiratory capacity (IC) manoeuvres during exercise. RESULTS: Twenty-one subjects exhibited DH (DH group) and 12 did not (non-DH group). The measurement results were given in mean ± SD and difference between the values measured during maximal load and rest also (ΔX = Xmax.load-Xrest). ΔSV and ΔCO were significantly higher in non-DH vs. DH patients (ΔSV: non-DH 9,7 ± 13,22 ml vs. DH -3,6 ± 14,34 ml, p = 0.0142; ΔCO: non-DH 2,26 ± 1,46 l/min vs. DH 0,88 ± 1,35 l/min, p = 0.0024). LVETi was not different between the two groups. Calculated oxygen delivery (DO2) during maximal load was significantly higher in non-DH group. CONCLUSION: We concluded that worse cardiovascular adaptation to exercise of COPD patients can be associated with exercise-induced DH in a similar cardiovascular aged COPD group.

Severe hypoxaemia without dyspnoe in COVID-19 pneumonia / Súlyos hypoxaemia légszomj nélkül COVID-19-pneumoniában.

Összefoglaló. Számos közlemény született arról, hogy a COVID-19-pneumoniás betegek jelentos hányadában az artériás parciális oxigéntenzió kifejezetten alacsony, mégsem jellemzo a dyspnoe, és a pulzusoximetria sem mutat - a csökkent oxigéntenzióval arányos - súlyos hypoxaemiát. A jelenséget "happy hypoxaemia" néven említik. Ugyanakkor a légszomjról nem panaszkodó, de súlyos alveolocapillaris O2-felvételi zavarban szenvedo COVID-19-pneumoniás betegek a legkisebb fizikai megterhelést sem turik, és állapotuk gyorsan kritikussá válhat, tehát a hypoxaemia mértékének idoben való felismerése kulcskérdés. A jelen közleményben egy ilyen eset rövid ismertetése után összefoglaljuk a súlyos, de tünetmentes hypoxaemia hátterében meghúzódó élettani okokat. Ezek között szerepel a hypocapnia (respiratoricus alkalosis) is, mely alacsony oxigéntenzió mellett is a hemoglobin viszonylag megtartott oxigénszaturációját eredményezi. Ezért a mindennapi COVID-19-ellátásban a megismételt artériásvérgáz-meghatározások jelentosége nem hangsúlyozható eléggé. Orv Hetil. 2021; 162(10): 362-365. Summary. Many COVID-19 patients have very low arterial partial oxigen tension while severe dyspnoe does not develop. Pulse oxymetry indicates only moderate reduction of arterial O2 saturation in these patients. The phenomenon is named "happy hypoxaemia". Lack of (severe) dyspnoe and only moderately decreased O2 saturation in severely impaired alveolo-capillary O2 uptake may partially be explained by an increased oxygen affinity of hemoglobin in the presence of low arterial partial pressure of CO2. The latter results from increased alveolar ventilation, while low partial pressure of O2 in COVID-19 patients reflects right-to-left shunting of pulmonary blood flow and ventilation-perfusion mismatch of the diseased lungs. While such patients may have mild complaints as related to the real impairment of alveolo-capillary oxygen exchange, severe hypoxaemia is a negative prognostic factor of outcome in this state where severe clinical deterioration may rapidly appear. The latter circumstance together with the unusual relationship of O2 partial pressure and O2 saturation of hemoglobin in COVID-19 emphasize the importance of repeated complete arterial blood gas analyses in these patients. Orv Hetil. 2021; 162(10): 362-365.

Seasonal changes of lower respiratory tract infections in lung transplant recipients during the first post-transplant year: The Hungarian experience.

BACKGROUND: After lung transplantation (LuTX) a high level of immunosuppression is needed to prevent rejection of the graft. Together with earlier colonization by pathogens, immunosuppression makes recipients more susceptible to infections, especially during the first postoperative year. As seasonality of lower respiratory tract infections (LRTI) is well-known in chronic lung diseases, we assessed seasonal changes of pathogen spectrum and number of infections in the first postoperative year in LuTX recipients. METHODS: LRTI were analyzed in 28 Hungarian adult LuTX patients. Incidence and spectrum of microorganism causing LRTI were evaluated according to post-transplant time and seasonal temperature and humidity changes. RESULTS: A total of 69 cases of LRTI were registered (average: 1.9 cases/patient; range: 0-14). Gram-negative=59, gram-positive=26, and fungal=31 pathogens were detected, with polymicrobial samples in 46% of all cases. Increased number of LRTI was observed in the cold season (1.68±1.54 vs 0.79±0.92 case/month/patient, P<.01) and significant negative correlations were identified between the incidence of polymicrobial and bacterial infections and temperature (r2 =0.1535, P<.05, r2 =0.3144, P<.01, respectively). In addition, positive correlation was observed between polymicrobial infections and humidity (r2 =0.1403, P<.05). Higher incidence of LRTI was also noted in the cold season, when accounting for the differences in immunosuppression. CONCLUSION: Seasons influenced the incidence of LRTI in the first postoperative year in LuTX recipients. More intensive vigilance for possible gram-negative and polymicrobial infections is needed in these patients in cold and wet seasons in the continental climate zone, regardless of underlying disease.

Tumor cell expression of heat shock protein (HSP) 72 is influenced by HSP72 [HSPA1B A(1267)G] polymorphism and predicts survival in small Cell lung cancer (SCLC) patients.

The inducible heat shock protein (HSP)72 plays a central role in antitumor immunomodulation. HSP72 expression was assessed on tumor samples of 43 patients with advanced and metastatic small cell lung cancer (SCLC) by immunohistochemistry and HSP72 [HSPA1B A(1267)G] polymorphism was determined. HSP72 expression of SCLC cells was significantly decreased in GG as compared to cells of AA or AG genotype patients, and was associated with significantly shorter survival in GG patients as compared to carriers of the A allele. Decreased HSP72 expression of SCLC cells associated with HSP72 GG genotype is a negative prognostic factor for survival in SCLC patients.

Effect of cigarette smoke and dexamethasone on Hsp72 system of alveolar epithelial cells.

Smoking is the leading risk factor of chronic obstructive pulmonary disease (COPD) and lung cancer. Corticosteroids are abundantly used in these patients; however, the interaction of smoking and steroid treatment is not fully understood. Heat shock proteins (Hsps) play a central role in the maintenance of cell integrity, apoptosis and cellular steroid action. To better understand cigarette smoke-steroid interaction, we examined the effect of cigarette smoke extract (CSE) and/or dexamethasone (DEX) on changes of intracellular heat shock protein-72 (Hsp72) in lung cells. Alveolar epithelial cells (A549) were exposed to increasing doses (0; 0.1; 1; and 10 µM/µl) of DEX in the medium in the absence(C) and presence of CSE. Apoptosis, necrosis, Hsp72 messenger-ribonucleic acid (mRNA) and protein expression of cells were measured, and the role of Hsp72 on steroid effect examined. CSE reduced the number of viable cells by significantly increasing the number of apoptotic and necrotic cells. DEX dose-dependently decreased the ratio of apoptosis when CSE was administered, without change in necrosis. CSE - DEX co-treatment dose-dependently increased Hsp72 mRNA and protein expression, with the highest level measured in CSE + DEX (10) cells, while significantly lower levels were noted in all respective C groups. Pretreatment with Hsp72 silencing RNA confirmed that increased survival observed following DEX administration in CSE-treated cells was mainly mediated via the Hsp72 system. CSE significantly decreases cell survival by inducing apoptosis and necrosis. DEX significantly increases Hsp72 mRNA and protein expression only in the presence of CSE resulting in increased cellular protection and survival. DEX exerts its cell protective effects by decreasing apoptotic cell death via the Hsp72 system in CSE-treated alveolar epithelial cells.