Background:Chronic Obstructive Pulmonary Disease(COPD) is an inflammatory airway disease characterized by the presence of expiratory flow limitation. Exacerbations of COPD are common acute events. During epidemic of COVID-19, concerns have been raised with regard to mask- using because of increasing respiratory resistance. In this study, we aimed to evaluate the relationship between the vital signs , inflammation index, hypercapnia, hypoxia and mask-using in AECOPD patients.Methods:This retrospective study was performed at a tertiary hospital, and enrolled 23 patients with AECOPD who were hospitalized three or more times in the respiratory department. Patients in Group C were hospitalized and used masks during the epidemic period of COVID-19. Patient’s data of the previous two hospitalizations from the medical record system divided into group A and group B according to the time sequence. Vital signs, inflammation index, artery blood gas from medical record system and questionnaires of three hospitalizations in the same patient were collected to perform paired test.Results: Surgical mask using increased the levels of PaCO2 (8.98mm Hg; p = 0.004), HCO3-act (4.1mmol/L; p =0.006), BE (3.01mmol/L; p =0.019) and systolic blood pressure (11.39mm Hg; p = 0.01) in patients with AECOPD compared to last hospitalization. Surgical mask using for 30 to 120 minutes is associated with hypercapnia. There were no significant differences observed between group B and group A without using mask in vital signs, inflammation index, and artery blood gas.Conclusions: In this study, we found that systolic blood pressures and PaCO2, HCO3-act, BE were significantly elevated in AECOPD patients using masks compared to the other groups without masks. In addition,the changes in PaCO2,HCO3-act,BE is closely related to serum chloride concentration. Therefore, it is need to increase awareness and understanding of the use of masks in patients with chronic cardiopulmonary diseases.
Objectives Pulmonary veno-occlusive disease (PVOD) is a rare type of pulmonary hypertension, with similar clinical presentation to pulmonary arterial hypertension (PAH) but poorer prognosis and higher possibility to develop sever pulmonary oedema after specific PAH therapy, which have manifest the significance to distinguish PVOD from PAH for proper diagnose and clinical management. Methods We reported a 40-year-old male patient with a history of progressive dyspnea, fatigue, try cough, with a diagnosis of PAH confirmed elsewhere, was ultimately diagnosed as PVOD via non-invasive approaches—pulmonary function test (PFT), high-resolution CT scan of chest and bronchoalveolar lavage. In this paper, we also reviewed some published literature and discussed the differences between PVOD and PAH in all kinds of clinical aspects and highlighted the cautious application of PAH specific therapy strategy. Results The arterial blood gas analysis revealed severe hypoxemia (pH 7.47, PaCO2 30mm Hg, PaO2 53 mmHg and SO2 89% in room air). The pulmonary function testing identified no restrictive ventilatory defects (FEV1/FVC was 79.55%, VC 61.9% of predicted value) but a marked reduction in CO diffusion (DLCO was 35.8% of predicted value). The plasma level of N-terminal pro-brain natriuretic peptide (NT-proBNP) was 3180 pg/mL. The transthoracic echocardiography showed an enlarged right ventricle and atrium, moderate tricuspid regurgitation, bilateral pulmonary artery dilated and a small pericardial effusion. High-resolution computed tomography (HRCT) scan of the chest revealed interstitial oedema, enlarged lymph nodes in the mediastinum, few inflammation lesions on the superior lobe of left lung and the both main bronchi were compressed by the dilated pulmonary artery. CT pulmonary angiography showed dilated pulmonary arteries without embolism. The right heart catherization revealed mean pulmonary artery pressure as 57 mm Hg, and mean pulmonary capillary wedge pressure 14 mm Hg, showed as the pre-capillary pulmonary hypertension. The bronchoalveolar lavage confirmed occult alveolar haemorrhage by detecting hemosiderin-laden macrophages. Considering the risk of pulmonary oedema, the patient declined the specific PAH therapy. After treatment with warfarin (kept INR 2.0–3.0), diuretics, digtoxin and oxygen therapy, his symptoms improved in 3 months follow-up while ultimately died of right heart failure 18 months later. Conclusions This case justifies that PVOD should be taken into consideration when a PAH patient demonstrate remarkably low diffusing capacity of the lung for carbon monoxide (DLCO). The lung biopsy is the gold diagnostic standard, but usually not feasible. High-resolution CT scan and bronchoalveolar lavage are valuable for non-invasive approaches of PVOD which reveal the interstitial edema of the lungs and occult alveolar hemorrhage respectively in the patients with diagnosis of PAH and low diffusing capacity of the lung. Lung transplantation remains a feasible option of treatment. The specific therapies for PAH ...
for 28 days, then the systolic, diastolic, mean pulmonary artery pressure (PASP, PADP, mPAP) and right ventricle hypertrophy index (RVHI) were measured; the pathological changes of small pulmonary arteries were observed, the thickness index (TI) and area index (AI) of the small pulmonary arteries in three groups were evaluated with microscopy for morphological analysis; echocardiography measuring the internal diameters of the pulmonary trunk assessed pulmonary hypertension in three groups. Results: ①The PAP(PASP, PADP, mPAP) and RVHI in air embolism group were all significantly higher than these in control group, respectively (P<0.05), and these in nicorandil treated group were significantly lower than these in air embolism group, respectively (20.47AE3.91 mmHg VS 32.37AE3.00 mmHg, 9.35AE1.48 mmHg VS 13.49AE1.62 mmHg, 13.74AE1.86 mmHg VS 21.93AE1.10 mmHg and 0.31AE0.03 VS 0.47AE0.13 P<0.05). ②The thickness of wall increased and the cavity became narrow in the small pulmonary arteries of air embolic group, and these were significantly ameliorated in the small pulmonary arteries of nicorandil treated group. The TI and AI in the small pulmonary arteries of air embolic group were significantly higher than these in control group, respectively (P<0.05), and these in the small pulmonary arteries of nicorandil treated group were significantly lower than these in air embolic group, respectively (0.38AE0.12 VS 0.75AE0.13, 0.60AE0.16 VS 0.93AE0.09 P<0.05). ③The internal diameters of the pulmonary trunk was higher in air embolic group than that in control group(P<0.05); That was redused in nicorandil treated group(0.78AE0.06cm VS 0.93AE0.14cm, P<0.05). Conclusions: Nicorandil can significantly attenuate the chronic air embolism-induced pulmonary hypertension, improve pulmonary vascular remodeling of the small pulmonary artery and right ventricular hypertrophy and reduse the internal diameters of the pulmonary trunk.Objectives: Studies have demonstrated that rennin angiotension system is involved in the pathogenesis and development of pulmonary arterial hypertension (PAH). However, it is controversial whether angiotensin II type I receptor blockers attenuate PAH.
Objectives The aim of this study is to summarise the clinical features of PPH of the elderly patients with portal hypertension.Methods 15 patients with PPH including nine males and six females were includes in the study. Clinical features about Symptoms, physical examination findings and laboratory test results were evaluated. Results Dyspnoea was seen in 15 patients (100%), accentuated P2 in 10 patients (66.7%), systolic murmur of tricuspid area in 12 patients (80%), PaO 2 <70 mm Hg in 15 patients (100%), with an average of (58.6±9.3) mm Hg. X-ray showed prominent pulmonary artery segment in 11 patients (73%), ECG with leads V1 R/S>1 in 9 patients (60%), echocardiography showed tricuspid regurgitation in 15 patients (100%), increase in right ventricular diameter of 10 patients (66.7%), right ventricular anterior wall thickening in 6 patients (40%). Child-Pugh Classification A of five cases, with an average of (64.4±8.1) mm Hg in PaO 2 and (53.6±8.4) mm Hg in pulmonary arterial systolic pressure. Child-Pugh Classification B of three cases, with an average of (60.7±8.4) mm Hg in PaO 2 and (68.3±12.6) mm Hg in pulmonary arterial systolic pressure. ChildPugh Classification C of seven cases, with an average of (53.6±8.6) mm Hg in PaO 2 and (75.7±16.4) mm Hg in pulmonary arterial systolic pressure. Conclusions Dyspnoea is an important clinical manifestation in PPH patients. Accentuated pulmonary second heart sound is the common features of pulmonary hypertension. X-ray, electrocardiogram could also show the increase of pulmonary arterial pressure. Our results suggest that the severity of PPH increases with lower blood oxygen pressure, as the liver function (Child Pugh classification higher) gets worse in elderly patients with portal hypertension.Heart 2012;98(Suppl 2): E1-E319
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