2017年 · 第40卷第02期

The monkey bids farewell to the old year, the rooster announces the new year, the festive sound of firecrackers in the Spring Festival seems to be still noisy in the ears, and the glutinous and soft glutinous rice balls in the Lantern Festival are still vaguely fragrant in the mouth. On the occasion of the Spring Festival, I would like to wish all the readers, authors and editors who have cared, supported and helped us for many years a good old age, and wish you all good health, smooth work and all the best in the new year!

The main cause of acute exacerbation of chronic obstructive pulmonary disease (COPD) is respiratory tract infection. Other non-infectious factors include air pollution, allergens, heart failure, pulmonary embolism, hypertension, diabetes and dyslipidemia^[1,2]。 The incidence and correlation of metabolic syndrome (Mets) in patients with COPD need further investigation^[3]。 Systemic inflammatory response is a common pathophysiological mechanism of COPD and Mets^[4,5]。 This study aimed to explore the relationship between Mets and COPD exacerbation and its possible mechanisms.

A 49-year-old male was admitted to the hospital on December 3, 2014 due to "cough, shortness of breath, cough of white mucous sputum, 30-40 ml daily". He was diagnosed with mucinous adenocarcinoma of both lungs by PET-CT and bronchoscopic lung tissue biopsy, and the TNM stage belonged to T4N2M0 (Figure 1)。 Five courses of chemotherapy (TP regimen: paclitaxel + cisplatin) were started on 11 December 2014. After the first 4 courses, the patient's symptoms improved, sputum was reduced, shortness of breath was reduced, and the lesions were reduced. After the fifth course of treatment, the patient's sputum volume increased, 80~120 ml/d, and shortness of breath worsened. Re-examination of chest CT showed the progression of the lesion. Switched to icotinib hydrochloride 125 mg orally, 3 times/d, starting on 31 Mar 2015. Within 6 months after taking the medicine, the patient's expectoration decreased, shortness of breath decreased, and the lesion decreased. From the 7th month, cough and sputum were aggravated, and a large amount of watery mucous foam sputum was coughed (Figure 2), which can reach 2 L/d when the dose is high, with fever for 1 week, and was readmitted on 10 October 2015. Admission physical examination: pulse 114 beats/min, breathing 32 beats/min, blood pressure 103/64 mmHg (1 mmHg =0.133 kPa), SPO₂86% (oxygen inhalation concentration 5 L/min). Cyanosis of the skin and lips, coarse breathing sounds in both lungs, and wet rales can be heard in both lower lungs. Imaging suggested lesion progression (Figure 3，Figure 4)。 Blood gas analysis: pH 7.448, carbon dioxide partial pressure 35.3 mmHg, oxygen partial pressure 43.7 mmHg. Serum potassium was 4.4 mmol/L, serum sodium was 102.4 mmol/L, and serum chlorine was 66.3 mmol/L. Non-invasive ventilation was given after admission [S/T mode with positive inspiratory phase pressure (IPAP) of 19 cmH₂O (1 cmH₂O =0.098 kPa) and positive end-expiratory pressure (EPAP) of 7 cmH₂O, inhaled oxygen concentration is 80%], corrected electrolyte, anti-infection and other treatments, the patient's symptoms did not improve significantly, oxygenation index<100 mmHg, still coughing a large amount of white watery mucous foamy sputum, with a sputum volume of about 1 500 to 2 000 ml/d. On the second day of admission, the patient sat upright and breathed, and watery sputum continuously gushed out of the mouth and nasal cavity, with a volume of watery sputum reaching 100 ml/min. The patient could not cooperate with non-invasive ventilator ventilation due to persistent cough and expectoration, and there was a possibility of asphyxia due to sputum at any time. Given aerosolized inhalation furosemide 40 mg, the cough was relieved, the amount of phlegm was significantly reduced, and the dyspnea was relieved on the day of aerosolization, which can be combined with non-invasive ventilation. Followed by aerosol inhalation of furosemide 40 mg once/d daily and active anti-infective treatment, the patient's sputum volume gradually decreased, and the sputum volume was less than 100 ml/24 h on the 12th day of hospitalization (Figure 5), normal body temperature, gradual relief of dyspnea, oxygenation index>250 mmHg, cough of a small amount of white phlegm, discharged on foot on the 18th day of hospitalization.

In 1918, Dr. Cheyne wrote a review of medical records that detailed a 60-year-old obese patient suffering from stroke and severe arrhythmias who developed an abnormal breathing pattern at the end of his life with intermittent respiratory arrest. This periodic abnormal breathing pattern was described again by Stokes in a monograph on cardiovascular diseases published in 1854. In honor of the contributions of these two scholars, this abnormal breathing pattern was named Cheyne-Stokes breathing, or CSR for short^[1]。 Since then, various textbooks, including diagnostics, respiratory diseases, cardiovascular and neurology textbooks have been using this name. Until recent years, it has been found that many CSRs occur during sleep, so this CSR occurring during sleep is called CSA. Because the relationship between the two is not fully understood, it is often collectively referred to as CSR-CSA^[1]。 Later, it was found that CSR often occurs in the first and second stages of NREM sleep, and some patients can also occur when they are awake.

adaptive servo-ventilation (ASV), which began in 2001, has a history of more than ten years from its invention to its widespread application. It is the main innovative noninvasive ventilation mode for the treatment of congestive heart failure complicated with CSR^[1]。 ASV is a kind of ventilation mode evolved from bileve positive airway pressure (BiPAP), which not only provides variable inspiratory pressure support (IPS), but also has automatic recognition and adjustment of frequency standby function. Clinically, two different algorithms are mainly used in the ASV mode^[2]One is aimed at achieving minute ventilation volume, and the other is aimed at achieving peak inspiratory flow rate. Despite the differences in parameter settings between these two types of ASV, the purpose of this type of ventilation mode design is mainly for the treatment of congestive heart failure with central sleep apnea or Chen-Shi respiration (CSA-CSB/CSR).

Tidal breathing is an independent risk factor for cardiac death and rehospitalization in patients with heart failure. The specific pathogenesis of heart failure complicated with tidal breathing is not fully understood at present. Chemoreceptors have an important effect on CO₂Increased sensitivity and prolonged circulation time caused by heart failure together lead to impaired feedback loop of respiratory regulatory circuit, which plays an important role in its pathogenesis. In CSR patients, breathing is unstable, and pulmonary congestion leads to excitation of vagus nerve receptors in the lungs and increased sensitivity of central and peripheral chemoreceptors. At the same time, slight hyperventilation caused by changes in apnea threshold and arousal of patients can cause PaCO₂Drop below the apnea threshold^[1]。 PaCO₂When lowered, the body responds to a large change in ventilation, but because of circulation delay, PaCO₂The changes of PaCO cannot be fed back to the hub in time, causing PaCO₂Being overcorrected, dropping below the apnea threshold results in central apnea. Apnea cannot be corrected in time after appearance, to PaCO₂It is perceived only after it is significantly elevated, causing deepening and accelerating respiration to correct PaCO₂So that it is over-corrected again below the apnea threshold, and so on, resulting in repeated CSR^[2]。

High altitude pulmonary edema (HAPE) is a life-threatening non-cardiogenic pulmonary edema, which usually occurs in plain people who reach an altitude of 2 500 to 3 000 m rapidly. Its susceptibility factors mainly include excessive climbing speed, High altitude reached, overwork, cold and upper respiratory tract infection. It was reported that the incidence of only 0.2% was reported in those who climbed 4 d to reach 4 500 m altitude, whereas the incidence reached 15% in those who reached 5 500 m altitude within 2 d, being the most common cause of death in altitude sickness^[1]。 At present, it is believed that the pathogenesis of HAPE mainly includes hypoxic pulmonary hypertension, changes in vascular permeability, decreased alveolar fluid clearance function, oxidative stress and inflammatory response. In addition, HAPE also shows ethnic specificity and individual differences, suggesting that it is influenced by genetic factors. In recent years, with the development of biotechnologies such as gene sequencing, gene knockout and high-throughput drug screening, the research focus of HAPE has gradually shifted from symptoms and signs to changes at the cellular and molecular level in vivo. Recent research on key molecules and related genes in the pathogenesis of HAPE is reviewed, in order to provide new ideas for screening HAPE susceptibility genes and find new targets for improving and treating HAPE.

Pulmonary hypertension is a pathophysiological state characterized by a progressive increase in pulmonary vascular resistance. It can be an independent disease or a complication of various pulmonary and cardiovascular diseases. Its pathogenesis includes pulmonary vascular endothelial dysfunction, pulmonary vasoconstriction dysfunction and continuous proliferation of pulmonary artery smooth muscle cells. The above comprehensive factors lead to continuous and irreversible increase of pulmonary artery pressure, resulting in symptoms and signs of pulmonary hypertension. Patients with pulmonary hypertension have poor long-term quality of life, high mortality and poor prognosis. Although many new drugs have been used in clinical practice in recent years, the 1-year survival rate of patients with pulmonary hypertension can reach 80% ~90%, but the 5-year survival rate is only 57%^[1]。 Therefore, it is still necessary to conduct in-depth research on the pathogenesis of pulmonary hypertension, find early diagnostic indicators and therapeutic targets with potential clinical application value, and provide a basis for early diagnosis and effective treatment of the disease, so as to reverse the disease process or delay the disease progression early, improve the quality of life of patients and improve the long-term survival rate.

Severe patients with invasive mechanical ventilation often experience a variety of adverse physical and psychological experiences^[1]The routine practice in the intensive care unit (ICU) is to take sedation measures for patients, which can not only relieve various discomfort of patients, but also ensure the smooth progress of mechanical ventilation and other treatments^[2]It can also play an organ protective role^[3]。 However, sedation therapy, while exerting its positive effects, also produces many adverse consequences, even the harm outweighs the good^[4]Therefore, how to choose the appropriate sedation strategy in ICU is always a difficult problem to be solved urgently. This article summarizes the research progress of mechanical ventilation sedation strategy in ICU as follows, aiming to help clinicians better understand and implement sedation treatment in ICU.

Most treatment effects of community-acquired pneumonia (CAP) occur around 3 days after treatment^[1]Therefore, the new edition of "Community Acquired Pneumonia Diagnosis and Treatment Guidelines"^[2]It is recommended in that the patient's condition and diagnosis be evaluated 3 days after the empirical initial treatment. Accurate and timely judgment of the treatment effect can help doctors actively adjust the treatment plan and reduce the fatality rate. The evaluation after initial treatment included the patient's clinical symptoms, such as body temperature, respiration, heart rate and blood pressure; Serological markers such as C-reactive protein, procalcitonin and D-dimer. Serum markers play an important role in evidence-based medicine because of their strong objectivity.

The patient was a 52-year-old female. He was admitted to hospital on August 20, 2015 for the main reason of "shortness of breath for 2 years after activity, dysphagia for half a year and aggravation for 1 month".

A 44-year-old male was admitted on 8 November 2013 due to "dyspnea after smoke inhalation for 20 d". On October 13, 2013, the patient continued to inhale black smoke (mainly unsaturated polyester, epoxy resin, styrene and toluene) for about 1 h due to spontaneous combustion in the oven, and then gradually developed chest tightness and dyspnea. On November 7, 2013, chest CT examination showed diffuse lesions in both lungs, considering aspiration pneumonia with lung injury (Figure 1)。 Past physical health, deny history of hypertension, diabetes, alcohol consumption, food and drug allergies. He has smoked for more than 20 years, with a smoking index of 400 years. He has been engaged in metal painting for nearly 30 years. In 2011, a similar oven spontaneous combustion accident occurred. Physical examination: body temperature 36.2 ℃, pulse rate 70 beats/min, respiratory rate 24 beats/min, blood pressure 130/81 mmHg (1 mmHg =0.133 kPa). The superficial lymph nodes were not palpable and swollen, breathing was slightly shortly, the breathing sounds of both lungs were clear, and no abnormalities were found in the heart and abdomen. Initial diagnosis: inhalation lung injury, lung infection.

High-flow nasal cannula (HFNC), as a new oxygen therapy mode, is a type of oxygen therapy mode that directly delivers high-flow gas mixed with air and oxygen to the patient through a nasal cannula without sealing. It consists of the following four parts: a flow sensor and a turbine system for keeping the flow at a set value, an active heating humidifier, a breathing tube with built-in heating line, and a nasal cannula connected to the patient end. Recently Frat et al.^[1]It was found that HFNC significantly improved 90-day survival in patients with acute hypoxemic respiratory failure (AHRF) compared with normal oxygen therapy and noninvasive positive pressure ventilation. At present, there have been no reports of HFNC in the treatment of adult AHRF patients in China. Our experience is summarized as follows.

Pulmonary ultrasound has developed rapidly and is currently used in ICU, emergency department and even respiratory ward, which can dynamically evaluate pulmonary edema, pneumothorax and pleural effusion. Pulmonary ultrasound has an auxiliary role in the diagnosis of pneumonia. At present, pulmonary ultrasound can replace chest X-ray or even CT to assist in the diagnosis of community acquired pneumonia (CAP)^[1,2,3]and ventilator associated pneumonia (VAP)^[4]。 The findings suggest that rapid, non-invasive and reproducible pulmonary ultrasound is expected to be one of the best options for pneumonia diagnosis. Because there are very few studies on pulmonary ultrasound in the diagnosis of VAP, this paper mainly introduces the value and application of pulmonary ultrasound with CAP as the object.

Multidrug-resistant bacterial infections, including Acinetobacter baumannii, in intensive care units (ICUs) have put tremendous pressure on the diagnosis and treatment of patients with ventilator-associated pneumonia (VAP). In order to avoid the unnecessary use of antibiotics, it is particularly important to identify the different states of infection and colonization in time in clinic. Current quantitative culture of bacteria in lower respiratory tract specimens relies on some invasive procedures. In order to find biomarkers of pathogenic origin, studies on the detection of volatile organic compounds (VOCs) in vivo and in vitro environments have been reported. In view of this, we designed this exploratory clinical pilot trial to predict that metabolites derived from Acinetobacter baumannii and their concentration values may be related to the presence of this bacterium and its different ecological microenvironments (infection and colonization status) in the lower respiratory tract of patients with invasive ventilation.