[The characteristics of biofilm formation in endotracheal tubes in ventilated patients].

OBJECTIVE: To evaluate the etiology and drug resistance of biofilms in endotracheal tubes in respiratory intensive care unit (RICU). METHODS: A prospective cohort study was conducted. The biofilms were observed by scanning electron microscopy at different times of ventilation. The pathogens were identified and their resistance to antibiotics were analyzed. RESULTS: Twenty one VAP cases were identified in 39 mechanically ventilated patients (53.85%). Patchy biofilms were observed 2 d to 7 d after the initiation of ventilation. After 7 d to 10 d, 87.5% of the endotracheal tubes were covered by biofilms. Biofilms were identified in all the tubes longer than 10 d. CONCLUSIONS: The incidence of VAP increased with prolonged mechanical ventilation. Meanwhile the antibiotic resistance rate increased and more pathogens isolated were consistent with those in the biofilms.

[The change and significance of the cardiopulmonary exercise test parameters in patients with obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To investigate the change of exercise cardiopulmonary function in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). METHODS: Thirty OSAHS patients and 18 normal healthy adults (control group) were studied by cardiopulmonary exercise test (CPET). The results including maximal oxygen uptake percent predicted (Vo(2)max% predicted), oxygen uptake to work rate (Vo(2)/WR), oxygen pulse percent predicted (Vo(2)/HRmax% predicted), anaerobic threshold to maximal oxygen uptake (AT/Vo(2)max), breathing reserve (V(E)max/MVV) and ventilatory equivalents for carbon dioxide (V(E)/V(CO2)) were compared between two groups. RESULTS: The levels of Vo(2)max% predicted, AT/Vo(2)max, Vo(2)/HRmax% predicted, Vo(2)/WR, and V(E)max/MVV in the OSAHS group [(83 +/- 5)%, (44 +/- 6)%, (79 +/- 5)%, (9.3 +/- 0.6) ml.min(-1).W(-1), (73 +/- 8)%] were lower than those in the control group [(88 +/- 5)%, (49 +/- 6)%, (83 +/- 4)%, (10.9 +/- 2.3) ml.min(-1).W(-1), (79 +/- 9)%, all P < 0.05]. The levels of V(E)/V(CO2) in the OSAHS group (29 +/- 3) was higher than the control group (26 +/- 3, P < 0.05). In the OSAHS group Vo(2)max% predicted, Vo(2)/HRmax% predicted, Vo(2)/WR AT/Vo(2)max and V(E)max/MVV correlated negatively with apnea-hypopnea index (AHI, r = -0.52, -0.62, -0.59, -0.37, -0.66, P < 0.05). Vo(2)max% predicted, Vo(2)/HRmax% predicted, Vo(2)/WR, AT/Vo(2)max and V(E)max/MVV correlated with lowest oxygen saturation (LSaO(2), r = 0.60, 0.63, 0.64, 0.40, 0.59, P < 0.05). V(E)/V(CO2) correlated with AHI (r = 0.57, P < 0.01) and correlated negatively with LSaO(2) (r = -0.62, P < 0.01). CONCLUSIONS: The cardiac output of patients with OSAHS can not meet the demand of hard exercise. At the same time, there is more significant ventilation-perfusion disturbance in OSAHS patients than normal subjects. The patients' exercise cardiopulmonary function has been compromised although there are no symptoms.

[Study on hemodynamic changes and cardiac troponin I level in pig model of acute experimental pulmonary embolism].

OBJECTIVE: To evaluate the hemodynamic effects and cardiac troponin I (cTn I), creatine kinase-MB (CK-MB), myoglobin (Mb) releasing kinetics of acute experimental pulmonary embolism of pigs. METHODS: Sixteen juvenile pigs, of either gender and weighing 30 to 40 kg were studied, 8 in the embolism group and 8 in the control group. The 8 embolism animals received 0.1 g/kg polystyrene beads (diameter range 0.65 to 0.67 mm) suspended in 0.9% saline by venous injection. Pulmonary arterial pressure (PAP), systemic arterial pressure (SAP), pulmonary capillary wedged pressure (PCWP), cardiac output (CO), blood gases and serum cTn I, CK-MB, and Mb were measured before and immediately, 30 min, 1 hour, 2 hour, and 3 hour after acute pulmonary embolism. RESULTS: PAP was increased to 2 - 3 fold of the baseline and the control level immediately, and then decreased to the baseline level in 2 to 3 hours. Serum cTn I and Mb increased significantly after embolism and remained at a higher level through the 3 hour experimental procedure. The CK-MB was not changed after acute pulmonary embolism. CONCLUSIONS: Acute pulmonary embolism caused lung gas exchange abnormality and acute pulmonary hypertension. The hemodynamic effects of acute pulmonary embolism include injury to the myocardial cells and releasing of cTn I and Mb to blood stream. cTn I can be detected in the early phase of acute pulmonary embolism, and maybe a useful marker in diagnosis and management of acute pulmonary embolism.