The artificial ventilation system is a multi-factor system with some high uncertain risks which should be under controlled by medical risk management of hospitals. The key suggestions for reducing the accidence caused by ventilator are recommented： 1 ） to clarify the risk factor of ventilators, 2 ） to set up management group of ventilators with a clinical engineer who is good at management and quality control of medical equipment on ventilators, 3 ） to develop ventilator clinical practice for safety use, 4 ） to explore the effective risk monitoring and early warning system and mechanism on ventilator application.
Objective To analyze the clinical and etiological characteristics and bacterial susceptibility in patients with ventilator-associated pneumonia (VAP) in Guangzhou area.Methods A retrospective study was conducted on VAP patients in four hospital of Guangzhou from Jan 2004 to Oct 2005.Totally 157 patients were enrolled in this study，whose flora was identified and tested by Kirby Bauer disk diffusion susceptibility test.The univariate analysis method was used to analyze the prognostic parameters.Results The average onset time of VAP was 7.7 days after mechanical ventilation with a mortality rate of 38.2%.The proportion of Gram-negative bacilli，Gram-positive cocci and eumycete was 68.0%，23.4% and 8.7% respectively in 184 isolated strains.The most common pathogens were Pseudomonas aeruginosa (18.5%)，Stenotrophomonas maltophilia (14.1％)，Burkholderia cepacia (10.9%)，Staphylococcus aureus (10.3%) and Acinetobacter baumannii (8.7%).Pseudomonas aeruginosa，Stenotrophomonas maltophilia，and Acinetobacter baumannii were resistant to most common antibacterials such as cephalosporin and imipenem.18 strains oxacillin resistant Staphylococcus aureus，7 strains oxacillin resistant Staphylococcus simulans and one vancomycin resistant Staphylococcus aureus were isolated.Expect for vancomycin，teicoplanin and fusidic acid，the resistance of Gram-positive cocci were above 50% to other 9 antibacterials.Conclusions The antibiotic resistance situation of VAP in Guangzhou is very serious with high mortality.It is important to reinforce the prevention and guidance on the proper treatment of VAP.
Objective To investigate the effects of mechanical ventilation( MV) via different tidal volume ( VT) in combination with positive end expiratory pressure( PEEP) on dogs with acute lung injury( ALI) . Methods Dog model of oleic acid-induced ALI was established. And after that animals were randomized into different MV groups ( included low VT group, VT =6 mL/kg; and high VT group, VT =20 mL/kg) and ventilated for 6 h with a PEEP of 10 cmH2O. Arterial blood gas wasmeasured before, during and after ALI model was established ( at 1 h,2 h, 4 h and 6 h during MV) . The albumin concentration in BALF and pathological change of the lung tissue were evaluated in order to determine the lung injury while animals were sacrificed after 6 h MV. Results ALI model was successfully established ( 2. 50 ±0. 80) hours after oleic acid injection. Arterial pH decreased much severer in the low VT group than the high VT group( P lt;0. 01) . PaO2 and SaO2 in ventilation groups decreased after modeling but increased after MV, and PaO2 and SaO2 were significantly higher in the low VT group than the high VT group after 6 h MV( P lt;0. 05) . PaCO2 fluctuated less in the high VT group, while it increased significantly in the low VT group after MV( P lt; 0. 01) . Oxygenation index( PaO2 /FiO2 ) was lowered after modeling( P lt; 0. 01) , decreased to about 190 mm Hg after 1 h MV. And PaO2 /FiO2 in low VT group was significantly higher than the high VT group after 6 h MV( P lt; 0. 05) . BALF albumin concentration and the lung injury score in the low VT group were both significantly lower than the high VT group( both P lt; 0. 05) . Conclusions Ventilation with PEEP could improve the oxygenation of ALI dogs, and low VT ventilation improves the oxygenation better than high VT. Otherwise, low VT could induce hypercapnia and ameliorate lung injury caused by high VT MV.
Objective To evaluate the efficacy and safety of Levofloxacin combined with Cefoperazone/Sulbactam on the patients with ventilator-associated pneumonia ( VAP) . Methods The clinical effect of Levofloxacin combined with Cefoperazone/ Sulbactam on ventilator-associated pneumonia in 58 paitiens with VAP were retrospectively analyzed. Results 26 patients ( 44. 8% ) were cured, 18 patients( 31. 1% ) were marked improved, and 14 patients ( 24. 1% ) were ineffective. The total clinical efficacy rate was 75. 9% . 55 strains of bacteria were isolated, and Gram-negative bacilli were dominant pathogens( 78. 2% ) . The bacterial clearance rate was 78. 2% . The prevalence of adverse reaction was 5. 1% . Conclusion Levofloxacin combined with Cefoperazone/ Sulbactam is effective and safe for patients with VAP.
Objective To study the influencing factors for duration of mechanical ventilation in chronic obstructive pulmonary disease ( COPD) patients with type II respiratory failure. Methods Twenty-eight cases of mechanical ventilated COPD patients with type II respiratory failure were enrolled from March 2006 to March 2008 in Beijing Shunyi Hospital. They were divided into two groups based on their duration of ventilation: ≤7 d group as group I, and gt; 7 d as group II. Data of heart rate and blood pressure were recorded before the trachea intubation. Clinical data of blood routine, blood gas analysis and serum biochemistry were collected and analyzed. Previous history, smoking history and subsequent complications were also recorded. Results Heart rate in the group II were significantly higher than which in the group I[ ( 121. 50 ±17. 20) /min vs ( 103. 08 ±19. 97) /min, P lt;0. 05] . The incidences of upper gastrointestinal hemorrhage and blood pressure fall immediately after intubation were 63% and 88% respectively in the group II, which were significantly higher than the group I ( 0 and 25% ) . The levels of albumin, pre-albumin, Na+ , PaO2 were ( 29. 06 ±5. 00) g /L, ( 66. 36 ±17. 72) mg/L,( 138. 45 ±4. 74) mmol /L and ( 49. 06 ±20. 11) mm Hg respectively in the group II. While in the group I, those were ( 37. 11 ±2. 73) g /L, ( 127. 70 ±35. 84) mg/L, ( 143. 29 ±3. 42) mmol /L and ( 72. 25 ±38. 69) mm Hg respectively, which showed significant differences compared with the grouop II. The incidence of previous concomitant cerebral infarction showed significant difference between the group I and group II( 33. 33% vs 0) .Conclusion The levels of albumin, pre-albumin, heart rate before the intubation, upper gastrointestinal hemorrhage and blood pressure fall immediately after the intubation are associated with duration of mechanical ventilation and may indicate the prognosis in COPD patients with type II respiratory failure.
Objective To analyze the risk factors for ventilator-associated pneumonia( VAP) in adult patients undergoing cardiac surgery with cardiopulmonary bypass ( CPB) . Methods A total of 127 consecutive adult patients who received postoperative ventilation for more than 48 hours between January 2002 and June 2008 in the cardiac surgical intensive care unit( CSICU) were included in this study. The patients were assigned into a VAPgroup( n =64) and a control group( n = 63) . Pre-, intra-, and postoperative factors were collected and analyzed between two groups, and the multivariate analysis( logistic regression)were used to identify the risk factors of VAP. Results The overall incidence of VAP was 5.1%. The mortality of VAP was 28. 1% . Compared to the control group, the patients in the VAP group had longer duration of cardiopulmonary bypass time, ventilation time, more blood products usage and the duration of stay in CSICU( P lt; 0. 001) , higher morbidity of low cardiac output syndrome and tracheotomy( P lt; 0. 01) and higher rate of aortic surgery and mortality( P lt; 0. 05) . The preoperative left ventricular ejection fraction ( LVEF) and postoperative oxygenation index( PaO2 /FiO2 ) were lower in the VAP group than those of the control group( P lt; 0. 001) . Five variables were found to be significantly related to the development of VAP by multivariate analysis: CPB time gt; 120 min( OR = 6. 352, P = 0. 000) ; PaO2 /FiO2 lt; 300 mm Hg( OR =3. 642, P = 0. 017) , transfusion of blood products ≥1500 mL( OR = 5. 083, P = 0. 039) , ventilation time≥5 days( OR = 9. 074, P = 0. 047) and tracheotomy( OR = 19. 899, P = 0. 021) . A total of 102 pathogens were obtained by sputum culture in 64 VAP patients. There were 62( 60. 8% ) cases of gram negative bacilli, 19 cases( 18. 6% ) of gram positive cocci and 21( 20. 6% ) cases of eumycetes. Conclusion This study shows that the cardiopulmonary bypass time, ventilation time, hypoxemia, blood products transfusion and tracheotomy are risk factors most likely associated with VAP development.
Objective To observe the effects of mechanical stretch on cytokines release from alveolar macrophages( AMs) and the expression of macrophage inflammatory protein-2( MIP-2) induced by lipopolysaccharide( LPS) . Methods AMs were divided into the following groups: ①AMs were subjected to 20% elongation by Flexercell 4000T cell stress system for 24 hours and the supernatant was collected to detect the levels of TNF-α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, IFN-γ, macrophage inflammatory protein-1α( MIP-1α) , MIP-2, monocyte chemoattractant protein-1( MCP-1) , granulocyte /macrophage colony stimulating factors( GM-CSF) , interferon inducible protein-10( IP-10) , regulated on activation in normal T-cell expressed and secreted( Rantes) and keratinocyte chemoattractant( KC) , by using LiquiChip system. ② AMs were subjected to 5% , 10% , 15% and 20% elongation for 24 hours and the supernatant was collected to detect the levels of MIP-2. ③AMs were subjected to 20% elongation and MIP-2 in supernatant was detected 1, 3,6, 12, and 24 hours later. ④ AMs were subjected to 20% elongation and/ or LPS at a concentration of 10 ng/mL, and MIP-2 in supernatant was detected 24 hours later. Unstretched AMs were used as control in all kind of test. Results ①The levels of IL-1β, IL-6,MIP-2, MCP-1, IFN-γand IP-10 secreted by stretched AMs were 8. 7, 4. 3, 38. 6, 4. 8, 14. 2 and 5. 0 times those of the control group( all P lt; 0. 001) . ② The levels of MIP-2 secreted by AMs subjected to 10% , 15% and 20% elongation were ( 480. 5 ±93. 1) pg /mL,( 806. 3 ±225. 9) pg/mL and ( 1335. 7 ±18. 5) pg/mL respectively, all significantly higher than those oft he control group [ ( 34. 6 ±11. 4) pg/mL, all P lt;0. 001] . ③ Three hours after the stimulation of stretch the level of MIP-2 began to increase gradually. And 6, 12, and 24 hours after the stimulation the levels of MIP-2 secreted by the AMs were ( 819. 4 ±147. 5) pg/mL, ( 1287. 6 ±380 ±3 ) pg/mL and ( 1455. 9 ±436. 7) pg/mLrespectively, all significantly higher than those of the control group[ ( 33. 4 ±10. 2) pg/mL, all P lt; 0. 001] . ④When the AMs were stimulated individually by LPS( 10 ng /mL) or mechanical stretch ( 20% ) , the levels of MIP-2 increased to ( 1026. 3 ±339. 5 ) pg/mL and ( 1335. 7 ±318. 5 ) pg/mL respectively( both P lt; 0. 001) . When the AMs were costimulated by LPS and mechanical stretch, the level of MIP-2 increased to ( 2275. 3 ±492. 1) pg/mL, implicating a synergistic effect between mechanical stretch and LPS ( F = 121. 983, P lt; 0. 001) . Conclusions Mechanical stretch activates AMs to produce multiple inflammatory cytokines and induce AMs to secret MIP-2 in a strength- and time-dependent manner.Mechanical stretch also has synergistic effect with LPS in inducing MIP-2 release, which might play an important role in the development of ventilator-induced lung injury.
Objective To establish a rabbit model of ventilator-induced lung injury. Methods Fourty healthy New Zealand rabbits were randomly divided into 3 groups: ie. a routine 8 mL/kg tidal volume group( VT8 group) , 25 mL/kg large tidal volume group( VT25 group) , and 40 mL/kg large tidal volume group( VT40 group) . VT25 and VT40 group were further divided into 2 hours and 4 hours ventilation subgroups. Arterial blood gas, lung mechanical force and hemodynamic parameters were monitored. Lungtissue was sampled for evaluate lung wet/dry ratio and lung injury by HE stain. Bronchoalveolar lavage fluid ( BALF) was collected for measurement of protein concentration, total and differential cell counts. Results Compared with VT8 group, lung injury score in both VT40 and VT25 groups were elevated significantly, ofwhich 4 hour VT40 subgroup was the highest. Lung pathology examination of VT40 group revealed apparent alveolar deformation, interstitial and alveolar space exudation, inflammatory cells infiltration, pulmonary consolidation and alveolar hemorrhage. Lung pathology examination of VT25 group showed pulmonary intervalthickening, inflammatory cells infiltration, while alveolar intravasation was mild. Blood gas analysis showed that PaO2 /FiO2 was deteriorated with time in VT25 and VT40 groups, and PaO2 /FiO2 at the 3 hours in VT40 group( lt; 300 mm Hg) had met the acute lung injury standard, while which in VVT25 group was above 300 mmHg. Lung wet/dry ratio, BALF protein concentration, total nucleated cell and neutrophilic leukocyte were elevated in both VT25 and VT40 groups, of which 4 hours VT40 group was the highest. Conclusion Using 4 hours ventilation at a tidal volume of 40 mL/kg can successfully establish the rabbit model of ventilator-induced lung injury.
为预防应激性溃疡和消化道出血, 质子泵抑制剂( PPI) 、组胺H2 受体拮抗剂( H2 RA) 以及硫糖铝在ICU中的应用非常普遍。既往的研究认为以PPI 或H2RA 为代表的抑酸剂( ASD) 可致胃液pH 值增高, 为细菌在胃腔内定植创造了条件, 并进而增加医院获得性肺炎( HAP) , 尤其是呼吸机相关性肺炎( VAP) 发生的风险。我们通过文献复习发现,ASD 与VAP 的关联性迄今仍无明确的证据, 已有的临床研究结论互为矛盾; 另一方面, 既往研究多集中于硫糖铝与H2RA 的比较, 有关PPI 和H2RA 导致VAP 的风险比较研究仍然缺乏, PPI 是否比H2 RA 更易发生VAP 也缺乏研究可资证明。为此我们将有关内容综述如下, 以供同道参考。
Objective To analyze the common causes of ventilator alarms during mechanical ventilation and their management. Methods A total of 104 ventilator alarms that were not instantly solved by first-line residents but referred to pulmonary therapist and attending physicians during September 2007 and August 2008 in the MICU of our hospital were analyzed retrospectively. Results Of all the 104 ventilator alarms, 27 ( 26%) were due to problems of ventilation circuits; 18 were due to patient effortagainst ventilator secondary to anxiety, horror or pain; 15 were due to inappropriate ventilator parameters;13 were due to airway problems; 5 were due to ventilator malfunction; 4 were due to worsening clinical status; 22 were due to other causes. Conclusion During mechanical ventilation, accurate assessment andprompt management of ventilator alarms are of great importance to patient safety and ventilation efficacy.