Chiung-Yuan Hsu

Tracheal rapid ultrasound exam (T.R.U.E.) for confirming endotracheal tube placement during emergency intubation

OBJECTIVES This study aimed to assess the diagnostic accuracy and timeliness of using tracheal ultrasound to examine endotracheal tube placement during emergency intubation. METHODS This was a prospective, observational study, conducted at the emergency department of a national university teaching hospital. Patients received emergency intubation because of impending respiratory failure, cardiac arrest, or severe trauma. The tracheal rapid ultrasound exam (T.R.U.E.) was performed during emergency intubation with the transducer placed transversely at the trachea over the suprasternal notch. Quantitative waveform capnography was used as the criterion standard for confirmation of tracheal intubation. The main outcome was the concordance between the T.R.U.E. and the capnography. RESULTS A total of 112 patients were included in the analysis, and 17 (15.2%) had esophageal intubations. The overall accuracy of the T.R.U.E. was 98.2% (95% confidence interval [CI]: 93.7-99.5%). The kappa (κ) value was 0.93 (95% CI: 0.84-1.00), indicating a high degree of agreement between the T.R.U.E. and capnography. The sensitivity, specificity, positive predictive value, and negative predictive value of the T.R.U.E. were 98.9% (95% CI: 94.3-99.8%), 94.1% (95% CI: 73.0-99.0%), 98.9% (95% CI: 94.3-99.8%) and 94.1% (95% CI: 73.0-99.0%). The median operating time of the T.R.U.E. was 9.0s (interquartile range [IQR]: 6.0, 14.0). CONCLUSIONS The application of the T.R.U.E. to examine endotracheal tube placement during emergency intubation is feasible, and can be rapidly performed.

Effect of different resuscitation fluids on cytokine response in a rat model of hemorrhagic shock

This study was designed to determine the effects of different resuscitation fluids on the production of proinflammatory and anti-inflammatory cytokines in an animal model of hemorrhagic shock. Wistar male rats (n = 24; 8/group) were subjected to a volume-controlled hemorrhagic shock for 30 minutes and resuscitated as follows: (1) sham group without resuscitation, (2) lactated Ringer solution (LR), 3:1; (3) 4% hydroxyethyl starch (HES) solution, 1:1; and (4) 4% modified fluid gelatin (GEL), 1:1. Hemodynamic parameters were recorded, and blood samples were collected at 0 min and 30, 90, 150, 210, 270, and 330 min after hemorrhage for plasma levels of IL-6, IL-10, and TNFα. The circulating concentrations of IL-6 at 90, 150, 210, 270, and 330 min and TNFα levels at 150, 210, and 270 min after hemorrhage were significantly elevated in animals resuscitated with GEL compared with HES or LR (P < 0.05). At 210, 270, and 330 min, IL-10 concentration was decreased significantly in GEL-resuscitated rats compared with rats resuscitated with LR or HES (P < 0.05). Mean blood pressure and serum levels of lactate after resuscitation were not different among three kinds of fluids. LR, HES, and GEL are comparable in volume efficacy for resuscitation of hemorrhagic shock but are associated with different postresuscitation immune responses. Resuscitation with GEL may be associated with cytokine production favoring a proinflammatory response. The marked elevation of IL-6 observed in the GEL-treated animals may play a role in the relatively high frequency of anaphylactoid reaction in clinical use of GEL.

Cardioprotective effect of therapeutic hypothermia for postresuscitation myocardial dysfunction.

Mild-to-moderate therapeutic hypothermia after resuscitation from cardiac arrest is neuroprotective, but its effect on postresuscitation myocardial dysfunction is not clear. We hypothesized that therapeutic hypothermia is cardioprotective in postresuscitation. Male adult Wistar rats underwent asphyxia-induced cardiac arrest and manual resuscitation with epinephrine. Therapeutic hypothermia is induced immediately after successful resuscitation and the return of spontaneous circulation (ROSC). One hour after ROSC, the rats achieved a target temperature of 30°C to 31°C, which was maintained for 1.5 h and then transitioned to the passive rewarming process in the hypothermia group. A temperature between 36.5°C and 37.5°C was maintained in the normothermia group. Echocardiography revealed that hypothermia resulted in significantly better systolic function of fractional shortening in 60 and 120 min after ROSC (both P < 0.05). The benefit of cardioprotection was also confirmed by the general linear mixed-models analysis of dP/dt, which revealed significantly better systolic function in positive dP/dtR(40) and diastolic function in maximal negative dP/dt (both P < 0.001). The 4-h and 3-day survival analyses both revealed better outcomes in the hypothermia groups in the log-rank test (P < 0.001 for the 4-h analysis, and P < 0.05 for the 3-day analysis). Serum level of heart-type, fatty acid-binding protein at 4 h after resuscitation as the myocardium damage marker was also significantly lower in the hypothermia group (52.4 ng/mL vs 186.5 ng/mL in the normothermia group; P < 0.05). Western blotting of myocardium showed that myocardial Akt and ERK1/2 were more activated in the hypothermia group 2 h after spontaneous circulation returned. In conclusion, postresuscitation mild-to-moderate therapeutic hypothermic is cardioprotective in the asphyxia-induced cardiac arrest animal model. It stabilizes hemodynamics, improves short-term survival, and decreases myocardial damage. The cardioprotective effect is associated with Akt and ERK1/2 activation in signal transduction.

Ultrasonographic lung sliding sign in confirming proper endotracheal intubation during emergency intubation.

AIM OF STUDY Unrecognized one-lung intubations (also known as main-stem intubation) can lead to hypoventilation, atelectasis, barotrauma, and even patient death. Many traditional methods can be employed to detect one-lung intubation; however, each of these methods has limitations and is not consistently reliable in emergency settings. This study aimed to assess the accuracy and timeliness of ultrasound to confirm proper endotracheal intubation. METHODS This was a prospective, single-center, observational study conducted at the emergency department of a national university teaching hospital. Patients received emergency tracheal intubation because of respiratory failure or cardiac arrest. After intubation, bedside ultrasound was performed with a transducer placed on the chest bilaterally at the mid-axillary line, to identify lung sliding over the lungs bilaterally during ventilation. Chest radiography was used as the criterion standard for confirmation of endotracheal tube position. RESULTS One hundred and fifteen patients needing tracheal intubation were included, and nine (7.8%) had one-lung intubations. The overall accuracy of ultrasound to confirm proper endotracheal intubation was 88.7% (95% confidence interval (CI): 81.6-93.3%). The positive predictive value was 94.7% (95% CI: 87.1-97.9%) in the non-cardiac-arrest group and 100% (95% CI: 87.1-100.0%) in the cardiac-arrest group. The median operating time of ultrasound was 88 s (interquartile range [IQR]: 55.0, 193.0), and of chest radiography was 1349 s (IQR: 879.0, 2221.0) post intubation. CONCLUSIONS In this study, the positive predictive value of bilateral lung sliding in confirming proper endotracheal intubation was high, especially among patients with cardiac arrest. Considerable time advantage of ultrasound over chest radiography was demonstrated.

Predictive model of diagnosing probable cases of severe acute respiratory syndrome in febrile patients with exposure risk

Abstract Study objective Since the World Health Organization issued a global alert about severe acute respiratory syndrome (SARS) on March 12, 2003, the illness has become a major public health challenge worldwide. The objective of this study is to identify the clinical risk factors of SARS and to develop a scoring system for early diagnosis. Methods The detailed clinical data of all patients presenting to the emergency department (ED) with a temperature higher than 38.0°C (100.3°F), documented at home or at the ED, and risks of exposure to SARS within 14 days were assessed. The diagnosis of probable SARS was made according to the definition of the Centers for Disease Control and Prevention. Items with significant differences among symptoms, signs, and laboratory tests on presentation between SARS and non-SARS groups were determined and used to develop the scoring system. Results Seventy patients were enrolled and 8 were diagnosed as probably having SARS. None of the initially discharged patients or their relatives developed SARS. Compared with the non-SARS group, the SARS group was younger (33.9±15.9 years versus 44±9.8 years; P=.02), had a higher percentage of fever prolonged more than 5 days (87.5% versus 6.5%; P<.01), myalgia (75% versus 27.4%; P=.01), and diarrhea (50% versus 9.7%; P=.02); had less occurrence of cough before or during fever (0% versus 64.5%; P=.01); and had lower absolute lymphocyte (0.9±0.3×109/L versus 1.5±1.1×109/L; P<.01) and platelet counts (144.1±36.3×109/L versus 211.6±78.8×109/L; P=.02). A 4-item symptom score based on the presence of cough before or concomitant with fever, myalgia, diarrhea, and rhinorrhea or sore throat detects SARS with 100% sensitivity and 75.9% specificity; a 6-item clinical score based on lymphopenia (<1.0×109/L), thrombocytopenia (<150×109/L) and the 4 symptom items detects SARS with 100% sensitivity and 86.3% specificity. Conclusion Certain symptoms and laboratory tests indicate higher risk of febrile probable SARS. In nonendemic areas, the febrile patients with recent contact with SARS or travel history to endemic areas could be screened for the probability of SARS by the use of clinical and symptom scores.

Erythropoietin improves the postresuscitation myocardial dysfunction and survival in the asphyxia-induced cardiac arrest model.

To investigate the effect of erythropoietin for the management of postresuscitation myocardial dysfunction following asphyxia-induced cardiac arrest. Male adult Wistar rats were used for the prospective controlled animal study. Asphyxia-induced cardiac arrest was performed by turning-off the ventilator and clamping the endotracheal tube. Cardiopulmonary resuscitation with an intravenous injection of 0.01 mg/kg epinephrine and mechanical ventilation were started after 6.5 minutes of asphyxia. The resuscitated animals received either erythropoietin (5000 U/kg) or equivalent volume of 0.9% saline as placebo intravenously 3 minutes after return of spontaneous circulation. The erythropoietin treatment produced better left ventricular dP/dt40 and −dP/dt in the invasive hemodynamic measurements, and left ventricular fraction shortening by echocardiography. Administration of erythropoietin also improved three days survival among those successfully resuscitated. The molecular effects of erythropoietin were shown by activation of its down streaming Akt and ERK 42/44 signaling pathways. EPO has the potential to improve postresuscitation myocardial dysfunction and short term survival in rats after asphyxia-induced cardiac arrest.

Circulating cell-free DNA levels correlate with postresuscitation survival rates in out-of-hospital cardiac arrest patients ☆ ☆☆

Early prediction of prognosis is helpful in cardiac arrest patients. Plasma cell-free DNA, which increases rapidly after cell death, is a novel biomarker for the prognosis of critical ill patients. Changes in the plasma cell-free DNA level and its role for the early prognosis of cardiac arrest patients remain unclear. We prospectively enrolled adult out-of-hospital cardiac arrest (OHCA) patients with sustained return of spontaneous circulation. The resuscitation variables were recorded following the Utstein recommendation. The plasma cell-free DNA concentration was determined by quantitative real-time polymerase chain reaction assay of β-globin gene. A total of 42 patients were enrolled for the study. The plasma cell-free DNA level within 2h after cardiac arrest was higher in the non-survival group than the survival-to-discharge group (median level 1659.9 g.e./mL vs. 1121.6g.e./mL, p=0.003 by non-parametric test). The plasma cell-free DNA level at 72 h became no difference between these two groups. The optimal cutoff value of plasma cell-free DNA for predicting survival-to-discharge was 1,170 g.e./mL by ROC curve analysis (area under curve 0.752, p=0.010). A plasma cell-free DNA level higher than 1,170 g.e./mL and was an independent predictor for in-hospital mortality by multiple logistic regression analysis (adjusted odds ratio of 12.35, p=0.023) and was also associated with higher 90 day mortality (p=0.021 by log-rank test). In conclusion, the plasma cell-free DNA level increases during the early post-cardiac arrest phase and can be an early prognostic factor for OHCA patients.

Acute cardiac dysfunction after short-term diesel exhaust particles exposure.

Epidemiological studies show an association between particulate matter exposure and acute heart failure. However, underlying mechanisms remain unclear. In this study, we investigated acute cardiac hemodynamic effects and related mechanisms after 1 day exposure to diesel exhaust particles (DEPs). Male Sprague-Dawley rats were randomized and instilled with 250 microg (low dose) or 500 microg (high dose) of DEP or saline placebo intra-tracheally. The cardiac systolic function by dP/dt(40) and diastolic functions by maximal negative dP/dt were both worse in DEP low dose and DEP high dose groups than the control group, respectively. In the heart rate variability analysis, SDNN in DEP low dose and DEP high dose groups were both lower than the control group. The low frequency heart rate variability was higher in the DEP groups compared to the control group. The cardiac IL-1beta expression and circulating cardiac troponin I level were higher in the DEP group than the control group. Plasma IL-1beta and IL-6 protein were significantly higher in the DEP groups than the control group. In conclusion, DEP exposure causes acute cardiac systolic and diastolic dysfunction. The changes may be related to decreased heart rate variability, increased cardiac inflammatory reaction and myocardial damage.

Antiapoptotic Cardioprotective Effect of Hypothermia Treatment Against Oxidative Stress Injuries

OBJECTIVES The effect of hypothermia on cardiomyocyte injury induced by oxidative stress remains unclear. The authors investigated the effects of hypothermia on apoptosis and mitochondrial dysfunction in cardiomyocytes exposed to oxidative stress. METHODS Cardiomyocytes (H9c2) derived from embryonic rat heart cell culture were exposed to either normothermic (37 degrees C) or hypothermic (31 degrees C) environments before undergoing oxidative stress via treatment with hydrogen peroxide (H(2)O(2)). The degree of apoptosis was determined by annexin V and terminal deoxynucleotidyl transferase (TUNEL) staining. The amount of reactive oxygen species (ROS) was compared after H(2)O(2) exposure between normo- and hypothermic-pretreated groups. Mitochondrial dysfunction in both groups was measured by differential reductase activity and transmembrane potential (DeltaPsim). RESULTS Hydrogen peroxide induced significant apoptosis in both normothermic and hypothermic cardiomyocytes. Hypothermia ameliorated apoptosis as demonstrated by decreased annexin V staining (33 +/- 1% vs. 49 +/- 4%; p < 0.05) and TUNEL staining (27 +/- 17% vs. 80 +/-25%; p < 0.01). The amount of intracellular ROS increased after H(2)O(2) treatment and was higher in the hypothermic group than that in the normothermic group (237.9 +/- 31.0% vs. 146.6 +/- 20.6%; p < 0.05). In the hypothermic group, compared with the normothermic group, after H(2)O(2) treatment mitochondrial reductase activity was greater (72.0 +/- 17.9% vs. 27.0 +/- 13.3%; p < 0.01) and the mitochondria DeltaPsim was higher (101.0 +/- 22.6% vs. 69.7 +/- 12.9%; p < 0.05). Pretreatment of cardiomyocytes with the antioxidant ascorbic acid diminished the hypothermia-induced increase in intracellular ROS and prevented the beneficial effects of hypothermia on apoptosis and mitochondrial function. CONCLUSIONS Hypothermia at 31 degrees C can protect cardiomyocytes against oxidative stress-induced injury by decreasing apoptosis and mitochondrial dysfunction through intracellular ROS-dependent pathways.

Post-cardiac arrest myocardial dysfunction is improved with cyclosporine treatment at onset of resuscitation but not in the reperfusion phase

AIM OF STUDY Significant myocardial dysfunction and high mortality occur after whole-body ischaemia-eperfusion injuries in the post-cardiac arrest status. The inhibition of mitochondrial permeability transition pore (mPTP) opening during ischaemia-reperfusion can ameliorate injuries in the specific organs. We investigated the effect and therapeutic window of pharmacological inhibition of mPTP opening in cardiac arrest. METHODS Forty male Wistar rats were resuscitated after cardiac arrest induced by 8.5 min of asphyxia. Cyclosporine (10 mg/kg) was administered intravenously at onset of resuscitation in protocol 1 study and administered 3 min after ROSC in protocol 2 with placebo control in both. RESULTS Left ventricular systolic (dP/dt 40), diastolic (maximal negative dP/dt) functions and cardiac output were improved in the group with cyclosporine treatment at onset of resuscitation compared to control group (p < 0.01, respectively). Seventy-two hour survival was better in the group with cyclosporine treatment at onset of resuscitation compared to control (p = 0.046). Left ventricular systolic and diastolic function, cardiac output and 72 h survival were not improved in the group with cyclosporine treatment 3 min after ROSC. The severity of mitochondrial damage under electronic microscopy, mPTP opening, mitochondrial respiratory control ratio and ADP:O ratio were ameliorated in the group with cyclosporine treatment at onset of resuscitation (p< 0.05, respectively) but not in the group with cyclosporine treatment at 3 min after ROSC. CONCLUSIONS Post-cardiac arrest myocardial dysfunction and survival can be improved by cyclosporine treatment at onset of resuscitation, but not by the cyclosporine treatment at 3 min after ROSC.