Department of Emergency and Disaster Medicine Hamamatsu University Hospital
1-20-1 Handa-yama, Higashi-ku, Hamamatsu, 431-3192, Japan
Tel: ++81-53-435-2759, Fax: ++81-53-435-2796
toshiaki[at]hama-med.ac.jp
Education: 1987 M.D. Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan 1999 Ph.D. Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan
Fellowships: 1989-1991 Fellow in Pediatric Anesthesia, Saitama Children's Medical Center, Hasuda, Saitama, Japan 1996-1998 Research Fellow in Division of Cardiothoracic Anesthesiology and Critical Care, The Emory Clinic, Atlanta, GA, USA
Hospital Appointments: 1991-1993 Physician in Anesthesiology, Shizuoka General Hospital, Shizuoka, Shizuoka, Japan 1993-1996 Physician in Anesthesiology, Hamamatsu University Hospital, Hamamatsu, Shizuoka, Japan 1998-2000 Physician in Anesthesiology, Tokyo-Metropolitan Hachiouji Children's Hospital, Hachiouji, Tokyo, Japan
Academic Appointments: 2000-2003 Assistant Professor in Intensive Care, Hamamatsu University Hospital, Hamamatsu, Shizuoka, Japan 2003-2009 Assistant Professor, Department of Anesthesiology and Intensive Care, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan 2009-present Senior Assistant Professor, Department of Emergency Medicine, Hamamatsu University Hospital, Hamamatsu, Shizuoka, Japan
Licensure and Certification: 1987 Medical License in Japan 1993 Fellow of the Japanese Society of Anesthesiologists 2006 Board certificated intensivist, the Japanese Society of Intensive Care Medicine 2007 Fellow of the Japanese Society of Reanimatology 2012 Councilor of the Japanese Society of Reanimatology
Teaching Licenses: 2006 Basic Life Support/Advanced Cardiovascular Life Support instructor, American Heart Association 2008 Difficult airway management instructor, Japanese Association for Medical Simulation 2009 Medical clinical instructor, Ministry of Health, Labour and Welfare, Japan 2010 Central venous catheterization instructor, Japanese Association for Medical Simulation
Grant: 2010-2012 Grant-in-Aid for Scientific Research (#22592012) from Japan Society of Promotion of Science
Award: 2011 A finalist of Best Abstract Prize Competition in Euroanaesthesia 2011 (Amsterdam, the Netherlands)
Abstract: We experienced a case of unexpected difficult nasal intubation due to lingual tonsil hyperplasia. A 43-year-old male was scheduled for pharyngoplasty to sleep apnea syndrome. After induction of general anesthesia, Macintosh laryngoscopy was failed to expose his glottis by two experienced anesthesiologists. We also found that the view of his larynx by fiberoptic bronchoscope (FOB) was poor, and nasal intubation guided by FOB was difficult. Finally, we made an oral intubation with Macintosh laryngoscopy under a gum elastic bougie guide. Ventilation and oxygenation were maintained throughout the procedure. A FOB guided intubation under general anesthesia is often difficult, because identification of glottis is interfered by deviated pharyngeal tissue and epiglottis, which were affected by the use of muscle relaxants. At present, since a selective relaxant binding agent âSugammadexâ is available in an anesthesiology field, to reverse the effect of non-depolarizing muscle relaxant by sugammadex and to resume breath spontaneously is advisable steps in this situation.
Abstract: The term âwide QRSâ is defined as a QRS interval ⥠120 ms on ECG (electrocardiogram). It is often difficult to differentiate whether the arrhythmia causing sustained (sustained time ⥠30 sec) wide QRS tachycardia is ventricular tachycardia, paroxysmal supraventricular tachycardia with aberrant conduction, atrial flutter with aberrant conduction, or WPW (Wolff-Parkinson-White) syndrome. A patient should be considered âunstableâ when a symptom and/or a sign such as loss of consciousness including syncope, ischemic chest pain, dyspnea, hypotension, or findings of shock are observed. These patients should receive immediate synchronized DC cardioversion. Patient diagnosed as âstableâ wide QRS tachycardia should be referred to cardiologists immediately and may be considered for drug therapy. A 12-leads ECG for further diagnosis is highly recommended in as many situations as possible.
Abstract: We experienced a case of a 74-year-old woman who did not respond to standard cardiopulmonary resuscitation (CPR). She had undergone aortic valve replacement (AVR) due to aortic valve stenosis (AS) 7 months ago. She was currently scheduled to have a biopsy of larynx due to a subglottis tumor and airway stenosis under general anesthesia. Immediately after the insertion of a direct laryngoscope for the biopsy, cardiac arrest occurred following sinus tachycardia and ST depression. Although we performed CPR vigorously, we could not resuscitate her. Myocardium of AS occasionally occurs, causing an imbalance in oxygen supply and demand even without coronary artery disease more than 6 months after AVR. We speculated that the origin of refractory cardiac arrest was the persistent pathology of AS despite AVR performed 7 months earlier.
Abstract: <br><b>Aim: <br></b>Therapeutic hypothermia (TH) is widely used as a cardioprotective treatment for cardiac arrest. TH at 30â32°C during ischaemia and reperfusion has a cardioprotective effect. The aims of the study were to examine whether TH at 34°C with late induction (immediately after the start of reperfusion) has a cardioprotective effect and to determine if this effect is mediated by nitric oxide (NO) and phosphatidylinositol 3â-kinase (PI3K).
<br><b>Methods: <br></b>Langendorff perfusion of Sprague-Dawley rat hearts was initiated at 75 mmHg at 37°C. Left ventricle infarct sizes were evaluated by triphenyltetrazolium chloride staining after Langendorff perfusion in 6 groups (each n=7): control group; ischaemia group, with 34ºC TH during ischaemia for 30 min and reperfusion for 180 min; reperfusion group, with 34ºC TH induced solely during the reperfusion period; and the L-NAME (NO synthase inhibitor), LY294002, and wortmannin (PI3K inhibitors) groups, which were treated similarly to the reperfusion group with the addition of each compound.
<br><b>Results: <br></b>TH reduced the left ventricle infarct size from 54.2%±14.8 of the control group to 11.9%±6.3 (ischaemia group, p<0.001) and to 23.5%±10.5 (reperfusion group, p<0.001). L-NAME, LY294002, and wortmannin reversed the cardioprotective effect of TH induced during reperfusion to 42.5%±10.6 (p=0.009), 40.9%±4.1 (p=0.021), and 51.9%±13.0 (p<0.001), respectively. Circulatory temperatures reached 34°C within 5 min in all groups subjected to TH.
<br><b>Conclusions: <br></b>TH of 34°C showed a cardioprotective effect even with late initiation of cooling during reperfusion. The effect was mediated by NO and PI3K.
Abstract: A 38-year-old male was transported to the operating room for emergency debridement of his right arm due to gas gangrene. Gas gangrene occurred as a consequence of self-injection of a psychostimulant using a dirty needle. He had been treated with benzodiazepine and levomepromazine for depression, and was addicted to psychostimulants. The anesthesia was maintained with air-oxygen-sevoflurane and narcotics, after induction with propofol and vecuronium. Hypotension was successfully managed with dopamine infusion. Surgery was performed twice because the patient ultimately required amputation of the upper arm. He was extubated and discharged from the intensive-care unit the day after amputation. Thereafter, transient restlessness was treated with diazepam. Psychostimulant abuse patients require careful management for acute hemodynamic changes and mental condition during the perioperative period.
Abstract: <br><b>Background</b><br>The medical studentsâ advanced life support workshop (Studentsâ ACLS WS) is the student-organized training course for cardiopulmonary resuscitation and emergent cardiac care (CPR and ECC) in Japan. We held the 14th Studentsâ ACLS WS of the Tokai region at the Hamamatsu University School of Medicine.<br><b>Methods</b><br>
Approximately one month after the 14th Studentsâ ACLS WS of the Tokai region, we conducted a questionnaire survey with the participants of the Studentsâ ACLS WSs, including instructors and learners. <br><b>Results</b><br>Our survey showed that the most frequent motivation of the instructors was to continue their activities and have repeated opportunities to improve their knowledge and skills of CPR and ECC. Our major problems were insufficient funds and time to participate in the Studentsâ ACLS WSs.<br><b>Conclusions</b><br>Our desire is to develop a standardized Studentsâ ACLS WS consensus under the supervision of our senior physicians and teachers to resolve these difficulties and to encourage as many medical students as possible to participate in the Studentsâ ACLS WSs; i.e. to reduce the work load of preparation for the Studentsâ ACLS WS and relieve our anxiety that we might provide wrong information to the learners.
Abstract: <br><b>Purpose<br></b>
Systemic alkalinization is recommended for resuscitation from local anesthetic-induced cardiotoxicity . Although it has been suggested that inducing hypocapnic alkalosis prior to exposure to toxic concentrations of local anesthetics may minimize cardiotoxicity , it remains unclear whether inducing severe hypocapnic alkalosis after administration of local anesthetics will minimize the duration of bradycardia. We investigated the effects of hypocapnic alkalosis on heart rate (HR) recovery from bupivacaine or levobupivacaine-induced bradycardia, using isolated rat hearts.
<br><b>Methods<br></b>
The time required for the HR to attain 90% of the baseline HR (recovery time) following bradycardia induced by 1 μg.mL-1 and 10 μg.mL-1 concentrations of either bupivacaine or levobupivacaine ,was measured in 24 isolated rat hearts, respectively. Normal pH perfusate (bupivacaine or levobupivacaine with normal pH washout groups) or severe hypocapnic alkalosis perfusate (bupivacaine or levobupivacaine with hypocapnic alkalosis washout groups) were reperfused after exposure to the local anesthetics.
<br><b>Results<br></b>
Severe hypocapnic alkalosis prolonged the recovery time, from 273±122 s at the 1 μg.mL-1 bupivacaine concentration with normal pH washout, to 1203±540 s in the bupivacaine with hypocapnic alkalosis washout (p=0.029). Severe hypocapnic alkalosis also prolonged the recovery time, from 1153±644 s at a 10 μg.mL-1 bupivacaine concentration in the normal pH washout, group, compared to 2065±617 s in the bupivacaine with hypocapnic alkalosis washout group (p=0.032). With levobupivacaine 10 μg.mL-1 in the normal pH washout group, heart rate recovery time increased from 863±186 s to 1565±567 s, compared to the hypocapnic alkalosis washout group (p=0.045).
<br><b>Conclusions<br></b>
Severe hypocapnic alkalosis prolonged the recovery time from bupivacaine or levobupivacaine-induced bradycardia in isolated rat hearts. When bradycardia occurs after intravascular bupivacaine or levobupivacaine administration, maintenance of normocapnia may minimize the duration of bradycardia.
Notes: <br><b>Implication Statement<br></b>
Severe hypocapnic alkalosis prolonged the recovery of heart rate from bupivacaine- or levobupivacaine-induced bradycardia, using an isolated rat heart model. When bradycardia occurs after intravascular bupivacaine- or levobupivacaine-administration, maintenance of normocapnia might minimize the duration of bradycardia.
Abstract: <br><b>Purpose</b> <br> Our purpose was to investigate whether the NO donor, 3-(2-hydroxy-1-methyl-2-nitroso-hydrazino)-N-methyl-1-propanamine (NOC7), restored cardiac function following global ischemia in an isolated rat heart model and whether intracellular messengers were involved in its effect.
<br><b>Methods</b> <br> Isolated rat hearts (n = 36) were randomly divided into six groups. The sham control group was perfused with modified Krebs-Henseleit bicarbonate buffer (KHB) alone. The ischemic control group and the NOC7 groups were subjected to 35 min of global ischemia, followed by 30 min of reperfusion with KHB alone, or reperfusion with KHB including NOC7 at 0.2, 2, 20, or 200 μM, respectively. Left ventricular developed pressure (LVDP), the maximum and the minimal rate of rise in LVP (±dP/dt), and coronary flow were measured continuously. Cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) levels were measured in myocardium homogenate, using enzyme immunoassay (EIA) methods.
<br><b>Results</b> <br> NOC7 at 2 and 20 μM rescued myocardial performance (LVDP, 111.9 ± 10.5% and 124.3 ± 12.5% of baseline, respectively; P < 0.05 vs ischemic control) at 30 min after reperfusion. However, NOC7 at 200 μM reduced the LVDP to 55.3 ± 6.0% of baseline. Coronary flows remain unchanged. The cAMP levels increased significantly from 0.83 ± 0.44 pmol·mgâ1 protein in the ischemic control group to 1.79 ± 0.39, 1.86 ± 0.25, and 2.63 ± 0.24 pmol·mgâ1 protein, in the groups with NOC7 at 2, 20, and 200 μM, respectively (P < 0.05). The cGMP level increased from 1.49 ± 0.61 pmol·mgâ1 protein in the ischemic control group to 3.92 ± 0.66 pmol·mgâ1 protein in the group with NOC7 at 200 μM alone (P < 0.05).
<br><b>Conclusion</b> <br> NOC7 appeared to exert a biphasic effect on the contractile force of the isolated rat heart after 35-min global ischemia. The balance between intracellular cAMP and cGMP levels seemed to be involved in its mechanism.
Notes: The nitric oxide donor, NOC7, improves cardiac dysfunction following global ischemia in a whole organ model of the isolated rat hearts. NO donors might be one option for the restoration of cardiac dysfunction after global ischemia when used at an appropriate dose.
Abstract: <br><b>AIM: </b><br>Dexmedetomidine is a highly specific and selective alpha-2 adrenergic agonist that is now widely used in the intensive care setting. Many intensive care unit (ICU) patients are at risk of respiratory or cardiac arrest. This study was conducted to determine whether dexmedetomidine exhibits a cardioprotective effect on global ischaemia and subsequent myocardial infarction. <br><b>METHODS: </b><br>Isolated rat hearts were subjected to 30 min of global ischaemia followed by 120 min reperfusion, with administration of 0, 1 and 10nM dexmedetomidine during the pre-ischaemic period (n=7 each group). Secondly, 1 microM yohimbine, an alpha-2 antagonist, was given during the pre-ischaemic period, alone or in combination with 10 nM dexmedetomidine (n=7 each group). <br><b>RESULTS: </b><br>Dexmedetomidine administration reduced coronary flow significantly (103.6+/-4.7%, 77.9+/-3.7, 63.7+/-6.1%, of the baseline values for 0, 1 and 10 nM dexmedetomidine, respectively), and yohimbine administration reversed this effect (88.0+/-2.2%). Dexmedetomidine improved the infarct size at each concentration (45.3+/-3.6, 30.2+/-3.3, and 21.2+/-2.3% of the total left ventricular mass for 0, 1, and 10nM dexmedetomidine, respectively), which was also reversed by yohimbine (43.6+/-1.4%). <br><b>CONCLUSION:</b><br> Dexmedetomidine exhibited a cardioprotective effect on global ischaemia in the isolated rat heart model, which was mediated by alpha-2 adrenergic stimulation.
Abstract: A 5-year-old boy developed anaphylactic shock during laparotomy. Since postoperative examination for allergens revealed that IgE anti-latex antibody was strongly positive, a possible cause of this shock should be latex allergy. The patient has past history of bronchial asthma and atopic predisposition. This patient is considered to gain the sensitivity against latex due to frequent previous operations. We conclude that great care should be taken to prepare for possible anaphylactic shock during operation in patients with atopic predisposition and history of frequent operations.
Abstract: <br><b>Background</b><br>Bleeding after cardiopulmonary bypass (CPB) is related to multiple factors. Excess protamine weakens clot structure and decreases platelet function; therefore, an increased activated clotting time (ACT) after protamine reversal of heparin may be misinterpreted as residual heparin anticoagulation. <br><b>Methods</b><br>We evaluated the effects of protamine, recombinant platelet factor 4 (rPF4), and hexadimethrine on ACT in blood obtained after CPB. In addition, we examined the effect of protamine on in vitro platelet aggregation. Incremental doses of protamine, rPF4, and hexadimethrine were added to heparinized blood from CPB, and ACTs were performed. Incremental concentrations of protamine were added to heparinized platelet-rich plasma, and aggregometry was induced by adenosine diphosphate (ADP) and collagen. <br><b>Results</b><br>The mean heparin concentration at the end of CPB was 3.3 U/mL. Protamine to heparin ratios >1.3:1 produced a significant prolongation of the ACT that was not seen with rPF4 and was observed only with 5:1 hexadimethrine to heparin ratios. ADP-induced platelet aggregation was reduced with protamine administration > or =1.3:1. <br><b>Conclusions</b><br>Excessive protamine reversal of heparin prolongs ACT and alters ADP-induced platelet aggregation in a dose-dependent manner in vitro. Additional protamine administered to treat a prolonged ACT may further increase clotting time, reduce platelet aggregation, and potentially contribute to excess bleeding after CPB.
Notes: <br><b>IMPLICATIONS:</b> <br>We found that excess protamine prolonged the activated clotting time and altered platelet function after cardiopulmonary bypass, whereas heparin antagonists, such as recombinant platelet factor 4 and hexadimethrine, exhibited a wider therapeutic range without adversely affecting the activated clotting time. Approaches to avoid excess protamine or use of alternative heparin antagonists after cardiopulmonary bypass may be beneficial.
Abstract: <br><b>Background<br></b>Coagulopathies in children after cardiopulmonary bypass (CPB) are complex. There are very limited data correlating coagulation tests with postoperative bleeding. We evaluated coagulation changes after CPB and after the administration of coagulation products to 75 children. <br><b>Methods<br></b>Baseline coagulation tests were obtained and repeated after protamine administration, after transfusion of individual coagulation products, and on arrival in the intensive care unit (ICU). Regression analysis demonstrated no baseline coagulation test to predict postoperative chest tube drainage. Weight and duration of CPB were determined to be the only predictors of bleeding. Further analyses demonstrated that children <8 kg had more bleeding and required more coagulation products than children >8 kg. <br><b>Results<br></b>Postprotamine platelet count and fibrinogen level correlated independently with 24-h chest tube drainage in children <8 kg, whereas postprotamine platelet count and thrombelastographic values did so in patients weighing >8 kg. Platelet administration alone was found to restore effective hemostasis in many patients. <br><b>Conclusions<br></b>With ongoing bleeding, cryoprecipitate improved coagulation parameters and limited blood loss. Fresh-frozen plasma administration after platelets worsened coagulation parameters and was associated with greater chest tube drainage and more coagulation product transfusions in the ICU. Objective data to guide post-CPB component therapy transfusion in children are suggested.
Notes: <br><b>Implications: <br></b>Children <8 kg can be expected to have more severe coagulopathies, require more coagulation product transfusions, and bleed more after cardiopulmonary bypass. Correlations between coagulation tests and postoperative chest tube drainage are defined. Platelets and, if necessary, cryoprecipitate optimally restore hemostasis. Fresh-frozen plasma offers no benefits in correcting postcardiopulmonary bypass coagulopathies in children.
Abstract: <br><br>To compare the effects of prostaglandin E1 (PGE1) with those of nitroglycerin (NTG) on whole body metabolism (oxygen uptake (VO2) and carbon dioxide elimination (VCO2) during induced hypotension, we have studied 16 patients undergoing elective surgery (radical mastectomy or tympanoplasty). <br><br>The patients were allocated randomly in a non-blinded manner to two groups. Baseline characteristics were similar in the two groups. Arterial pressure was controlled at about 70% of the baseline value using PGE1 or NTG. VO2, VCO2, gas exchange ratio (RQ) and deadspace ventilation ratio (VD/VT) were measured continuously with mass spectrometry. The values for all variables were measured for 10 min at five times (1 = start of surgery (baseline value); 2 = start of drug infusion; 3 = 60 min after start of drug infusion; 4 = drug infusion stopped; 5 = surgery finished). VO2, VCO2, RQ and VD/VT values were relatively constant in both groups during surgery. <br><br>The balance between oxygen supply and oxygen demand was maintained during induced hypotension with PGE1 or NTG.
