The Experts below are selected from a list of 216 Experts worldwide ranked by ideXlab platform
Michihisa Jougasaki - One of the best experts on this subject based on the ideXlab platform.
-
suppression of Hyperventilation induced attacks with infusion of atrial natriuretic peptide in patients with variant angina pectoris
American Journal of Cardiology, 1993Co-Authors: Etsuo Morita, Michihisa Jougasaki, Michihiro Yoshimura, Hidenori Tanaka, Hirofumi YasueAbstract:Abstract Atrial natriuretic peptide (ANP) is reported to dilate a major coronary artery in both experimental animals and humans. Spasm of a major coronary artery is the cause of variant angina pectoris and can be induced by Hyperventilation. The effect of the ANP infusion on anginal attack induced by Hyperventilation was studied in patients with variant angina pectoris. The study was performed in the early morning on 3 consecutive days in 11 patients with variant angina pectoris in whom the attacks were reproducibly induced by Hyperventilation. On days 1 and 3 (saline solution infusion), and day 2 (ANP infusion), Hyperventilation was started 14 minutes after beginning infusion of ANP (0.1 μg/kg/min) or saline solution for 6 minutes. The attacks were induced in all 11 patients by Hyperventilation on days 1 and 3. However, the attacks were not induced in any patient on day 2 of the ANP infusion. The plasma ANP level increased from 33 ± 7 pg/ml to the peak level of 2,973 ± 479 pg/ml (p
Francisco Carlos De Andrade - One of the best experts on this subject based on the ideXlab platform.
-
Uses and abuses of the Hyperventilation in severe traumatic brain injury
Academia Brasileira de Neurologia - ABNEURO, 2000Co-Authors: Francisco Carlos De AndradeAbstract:É feita avaliação crítica sobre as diretrizes atuais e consequências da manobra de hiperventilação (MHV) na prevenção e tratamento da hipertensão intracraniana (HIC) que segue aos traumatismos crânio-encefálicos (TCE) graves. O uso profilático da MHV deve ser evitado na fase aguda de TCE grave, a menos que se registrem altos valores de O2 no sangue venoso medido no bulbo jugular, ou para ganhar tempo quando o paciente apresenta evidentes sinais posturais de deterioração neurológica. A falta de resposta cerebrovascular à MHV para baixar a HIC significa que a barreira hemato-encefálica (BHE) está difusamente lesada. Então, a MHV pode ser utilizada como um crivo nos TCE graves, uma vez que a lesão da BHE atesta que os demais tratamentos disponíveis para combater a HIC (sedação, paralisia e diuréticos osmóticos) não funcionarão. Uma nova hipótese patogênica do edema encefálico traumático e abordagem terapêutica é apresentada.A critical evaluatin was done about the guidelines and effects of the Hyperventilation maneuver on prevention and treatment of increased intracranial pressure (ICP) that follows severe traumatic brain injury (TBI). The prophylatic use of Hyperventilation should be avoided after severe TBI acute phase, unless high venous O2 values are recorded at jugular bulb blood (SjO2), or to allow time when there are evidences of neurologic deterioration with posturing. The lack of cerebrovascular response to Hyperventilation to low the ICP means that the blood brain barrier (BBB) function is extensively impaired. Then, hyperventilacion may be used as a screening therapeutic test in acute severe TBI, since BBB impairment is the pointer that other available clinical procedures for high ICP control (sedation, paralysis and osmotic diuretics) are not workable. A new pathogenetic hypothesis about traumatic brain edema and its therapeutic approach is presented
-
Usos e abusos da hiperventilação nos traumatismo crânio-encefálicos graves
Arquivos de neuro-psiquiatria, 2000Co-Authors: Francisco Carlos De AndradeAbstract:A critical evaluatin was done about the guidelines and effects of the Hyperventilation maneuver on prevention and treatment of increased intracranial pressure (ICP) that follows severe traumatic brain injury (TBI). The prophylatic use of Hyperventilation should be avoided after severe TBI acute phase, unless high venous O2 values are recorded at jugular bulb blood (SjO2), or to allow time when there are evidences of neurologic deterioration with posturing. The lack of cerebrovascular response to Hyperventilation to low the ICP means that the blood brain barrier (BBB) function is extensively impaired. Then, hyperventilacion may be used as a screening therapeutic test in acute severe TBI, since BBB impairment is the pointer that other available clinical procedures for high ICP control (sedation, paralysis and osmotic diuretics) are not workable. A new pathogenetic hypothesis about traumatic brain edema and its therapeutic approach is presented.
-
Usos e abusos da hiperventilação nos traumatismo crânio-encefálicos graves Uses and abuses of the Hyperventilation in severe traumatic brain injury
Academia Brasileira de Neurologia (ABNEURO), 2000Co-Authors: Francisco Carlos De AndradeAbstract:É feita avaliação crítica sobre as diretrizes atuais e consequências da manobra de hiperventilação (MHV) na prevenção e tratamento da hipertensão intracraniana (HIC) que segue aos traumatismos crânio-encefálicos (TCE) graves. O uso profilático da MHV deve ser evitado na fase aguda de TCE grave, a menos que se registrem altos valores de O2 no sangue venoso medido no bulbo jugular, ou para ganhar tempo quando o paciente apresenta evidentes sinais posturais de deterioração neurológica. A falta de resposta cerebrovascular à MHV para baixar a HIC significa que a barreira hemato-encefálica (BHE) está difusamente lesada. Então, a MHV pode ser utilizada como um crivo nos TCE graves, uma vez que a lesão da BHE atesta que os demais tratamentos disponíveis para combater a HIC (sedação, paralisia e diuréticos osmóticos) não funcionarão. Uma nova hipótese patogênica do edema encefálico traumático e abordagem terapêutica é apresentada.A critical evaluatin was done about the guidelines and effects of the Hyperventilation maneuver on prevention and treatment of increased intracranial pressure (ICP) that follows severe traumatic brain injury (TBI). The prophylatic use of Hyperventilation should be avoided after severe TBI acute phase, unless high venous O2 values are recorded at jugular bulb blood (SjO2), or to allow time when there are evidences of neurologic deterioration with posturing. The lack of cerebrovascular response to Hyperventilation to low the ICP means that the blood brain barrier (BBB) function is extensively impaired. Then, hyperventilacion may be used as a screening therapeutic test in acute severe TBI, since BBB impairment is the pointer that other available clinical procedures for high ICP control (sedation, paralysis and osmotic diuretics) are not workable. A new pathogenetic hypothesis about traumatic brain edema and its therapeutic approach is presented
Takao Ayuse - One of the best experts on this subject based on the ideXlab platform.
-
management of post Hyperventilation apnea during dental treatment under monitored anesthesia care with propofol
Biopsychosocial Medicine, 2014Co-Authors: Masato Kobayashi, Ichiro Okayasu, Shinji Kurata, Takuro Sanuki, Takao AyuseAbstract:Although Hyperventilation syndrome generally carries a good prognosis, it is associated with the risk of developing severe symptoms, such as post-Hyperventilation apnea with hypoxemia and loss of consciousness. We experienced a patient who suffered from post-Hyperventilation apnea. A 17-year-old female who suffered from Hyperventilation syndrome for several years developed post-Hyperventilation apnea after treatment using the paper bag rebreathing method and sedative administration during a dental procedure. We subsequently successfully provided her with monitored anesthesia care with propofol. Monitored anesthesia care with propofol may be effective for the general management of patients who have severe Hyperventilation attacks and post-Hyperventilation apnea. This case demonstrates that appropriate emergency treatment should be available for patients with Hyperventilation attacks who are at risk of developing post-Hyperventilation apnea associated with hypoxemia and loss of consciousness.
Soejima Yuji - One of the best experts on this subject based on the ideXlab platform.
-
Prolonged post-Hyperventilation apnea in two young adults with Hyperventilation syndrome
BioPsychoSocial medicine, 2013Co-Authors: Takao Munemoto, Akinori Masuda, Nobuatsu Nagai, Muneki Tanaka, Soejima YujiAbstract:Background The prognosis of Hyperventilation syndrome (HVS) is generally good. However, it is important to proceed with care when treating HVS because cases of death following Hyperventilation have been reported. This paper was done to demonstrate the clinical risk of post-Hyperventilation apnea (PHA) in patients with HVS.
Hirofumi Yasue - One of the best experts on this subject based on the ideXlab platform.
-
Hyperventilation as a specific test for diagnosis of coronary artery spasm
American Journal of Cardiology, 1997Co-Authors: Koichi Nakao, Michihiro Yoshimura, Masamichi Ohgushi, Kimihiko Morooka, Ken Okumura, Hisao Ogawa, Kiyotaka Kugiyama, Yuichi Oike, Kazuteru Fujimoto, Hirofumi YasueAbstract:The Hyperventilation test has been used as a clinical tool to induce coronary spasm. However, its diagnostic and prognostic values have not been fully elucidated. This study was designed to establish the sensitivity and specificity of the Hyperventilation test and to clarify the characteristics of Hyperventilation test-positive patients. We examined 206 patients in whom coronary spasm was documented by angiography (spasm group), and 183 patients without angina at rest in whom acetylcholine failed to induce spasm (nonspasm group). All patients performed vigorous Hyperventilation for 6 minutes in the early morning. Of the spasm group patients, 127 showed positive responses to the test, including ST elevation (n = 111), ST depression (n = 15) and negative U wave (n = 1). None in the nonspasm group showed any ischemic electrocardiographic change. Thus, the sensitivity and specificity of this test for diagnosis of coronary spasm were 62% and 100%, respectively. In the spasm group, there were no significant differences between Hyperventilation test-positive and test-negative patients in age, sex, the prevalence of hypertension, diabetes mellitus, obesity, smoking, and the number of diseased vessels. When clinical characteristics were compared, the proportions of the patients with high disease activity (> or =5 attacks a week), with severe arrhythmias (second- or third-degree atrioventricular block and/or ventricular tachycardia) during attacks, and with multivessel spasm were significantly higher in the Hyperventilation test-positive patients than in the negative patients (69% vs 20%, p <0.0001; 31% vs 11%, p <0.005; and 58% vs 34%, p <0.01, respectively). These findings imply that Hyperventilation is a highly specific test for the diagnosis of coronary artery spasm, and that Hyperventilation test-positive patients are likely to have life-threatening arrhythmias during attacks and multivessel spasm.
-
suppression of Hyperventilation induced attacks with infusion of atrial natriuretic peptide in patients with variant angina pectoris
American Journal of Cardiology, 1993Co-Authors: Etsuo Morita, Michihisa Jougasaki, Michihiro Yoshimura, Hidenori Tanaka, Hirofumi YasueAbstract:Abstract Atrial natriuretic peptide (ANP) is reported to dilate a major coronary artery in both experimental animals and humans. Spasm of a major coronary artery is the cause of variant angina pectoris and can be induced by Hyperventilation. The effect of the ANP infusion on anginal attack induced by Hyperventilation was studied in patients with variant angina pectoris. The study was performed in the early morning on 3 consecutive days in 11 patients with variant angina pectoris in whom the attacks were reproducibly induced by Hyperventilation. On days 1 and 3 (saline solution infusion), and day 2 (ANP infusion), Hyperventilation was started 14 minutes after beginning infusion of ANP (0.1 μg/kg/min) or saline solution for 6 minutes. The attacks were induced in all 11 patients by Hyperventilation on days 1 and 3. However, the attacks were not induced in any patient on day 2 of the ANP infusion. The plasma ANP level increased from 33 ± 7 pg/ml to the peak level of 2,973 ± 479 pg/ml (p
