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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The post-operative review of 81 patients operated for a large interventricular communication before the age of two years reveals excellent results: the mean age at operation was 7 months, extracorporeal circulation was performed in 25 patients for a mean duration of 77 minutes and profound hypothermia to 18 degrees C was induced in 56 patients. The atrial approach was used in 30% of cases. The mean follow-up period is 26 months. There was one case of complete bundle branch block, which was subsequently fitted with a pacemaker, 7 cases of bifascicular branch block and a right bundle branch block in the majority of cases. The pulmonary vascular resistance was virtually normal (a mean of 3.2 U.m-2 prior to the operation and a mean of 1.9 U.m-2 after the operation). The left ventricular volume, which was markedly increased in all patients preoperatively, returned to normal with maintenance of a normal ejection fraction. The neuro-psychomotor behaviour was abnormal in 13 of the 63 patients tested. These abnormalities are not related to the correction procedure, but to pre-existing pathology (small birth weight). 52 patients from a series of 63 cases operated for tetralogy of Fallot before the age of 2 years (median age 12 months) were also reviewed. Extracorporeal circulation lasting a mean of 115 minutes was performed in 31 patients, cardiac arrest under profound hypothermia was induced in the other cases, for a mean duration of 61 minutes. The mean follow-up period was 29 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Results of the intracardiac repair of tetralogy of Fallot and interventricular communication before the age of 2 years]. 397 71

The indications for and results of surgical closure of ventricular septal defect (VSD), uncomplicated by other congenital cardiac defects, depend on the size of the VSD and its haemodynamic consequences. In infants the timing of surgical closure is determined largely by the persistence of symptoms of congestive cardiac failure unresponsive to maximal medical treatment. There is a high incidence of spontaneous closure of VSD with age, especially in defects of small size. Accompanying aortic regurgitation is a serious complication. Progress in surgical technique (e.g. deep hypothermia, cardioplegia, identification of the conduction tissue) has substantially decreased the hospital mortality of surgical closure and the incidence of late deaths. In selected series the hospital mortality has been reduced to as low as 1-2% in patients over one year of age. Unless there is intractable cardiac failure (rarely observed beyond infancy), surgical closure can be delayed: pulmonary vascular obstructive disease develops only very exceptionally below the age of two years. Late complications include re-opening of the patch repair, arrhythmias and conduction disorders. The prognosis of post-operative left axis deviation plus right bundle branch block (left anterior hemiblock) is good in the absence of serious arrhythmias. Late deaths are rare. Operation in early childhood prevents the occurrence or persistence of abnormal right ventricular function. Exercise tolerance is normal in the absence of complications in practically all patients, who can therefore lead a normal life in all respects. There is, however, still slight doubt to what extent surgical closure is truly "curative" rather than "corrective".
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PMID:The outlook for children after cardiac surgery: ventricular septal defects. 665 3

A 56-year-old man was admitted to our hospital after successful resuscitation for out-of-hospital cardiac arrest. Electrocardiogram on admission showed right bundle branch block and ST segment elevation in leads V1-3. Subsequent intravenous infusion of isoproterenol rapidly resolved ST segment elevation, suggesting Brugada syndrome. Therapeutic hypothermia, that was performed with a target temperature of 34.0 degrees C did not induce ST segment elevation in leads V1-3. The J-ST segment elevation rather became much more normal, suggesting a beneficial effect of mild therapeutic hypothermia. Serial ECG showed the temporal variation of ST segment elevation, and pilsicainide challenge test showed the occurrence of ST segment elevation, confirming the diagnosis of Brugada syndrome. Clinical observation suggested that mild therapeutic hypothermia reversed the Brugada phenotype through the prevention of fever as well as being indicated for cerebral protection after cardiac arrest. In conclusion, therapeutic hypothermia with a temperature of 34.0 degrees C can be used safely in Brugada syndrome.
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PMID:Therapeutic hypothermia after out-of-hospital cardiac arrest due to Brugada syndrome. 1862 Jul 95

When an ECG shows (or is suspicious for) a Brugada pattern, i.e., the association of a positive terminal deflection and ST segment elevation in the right precordial leads, the cardiologist often faces several problems. Three important questions are raised by this ECG pattern: (1) is this really a Brugada ECG pattern? (2) How can be determined whether this patient is at risk for sudden death? and (3) Should this patient receive an implantable cardioverter-defibrillator (ICD)? The term "Brugada syndrome" should be restricted to patients who have diagnostic ECG changes, as well as a history of symptoms. Asymptomatic subjects, in contrast, should be categorized as having a "Brugada ECG pattern" rather than the syndrome. Diagnostic ECG (type 1) is characterized by a J wave (a terminal positive wave) whose amplitude is > or =2 mm, and a "coved" type ST segment elevation located in the right precordial leads. These signs are usually present in leads V1 and/or V2 (lead V3 is more rarely involved, and is never the only affected one), but occasionally also can be observed in some of the limb leads. Types 2 and 3 ECGs, which are not truly diagnostic of Brugada pattern, are characterized by a "saddle back" ST segment elevation, that is > or =1 mm in type 2 and <1 mm in type 3. In Brugada ECG pattern, the QRS complex characteristically shows a positive terminal deflection that mimics an r' prime wave (the wave occurring in right bundle branch block), in the right precordial leads. Actually, it is a J wave that is very similar to the "Osborn" one observed during hypothermia. The J wave of Brugada ECG pattern is generated by a voltage gradient across the myocardial wall of the right ventricular outflow tract. This abnormal potential can be recorded only by electrodes located very close to the site where that phenomenon is originating. Displacement of the right precordial leads electrodes one or two intercostal spaces above their normal positions may, at times, disclose the diagnostic pattern when conventional leads, recorded at the fourth intercostal space, are non-diagnostic or even normal. High right precordial leads should be recorded whenever standard V1-V3 leads raise the suspicion of Brugada pattern. For example, when a relatively large positive terminal wave, even of low amplitude, is recorded, placing high right precordial leads is an option that should be considered. The ECG may show a marked variation over time, ranging from the typical pattern to a completely normal ECG and back again. In subjects with a non-diagnostic ECG, a pharmacological test with sodium channel blockers may disclose the typical Brugada pattern. In order to establish the diagnosis, several conditions that can mimic Brugada pattern must be excluded. These include right bundle branch block, early repolarization, acute myocardial ischemia, pericarditis, hypercalcemia, hyperkalemia, hypothermia and primary right ventricular diseases, particularly arrhythmogenic right ventricular dysplasia. Some drugs (e.g., some antiarrhythmic drugs, psychotropic agents or antihistamines), hyperthermia and enhanced vagal tone, as it occurs after a full meal, may render Brugada pattern more evident on the ECG. Typical ventricular arrhythmia in Brugada syndrome is a polymorphic ventricular tachycardia, that can evolve into ventricular fibrillation; its mechanism is assumed to be phase 2 reentry. Monomorphic ventricular tachycardia is rarely seen. Atrial fibrillation occurs more frequently in patients with the Brugada ECG pattern than in the general population. A mutation in the SCN5A gene, which encodes the alpha subunit of the cardiac sodium channel, is found in about 20% of the subjects with Brugada pattern; mutations in other genes have less frequently been described. Genetic testing is not very helpful in formulating the diagnosis, but when a mutation is found it could be useful to extend testing to first degree relatives, enabling early detection of abnormal gene carriers. Patients who have experienced an aborted sudden death have a high risk of recurrence and should receive an ICD. A history of syncope, spontaneous type 1 ECG and male sex, not family history of sudden death, are independent risk factors. The role of programmed ventricular stimulation in risk stratification remains the subject of debate. Asymptomatic patients with a Brugada ECG pattern should: (1) receive adequate information on current knowledge concerning this topic, (2) be given the list of forbidden drugs, (3) be informed to promptly treat hyperthermia, (4) be informed that clinical evaluation should be extended to their first degree relatives, 5) undergo regular cardiology follow-up. Also in this group the role of programmed ventricular stimulation in risk stratification is debated. Subjects showing a Brugada pattern after a pharmacological challenge should be followed-up with ECG and 12-lead Holter monitoring, if available, to identify the appearance of spontaneous type 1 ECG. Symptoms should be promptly reported.
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PMID:[Doubts of the cardiologist regarding an electrocardiogram presenting QRS V1-V2 complexes with positive terminal wave and ST segment elevation. Consensus Conference promoted by the Italian Cardiology Society]. 2156 Apr 82

Out-of-hospital cardiac arrest (OHCA) is a crucial public health problem. To improve outcomes of patients after cardiac arrest, the American Heart Association promotes the concept of the chain of survival.We report a case of a 19-year-old man with no markedly past medical history who suffered from OHCA, and he was resuscitated with cardiopulmonary resuscitation, without interruption, during the rescue process for 120 minutes until return of spontaneous circulation (ROSC). Electrocardiogram on admission showed right bundle branch block and ST segment elevation in leads V1-V2, and the patient's uncle had experienced the same event and had received implantable cardioverter defibrillator (ICD) treatment. Therefore, the patient was diagnosed with Brugada syndrome. Postcardiac arrest care was performed after ROSC, including mild therapeutic hypothermia, hemodynamic monitoring and management, and ICD implantation, and then the patient completely recovered without any noticeable neurological or intellectual deficits in the follow-up examinations.Our case demonstrates that even after an OHCA with prolonged time (120 minutes) until ROSC, survival with a favorable neurological outcome is possible, provided implementation of an extremely effective rescue chain.
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PMID:Complete Recovery With the Chain of Survival After a Prolonged (120 Minutes) Out-of-Hospital Cardiac Arrest Due to Brugada Syndrome: A Case Report. 2616 3

BACKGROUND The clinical presentation of pulmonary embolism (PE) is highly variable, ranging from no symptoms to shock or sudden death, often making the diagnosis a challenge. An electrocardiogram (EKG) is not a definitive diagnostic tool; however, it can alter the clinical suspicion of acute PE. PE has nonspecific electrocardiographic patterns ranging from a normal EKG in almost 33% of patients to sinus tachycardia, S1Q3T3 pattern (McGinn-White Sign), right axis deviation, and incomplete right bundle branch block (RBBB). ST-segment elevation associated with PE is exceedingly rare, and to date, only a few cases have been reported. CASE REPORT We present a case of a middle-aged male patient with no medical comorbidities other than obesity, who presented with initial symptoms and EKG findings concerning an ST-elevation myocardial infarction (STEMI). He was later found to have rather patent coronary arteries on cardiac catheterization but bilateral sub-massive pulmonary embolism on computed tomography angiogram (CTA) of the chest. CONCLUSIONS The differential diagnosis of STEMI is broad, including, but not limited to, Prinzmetal's angina, takotsubo cardiomyopathy, Brugada syndrome, left ventricular aneurysm, hypothermia, hyperkalemia, and acute pericarditis. Pulmonary embolism may present with abnormal EKG and biomarkers that appear to be an acute coronary syndrome, even STEMI. Physicians must maintain a high index of clinical suspicion through risk stratification to identify PE in these settings, as the frequency of such an occurrence is extremely low. A bedside echocardiogram can be an invaluable diagnostic tool in such cases.
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PMID:Pulmonary Embolism Presenting as ST-Elevation Myocardial Infarction: A Diagnostic Trap. 3324 83