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

This article examines specific electrocardiographic (ECG) and electrophysiological features of ventricular repolarization in rats and mice, and the role of depolarization-activated potassium currents in mediating the unique features of ECG recordings in these rodents. This article describes the currents that underlie ventricular repolarization in these rodents, identifies terminology that appropriately describes the unique features of murine ECG recordings, and correlates these unique findings with selected human ECG ventricular repolarization abnormalities. The absence of a distinct isoelectric interval between the QRS complex and the T wave, accompanied by a relatively short QT interval, are common features of ECG recordings in mice and rats, but not in ECGs in guinea pigs. The murine ECG morphology is apparently attributable to the presence of large outward K+ currents that dominate the early phase of ventricular repolarization. In rats and mice, the predominant current underlying the early phase of repolarization appears to be the rapidly activating and inactivating 4-aminopyridine-sensitive transient outward current (ie, I(to)). Importantly, the density of I(to) in rats and mice is high, whereas this current is not evident in the ventricular myocytes of guinea pigs. The high density of I(to) appears to underlie the prominent J wave or downsloping ST-segment elevation seen in rats and mice, whereas the ST-segment is isoelectric in guinea pigs. The unusual J wave and ST-segment pattern in murine ECGs, however, does bear some resemblance to ECG features observed in humans with Brugada syndrome, and with hypothermia and ischemia. These patterns in rats and mice might, therefore, serve as an experimental model for the idiopathic J wave.
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PMID:Rapid ventricular repolarization in rodents: electrocardiographic manifestations, molecular mechanisms, and clinical insights. 1081 9

Incidence of electrocardiographic abnormalities in subarachnoid hemorrhage secondary to aneurysm rupture is 50-100%. The most frequent electrocardiographic abnormalities described include acuminated, inverted or flat T waves, inverted T waves associated with prolonged QT interval, positive or negative ST segment levels, prominent U waves, PR segment enlargement, acuminated P waves, and pathologic Q waves. J point is the isoelectric union of QRS complex with ST segment. It represents the end of depolarization and the beginning of repolarization. Prominent and positive J point level is named J wave, considered pathognomonic of severe hypothermia, although it has also been described in other clinical entities not associated with hypothermia, such as hypercalcemia, Brugada syndrome, acute brain injury, cardiac arrest, and dysfunction of cervical sympathetic system. Non-hypothermic J wave is an infrequent electrocardiographic manifestation of subarachnoid hemorrhage. We describe a clinical case of non-hypothermic J wave in a patient with subarachnoid hemorrhage.
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PMID:[Non-hypothermic J wave in subarachnoid hemorrhage]. 1517 30

We report, at the time of a hypothermia major, the observation of an anomaly of the repolarisation on the electrocardiogram of surface, called "J wave", and described in an exhaustive way by Osborn, which attached its name there. It corresponds to the picking of the terminal section of the QRS, with heightening in dome, the J point is then elevated compared to the base line. It can be also seen among patients normothermic in physiological or pathological circumstances. Its physiopathology from now on is understood better, the J wave is the result of the difference of potential action between the epicarde and endocarde during phases 1 and 2 of the ventricular repolarisation. This gradient is related to the Ito current, also accused in the "channel pathologies", of which Brugada syndrome.
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PMID:[Osborn J wave. A new "channel pathology"? A case report]. 1707 66

The "J wave" (also referred to as "the Osborn wave,""the J deflection," or "the camel's hump") is a distinctive deflection occurring at the QRS-ST junction. In 1953, Dr. John Osborn described the "J wave" as an "injury current" resulting in ventricular fibrillation during experimental hypothermia. Although "J Wave" is supposed to be pathognomonic of hypothermia, it is seen in a host of other conditions such as hypercalcemia, brain injury, subarachnoid hemorrhage, cardiopulmonary arrest from over sedation, the Brugada syndrome, vasospastic angina, and idiopathic ventricular fibrillation. However, there is paucity of literature data as regards to ischemic etiology of "J Wave." In this article, we present a case where "J waves" were probably induced by ischemia. We also discuss the mechanism of ischemia-induced "J wave" accentuation and its prognostic implications.
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PMID:Occurrence of "J waves" in 12-lead ECG as a marker of acute ischemia and their cellular basis. 1754 22

Commotio cordis or ventricular fibrillation caused by a blow to the chest is a rare cause of cardiac arrest in a well child. We report a case of a young child falling from a low height landing chest first with rapid onset of unconsciousness, apnoea and cyanosis. Cardiopulmonary resuscitation was given by parents under telephone instruction from an ambulance dispatch centre. On arrival of officers, 7 min after the fall, ventricular fibrillation was present but responded to defibrillation (biphasic 3 J/kg). No clinical or CT evidence of chest or brain trauma was present and investigations (ECGs, cardiac MRI, echocardiography, viral tests, metabolic tests, drug tests, serum electrolytes) did not reveal any cardiac illness or abnormal cardiac anatomy. Specifically, a long QT was absent and a Flecainide challenge for Brugada syndrome was negative. There was no family history of sudden death. No further dysrrhythmia occurred and the child recovered neurologically well after 3 days of therapeutic hypothermia (for cerebral ischaemia) and 7 days of mechanical ventilation.
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PMID:A case of Commotio cordis in a young child caused by a fall. 1816 18

A patient in whom moderate hypothermia developed after prolonged cardiopulmonary resuscitation is described. Hypothermia was manifested by transient electrocardiogram changes, including long QT, precordial J waves, and downsloping ST-segment elevation ending in a negative T wave in leads V(1) and V(2) resembling the Brugada syndrome. The physiopathologic mechanisms of these electrocardiographic findings are discussed.
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PMID:Hypothermia-induced Brugada-like electrocardiogram pattern. 1853 79

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

Brugada syndrome (BrS), caused by ion channel abnormalities, is characterized by ST segment elevation and negative T waves in the right precordial electrocardiographic (ECG) leads recorded over the right ventricular outflow tract (RVOT). BrS is sensitive to body temperature and can lead to T-wave alternans (TWA), ventricular tachycardia, and sudden death. Recent studies in an isolated canine RVOT model of BrS demonstrated that reversal of the transmural gradient of repolarization caused the ECG characteristics and that major intraepicardial and transmural dispersion of action potentials (APs) initiated phase 2 reentry, premature ventricular activations, and tachyarrhythmias. Hypothermia enhanced the heterogeneity of the AP and promoted the origination of phase 2 reentry in the epicardium of the RVOT, but the prolonged AP duration frequently blocked reentry. Hyperthermia abbreviated the AP and facilitated the maintenance of reentry and tachyarrhythmias. Bradycardia promoted alternans in the phase 2 dome of the AP within the epicardium of the RVOT, resulting in TWA. The above phenomena were localized in the epicardium of the RVOT. Blockade of the transient outward current, I(to), reduced AP heterogeneity and prevented arrhythmias in the BrS model. In addition, epicardial activation delay led to fragmented QRS, a risk marker of prognosis in BrS. Body surface mapping in patients with BrS supported these experimental findings. In conclusion, the AP heterogeneity within the epicardium of the RVOT contributes to the ECG characteristics, temperature sensitivity, TWA, and arrhythmias in BrS, and body surface mapping and fragmented QRS can be effective predictors of risk in patients with BrS.
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PMID:Brugada syndrome: insights of ST elevation, arrhythmogenicity, and risk stratification from experimental observations. 1988 72

The J wave, also referred to as an Osborn wave, is a deflection immediately following the QRS complex of the surface ECG. When partially buried in the R wave, the J wave appears as J-point elevation or ST-segment elevation. Several lines of evidence have suggested that arrhythmias associated with an early repolarization pattern in the inferior or mid to lateral precordial leads, Brugada syndrome, or arrhythmias associated with hypothermia and the acute phase of ST-segment elevation myocardial infarction are mechanistically linked to abnormalities in the manifestation of the transient outward current (I(to))-mediated J wave. Although Brugada syndrome and early repolarization syndrome differ with respect to the magnitude and lead location of abnormal J-wave manifestation, they can be considered to represent a continuous spectrum of phenotypic expression that we propose be termed J-wave syndromes. This review summarizes our current state of knowledge concerning J-wave syndromes, bridging basic and clinical aspects. We propose to divide early repolarization syndrome into three subtypes: type 1, which displays an early repolarization pattern predominantly in the lateral precordial leads, is prevalent among healthy male athletes and is rarely seen in ventricular fibrillation survivors; type 2, which displays an early repolarization pattern predominantly in the inferior or inferolateral leads, is associated with a higher level of risk; and type 3, which displays an early repolarization pattern globally in the inferior, lateral, and right precordial leads, is associated with the highest level of risk for development of malignant arrhythmias and is often associated with ventricular fibrillation storms.
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PMID:J wave syndromes. 2015 65

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


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