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The Osborn wave J wave is a positive deflection seen at the J point in precordial and true limb leads. It is most commonly associated with hypothermia. These changes will appear as a reciprocal, negative deflection in aVR and V1. It represents the approximate end of depolarization and the beginning of repolarization as determined by the surface ECG. There is an overlap of around 10ms. The J wave is a much less common, slow deflection of uncertain origin originally described in relation to hypothermia. Causes of non-hypothermic Osborn waves include:. No definitive physiological cause for the deflection has been described, despite numerous postulates. Compared to other hypothermia-induced ECG abnormalities e. See below for a deep dive into the eponymous history. Osborn Wave ECG examples. Example 1. Example 2. Example 3. Example 4. Occasionally you may encounter other terms used to describe Osborn waves J waves. Some authors have used the term J wave deflection to describe such a large, prominent deviation of the J point from the baseline. There is little consensus regarding terminology, nature, and prognostic significance of the J wave. In the setting of hypothermia, this phenomenon is most commonly referred to as an Osborn wave. They noted that a widening of the secondary deflection on the QRS complex and supraventricular arrhythmias were accompanied by a parallel increase of carbon dioxide in alveolar air during body cooling. Bigelow et al described ECG changes in hypothermic dogs as:. The T-wave is long and irregular, and usually inverted. Experimentally-induced hypothermia caused the development of a distinct deflection at the J point on the ECG and resulted in ventricular fibrillation. Osborn considered acidaemia induced by hypothermia as a primary cause of the Osborn wave, because it disappeared if the arterial pH was normalized by hyperventilation during the same degree of cooling. He postulated:. They questioned the participation of acidosis in J wave genesis and the ability of this deflection to predict development of ventricular fibrillation. The characteristic deflection of hypothermia has sometimes been named after Osborn who discussed it in Procter Harvey, MD. J wave deflections were found in the settings of acute ischaemic events, cocaine use, haloperidol overdose, and left ventricular hypertrophy due to hypertension. They concluded that the Osborn wave is not pathognomonic of hypothermia. The presence of a prominent action potential notch in epicardium but not endocardium is shown to provide a voltage gradient that manifests as a J Osborn wave or elevated J-point in the ECG. Over the years it has been increasingly common for clinicians to label the J-wave deflection seen in hypothermia as an Osborn wave. Emergency physician, Sir Charles Gairdner Hospital. Passion for rugby; medical history; medical education; and asynchronous learning FOAMed evangelist. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. This site uses Akismet to reduce spam. Learn how your comment data is processed. J point in a normal; b J point elevation; c with Osborn wave J wave ; d J point depression. Rectal temperature: a. Fig 4. Electrocardiogram during hypothermia lead II. Hypothermic dog 7 min. Animal showed early alkalosis followed by acidosis. Rectal temp. Diagram of ECG shown in A, identifying current of injury. Osborn JJ. Am J Physiol. Serial lead II electrocardiograms taken during rewarming process. Note loss of muscular tremors, emergence of P waves, increase in heart rate, and gradual diminution of the size of J waves arrows. Fernandez Mike Cadogan. Robert Buttner. Leave a Reply Cancel reply.

Osborn Wave (J Wave)

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Official websites use. Share sensitive information only on official, secure websites. Mad-honey poisoning can occur after the eating of honey that contains grayanotoxin. Mad honey is intentionally produced from the nectar of Rhododendron ponticum , which grows in Japan, Nepal, Brazil, parts of North America and Europe, and the eastern Black Sea region of Turkey. Low doses of grayanotoxin can cause dizziness, hypotension, and bradycardia, and high doses can cause impaired consciousness, syncope, atrioventricular block, and asystole due to vagal stimulation. Reports of acute coronary syndrome are very rare. Herein, we present the case of a year-old husband and year-old wife who, to improve sexual performance, intentionally ate honey from the Black Sea area of Turkey for 1 week. Within 3 hours of consuming increased amounts of the honey, they presented at our emergency department with acute inferior myocardial infarctions. Coronary angiography revealed normal coronary arteries in both patients. Supportive treatment with atropine rapidly resolved the clinical symptoms and electrocardiographic irregularities. Grayanotoxin-containing rhododendron pollen was detected in the honey. In patients from geographic regions where mad honey can be obtained, mad-honey poisoning should be considered in the differential diagnosis of chest pain, particularly in the presence of unexplained bradyarrhythmia and hypotension. Sexual performance is a chief reason for the purchase of mad honey and self-treatment with it by persons of our patients' ages. Mad-honey poisoning can occur after eating honey that contains grayanotoxin. Grayanotoxin-containing honey is intentionally produced from the nectar of Rhododendron ponticum , which grows in Japan, Nepal, Brazil, parts of North America and Europe, and the eastern Black Sea region of Turkey. In September , a year-old husband and his year-old wife presented at our emergency department with confusion and chest pain. Their medical histories could not immediately be taken. Neither ECG revealed right ventricular infarction. After both patients were given 1 mg of atropine, their blood pressures and heart rates recovered dramatically, and their chest pain and ST-segment elevations resolved within 5 minutes. In the catheterization laboratory, coronary angiography showed normal coronary arteries in both patients Figs. Both were then taken to the coronary intensive care unit, where ECGs 30 minutes after admission showed complete ST-segment resolution in the inferior leads. By this time, the patients were clinically and hemodynamically stable. Levels of cardiac troponin I were The couple revealed that they had eaten mad honey 3 hours before admission to the hospital. During their weeklong consumption of the honey for reasons of sexual performance, mild headaches and dizziness had occurred, but they had not cared. They had increased their intake of honey from 1 teaspoon each to 1 tablespoon each on the morning of their hospitalization. Electrocardiogram upon hospital admission shows complete atrioventricular block and ST-segment elevation in the inferior leads. Electrocardiogram upon hospital admission shows atrioventricular nodal rhythm and ST-segment elevation in the inferior leads. Coronary angiography shows no evidence of flow-limiting lesions in A the right coronary artery or B the left coronary arteries. Analysis of the honey revealed grayanotoxin-containing rhododendron pollen. The patients were discharged on the 5th day of hospitalization, and no medications were prescribed. One month later, both were asymptomatic, and results of ECGs and echocardiography were normal. Mad-honey poisoning is caused by the ingestion of grayanotoxin. Honey with grayanotoxin is intentionally produced from the nectar of Rhododendron ponticum , which grows extensively in the mountains of the eastern Black Sea region of Turkey. First, grayanotoxin binds to the voltage-dependent sodium channel in its open state. Second, the modified sodium channels are unable to inactivate. Third, the activation potential of the modified sodium channel is shifted in the direction of hyperpolarization. Thus, grayanotoxin creates increased sodium channel permeability and activates the vagus nerve, causing dizziness, hypotension, and bradycardia in low doses, and impaired consciousness, syncope, atrioventricular block, and asystole in high doses due to vagal stimulation. A clinical evaluation that includes close questioning of the patient is typically sufficient to establish the diagnosis of mad-honey poisoning; but in difficult cases, or when a dietary and travel history cannot be taken, pollen analysis can be definitive. Acute inferior MIs occurred within 3 hours after the patients ingested increased amounts of the honey; after atropine was given, their blood pressures and heart rates returned to normal, and their angina and ST-segment elevations resolved. Upon analysis, the rhododendron pollen in the honey was determined to be the precipitant of the patients' acute MIs. To our knowledge, no fatal cases of mad-honey poisoning have been reported since ancient Roman times. Typically, the effects of inadvertent poisoning last no longer than 24 hours, and supportive care is sufficient as treatment. Severely depressed blood pressure usually responds to atropine and saline infusion therapy; vasopressor therapy is rarely required. Therefore, our patients did not require long-term antiplatelet therapy. In persons with normal coronary arteries, prolonged vagal tonus may lead to transient ST-segment elevation because of hypotension and bradycardia. In our patients, the main mechanism of the transient ST elevation probably depended upon a prolonged vagal tonus that was induced by the grayanotoxin in the honey. Their rapid recovery after atropine administration also supports this reasoning. To our knowledge, acute coronary syndrome from mad-honey poisoning has been reported only twice. The earlier reports suggest that mad-honey poisoning should be kept in mind as a differential diagnosis in the presence of STEMI and the absence of coronary lesions. In a survey of Turkish beekeepers who produced and sold mad honey as an alternative medicine, 16 men aged 41 to 60 years purchased mad honey chiefly for self-treatment of sexual dysfunction. This was the second most common reason for purchase by women of that age. Our married patients in this report fit that demographic category. As a library, NLM provides access to scientific literature. Tex Heart Inst J. Find articles by Mikail Yarlioglues. Find articles by Mahmut Akpek. 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