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LETTER TO EDITOR
Year : 2015  |  Volume : 5  |  Issue : 4  |  Page : 268-270

Osborn waves in normothermic patient with hydropneumothorax and myocardial ischemia


Department of Medicine, Dr. Rajendra Prasad Government Medical College, Tanda, Himachal Pradesh, India

Date of Web Publication1-Dec-2015

Correspondence Address:
Vivek Chauhan
Department of Medicine, Dr. Rajendra Prasad Government Medical College, Tanda, Kangra - 176 001, Himachal Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2229-5151.170843

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How to cite this article:
Chauhan V, Brahma RS. Osborn waves in normothermic patient with hydropneumothorax and myocardial ischemia. Int J Crit Illn Inj Sci 2015;5:268-70

How to cite this URL:
Chauhan V, Brahma RS. Osborn waves in normothermic patient with hydropneumothorax and myocardial ischemia. Int J Crit Illn Inj Sci [serial online] 2015 [cited 2021 Aug 3];5:268-70. Available from: https://www.ijciis.org/text.asp?2015/5/4/268/170843

Dear Editor,

A 55-year-old male was admitted with a complaint of cough and left sided chest pain for two weeks. He had fever and progressive dyspnea for one week before admission. He was worked up at some private clinic where his chest X-ray, CT thorax and blood investigations were already done. His chest X-ray showed hydropneumothorax on left side. His CT thorax showed large hydropneumothorax on left side with collapse consolidation of left lower lobe with mediastinal lymphadenopathy suggestive of infective changes [Figure 1]. Possibility of pulmonary tuberculosis was kept. His ECG showed tachycardia with normal axis and deep S waves in lead V1. Incidentally, we noticed that there were Osborn waves in inferior and lateral chest leads [Figure 2]. We checked his temperature, which was 99°F. His blood pressure was 110/72 mm Hg. Other causes of Osborn waves were not found and his calcium level was 7.1 mg/dl, and serum creatinine was 2 mg/dl. However, his CK-MB enzyme level was high (120 IU/L). We planned an echocardiography for this patient to rule out myocardial infarction (MI). Unfortunately, before we could do anything further, even before a chest tube could be put in he developed a sudden cardiac arrest and could not be revived.{Figure 1}{Figure 2}

The questions that remained unanswered were whether our patient had an MI which was shadowed by the massive hydropneumothorax and what caused appearance of Osborn waves in this patient. Though hydropneumothorax had produced a lot of distortion of cardiac axis in our patient, Osborn waves have never been described in a patient of hydropneumothorax before. These waves have been given various names in the past like "camel-hump sign", "late delta wave", "hathook junction", "hypothermic wave", "J point wave", "K wave", "H wave" and "current of injury".[1] Osborn waves are most commonly seen in hypothermia patients but have been reported in many other conditions like hypercalcemia, brain injury, subarachnoid hemorrhage, cardiopulmonary arrest from oversedation, vasospastic angina, Brugada syndrome or idiopathic ventricular fibrillation.[1],[2],[3],[4]

Osborn waves of hypothermia are most commonly observed in leads II, III, aVF, V5 and V6.[2] In our patient however, they were best seen in lead III and V2, however other leads that showed this wave were lead II, aVF, V3-V5 [Figure 2]. The ECG changes in our patient were not suggestive of cardiac ischemia but he had creatinine kinase MB fraction levels of 120 IU/L which was suggestive of significant myocardial injury. Osborn waves in myocardial ischemia in absence of hypothermia have been very well described as an early manifestation of left circumflex (LCx) artery infarction.[4] Pathophysiologically, the heterogeneous distribution of a transient outward current-mediated spike-and-dome morphology of the action potential across the ventricular wall has been shown to lead to the manifestation of the electrocardiographic J wave.[5] It is known that ischemic events in the territory of LCx are likely to be missed as these may not be associated with classical ST segment elevations and that the posterior wall of myocardium is one of the "silent areas" of the routine 12-lead ECG. There are case reports where the diagnosis of true posterior wall infarction was made only after the appearance of the classical ECG changes after 24 hours. The J waves seen in the first ECG represent the "current of injury" and are indicative of severe ischemia in the territory of LCx.[4] Experimental data in laboratory animals shows that simulated acute ischemia produces similar waves secondary to transmural voltage gradient in the early phases of ischemia. Acute ischemia may cause opening of KATP channels and reduction of calcium channel current, leading to an increase in the magnitude of the epicardial action potential and this to inscription of the J waves.[6] Osborn waves have generally been considered to be benign waves which reverse once temperature is normalized. An interesting case report shows that in a patient of cardiac arrest where they were trying to induce therapeutic hypothermia, whenever Osborn waves appeared, there was a ventricular fibrillation. This case highlights the arrhythmogenic potential of Osborn waves.[7] The association of Osborn wave with myocardial ischemia in our patient which was not evident from the ECG but was revealed by highly raised CK-MB levels. Our patient developed sudden cardiac arrest most probably due to ventricular fibrillation which was not documented. The correlation of Osborn waves with ventricular fibrillation is another area where research is needed, especially in the light of routine induction of hypothermia post return of spontaneous circulation in cardiac arrest patients, where Osborn waves are likely to appear. Moreover, the presence of left sided hydropneumothorax in our patient makes this ECG interesting and this case may put some more light on the genesis of Osborn waves.

 
   References Top

1.
Maruyama M, Kobayashi Y, Kodani E, Hirayama Y, Atarashi H, Katoh T, et al. Osborn waves: History and significance. Indian Pacing Electrophysiol J 2004;4:33-9.  Back to cited text no. 1
    
2.
Patel A, Getsos JP, Moussa G, Damato AN. The osborn wave of hypothermeia in normothermic patients. Clin Cardiol 1994;17:273-6.  Back to cited text no. 2
    
3.
Otero J, Lenihan DJ. The "Normothermic" Osborn wave induced by severe hypercalcemia. Tex Heart Inst J 2000;27:316-7.  Back to cited text no. 3
    
4.
Shinde R, Shinde S, Makhale C, Grant P, Sathe S, Durairaj M, et al. Occurrence of "J waves" in 12-Lead ECG as a marker of acute ischemia and their cellular basis. Pacing Clin Electrophysiol 2007;30:817-9.  Back to cited text no. 4
    
5.
Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996;93:372-9.  Back to cited text no. 5
    
6.
Cellular basis for ST-segment changes observed during ischemia.-PubMed-NCBI. Available from: . [Last accessed on 2015 Jul 21].  Back to cited text no. 6
    
7.
Kim CY, Bae MH, Kim NK, Yang YA, Kim KY, Lee JH, et al. Case of recurrent ventricular fibrillations with osborn wave developed during therapeutic hypothermia. Korean Circ J 2015;45:81-4.  Back to cited text no. 7
    




 

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