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Head and Neck
Published in Bobby Krishnachetty, Abdul Syed, Harriet Scott, Applied Anatomy for the FRCA, 2020
Bobby Krishnachetty, Abdul Syed, Harriet Scott
Other Hypocalcaemia. This may present as neuromuscular excitability, tetany or perioral tinging. Facial twitching may be seen when tapping over the facial nerve at the parotid gland. ECG may demonstrate a prolonged QT interval.Thyroid stormPneumothorax (if retro-sternal dissection)
Medicinal poisons
Published in Jason Payne-James, Richard Jones, Simpson's Forensic Medicine, 2019
Jason Payne-James, Richard Jones
Since the 1990s, the concept of primary ‘inherited’ arrhythmia syndromes, or ion channelopathies, has developed from advances in molecular genetics. Alterations in genes coding for membrane proteins, such as ion channels or their associated proteins responsible for the generation of cardiac action potentials (AP), cause specific malfunctions which eventually lead to cardiac arrhythmias. These arrhythmic disorders include a wide variety of conditions. Among these, long QT, and Brugada, syndromes are the most extensively studied, and drugs cause a phenocopy of these two diseases. More than 10 different genes have been reported to be responsible for each syndrome. Individuals with long QT syndrome (LQTS) experience abnormal prolongation of the QT interval – the portion of the electrocardiogram (ECG) that represents repolarisation of cardiomyocytes (Figure 25.1). The QT interval extends from the onset of the Q wave to the end of the T wave. The normal rate-adjusted length for the QT interval is less than 440 milliseconds. A prolonged QT interval favours the occurrence of a lethal form of ventricular tachycardia known as torsades des pointes. The QT prolongation may be caused by genetic aberration or it may be acquired. Even those with the genetic form of the disease may have a perfectly normal-appearing electrocardiogram until some event causes the QT interval to lengthen, become pathologically long and produce an arrhythmia. The diagnosis is made by DNA resequencing.
The QT interval
Published in Andrew R Houghton, Making Sense of the ECG, 2019
When you assess the QT interval, therefore, ask yourself the following two questions: Is the QTc interval long?Is the QTc interval short?
Characterization and management of adverse events observed with mobocertinib (TAK-788) treatment for EGFR exon 20 insertion–positive non–small cell lung cancer
Published in Expert Review of Anticancer Therapy, 2023
James Chih-Hsin Yang, Caicun Zhou, Pasi A. Jänne, Suresh S. Ramalingam, Tae Min Kim, Gregory J Riely, Alexander I Spira, Zofia Piotrowska, Tarek Mekhail, Maria Rosario Garcia Campelo, Enriqueta Felip, Lyudmila Bazhenova, Shu Jin, Manmit Kaur, Paul M. Diderichsen, Neeraj Gupta, Veronica Bunn, Jianchang Lin, Eric N. Churchill, Minal Mehta, Danny Nguyen
Treatment-related cardiac disorders, which include cardiac failure and QTc interval prolongation, were observed in 12% of the patients; Grade ≥3 treatment-emergent cardiac disorders were observed in 13% of the patients, 11% with SAEs, and 2% discontinuing. Cardiac failure (including congestive cardiac failure, decreased ejection fraction, and cardiomyopathy) occurred in 2.3% of the patients. Grade 3 cardiac failure occurred in 0.8% of the patients. Grade 4 and fatal cardiac failure occurred in one patient each (0.4%). QTc interval prolongation (including electrocardiogram QT prolongation and ventricular arrhythmia) occurred in 8% of the patients. Grade 3 QTc interval prolongation occurred in 1.6% of the patients and Grade 4 QTc interval prolongation occurred in 1 patient (0.4%).
Prolonged QTc Interval in Nigerian Children with Sickle Cell Anemia
Published in Hemoglobin, 2021
Maxwell U. Anah, Anthony C. Nlemadim, Chigozie I. Uzomba, Egorp O. Ineji, Friday A. Odey
There are other established causes of prolonged QTc interval, the majority of which have been excluded in the subjects of this study [8]. One of them is hypocalcemia, which appears to be a constant factor in sickle cell anemia, and together with myocardial ischemia, may be the fundamental reason for the occurrence of prolonged QTc interval in sickle cell anemia unlike in non sickle cell anemia patients with anemia due to other hematological diseases [3,4,21]. Hypomagnesemia also causes prolonged QTc interval by impairing release of parathormone and tissue response to parathormone that leads to secondary hypocalcemia [22]. Therefore, if serum calcium levels were measured in this study, one may have found hypocalcemia in both clinical states similar to that obtained in previous studies [3–7].
A pharmacological profile of intravenous amisulpride for the treatment of postoperative nausea and vomiting
Published in Expert Review of Clinical Pharmacology, 2020
Several unwanted, ‘off-target’ effects of dopamine-antagonist antiemetics have limited their clinical use, the most important being a prolongation of the QT interval of the electrocardiogram, mediated by binding to the potassium ion channel known as the hERG channel, after the human ether-à-go-go-related gene (hERG) which codes for its alpha subunit. The QT interval represents the electrical repolarization of the heart in preparation for a new beat. QT prolongation can, therefore, lead to rhythm disturbances, including the potentially fatal torsade de pointes. Numerous dopaminergic antiemetics have been shown to bind hERG with high affinity, including droperidol (half-maximal inhibitory concentration [IC50] = 0.6–0.9 µM), haloperidol (~1 µM) and prochlorperazine (0.7–0.9 µM) [28–30]. These agents are also associated with a significant prolongation of the QT interval and cases of torsade de pointes in clinical practice [31–33].