Paper 3 Answers
James Day, Amy Thomson, Tamsin McAllister, Nawal Bahal in Get Through, 2014
The QT interval is a measure of the time taken for a cycle of ventricular depolarization and repolarization, and is measured as the time between the beginning of the electrocardiogram Q wave and the end of the T wave. It varies with heart rate and is therefore corrected to give the QTc. Prolongation of the QT interval can be due to genetic or acquired causes but is often due to a combination of a genetic predisposition and acquired factors. Prolongation of QT interval leads to impairment of ventricular repolarization, which can predispose to polymorphic ventricular tachycardia (torsade de pointes). Drugs that prolong QT interval include most volatile anaesthetic agents, amiodarone, flecainide, thiazides, phenothiazines, tricyclic antidepressants and suxamethonium. In addition, excessive stress can trigger torsades de pointes in patients with prolonged QT interval. Care must therefore be taken in administering general anaesthesia in such patients.
Thorax
Bobby Krishnachetty, Abdul Syed, Harriet Scott in Applied Anatomy for the FRCA, 2020
The QT interval is the time from the start of the Q wave to the end of the T wave, thus representing the time taken for ventricular depolarisation and repolarisation. The maximum slope intercept method defines the end of the T wave as the intercept between the isoelectric line with the tangent drawn through the maximum down slope of the T wave.Normal value: 380–440 msIt is inversely proportional to heart rate, thus changing with higher and lower heart rates. Hence the corrected QT interval (QTc) is used to estimate the QT at a standard heart rate of 60/min to improve recognition of patients at increased risk of arrhythmias.
Medicinal poisons
Jason Payne-James, Richard Jones in Simpson's Forensic Medicine, 2019
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.
A pharmacological profile of intravenous amisulpride for the treatment of postoperative nausea and vomiting
Published in Expert Review of Clinical Pharmacology, 2020
Gabriel Fox, Peter Kranke
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].
Comparison of different QT correction methods for nonclinical safety assessment in ketamine-anesthetized Indian rhesus monkeys (Macaca mulatta)
Published in Toxicology Mechanisms and Methods, 2023
Laxit K. Bhatt, Chitrang R. Shah, Rajesh J. Patel, Shital D. Patel, Sudhir R. Patel, Vipul A. Patel, Jitendra H. Patel, Pankaj Dwivedi, Niraj A. Shah, Rajesh S. Sundar, Mukul R. Jain
QT interval is the measure of the length from the onset of the QRS complex to the end of the T wave in one cardiac cycle, representing ventricular depolarization and repolarization (Chaves et al. 2006). QT interval varies with heart rate (HR); an inversely proportional relationship wherein a shorter QT interval is recorded for faster heart rates and vice versa (Chaves et al. 2006; Guth 2007). This has prompted researchers to develop a QT correction formula that adjusts the impact of HR on QT interval. The corrected QT interval (QTc) has widespread clinical and pharmaceutical significance (Chaves et al. 2006; Guth 2007). Various QT correction formulas are available currently. They can be divided into three types: population correction methods, test specific/individual correction methods and Holter bin methods. The population correction method can be used at any time and is the most popular (Holzgrefe et al. 2014).
A case of celiac disease presenting with celiac crisis: rare and life threatening presentation
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
Rakshya Poudyal, Saroj Lohani, William B. Kimmel
Other labs on admission revealed magnesium of 1 mg/dl (normal 1.9–2.7 mg/dl), potassium of 3.1 meq/L (normal 3.5–5.1 meq/L), 25 Hydroxy vitamin D of 10.1 ng/ml (normal >20 ng/ml), parathyroid hormone of 140 pg/ml (normal 12–88 pg/ml), albumin of 2.7 g/dL (normal 3.5–5.7 g/dL), venous PH of 7.314 (normal 7.32–7.43), bicarbonate of 19.8 meq/L (normal 21–31 meq/L), ferritin of 7 ng/ml (normal 27–300 ng/ml), iron of 14 mcg/dL (normal 50–212 mcg/dL), iron sat of 7 (20–50%). His hemoglobin was 8.6 g/dL (14–17.5 g/dL), Mean Corpuscular Volume (MCV) 79 fl (normal 80–99 fl), Mean Cellular Hemoglobin (MCH) 24.8 pg (normal 27–34 pg) and total leucocyte count was 16,600/microL (normal 4800–10,800/microL) . Renal function was normal. Electrocardiogram revealed prolonged QT interval. Computerized Tomography (CT)scan of abdomen revealed diffuse enteritis with reactive mesenteric adenopathy.
Related Knowledge Centers
- Arrhythmia
- Cardiac Arrest
- T Wave
- Ventricle
- Heart
- Electrocardiography
- Qrs Complex
- Genetics
- Long Qt Syndrome
- Sotalol