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Thorax
Published in Bobby Krishnachetty, Abdul Syed, Harriet Scott, Applied Anatomy for the FRCA, 2020
Bobby Krishnachetty, Abdul Syed, Harriet Scott
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
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
An alternative way to assess a QT interval is to correct it to what it would be if the patient's heart rate was 60 beats/min. By doing this, all you will need to remember is the normal range for the QT interval at a heart rate of 60 beats/min: 350–450 msec in men and 350–460 msec in women.
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).
QTc interval diurnal variations in patients treated with psychotropic medications: implications for the evaluation of drug induced QTc changes
Published in International Review of Psychiatry, 2022
A. Cuomo, C. Libri, G. Barillà, M. Cattolico, P. Carmellini, A. Fagiolini
QT interval is defined as the time going from the start of the Q wave to the end of the T wave on the electrocardiogram (EKG). QT interval shortens at faster heart rates and lengthens at slower heart rates. Corrected QT interval (QTc) estimates the QT interval at a standard heart rate of 60 bpm, and this permits a comparison of QT values over time at different heart rates and improves detection of patients at increased risk of arrhythmias. Prolonged QTc interval is considered a marker to detect the risk of torsades de pointes (TdP), which frequently leads to sudden cardiac death (Vandael et al., 2017). According to the European Medicines Agency (EMA) guidelines, a QTc interval is defined as prolonged if its value is greater than 450 ms in adult men and 470 ms in adult women; for QTc values greater than 500 ms, QTc prolongation is considered severe and is associated with a higher risk of TdP (Nachimuthu et al., 2012; van Noord et al., 2010). In a Swiss study conducted on 6790 psychiatric patients, abnormal EKGs were detected in 27.3% of patients with a prevalence of prolonged QTc interval (≥ 470–499 ms) in 6.1% of patients and another 1.6% with long QTc interval (≥ 500 ms) with 58% of the latter qualifies as induced by drug, of whom 19.4% had torsade de pointes or sudden death within 72 h of detection (Girardin et al., 2013).
Pseudohypoparathyroidism presenting in children at a tertiary hospital in Johannesburg, South Africa
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2020
N Madi, FY Moosa, KB Parbhoo, JM Pettifor, K Thandrayen
A 13-year-old black African male presented with generalised tonic-clonic seizures. He had no clinical signs of hypocalcaemia (tetany, muscle spasms) and negative Trousseau and Chvostek signs. He was wasted and mildly stunted. He had no dysmorphic features, and no signs of AHO. He was unable to walk, with decreased power in the lower limbs but no other positive neurological findings. He did have a lower respiratory tract infection with digital clubbing and subsequently was confirmed to have pulmonary tuberculosis (TB) on sputum microscopy and cultures. Biochemistry on admission showed severe hypocalcaemia, an elevated PTH level and hyperphosphataemia (see Table 1). His renal function, thyroid function tests and albumin were normal. The ECG showed a slightly prolonged QT interval. The CT scan of the brain showed extensive bilateral calcifications in the basal ganglia and cerebral parenchyma, with age-inappropriate involutional changes and the brain MRI showed multiple symmetrical foci of calcifications in the basal nuclei, cerebellar hemispheres and cortex, with ventriculomegaly and prominent sulci (Figure 3).