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Paper 1
Published in Aalia Khan, Ramsey Jabbour, Almas Rehman, nMRCGP Applied Knowledge Test Study Guide, 2021
Aalia Khan, Ramsey Jabbour, Almas Rehman
On an ECG, Q-waves are thought to be non-significant if small and present in the left ventricular leads. If the Q-wave is >0.04 seconds in width and >2mm in depth, it is thought to be pathological. Although indicative of infarction, there is no correlation with the age of an infarct. They directly precede the R-wave.
Bioelectric and Biomagnetic Signal Analysis
Published in Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam, Introduction to Computational Health Informatics, 2019
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam
The thickening of the right-ventricle in a heart causes Q-wave to become pronounced. Since part of the depolarization wave is embedded inside the R-wave in a negative direction (vector points away in lead V4), the amplitude of R-wave in lead V6 becomes smaller. In the case of left ventricular hypertrophy, the amplitude of QRS-complex becomes very pronounced and spike-like (>25 mm) in the lead V5 or V6, and the conduction is delayed causing QRS interval to become bigger (> 0.12 ms). The sum of S-wave amplitude in V2 and R-wave amplitude in V5 increases beyond 35 mm. Figure 7.11 illustrates the effect of ventricular hypertrophy on QRS and T waveforms.
Electrocardiography and arrhythmias
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
The rapid depolarization of a large mass of ventricular muscle produces a large deflection, the QRS complex (Figure 5.3), which occurs just before the first heart sound. The Q wave is defined as the first downward spike (negative deflection), the R wave as the first upward spike (positive deflection) and the S wave as the second downward spike. All three components are not necessarily present in every record; the complex may be just RS (e.g. Figure 5.2, Lead I) or just QR. The complex normally lasts <0.12 s. Wider QRS complexes indicate slower activation of the ventricles, caused by either a ventricular ectopic beat or a block in one of the bundle branches. In bundle branch block, the R wave has a characteristic ‘M or W'-shaped notch (depending on the lead and if it is the left or right bundle branch that is blocked), because of the staggered activation of the ventricles. The first heart sound follows just after the QRS complex (Figure 2.5). Hypertrophy of the ventricles can lead to particularly tall QRS complexes, although their size is also influenced by the amount of tissue between the heart and electrode.
Spontaneous coronary artery dissection and acute myocardial infarction in women
Published in Baylor University Medical Center Proceedings, 2022
Ali Farzad, William Giesing, Cara Norvell, John S. Garrett, Carlos Velasco
On examination, she appeared uncomfortable and had an initial blood pressure of 211/104 mm Hg. Initial electrocardiogram (ECG) obtained on arrival (Figure 1) was nondiagnostic and revealed normal sinus rhythm with nonspecific T wave abnormality. Q waves were noted in the septal leads with poor R wave progression. No prior ECGs were available for comparison. During evaluation she had changes in cardiac telemetry with ongoing pain. A repeat ECG demonstrated dynamic ischemic changes with new ST elevation (leads V1, V2, and aVR) and ST depression (leads I, II, aVF, V5, and V6) (Figure 2). These were suggestive of acute anteroseptal infarction; hence, interventional cardiology was consulted, and she was taken for emergent coronary angiography. Aspirin, clopidogrel, nitroglycerin, and heparin were initiated and improved her pain and blood pressure.
The electrocardiographic changes associated with hypothermia: the Osborn wave
Published in Acta Cardiologica, 2020
Francesca Cortese, Alessandra Paglia, Rocco Contuzzi, Andrea Andriani, Luigi Truncellito, Giacinto Calculli
It consists of an electrocardiographic deflection which is manifested as a late delta wave or as a small r ’wave following the QRS. It is the manifestation on the surface ECG of the electric gradient between a more prominent spike and dome action potential of epicardial cells than that of endocardial cells, an effect that is believed to be linked to a slowing down of the kinetics of activation of K + channels Ito compared to calcium channels, associated with low temperature. This wave is not specific for hypothermia but can also occur in other clinical conditions such as subarachnoid haemorrhage, myocardial ischaemia, acidosis, in the presence of hypercalcemia, early repolarization and even in normal subjects. Its amplitude also tends to increase in conjunction with the reduction in body temperature. The bradyarrhythmias and conduction disorders associated with hypothermia cease spontaneously with an increase in body temperature, so the use of beta stimulating drugs and the insertion of transvenous pacemakers, the latter for the mechanical irritation effect on the endocardium, should be considered with caution due to the high risk of inducing ventricular tachyarrhythmias and ventricular fibrillation.
The validity of hospital discharge register data on non-ST-elevation and ST-elevation myocardial infarction in Finland
Published in Scandinavian Cardiovascular Journal, 2020
Marjo Okkonen, Aki S. Havulinna, Olavi Ukkola, Heikki Huikuri, Matti Ketonen, Y. Antero Kesäniemi, Juha Mustonen, Juhani Airaksinen, Veikko Salomaa
Before the current diagnostic criteria, MIs were usually divided to Q-wave and non-Q-wave infarctions. Even though Q-wave mainly develops from STEMI and non-Q-wave MI from NSTEMI, some crossing between the infarct types is seen in a small proportion of cases [23]. Previously it was thought that the appearance of a Q-wave determined whether the infarct was transmural or subendocardial [24]. However, this has been shown not to be the case [25] and a Q-wave rather shows the size of the infarct [23]. The latest clinical definitions of MI have changed emphasis from the later ECG’s to the start of the event (primary ECG) and especially to NSTEMI and STEMI classification [26]. Accordingly, we excluded all cases where the ECG of the attack date was not available. The ICD-10 codes were used in Finland during our whole study period and they clearly divide the diagnoses to STEMI and NSTEMI. A Q-wave infarction is included in only mentioned in small print as an additional clarification for STEMI diagnoses [27]. Q-wave is not in the definition of STEMI in the ESC guidelines for management of STEMI [5]. Some confusion between the STEMI/NSTEMI and other transmural/subendocardial MI classifications in HDR diagnoses cannot be excluded but the study results mentioned above are well known for experienced clinicians in specialist hospitals. Thus, it is unlikely that they have caused substantial problem in STEMI vs NSTEMI classification [23–27].