![]() Q waves are not sacred to diagnose MI.It can be generated even by live myocytes when it behaves like an electrically dead ones. ![]() severe RVH) Are absent in the left precordial leads (LBBB) Are abnormally deep (ventricular. Transient Q waves have been described during myocardial ischemia without evidence of infarction. Such Q waves are usually permanent, though may regress and disappear over months to years. In fact this could be very common cause for labeling LVH as MI. Q wave Appear in the right precordial leads i.e. The development of Q waves on the surface electrocardiogram generally is considered indicative of myocardial infarction. As the heart rotates counterclockwise, septal activity instead of recording a r wave, merges with the s wave mimicking q waves. About 10% of LVH due HT can manifest q waves.In fact, who will develop pathological LVH (and who will not ) is predetermined by our ancestral genes. Note: Pathological LVH grows well with excellent nourishment from ACE gene dependent growth factors. Th q waves, gets amplified by the fibrotic process which is technically dead cells for the ECG machine at least !. Ultimately it many cases q waves are inscribed. Since the ECG is the summation of action potentials, it gets distorted with local delay, notch ,slur etc. Look For A negative deflection that is either broad or deep: Broad: >40ms (1mm) in duration Deep: >0.2mV (2mm) or >1/3 of R wave size. When the architecture of contractile units are altered, it finds difficult to generate good quality action potentials. While T wave and ST changes revert post myocardial infarction, Q waves are permanent and thus their presence may indicate previous infarction. This interferes with the alignment of sarcomeres of myocytes. ![]() Here LVH is predominately due to proliferation of fibroblasts and interstitial cells. Any LVH due to increased loading conditions( In the initial stages ).It robustly produce good quality electricity and the ECG inscribes a tall r waves It simply reflects hypertrophy of individual contractile units. In physiological LVH there is not much proliferation of interstitium. These non contractile cells have little electrical energy to show off. We know, cardiac muscle is made up of not only myocytes, it is enriched with, fibroblasts, interstitial cells, collagen and other extracellular matrix. In LVH how the direction of current get reversed ? In infarction it is obvious the dead cells form a distinct electrically inert window so that the muscle mass located in the opposite pole (If viable ) will record q waves. If it comes towards the electrode, R wave is recorded and if it goes away Q is recorded. It’s job is to simply tell which direction the current is traveling with reference to the recording electrode. One need to realise, ECG does not function as a tissue identifying machine. How can the ECG produce similar changes in both ? Infarct tissue is a cluster of dead cells, while LVH is a bundle of live cells. (With deep q waves* in v1 to v3 and sometimes q in inferior leads as well) ![]() But, we know often LVH is misdiagnosed as myocardial infarction especially anterior MI. ![]()
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