st elevation myocardial infarctions (stemis) have different characteristic ecg findings based on the amount of time elapsed since the mi first occurred. the earliest sign is hyperacute t waves, peaked t waves due to local hyperkalemia in ischemic myocardium. this then progresses over a period of minutes to elevations of the st segment by at least 1 mm. over a period of hours, a pathologic q wave may appear and the t wave will invert. over a period of days the st elevation will resolve. pathologic q waves generally will remain permanently. the coronary artery that has been occluded can be identified in an stemi based on the location of st elevation. the left anterior descending (lad) artery supplies the anterior wall of the heart, and therefore causes st elevations in anterior leads (v1 and v2). the lcx supplies the lateral aspect of the heart and therefore causes st elevations in lateral leads (i, avl and v6). the right coronary artery (rca) usually supplies the inferior aspect of the heart, and therefore causes st elevations in inferior leads (ii, iii and avf). artifacts an ecg tracing is affected by patient motion. some rhythmic motions (such as shivering or tremors) can create the illusion of cardiac arrhythmia. artifacts are distorted signals caused by a secondary internal or external sources, such as muscle movement or interference from an electrical device. distortion poses significant challenges to healthcare providers, who employ various techniques and strategies to safely recognize these false signals. accurately separating the ecg artifact from the true ecg signal can have a significant impact on patient outcomes and legal liabilities. improper lead placement (for example, reversing two of the limb leads) has been estimated to occur in 0.4% to 4% of all ecg recordings, and has resulted in improper diagnosis and treatment including unnecessary use of thrombolytic therapy. a method for interpretation whitbread, consultant nurse and paramedic, suggests ten rules of the normal ecg, deviation from which is likely to indicate pathology. these have been added to, creating the 15 rules for 12-lead (and 15- or 18-lead) interpretation. rule 1: all waves in avr are negative. rule 2: the st segment (j point) starts on the isoelectric line (except in v1 & v2 where it may be elevated by not greater than 1 mm). rule 3: the pr interval should be 0.12–0.2 seconds long. rule 4: the qrs complex should not exceed 0.11–0.12 seconds. rule 5: the qrs and t waves tend to have the same general direction in the limb leads. rule 6: the r wave in the precordial (chest) leads grows from v1 to at least v4 where it may or may not decline again. rule 7: the qrs is mainly upright in i and ii. rule 8: the p wave is upright in i ii and v2 to v6. rule 9: there is no q wave or only a small q (<0.04 seconds in width) in i, ii and v2 to v6. rule 10: the t wave is upright in i ii and v2 to v6. the end of the t wave should not drop below the isoelectric baseline. rule 11: does the deepest s wave in v1 plus the tallest r wave in v5 or v6 equal >35 mm? rule 12: is there an epsilon wave? rule 13: is there an j wave? rule 14: is there a delta wave? rule 15: are there any patterns representing an occlusive myocardial infarction (omi)? diagnosis numerous diagnoses and findings can be made based upon electrocardiography, and many are discussed above. overall, the diagnoses are made based on the patterns. for example, an "irregularly irregular" qrs complex without p waves is the hallmark of atrial fibrillation; however, other findings can be present as well, such as a bundle branch block that alters the shape of the qrs complexes. ecgs can be interpreted in isolation but should be applied – like all diagnostic tests – in the context of the patient. for example, an observation of peaked t waves is not sufficient to diagnose hyperkalemia; such a diagnosis should be verified by measuring the blood potassium level. conversely, a discovery of hyperkalemia should be followed by an ecg for manifestations such as peaked t waves, widened qrs complexes, and loss of p waves. the following is an organized list of possible ecg-based diagnoses. rhythm disturbances or arrhythmias: atrial fibrillation and atrial flutter without rapid ventricular response premature atrial contraction (pacs) and premature ventricular contraction (pvcs) sinus arrhythmia sinus bradycardia and sinus tachycardia sinus pause and sinoatrial arrest sinus node dysfunction and bradycardia-tachycardia syndrome supraventricular tachycardia atrial fibrillation with rapid ventricular response atrial flutter with rapid ventricular response av nodal reentrant tachycardia atrioventricular reentrant tachycardia junctional ectopic tachycardia atrial tachycardia ectopic atrial tachycardia (unicentric) multifocal atrial tachycardia paroxysmal atrial tachycardia sinoatrial nodal reentrant tachycardia torsades de pointes (polymorphic ventricular tachycardia) wide complex tachycardia ventricular flutter ventricular fibrillation ventricular tachycardia (monomorphic ventricular tachycardia) pre-excitation syndrome lown–ganong–levine syndrome wolff–parkinson–white syndrome j wave (osborn wave) heart block and conduction problems: aberration sinoatrial block: first, second, and third-degree av node first-degree av block second-degree av block (mobitz i and ii) third-degree av block or complete av block right bundle incomplete right bundle branch block (irbbb) complete right bundle branch block (rbbb) left bundle incomplete left bundle branch block (ilbbb) complete left bundle branch block (lbbb) left anterior fascicular block (lafb) left posterior fascicular block (lpfb) bifascicular block (lafb plus lpfb) trifascicular block (lafp plus fpfb plus rbbb) qt syndromes brugada syndrome short qt syndrome long qt syndromes, genetic and drug-induced right and left atrial abnormality electrolytes disturbances and intoxication: digitalis intoxication calcium: hypocalcemia and hypercalcemia potassium: hypokalemia and hyperkalemia serotonin toxicity ischemia and infarction: wellens' syndrome (lad occlusion) de winter t waves (lad occlusion) st elevation and st depression high frequency qrs changes myocardial infarction (heart attack) non-q wave myocardial infarction nstemi stemi sgarbossa's criteria for ischemia with a lbbb structural: acute pericarditis right and left ventricular hypertrophy right ventricular strain or s1q3t3 (can be seen in pulmonary embolism) history an early commercial ecg device (1911) ecg from 1957 in 1872, alexander muirhead is reported to have attached wires to the wrist of a patient with fever to obtain an electronic record of their heartbeat. in 1882, john burdon-sanderson working with frogs, was the first to appreciate that the interval between variations in potential was not electrically quiescent and coined the term "isoelectric interval" for this period. in 1887, augustus waller invented an ecg machine consisting of a lippmann capillary electrometer fixed to a projector. the trace from the heartbeat was projected onto a photographic plate that was itself fixed to a toy train. this allowed a heartbeat to be recorded in real time. in 1895, willem einthoven assigned the letters p, q, r, s, and t to the deflections in the theoretical waveform he created using equations which corrected the actual waveform obtained by the capillary electrometer to compensate for the imprecision of that instrument. using letters different from a, b, c, and d (the letters used for the capillary electrometer's waveform) facilitated comparison when the uncorrected and corrected lines were drawn on the same graph. einthoven probably chose the initial letter p to follow the example set by descartes in geometry. when a more precise waveform was obtained using the string galvanometer, which matched the corrected capillary electrometer waveform, he continued to use the letters p, q, r, s, and t, and these letters are still in use today. einthoven also described the electrocardiographic features of a number of cardiovascular disorders. in 1897, the string galvanometer was invented by the french engineer clément ader. in 1901, einthoven, working in leiden, the netherlands, used the string galvanometer: the first practical ecg. this device was much more sensitive than the capillary electrometer waller used. in 1924, einthoven was awarded the nobel prize in medicine for his pioneering work in developing the ecg. by 1927, general electric had developed a portable apparatus that could produce electrocardiograms without the use of the string galvanometer. this device instead combined amplifier tubes similar to those used in a radio with an internal lamp and a moving mirror that directed the tracing of the electric pulses onto film. in 1937, taro takemi invented a new portable electrocardiograph machine. in 1942, emanuel goldberger increases the voltage of wilson's unipolar leads by 50% and creates the augmented limb leads avr, avl and avf. when added to einthoven's three limb leads and the six chest leads we arrive at the 12-lead electrocardiogram that is used today. in the late 1940s rune elmqvist invented an inkjet printer - thin jets of ink deflected by electrical potentials from the heart, with good frequency response and direct recording of ecg on paper - the device, called the mingograf, was sold by siemens elema until the 1990s. etymology the word is derived from the greek electro, meaning related to electrical activity; kardia, meaning heart; and graph, meaning "to write".