qrs complexes appear 1-to-1, thus implying that the p wave causes the qrs complex. once sinus rhythm is established, or not, the second question is the rate. for a sinus rhythm, this is either the rate of p waves or qrs complexes since they are 1-to-1. if the rate is too fast, then it is sinus tachycardia, and if it is too slow, then it is sinus bradycardia. if it is not a sinus rhythm, then determining the rhythm is necessary before proceeding with further interpretation. some arrhythmias with characteristic findings: absent p waves with "irregularly irregular" qrs complexes is the hallmark of atrial fibrillation. a "saw tooth" pattern with qrs complexes is the hallmark of atrial flutter. a sine wave pattern is the hallmark of ventricular flutter. absent p waves with wide qrs complexes and a fast heart rate is ventricular tachycardia. determination of rate and rhythm is necessary in order to make sense of further interpretation. axis diagram showing how the polarity of the qrs complex in leads i, ii, and iii can be used to estimate the heart's electrical axis in the frontal plane. the heart has several axes, but the most common by far is the axis of the qrs complex (references to "the axis" imply the qrs axis). each axis can be computationally determined to result in a number representing degrees of deviation from zero, or it can be categorized into a few types. the qrs axis is the general direction of the ventricular depolarization wavefront (or mean electrical vector) in the frontal plane. it is often sufficient to classify the axis as one of three types: normal, left deviated, or right deviated. population data shows that a normal qrs axis is from −30° to 105°, with 0° being along lead i and positive being inferior and negative being superior (best understood graphically as the hexaxial reference system). beyond +105° is right axis deviation and beyond −30° is left axis deviation (the third quadrant of −90° to −180° is very rare and is an indeterminate axis). a shortcut for determining if the qrs axis is normal is if the qrs complex is mostly positive in lead i and lead ii (or lead i and avf if +90° is the upper limit of normal). the normal qrs axis is generally down and to the left, following the anatomical orientation of the heart within the chest. an abnormal axis suggests a change in the physical shape and orientation of the heart or a defect in its conduction system that causes the ventricles to depolarize in an abnormal way. classification angle notes normal −30° to 105° normal left axis deviation −30° to −90° may indicate left ventricular hypertrophy, left anterior fascicular block, or an old inferior stemi right axis deviation +105° to +180° may indicate right ventricular hypertrophy, left posterior fascicular block, or an old lateral stemi indeterminate axis +180° to −90° rarely seen; considered an 'electrical no-man's land' the extent of a normal axis can be +90° or 105° depending on the source. amplitudes and intervals animation of a normal ecg wave all of the waves on an ecg tracing and the intervals between them have a predictable time duration, a range of acceptable amplitudes (voltages), and a typical morphology. any deviation from the normal tracing is potentially pathological and therefore of clinical significance. for ease of measuring the amplitudes and intervals, an ecg is printed on graph paper at a standard scale: each 1 mm (one small box on the standard 25mm/s ecg paper) represents 40 milliseconds of time on the x-axis, and 0.1 millivolts on the y-axis. feature description pathology duration p wave the p wave represents depolarization of the atria. atrial depolarization spreads from the sa node towards the av node, and from the right atrium to the left atrium. the p wave is typically upright in most leads except for avr; an unusual p wave axis (inverted in other leads) can indicate an ectopic atrial pacemaker. if the p wave is of unusually long duration, it may represent atrial enlargement. typically a large right atrium gives a tall, peaked p wave while a large left atrium gives a two-humped bifid p wave. <80 ms pr interval the pr interval is measured from the beginning of the p wave to the beginning of the qrs complex. this interval reflects the time the electrical impulse takes to travel from the sinus node through the av node. a pr interval shorter than 120 ms suggests that the electrical impulse is bypassing the av node, as in wolf-parkinson-white syndrome. a pr interval consistently longer than 200 ms diagnoses first degree atrioventricular block. the pr segment (the portion of the tracing after the p wave and before the qrs complex) is typically completely flat, but may be depressed in pericarditis. 120 to 200 ms qrs complex the qrs complex represents the rapid depolarization of the right and left ventricles. the ventricles have a large muscle mass compared to the atria, so the qrs complex usually has a much larger amplitude than the p wave. if the qrs complex is wide (longer than 120 ms) it suggests disruption of the heart's conduction system, such as in lbbb, rbbb, or ventricular rhythms such as ventricular tachycardia. metabolic issues such as severe hyperkalemia, or tricyclic antidepressant overdose can also widen the qrs complex. an unusually tall qrs complex may represent left ventricular hypertrophy while a very low-amplitude qrs complex may represent a pericardial effusion or infiltrative myocardial disease. 80 to 100 ms j-point the j-point is the point at which the qrs complex finishes and the st segment begins. the j-point may be elevated as a normal variant. the appearance of a separate j wave or osborn wave at the j-point is pathognomonic of hypothermia or hypercalcemia. st segment the st segment connects the qrs complex and the t wave; it represents the period when the ventricles are depolarized. it is usually isoelectric, but may be depressed or elevated with myocardial infarction or ischemia. st depression can also be caused by lvh or digoxin. st elevation can also be caused by pericarditis, brugada syndrome, or can be a normal variant (j-point elevation). t wave the t wave represents the repolarization of the ventricles. it is generally upright in all leads except avr and lead v1. inverted t waves can be a sign of myocardial ischemia, left ventricular hypertrophy, high intracranial pressure, or metabolic abnormalities. peaked t waves can be a sign of hyperkalemia or very early myocardial infarction. 160 ms corrected qt interval (qtc) the qt interval is measured from the beginning of the qrs complex to the end of the t wave. acceptable ranges vary with heart rate, so it must be corrected to the qtc by dividing by the square root of the rr interval. a prolonged qtc interval is a risk factor for ventricular tachyarrhythmias and sudden death. long qt can arise as a genetic syndrome, or as a side effect of certain medications. an unusually short qtc can be seen in severe hypercalcemia. <440 ms u wave the u wave is hypothesized to be caused by the repolarization of the interventricular septum. it normally has a low amplitude, and even more often is completely absent. a very prominent u wave can be a sign of hypokalemia, hypercalcemia or hyperthyroidism. limb leads and electrical conduction through the heart formation of limb waveforms during a pulse the animation shown to the right illustrates how the path of electrical conduction gives rise to the ecg waves in the limb leads. recall that a positive current (as created by depolarization of cardiac cells) traveling towards the positive electrode and away from the negative electrode creates a positive deflection on the ecg. likewise, a positive current traveling away from the positive electrode and towards the negative electrode creates a negative deflection on the ecg. the red arrow represents the overall direction of travel of the depolarization. the magnitude of the red arrow is proportional to the amount of tissue being depolarized at that instance. the red arrow is simultaneously shown on the axis of each of the 3 limb leads. both the direction and the magnitude of the red arrow's projection onto the axis of each limb lead is shown with blue arrows. then, the direction and magnitude of the blue arrows are what theoretically determine the deflections on the ecg. for example, as a blue arrow on the axis for lead i moves from the negative electrode, to the right, towards the positive electrode, the ecg line rises, creating an upward wave. as the blue arrow on the axis for lead i moves to the left, a downward wave is created. the greater the magnitude of the blue arrow, the greater the deflection on the ecg for that particular limb lead. frames 1–3 depict the depolarization being generated in and spreading through the sinoatrial node. the sa node is too small for its depolarization to be detected on most ecgs. frames 4–10 depict the depolarization traveling through the atria, towards the atrioventricular node. during frame 7, the depolarization is traveling through the largest amount of tissue in the atria, which creates the highest point in the p wave. frames 11–12 depict the depolarization traveling through the av node. like the sa node, the av node is too small for the depolarization of its tissue to be detected on most ecgs. this creates the flat pr segment. frame 13 depicts an interesting phenomenon in an over-simplified fashion. it depicts the depolarization as it starts to travel down the interventricular septum, through the bundle of his and bundle branches. after the bundle of his, the conduction system splits into the left bundle branch and the right bundle branch. both branches conduct action potentials at about 1 m/s. interestingly, however, the action potential starts traveling down the left bundle branch about 5 milliseconds before it starts traveling down the right bundle branch, as depicted by frame 13. this causes the depolarization of the interventricular septum tissue to spread from left to right, as depicted by the red arrow in frame 14. in some cases, this gives rise to a negative deflection after the pr interval, creating a q wave such as the one seen in lead i in the animation to the right. depending on the mean electrical axis of the heart, this phenomenon can result in a q wave in lead ii as well. following depolarization of the interventricular septum, the depolarization travels towards the apex of the heart. this is depicted by frames 15–17 and results in a positive deflection on all three limb leads, which creates the r wave. frames 18–21 then depict the depolarization as it travels throughout both ventricles from the apex of the heart, following the action potential in the purkinje fibers. this phenomenon creates a negative deflection in all three limb leads, forming the s wave on the ecg. repolarization of the atria occurs at the same time as the generation of the qrs complex, but it is not detected by the ecg since the tissue mass of the ventricles is so much larger than that of the atria. ventricular contraction occurs between ventricular depolarization and repolarization. during this time, there is no movement of charge, so no deflection is created on the ecg. this results in the flat st segment after the s wave. frames 24–28 in the animation depict repolarization of the ventricles. the epicardium is the first layer of the ventricles to repolarize, followed by the myocardium. the endocardium is the last layer to repolarize. the plateau phase of depolarization has been shown to last longer in endocardial cells than in epicardial cells. this causes repolarization to start from the apex of the heart and move upwards. since repolarization is the spread of negative current as membrane potentials decrease back down to the resting membrane potential, the red arrow in the animation is pointing in the direction opposite of the repolarization. this therefore creates a positive deflection in the ecg, and creates the t wave. ischemia and infarction main article: electrocardiography in myocardial infarction ischemia or non-st elevation myocardial infarctions (non-stemis) may manifest as st depression or inversion of t waves. it may also affect the high frequency band of the qrs.