Aswell as being able to recognise the 3 different parts of the cardiac cycle, each stage should be completed within a specific time period to be considered normal. Although these measurements are in fractions of a second, the ECG paper allows you to count the time in small squares. Measurement in small squares is more universally used than tenths and hundredths of seconds.
The first measurement is known as the "P-R interval" and is measured from the beginning of the upslope of the P wave to the beginning of the QRS wave. This measurement should be 0.12-0.20 seconds, or 3-5 small squares in duration.The second measurement is the width of the QRS which should be less than 3 small squares, or less than 0.12 seconds in duration.
The third measurement is to check for regularity. This can be done by measuring the "p-p interval" or the "R-R interval".To measure the P-P interval, place the edge of a piece of paper along the line of the rhythm and mark the centre of 2 consecutive P waves. Compare this measurement with the next 2 P waves. If the measurements are the same then the rhythm is regular.
You do not need to be able to recognise a "T wave" for it to be sinus rhythm. Many abnormalities obscure the t wave. Suffice to say, if the patient is alive then the ventricles are definitely repolarising.
A well-planned approach to 12-lead ECG interpretation will prevent the interpreter from missing crucial information. Key aspects in the interpretation of the 12-lead ECG include the heart rate, the heart rhythm (both atrial and ventricular), the electrical axis (both the P-wave axis and the QRS axis), and knowledge of the normal intervals. Next, determine the relationship of P waves to QRS complexes. Finally, analyze the QRS morphology and ST and T-wave segments.
ECG paper commonly moves at 25 mm/second; thus, each small box (1 mm) is equivalent to 0.04 seconds (40 milliseconds), and each large box (5 mm) is equivalent to 0.2 seconds (200 milliseconds). At the beginning of an ECG, make note of the standardization square, normally 10 mm high by 5 mm wide. This will alert you to the correct paper speed and standard amplification of P, QRS, and T-wave complexes.
Physiologically, ECG tracing represents the conduction pathway through the heart. The normal conduction pathway originates in the sinoatrial (SA) node, which initiates sinus impulses, and a wave of depolarization spreads out over the right and left atria, forming the P wave. At the level of the atrioventricular (AV) node, the beat is conducted to the ventricles over the His bundle to the right and left bundle branches and the Purkinje system. The resulting atrial repolarization and early ventricular depolarization result in the QRS complex. Ventricular depolarization and subsequent repolarization lead to the completion of the cycle, forming the T-wave. The periods between each wave and complex are made up of intervals and segments. The PR, QT, and RR intervals represent the duration of conduction through the AV node, the duration of ventricular depolarization to repolarization, and the duration between each cardiac cycle, respectively. The PR and ST segments represent the isoelectric interval between depolarization and repolarization of the atria and ventricles.
The cardiac action potential cycle comprises five phases. The rapid upstroke of the ventricular myocyte action potential in phase 0 is caused by the rapid influx of sodium ions into the cell, generating a depolarizing (positive) current. When net intracellular charge reaches a well-defined threshold, cellular depolarization occurs. During the next 4 phases, the cardiac cell enters repolarization, which is the electrical reset allowing for the next beat.
Phase 1 results from inactivation of the inward sodium current and activation of a short-lived outward current. Phase 2 represents the plateau phase and consists of inward, depolarizing calcium currents and outward, repolarizing potassium currents. As the calcium currents decay, the potassium currents increase, ending the plateau phase. Phase 3 includes more rapid repolarizing currents and is generated by a family of potassium channels. The two main currents are described by their kinetics (slow and fast), and these channels are the targets for many class-III antiarrhythmic drugs. Phase 4 represents the resting state or electric diastole.
Cardiac arrhythmias are believed to result from abnormalities of impulse formation, impulse propagation, or repolarization. Tachycardias that result from impulse formation are termed automatic. Tachycardias that result from impulse propagation are considered reentrant. Tachycardias generated from abnormal repolarization result from genetic defects in ion channels (so-called channelopathies) and can be lethal. In addition, catecholamines, ischemia, cellular ion concentrations (potassium), and cardioactive medicines all influence the development of cardiac arrhythmias.
Lawrence Rosenthal, MD, PhD, FACC, FHRS Professor of Medicine, Director, Section of Cardiac Pacing and Electrophysiology, Director of EP Fellowship Program, Division of Cardiovascular Disease, University of Massachusetts Memorial Medical Center
Lawrence Rosenthal, MD, PhD, FACC, FHRS is a member of the following medical societies: American College of Cardiology, American Heart Association, Heart Rhythm Society, Massachusetts Medical Society
Disclosure: Nothing to disclose.
The basic way to calculate the rate is quite simple. You takethe duration between two identical points of consecutive EKG waveforms such as the R-Rduration. Take this duration and divide it into 60. The resulting equation would be:
Normal sinus rhythm (NSR): indicates that the rate is between 60 and 100, inclusive, and that the P waves are identifiable and are of the same morphology throughout. The RR interval or PP intervals between beats are same.
Sinus arrhythmia: There is a cyclical acceleration of heart rate with inspiration and slowing with expiration. The beat to beat interval is slightly different.The rhythm is regularly irregular, in the sense that there is a pattern to irregularity. This is termed sinus arrhythmia.
Normal duration: 0.12-2.0 seconds (3-5 horizontal boxes). Thisis measured from the onset of the P wave to the onset of the QRS complex regardless if theinitial wave is a Q or R wave.
Providing the paper speed is standard at 25 mm/second, then each small square = 0.04 seconds. So the only other thing you need to know, in order to correctly identify ECG abnormalities, is your 4 times table! Simple.
Always bear in mind the direction of a normal electrical impulse through the myocardium, and the position of the electrodes on the external chest wall/limbs. That way, you should be able to remember, which lead complexes/waveforms should always be positive. For this reason the QRS wave aVR should always be negative.
Thank you for emphasising a really important point: factual descriptions of an ECG, provided they are based on accurate observation will never be wrong. There should be no attempt to guess or to bluff, because that is sure to lead to incorrect interpretation in some cases and that could lead to incorrect decisions about treatment. Provided the ECG is interpreted in this way in full clinical context, it will usually allow correct decisions to be made about the need for and choice of first-line treatment (i.e. treating the patient, not the ECG).
For example, assessment of rhythm can be made safely and accurately using the six-stage method that is taught in life-support courses throughout Europe. This describes cardiac electrical activity by ventricular rate (fast, slow or normal), rhythm (regular or irregular) and QRS width (broad or normal/narrow). The observer then goes on to look for atrial activity and should describe this and its relationship to ventricular activity only if they are confident of its presence and its nature. The resulting description of rhythm allows safe, effective decisions about first-line treatment without necessarily giving the arrhythmia a precise name.
Unfortunately the ECG that you have shown as an example of a normal ECG may not be normal. It shows a negative T wave in lead aVL in the presence of a dominant R wave, a feature that is best considered abnormal and requiring further assessment. It could reflect lateral ischaemic myocardial disease, or possibly a myocardial abnormality such as hypertensive heart disease, despite the absence of voltage criteria for left ventricular hypertrophy. There is subtle ST segment sagging in lead I, which may support suspicion that the negative T wave in aVL is pathological, rather than just an axis phenomenon. Furthermore the P wave morphology raises some suspicion of left atrial overload, raising further concern that there could be some underlying left ventricular myocardial disease. The heart rate shows borderline sinus bradycardia at 59 beats per minute and the PR interval is right at the upper limit of normal at 198 msec.
These features emphasise the importance of interpreting ECGs in full clinical context. If the subject was (for example) a very fit, normotensive person in their 20s, with no symptoms or other clinical reason to suspect cardiovascular disease, the T-wave and other features that I have described would be more likely to be physiological or normal variants, but in an older person with a greater likelihood of cardiovascular disease they are much more likely to be abnormal.
On each box, the central mark indicates the median, and the bottom and top edges of the box indicate the 25th and 75th percentiles, respectively. The whiskers extend to the most extreme data points not considered outliers, and the outliers are plotted individually using the '+' marker symbol.
The box plot shows that the difference between the medians of the two groups is approximately 1. Since the notches in the box plot do not overlap, you can conclude, with 95% confidence, that the true medians do differ.
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