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Review of the Basics (The Systematic Approach) o Lead reversal Rate & Rhythm o Heart rate calculation o Sinus Mechanism Rhythms & Arrhythmias o Atrial Fibrillation o Multifocal Atrial Tachy (MAT) o Atrial Flutter o PSVT o Vagal maneuvers o Junctional Rhythms o PACs/PJCs/PVCs o Blocked/Aberrant PACs o QRS Morphology: PVC or Aberrancy o Ventricular Rhythms (AIVR/VT) The 2 KEY Lists for Tachycardias o Common Causes of a Regular SVT o Causes of a WCT (Wide Complex Tachycardia) The PR Interval The QRS Interval & Bundle Branch Block o RBBB o LBBB
WPW (Wolff-Parkinson-White) Syndrome The QT Interval & Causes of QT Prolongation Axis (and Hemiblocks) o Pathologic LAD (i.e. LAHB) o LPHB Chamber Enlargement o LVH o LAA/RAA o RVH / COPD o Pulmonary Embolus QRST Changes o Basic Lead Groups/Lead location o Leads with normal Q waves/T inversion o ST elevation o ST depression (Common Causes) Acute MI/Ischemia o Coronary circulation Use of Mirror Test o Tall R in V1 Electrolytes (hyper/hypokalemia) Pericarditis
12-LEAD ECG's - A "Web Brain" for Easy Interpretation
Starting Out: Review of the Basics
The KEY to interpretation of any ECG is to utilize a systematic approach. The approach we suggest for interpreting each 12-lead ECG that you encounter entails a systematic assessment of each of the following:
Rate Rhythm Intervals (PR/QRS/QT) Axis Hypertrophy Infarct (QRST changes)
We outline key elements to assess for each of the above parameters in the "Analyze an ECG" section of this ebook. Discussion is limited here to the following points:
The purpose of having (and regularly using) a systematic approach is simple: It prevents you from overlooking potentially important findings.
Additional benefits include increased accuracy, improved organization, and increased speed in completing your interpretation.
The process of 12-lead ECG interpretation should be thought of as consisting of two major steps:
1. Descriptive Analysis: Simply describe what is seen on the tracing (as
per the "Analyze an ECG" section of this ebook). Ideally, WRITE OUT your findings
2. The Clinical Impression: should only come after the first step has
been completed. Those specific findings identified in descriptive analysis should now be interpreted in light of the clinical context (i.e., as defined by the patient's age, presenting complaint, and additional relevant clinical history). KEY Clinical Point: The secret of successful ECG interpretation depends on keeping these 2 steps separate in your mind.
Why 2 separate steps?
Consider the following: Symmetric T wave inversion is often seen in the anterior leads (V1, V2, and V3) of pediatric patients. In an otherwise healthy child (with no heart murmur), this finding represents a completely benign normal variant that is commonly referred to as a Juvenile T Wave Pattern. However, the same ECG (with identical T wave inversion) would have to be interpreted very differently if the patient in question was an older adult with new-onset chest pain (in whom this finding should strongly suggest ischemia). Thus, descriptive analysis is the same in both cases (i.e., "symmetric T wave inversion in leads V1-3"), but the clinical impression is very different!
Tips for Applying the Systematic Approach
Be sure to carefully survey all 12 leads on the ECG, except perhaps for lead aVR, which can usually be ignored unless you suspect dextrocardia or lead misplacement (see below).
Always assess intervals at an early point in the process! If the rhythm is sinus and the QRS complex is wide, determine why the QRS is wide before going further (i.e., RBBB, LBBB, IVCD,). Remember the concept of "patterns of leads". For example, when looking at lead I. also look at lead aVL at the same time (since both leads view a similar area of the heart). When looking at lead III, look also at leads II and aVF (the other inferior leads). (review an example of this concept) With time, your experienced eye learns to simultaneously assess the two or three leads in each lead group. (review the basic lead groups)
Lead Reversal or Dextrocardia
They should be suspected if there is:
Global negativity in lead I (negative P wave, QRS complex and T wave) An upright QRS complex in lead aVR; and/or A negative P wave in lead II.
Dextrocardia is much less common than lead reversal. Suspect it if R wave progression is reversed and if you hear heart sounds on the right!).
12-LEAD ECG's - A "Web Brain" for Easy Interpretation
12-LEAD ECG's - A "Web Brain" for Easy Interpretation
Rate & Rhythm
Rhythm Analysis: Assessing the 5 Parameters
The most important clinical point (and the real KEY to rhythm interpretation) is to utilize a systematic approach. The system we favor is based on assessing for the following 5 parameters:
P waves QRS width Regular rhythm P waves Related to the QRS? Heart Rate
Memory Aid: "Watch your P's and Q's and the 3 R's".
Heart Rate: Calculating the Rate
The easiest way to estimate heart rate is to use the... Rule of 300 - Provided that the rhythm is regular, heart rate can be estimated by dividing 300 by the number of large boxes in the R-R interval. With the ECG machine set at the standard recording speed of 25 mm/second, the time required to record each little box on ECG grid paper is 0.04 second. Vertically,
Normal sinus rhythm (NSR) . 2. 5 beats occur each second X 60 seconds/minute = 300/minute)..04 = 0.then the R-R interval will be 0. . Sinus Mechanism Rhythms/Arrhythmias By definition. rate below 60 beats/minute..20 second. 3. rate between 60-99 beats/minute.regular rhythm. rate = 150 beats/minute (300 ÷ 2) R-R interval is 3 large boxes. . and 5 X 0. rate at 100 beats/minute or faster in an adult patient. Sinus bradycardia . the P wave will always be upright in standard lead II when the mechanism of the rhythm is sinus. if a QRS complex occurs with each large box (as in the figure).regular rhythm. By the Rule of 300 the rate of the sinus rhythm shown in this figure is 85 beats/minute. and the rate of the rhythm is 300 beats/minute (i. or between 100 and 75 beats/minute.20 X 5 = 1.regular rhythm.0 second). rate = 75 beats/minute (300 ÷ 4) and so on . R-R interval is 2 large boxes.e. KEY Clinical Point. Sinus tachycardia .20).20 second (because there are 5 little boxes in each large box. Thus. rate = 100 beats/minute (300 ÷ 3) R-R interval is 4 large boxes.each little box is 1 mm in amplitude. There are four basic types of sinus mechanism rhythms: 1. The time required to record each large box on ECG grid paper is 0. It can therefore be seen that the time required to record 5 large boxes will be one full second (0. since the R-R interval is between 3 and 4 large boxes. then sinus rhythm is not present (unless there is dextrocardia or lead reversal).If the P wave in lead II is not upright.
e. at or above the double dotted line in this figure. Sinus arrhythmia .irregular rhythm despite the presence of a sinus mechanism. A Fib is therefore described as having one of the following: . Sinus arrhythmia is a common normal variant that is frequently seen in otherwise healthy children and young adults.. Other Supraventricular (Narrow QRS) Arrhythmias A supraventricular rhythm is defined to be one in which the electrical impulse originates at or above the AV node (i. the other principal entities in this category include: • • • Atrial fibrillation Atrial flutter (distinguish from MAT) PSVT (paroxysmal supraventricular tachycardia) & Vagal Manuevers Junctional (AV nodal) rhythms • Atrial Fibrillation (A Fib) Atrial fibrillation is characterized by the presence of an irregularly irregular rhythm in the absence of P waves. Undulations in the baseline (known as "fib waves") may sometimes be seen (see figure). In addition to the sinus mechanism rhythms just described.4.
Atrial flutter typically manifests a sawtooth appearance that is usually best seen in the inferior leads. Clinically. A controlled (moderate) ventricular response. MAT is most often seen in patients with either pulmonary disease or multi-system problems (sepsis.). At times. Treat the underlying cause! Atrial Flutter (A Flutter) Atrial flutter is characterized by a special pattern of regular atrial activity that in adults almost always occurs at a rate of 300/minute. . if the rate averages less than 60 beats/minute. if the rate averages between 70-110 beats/minute. flutter waves may be very subtle (arrows in figure). if the rate averages over 120 beats/minute.• A rapid ventricular response. A slow ventricular response. but in which definite P waves are present. etc. electrolyte abnormalities. shock. in which the rhythm is also irregularly irregular. • • MAT (Multifocal Atrial Tachycardia) A Fib should be distinguished from MAT.
Less commonly with flutter there is 4:1 AV conduction (vent..The most common ventricular response to atrial flutter (by far!) is with 2:1 AV conduction.e.e. 3:1. Atrial activity is usually not evident. Note how much easier it is to identify flutter with 4:1 conduction (figure left) compared with 2:1 (figure above). although subtle notching or a negative deflection (representing retrograde atrial activity) may sometimes be seen at the tail end of the QRS complex. PSVT is a reentry tachycardia that almost always involves the AV node (ergo the most recent name for this rhythm which is AVNRT = AV Nodal Reentry Tachycardia). KEY Point . vagal maneuvers or stops spontaneously.. Odd conduction ratios (i. 1:1. This means that the ventricular rate with untreated atrial flutter is usually close to 150/min (i. Formerly this rhythm was known as PAT or PJT (paroxysmal atrial or junctional tachycardia). rate 75/minute)or a variable (irregular) ventricular response. Mechanistically. calculating the rate is most easily accomplished using the "Every- . The impulse continues to circulate within the AV node until the reentry pathway is interrupted by drugs. 300 ÷ 2). 5:1) are rare. When the rhythm is regular and the rate is fast (as in the above figure). PSVT (Paroxysmal Supra-Ventricular Tachycardia) PSVT is a regular supraventricular tachycardia that most often occurs at a rate of between 150 to 240 beats/minute.Accurate determination of heart rate is essential for assessment of the SVTs.
200/min). Vagal maneuvers work by producing a transient increase in parasympathetic tone. If there is no response. If properly performed. so that half the rate is approx. the R-R interval of every other beat in the figure is 3 large boxes.other-Beat" Method (i. Valsalva Have patient forcibly exhale (bear down) against a closed glottis (as if trying to go to the bathroom) for up to 15 seconds at a time. Vagal Manuevers Vagal maneuvers are commonly used to facilitate ECG diagnosis and/or to treat certain cardiac arrhythmias.CSM typically slows the ventricular rate (which may facilitate rhythm diagnosis). may be even more effective than CSM! Patient should be supine when attempting Valsalva.responds with either abrupt termination of PSVT (and conversion to sinus rhythm) or there is no response at all. thus slowing conduction through the AV node. resumption of tachycardia on release of pressure.e.gradual slowing with CSM. This means that the actual rate must be twice this (approx. • • • .100/minute. Usual Response to Vagal Maneuvers • Sinus Tachycardia . Never press on both carotids at the same time. Atrial Fib or Flutter . Carotid Sinus Massage (CSM) Always perform under constant ECG monitoring. Use the right carotid first. Ventricular Tachycardia . Don't do CSM if patient has a carotid bruit (as you may dislodge a plaque!). Remember that the carotid sinus is located high in the neck (at the angle of the jaw). PSVT . Rub for no more than 3-5 seconds at a time.. Warn patient that the maneuver will be uncomfortable (as very firm pressure is needed for success).does not respond to CSM. you may repeat CSM on the left side (possibly after giving medication).
the rate of an AV nodal escape rhythm is normally between 40-60 beats/minute. If the rate is faster than this and the patient is taking digoxin. 3. 2. They are of 3 basic types: . There are three basic types of junctional rhythms (with the type determined by the rate of the rhythm): 1.The rate exceeds 100/minute.The junctional rate speeds up to between 61-99 beats/minute and takes over the pacemaking function. the P wave in lead II will either be negative (preceding or following the QRS) or absent completely. The rhythm arises because the SA node is either delayed or fails in its pacemaking function. AV nodal escape rhythm . Premature Beats Premature beats are QRS complexes that interrupt the underlying rhythm by occurring earlier than expected. KEY Clinical Point. As a result. Junctional tachycardia . strongly suspect digitalis toxicity.Junctional (AV Nodal) Rhythms Junctional (or AV Nodal) rhythms are regular supraventricular rhythms in which atrial activity reflects an AV nodal site of origin.The junctional rate in an adult is between 40-60 beats/minute. Accelerated junctional rhythm .In adults.
2. 3. PVCs (Premature Ventricular Contractions) The underlying rhythm is interrupted by an early beat arising from the ventricles. PVCs are wide and have an appearance that is very different from that of the normal sinus-conducted beats. PJCs (Premature Junctional Contractions) The underlying rhythm is interrupted by an early beat arising from the AV node or junction. Instead. Blocked PACs and Aberrant Conduction Although most premature supraventricular beats (PACs or PJCs) are conducted to the ventricles normally (i.. see figure right). PACs (Premature Atrial Contractions) The underlying rhythm is interrupted by an early beat arising from somewhere in the atria other than the SA node (different shape P Wave. with a narrow QRS complex). this is not always the case.1.e. The P wave in lead II is negative or absent . Most often the impulse is conducted with a narrow QRS complex that is similar (or identical) in appearance to that of normal sinus-conducted beats. Most often the impulse will be conducted with a narrow QRS complex that is identical in appearance to that of normal sinus-conducted beats. PACs or PJCs may sometimes occur so early in the cycle as to be .
e. Other times.in which case aberrant conduction (with a widened QRS) occurs. premature beats may occur during the relative refractory period. non-conducted). Attention to QRS morphology may help to distinguish between aberrancy and ventricular beats."blocked" (i. QRS Morphology Assess the etiology of wide beats when the QRS complex is upright in V1. Practically speaking. because the conduction system is still in an absolute refractory state. aberrant conduction is most likely to take the form of some type of bundle branch block/hemiblock pattern (most commonly RBBB). (figure below) KEY Clinical PointBlocked .. (figure below) Assess the etiology of wide beats when the QRS complex is negative in V1.
(see "2 Key Lists for Interpreting Tachycardias) . AIVR (Accelerated Idio Ventricular Rhythm) The rate is more than 40/min.. or retrograde. they'll often be hiding (notching) a part of the preceding T wave (see subtle T wave notching in the figure right). Sustained Ventricular (Wide QRS) Arrhythmias With the exception of the chaotic variability of ventricular fibrillation. Ventricular rhythms may arise either as escape rhythms (if supraventricular pacemakers fail).PACs are often subtle and difficult to detect. They will be found if looked for. Atrial activity with the ventricular rhythms may be absent. Slow Idioventricular escape rhythm The ventricular rate is "slow" (i.e. the QRS complex is wide and very different in appearance from that of normal sinus-conducted beats (see figure right). between 20-40 beats/ minute. or usurping rhythms (when the ventricular focus accelerates and takes over the pacemaking function from the preexisting supraventricular pacemaker). VT is always a usurping rhythm. unrelated to the QRS complex. but does NOT exceed 110-120 beats/minute (see figure above). which is the usual rate range of an intrinsic ventricular escape focus). sustained ventricular rhythms are most often regular (or at least fairly regular) rhythms that originate from the ventricles. As a result of their ventricular origin. Ventricular tachycardia (VT) The rate exceeds 120-130/minute.
A "Web Brain" for Easy Interpretation 12-LEAD ECG's . If the QRS is narrow (in all 12 leads!). immediately cardiovert! If the patient is unstable. if the patient is stable hemodynamically. it no longer matters what the rhythm may be (i.A "Web Brain" for Easy Interpretation 2 Key Lists for Interpretating Tachycardias The 1st priority in evaluating any tachycardia is to ensure that the patient is hemodynamically stable. 1st Key List Common Causes of a Regular SVT (without sign of atrial activity) • • • Sinus Tachycardia Atrial Flutter PSVT .. then the rhythm is an "SVT" (SupraVentricular Tachycardia).12-LEAD ECG's . VT or SVT with aberrant conduction). an attempt can be made to determine the etiology of the tachycardia before proceeding further. If not. However. since the need for immediate synchronized cardioversion will be the same.e.
Fib. Use of a vagal maneuver and/or obtaining a 12-lead ECG during the tachycardia may help to determine the cause. the first priority is to determine if the patient is hemodynamically stable. Once again. espec ially if patie nt older and has heart disea se) SVT with preexisti . A. If the QRS is wide then the rhythm is a WCT (Wide Complex Tachycardia). is ruled out if the rhythm is regular. If not. consider the possible causes: 2nd Key List Common Causes of a Regular WCT of Uncertain Etiology • • VT (mos t com mon. look at the rate. sinus tachycardia rarely exceeds 150/minute in an adult patient & atrial flutter most often conducts at a ventricular rate close to 150 beats/min.To distinguish between the above 3 entities. cardiovert! If the patient with WCT is stable.
A "Web Brain" for Easy Interpretation 12-LEAD ECG's .A "Web Brain" for Easy Interpretation . Remember some patients with VT may remain awake and alert for long periods of time! 12-LEAD ECG's . Obtaining a 12-lead ECG during the tachycardia may help with diagnosis. Pay special attention to QRS morphology in leads V1 and V6.ng bund le branc h block • SVT with aberr ant cond uctio n KEY Points . Compare QRS morphology of the WCT with prior tracings (if available). as well as the axis (extensive LAD or RAD during the tachycardia suggests VT).Always assume VT until proven otherwise! Treat the patient accordingly.
20 second (i.The PR Interval As shown in the figure.. The PR is short if it is less than . if clearly more than a LARGE box in duration). Note: The isolated finding of 1° AV block (in the absence of other cardiac pathology) has virtually no clinical significance (and no effect on long-term outcome). in this situation it suffices to say that the PR interval is "normal". 12-LEAD ECG's . Precise determination of a PR interval that falls within the normal range is not necessary.A "Web Brain" for Easy Interpretation . if there is sinus mechanism) the PR interval is considered normal if between ..12 second in lead II (as may occur with WPW when the AV node is bypassed ) The PR is long if more than . (i. even if the PR interval is very long. Clinically.e.e.A "Web Brain" for Easy Interpretation 12-LEAD ECG's .12 and . The best lead to use for measuring the PR interval is lead II. In adults.20 second. if the P wave is upright in lead II. the PR interval is defined as the period that extends from the onset of atrial depolarization (beginning of the P wave) until the onset of ventricular depolarization (beginning of the QRS complex).
we suggest you short-circuit your systematic approach. This algorithm assumes that the rhythm is supraventricular (i. Instead. Thus. Practically speaking.10 second is the upper normal limit for QRS duration in adults.The QRS Interval & Bundle Branch Block The QRS interval represents the time it takes for ventricular depolarization to occur. all that matters is whether the QRS is normal or wide.. Key points to keep in mind are that: • QRS duration can be measured from any of the 12 leads of a standard ECG. Select the lead in which the QRS complex appears to be longest. Practically speaking. if the QRS is wide. .e. With sinus rhythm in adults. Given that 0. Precise measurement of QRS duration for a complex that is clearly within the normal range is not necessary. There may be typical RBBB (Right Bundle Branch Block).10 second. These limits do not hold true for children (for whom lesser degrees of QRS prolongation are abnormal). there are only 3 possibilities: 1. • • • If the QRS Complex is Wide If the rhythm is supraventricular and the QRS complex is wide. not VT) and that QRS widening is not due to WPW. look at V1 & V6 and immediately branch to this algorithm. the QRS complex is said to be wide if it is more than half a large box in duration. the process of ventricular activation should normally be complete in no more than 0. determine why it is wide before proceding further with your interpretation.
(There is incomplete RBBB if morphology is typical but the QRS is not prolonged to at least 0. "RBBB-Equivalent" Patterns (in lead V1) The shape of the QRS complex in lead V1 may vary greatly with RBBB. Typical RBBB The appearance of typical complete RBBB in the three KEY leads (I. LBBB. V1). It will not always show a neat rSR' (or rsR') in this lead. any of the patterns in this figure qualify for the diagnosis of . A wide terminal S wave in leads I and V6.. Instead.) An rSR' or rsR' in right-sided lead V1. The key to the diagnosis of RBBB is the wide terminal S wave in these leads. the reason for QRS widening must be the presence of IVCD (IntraVentricular Conduction Delay).e. or IVCD) are leads I. think of RBBB and the "r's" -. Note: The 3 key leads (and the only 3 leads needed) to determine the type of conduction defect (RBBB. V1.11 second. but neither typical RBBB nor typical LBBB is present. The QRS is usually predominantly positive in these left-sided leads with RBBB. In this case. and V6) is schematically shown in this figure. 3.11 second. and V6.rSR' complex with the taller right rabbit ear (the R') in a right-sided lead (i. • • As a memory aid to the ECG appearance of the QRS complex in the 3 key leads with typical complete RBBB. V1. Diagnostic criteria include: • QRS widening to at least . There may be typical LBBB (Left Bundle Branch Block).2. The QRS complex is wide. There may or may not be an initial small q wave.
• Note: normally. There may or may not be an initial small r wave in lead V1. many patients with IVCD have at least some type of underlying heart disease. IVCD (IntraVentricular Conduction Delay) The ECG appearance of IVCD is difficult to characterize. there should never be a Q wave in a left-sided leads (I. cardiomyopathy with ventricular fibrosis. and V6) is schematically shown in this figure.11 second) and a wide terminal S wave is present in left-sided leads (I and V6). rather than reflecting a discrete defect in the conduction system (as usually occurs with RBBB or LBBB). Diagnostic criteria include: • • QRS widening to at least . Thus. According to the previously mentioned algorithm. Finding a Q in I. An upright (monophasic) QRS complex in leads I and V6. IVCD is present if : . as long as the QRS is widened (>0. or V6 suggests that the patient has had an infarction at some point in the past. lead V1 may show either a QS or rS complex. Examples of conditions that may lead to IVCD include myocardial infarction. but there should not be any q wave in either lead I or lead V6. This is because IVCD is often the end result of a number of different pathophysiologic processes. aVL.RBBB.12 second. chamber enlargement and/or any combination of these (with or without a component of bundle branch block). That is. V6) with typical LBBB. V1. The QRS may be notched. A predominantly negative QRS complex in lead V1. Typical LBBB The appearance of typical complete LBBB in the three KEY leads (I.
which leads to development of secondary (2°) ST-T wave changes .e.. R B B B LBBB Typical Secondary ST-T Wave Changes RBBB and LBBB each alter the sequence of ventricular depolarization. leads I and V1 are consistent with RBBB.e.. IVCD • Neither typical RBBB nor typical LBBB is present. >0. there is a sinus rhythm and QRS widening. As a direct result of this altered sequence of activation these conduction defects also alter the sequence of ventricular repolarization. This is why they produce the alterations in QRS morphology that we have just discussed. In this figure depicting IVCD (right).11 second).• The QRS complex is wide (i. These ST-T wave changes are called secondary because . but lead V6 suggests LBBB!). but QRS morphology is not typical for either RBBB or LBBB in all 3 of the KEY leads (i.
Key Rule: The ST segment and T wave should normally be oriented opposite (arrows in the figure) in the 3 KEY leads when there is typical RBBB or LBBB. 12-LEAD ECG's . aVL. Extras Diagnosis of Infarction with BBB This is difficult. and indicates a primary (1°) ST-T wave change suggesting that ischemia or infarction may be occurring.A "Web Brain" for Easy Interpretation 12-LEAD ECG's .A "Web Brain" for Easy Interpretation Wolff-Parkinson-White . LVH is probably present with RBBB if the R in aVL is >12 and/or R in V5 or V6 is >25. Diagnosis of LVH with BBB Suspect LVH with LBBB if there is LAA and/or very deep S waves (>30 mm) in V1. Look for 1° ST-T wave changes or new Q waves in left-sided leads (I. but not necessarily impossible. V2 or V3. V6) with LBBB. Deviation from this pattern in any of the 3 KEY leads is abnormal.they are the result of the conduction defect itself. ST-T changes) is easier to see with RBBB. Evidence of infarction (Q waves.
QRS widening 2.In the setting of normal sinus rhythm the only exception to the simplified algorithm (figure) presented in the disscussion of BBB (for assessment of QRS widening) is the WolffParkinson-White (WPW) syndrome. When negative (as in leads II. a delta wave is present in only some of the leads in the figure.A "Web Brain" for Easy Interpretation . a short PR interval. Thus. Although admittedly uncommon (with an estimated incidence of 2 per 1. a delta wave (arrows in figure left) 3. aVF). Note the tall R wave complex in lead V1 that simulates RBBB. Not all leads necessarily show each of these findings. This is why WPW is known as "the great mimic"! 12-LEAD ECG's . The syndrome of WPW is recognized by the presence of three ECG findings: 1. III. the delta looks like a Q wave (and may simulate infarction). WPW occurs just often enough to cause problems for the unwary (principally by its role in facilitating reentry arrhythmias and very rapid A Fib).000 in the general population).
In contrast. . the QT is obviously prolonged on the right. For practical purposes. in which case measurement of the QT interval has little clinical significance.KEY Points: • The QT interval is measured from the onset of the Q wave (or the onset of the R wave if there is no Q) until the termination of the T wave. since it far exceeds half the R-R interval.A "Web Brain" for Easy Interpretation The QT Interval The QT interval is the period that extends from the beginning of ventricular depolarization until the end of ventricular repolarization (figure). since the QT is much less than half the R-R interval).. or so).12-LEAD ECG's .e. The principal exception to this general rule occurs when the heart rate is rapid (i. The QT Interval . more than 100 beats/minute. The QT interval is clearly normal on the left. the QT interval is prolonged if it clearly measures more than half the R-R interval.
Precise measurement of the QT interval is usually not necessary.e. quinidine. Select that lead in which the QT interval appears to be longest. • • Common Causes of QT Prolongation Drugs • Type 1A antiarrhythmic agents (i. the presence of these other conditions will usually be obvious from inspection of the ECG. procainamide.• Select a lead in which you can clearly see the terminal boundary of the T wave. seizure. and ischemia) may also cause QT prolongation. coma. (Hypercalcemia produces QT shortening but this is very difficult to recognize clinically. bundle branch block. intracerebral or brainstem bleeding Note . Practically speaking one only cares if the QT interval is normal or prolonged..A "Web Brain" for Easy Interpretation .e.. However.) Determination of the QT interval means little when the heart rate is rapid (faster than about 90-100/minute). hypocalcemia or hypomagnesemia CNS • catastrophes such as stroke. infarction. 12-LEAD ECG's .Several other conditions (i. disopyramide) & tricyclic antidepressants/phenothiazines "Lytes" • Hypokalemia.
Each lead records the heart's electrical potential from its own particular vantage point. The three standard limb leads are I. and III as derived from Einthoven's equilateral triangle. The augmented limb leads are each separated from each other by 120° and form a "Mercedes-Benz" triangle (dotted lines in figure). starting with lead I (at 0°). Key Points: • • • Each of the limb leads (I. III) is separated by 60°. each of these leads is separated from each other by 60°. As a result. Lead aVL bisects lead I (at 0°) and lead -III (at -60°). Lead III is 60° away from lead I (in the negative direction). The 2 key leads that are used for axis determination are leads I and aVF. it is easy to remember that this horizontal lead is . II.12-LEAD ECG's . Calculation of Axis: Basic Principles Mean QRS axis is calculated in the frontal plane. lateral lead aVL (at -30°) and distant lead aVR (which we can usually ignore and need not recall its degree location).A "Web Brain" for Easy Interpretation Axis & Hemiblocks A standard ECG is recorded by viewing the heart's electrical activity from 12 leads. beginning with vertical lead aVF (at +90°). II. As such. Think of lead I as the "starting" point. followed by lead II (at +60°) and lead III (60° further away at +120°).
It is easiest to define axis by quadrants. or at +90°.e. net QRS deflection) of lead I is about the same as that for lead aVF..oriented toward 0° (see figure below left). then the mean QRS axis lies closer to lead I (i. Lead aVF is oriented perpendicular to lead I (i.. "The axis lies between +40° and +50° "). Key Points • If the approximate size (i.e. then the mean QRS axis should lie midway between these leads. We often provide a range for our answer (i.. Lead aVF is therefore located 90° away from lead I. An indeterminate axis lies between +180° and +270° (or between -90° and -180° depending on the observer's perspective. looking straight up from the feet). LAD (Left Axis Deviation) and RAD (Right Axis Deviation) are defined as shown in the figure. A normal axis is defined as lying within the limits of 0° and +90°.. which is close to +45° (see figures above). between 0° and +40°).) Rapid Determination of Axis Determination of the mean axis quadrant can be made at a glance by inspection (and comparison) of the net QRS deflection in leads I and aVF. • .e. If the net QRS deflection of lead I is positive and clearly exceeds that for lead aVF.e.
or so) !!! • • Pathologic Left Axis Deviation Left Anterior HemiBlock (LAHB) is far more common than Left Posterior HemiBlock (LPHB).... the deflection corresponds to an axis that is less negative than -30°.. For practical purposes. whereas the anterior hemifascicle does not. If the net QRS deflection in lead II is more negative than positive. Axis calculation need not be exact as long as you are in the "ballpark" (that is. the deflection corresponds to an axis that is 90° away (or exactly at -30°). In the third .e. between +50° and +90°) if the net deflection in aVF is greater. It also has a dual blood supply (from the left and right coronary arteries). we equate the ECG diagnosis of LAHB with the finding of pathologic LAD.• The axis lies closer to lead aVF (i. This is because the left posterior hemifascicle is much thicker than the anterior hemifascicle.. KEY Point • One need only look at lead II to make the diagnosis of pathologic LAD.e. If there is LAD (as determined by the presence of a positive deflection in lead I and a net negative deflection in lead aVF). The axis is perpendicular to (i. 90° away from) a lead where the QRS complex is isoelectric (equal parts positive and negative). look next at lead II. In the first frame of the figure to the right. which we define as a mean QRS axis more negative than -30°. then the mean QRS axis must be more negative than -30° (which means LAHB). within about 2030°. In the second frame. All you are doing is approximating.
so that you understand their overall effect on the axis determination. tall R). LAHB is diagnosed because the net QRS deflection in lead II is negative (See previous section above). the deflection corresponds to an axis more negative than -30° (LAHB) Compare each of the deflections in the figure to the right with lead II in the figure above it. Visual Recognition of the Hemiblocks There is bifascicular block in the form of RBBB and LAHB.frame. in this case from RBBB and LPHB (diagnosed by the finding of a very deep straight component to the S wave in lead I). Again there is bifascicular block. 12-LEAD ECG's . Lead II (and also lead III) show the opposite configuration of lead I when there is LPHB (small q.A "Web Brain" for Easy Interpretation .
Even in the best of hands. We favor any of the following: • An R wave > 20 in any inferior lead (II.Clinical Detection The unfortunate clinical reality is that the ECG is not very accurate as a diagnostic tool for determining chamber enlargement. Only one of these criteria (35 or 12) need be met to diagnose LVH. These criteria are not valid for younger patients (under 35). Patient > 35 years old. Additional Voltage Criteria may occasionally be needed to diagnose LVH. • • For adults 35 or over. If "strain" is present in addition to voltage the specificity (accuracy) for true LVH is greatly increased. Simplified Criteria for Diagnosing LVH • Deepest S wave in lead V1 or V2. III. Diagnostic accuracy for determining RVH (Right Ventricular Hypertrophy) and atrial enlargement is even less. or aVF). remembering the numbers 35 and 12 allows diagnosis of LVH most of the time when it is possible to do so by 12-lead ECG. Left ventricular (LV) "Strain" (see below).A "Web Brain" for Easy Interpretation Chamber Enlargement LVH. plus tallest R wave in lead V5 or V6 > 35 and/or R wave in lead aVL > 12. Echo-cardiography is far superior to the ECG for diagnosing enlargement of any cardiac chamber.12-LEAD ECG's . . the sensitivity for detecting LVH (Left Ventricular Hypertrophy) does not exceed 60% (although specificity may approach 90 to 95% when certain criteria are met).
If a strain equivalent pattern (See figure) occurs in association with voltage for LVH. A tall R wave ( > 20) in lead V6. V4. V6). It is probably best not to even bother trying to diagnose RVH when LBBB. aVL. RBBB.• • • A deep S wave ( > 20-25) in lead V1 or lead V2. Suspect LVH despite LBBB or IVCD. negative. "Strain" is a pattern of asymmetric ST segment depression and T wave inversion (See Figure). or the R wave in V5 or V6 is > 25. if the S wave in V1. or IVCD is present. specificity for true LVH is greatly enhanced compared to the voltage criteria alone. V5. The P may normally be positive. Atrial Abnormality (P Wave Appearance) NSR (Normal Sinus Rhythm) • The P wave should normally be upright in lead II if there is NSR. or V3 is very deep ( > 30). LV strain is most commonly seen in one or more leads that look at the left ventricle (leads I. A tall R wave ( > 25) in lead V5. RAA (Right Atrial Abnormality) . What if there is a conduction defect? (See LVH + BBB) Suspect LVH despite RBBB if the R in aVL is > 12. V2. or biphasic in lead V1. less commonly it can be seen in inferior leads.
in a patient . III.• diagnosed by the finding of tall Peaked and Pointed P waves in the Pulmonary leads (II.None of the criteria listed above by itself is enough to make the diagnosis of RVH.. Persistent precordial S waves. If the P wave looks "uncomfortable to sit on". ECG Diagnosis of RVH Detection of right ventricular enlargement in adults by ECG criteria is often exceedingly difficult. KEY Points . the presence of several of these criteria (when seen together on a single tracing) is very suggestive of RVH. from identifying a combination of the following ECG findings): Findings Suggestive of RVH in Adults: • • • • • • • RAD or indeterminate axis. As a result. aVL) and/or a deep negative component to the P in lead V1.e. RAA (which very often accompanies RVH). Think of the ECG diagnosis of RVH as similar to making a "detective" diagnosis. Rarely will any one finding clinch the diagnosis. "Strain" in right ventricular leads Tall R wave in lead V1. think RAA!!! LAA (Left Atrial Abnormality) • diagnosed by finding an m-shaped (notched) and widened P wave ( > 0.12 second) in a "mitral" lead (I. This is because the left ventricle is normally so much larger and thicker than the right ventricle in adults that it masks even moderate increases in right ventricular chamber size. aVF).. II. especially when they occur in a likely setting (i.e. Incomplete RBBB (or an rSr' in lead V1). Low voltage (especially if emphysema present). many patients with RVH won't be identified if assessment for chamber enlargement is limited to obtaining an ECG. However. Instead determination of RVH is most often made by deduction (i.
RAA. Atrial Abnormality .V2 plus the tallest R in V5. aVL. Note also that there is "RV strain" (which is typically seen in inferior and/or anterior leads.V6) or use the R wave in lead aVL (dotted box) (35 and 12 are the KEYs) • • 12-LEAD ECG's . LVH Summary: Which Leads for What? • LV "strain" is usually seen in at least one of the following leads: I. which entails similar findings as RVH. tall R in V1. pulmonary hypertension and/or pulmonary stenosis). V4. Pulmonary Embolism . may suggest this diagnosis. Pulmonary Disease (such as COPD) may sometimes be suggested by ECG if at least two of the first 5 findings noted above are seen. deep S waves in V5.Most of the ECG criteria for RVH are present in this figure (RAD.A "Web Brain" for Easy Interpretation . and/or V6. Voltage for LVH . right-sided heart failure.with COPD. The ECG is usually not diagnostic.the two leads to look at for detecting LAA (or RAA) are leads II and V1 (arrows in the figure). V6).Use the leads within the heavy line in the figure (deepest S in V1. V5. both of which are present here).is most often associated with sinus tachycardia and/or non-specific STT wave changes. Example of RVH . although sudden development of A Fib and/or ECG findings of acute right heart "strain".
R .S . Assessing for Q .S .T is to ensure a systematic approach so that nothing is left out. while subtler (but equally important findings) go unnoticed. Scan each of the other 11 leads for Q waves.T Changes • • Ignore lead aVR.12-LEAD ECG's .R . The most common mistake that occurs when a systematic approach is not closely followed is to allow more dramatic ST segment and T wave changes to consume one's attention. • Check for R wave progression: o Does transition occur in the usual place? o Is there a tall R wave (or rSr') in lead V1 ? . Routine adherence to a systematic approach not only prevents such findings from being overlooked. The purpose of this mnemonic Q . Examples of such all-too-easy-to-overlook findings include recognition of a dominant R wave in lead V1 and poor R wave progression. but ends up saving time in the long run. o Note the leads in which Q waves are found.A "Web Brain" for Easy Interpretation QRST Changes The "heart" of ECG interpretation resides with assessing the tracing for QRST changes.
III.e. elevation or depression) and/or changes in the T wave.V1. whereas leftsided leads (V5 and V6) are predominantly positive. between V2 to V4). in which arrows depict the general direction of LV (left ventricular) depolarization.e.. V2 Anterior leads . right-sided precordial leads (V1 and V2) are predominantly negative.V4 to V6 . The area where the R wave becomes greater than the S wave (transition) occurs normally in this figure (i.• Look at all leads (except aVR) for: o Changes in the ST segment (i.II. The smaller RV (right ventricle) predominantly sees electrical activity as moving away from the right (and toward the larger and thicker left ventricle). anterior. This accounts for the fact that. The Basic Lead Groups: • • • • Inferior leads . Note the overlap between leads viewing the septal.V2 to V4 Lateral (left-sided) leads: o Lateral precordial leads .. in a normal ECG. Precordial Lead Appearance The figure shows a schematic cross-sectional view of the heart. aVF Septal leads . and lateral precordial areas.
e. Causes of Poor R Wave Progression (PRWP): • • • • • • • • • LVH RVH Pulmonary disease (i. anterior infarction is less likely in this tracing .I. LAHB. LBBB.e. Despite the PRWP. aVL R Wave Progression Normally the R wave becomes progressively taller as one moves across the precordial leads (see figure right) A number of conditions may be associated with "poor" R wave progression. RAA. COPD.. persistent precordial S waves). IVCD) Cardiomyopathy Chest wall deformity Normal variant Lead misplacement Examples of PRWP: The patient (see figure right) has COPD (suggested by RAD. or only increases very slowly in size.o High lateral leads . in which the R wave in leads V1 through V3-V4 either does not become bigger. chronic asthma) Anterior or anteroseptal infarction Conduction defects (i..
because an r wave is present in all precordial leads (albeit the r wave is small). Q Waves/T Wave Inversion: When is it "normal"? Leads III. or aVL is most likely not to reflect ischemia when the QRS is also negative in these leads. and V1 may normally display moderate-tolarge size Q waves and/or T wave inversion. In general we can ignore lead aVR. Isolated T wave inversion in lead III. Small and narrow normal septal q waves will often be seen in one or more of the lateral leads (I. This figure (left) shows PRWP from anteroseptal infarction (suggested by the complete lack of any r wave at all in leads V1. and V3). aVL. Statistically. or V6) in asymptomatic individuals who do not have heart disease. V5. One can't be nearly as sure about infarction in this next figure (right) compared to the one above (left) because a small r wave does develop by lead V3 (we'd say "possible" anteroseptal infarction). V2. . aVR. V4. aVL. realize that finding a QS in leads V1-V2 is more likely not to be due to infarction. aVF. aVF. since it rarely contributes useful clinical information.
.e. ST segment elevation with coving or a downward convexity ("frowny" configuration) is much more likely to be due to acute injury (from acute infarction). KEY Point History is ever important. Although ST elevation with a "smiley" configuration and J point notching often reflect a normal variant. This is known as early repolarization. "smiley" configuration) is usually benign. Common Causes of ST Segment Depression • • • Ischemia "Strain" Digitalis effect • • • Hypokalemia/Hypomagnesemia Rate-related changes Any combination of the above . In contrast. An identical ST pattern from a patient with chest pain must be assumed abnormal (and possibly indicative of acute infarction) until proven otherwise. especially when seen in an otherwise healthy.The Shape of ST Segment Elevation ST segment elevation with an upward concavity (i. asymptomatic individual (and when seen with notching of the J point in one or more leads). this is only true if the patient is asymptomatic.
e. 12-LEAD ECG's . Digoxin ("Dig effect") may produce either ST "scooping" or a "strain"-like pattern or no change at all. Finally. .The specific cause of ST segment depression in a given tracing may be suggested by the appearance of the ST segment and T wave itself.A "Web Brain" for Easy Interpretation 12-LEAD ECG's . there are Non-Specific STT wave Abnormalities such as ST flattening or slight depression. especially when seen in two or more leads of a group (i. in II. III. "strain" (for LVH) is suggested by asymmetric ST depression in lateral leads. and aVF). especially if voltage criteria are met. Ischemia is suggested by symmetric T wave inversion.. For example. "RV strain" is suggested if the tracing depicted in the figure is seen in right-sided leads in a patient with RVH. By doing so we hope to determine: • If any acute changes are present.A "Web Brain" for Easy Interpretation Infarction and Ischemia One of the most important reasons for obtaining an ECG is to help evaluate the patient who presents with new-onset chest pain.
... which is the earliest change of Acute MI. is the patient a candidate for acute intervention (i. or no symptoms at all. C shows the "hyperacute" stage. mental status changes. not associated with chest pain). Development of Q waves 4. fax tracings.e.e. A and B (figure below right) show a normal QRS complex before any changes develop. Note that a small narrow q wave may often be present (as in A) as a normal finding (reflecting normal septal Q waves that are commonly seen in lateral leads). Q waves of infarction tend to be bigger and wider. how extensive is the involvement. arrhythmias) and most importantly. are other abnormalities present (i. conduction defects. This . with thrombolytic therapy or angioplasty)? KEY Point Be aware that as many as 1/3 of all infarcts are "silent" MIs (i. Instead there may be dyspnea. If so. ST segment elevation 2. T wave inversion 3. in which the T wave becomes broader and peaks (almost as if "trying" to lift the ST segment). Use of a prior ECG may be invaluable for determining if abnormalities seen on a current tracing are new or old. we want to determine if the patient being evaluated is acutely infarcting or ischemic.• If there is evidence of prior infarction. To facilitate comparison. AV block. what area of the heart is involved. Specifically. Reciprocal ST segment depression. Acute Infarction: What are the Changes? There are 4 principal ECG indicators of acute infarction: 1.e.
Look for reciprocal changes (ST depression in leads not showing ST elevation) to help determine if ECG findings are acute. As many as 1/3 do not develop changes. many patients don't read the textbook! Variations on this theme are common (i. ST elevation is maximal. T waves evolve as ST segments return to baseline (in F)..change may be subtle (and easy to miss!). admit the patient to rule out Acute MI! Acute ECG changes may be subtle (as in the hyperacute). ST depression or T wave inversion may be the only change.). G shows ST-T wave abnormalities resolving (or nearly resolving) but there is persistence of Q waves. In general.e. E and F show Q waves becoming bigger. Non-Q wave infarctions may occur. The A thru F sequence in the figure above represents the "typical" evolution of Acute MI. D shows conventional ST elevation follows (with ST coving/"frowny" shape) and developing Q waves. troponin) may initially be negative. Q waves sometimes resolve with time. and serum markers (CK-MB. These tend to be "incomplete" infarctions (often not transmural) and pose a high risk for reinfarction (i. KEY Points regarding the ECG with Acute MI: • Not all patients with Acute MI develop ECG changes. it usually is short-lived. Q waves don't always develop. "completing" the infarct). Consider early revascularization ! Because ECG changes are not always seen with Acute MI. if uncertain about whether a Q wave or T wave inversion in lead III or aVF is clinically significant. a key determinant of whether or not to admit a patient with chest pain to the hospital must be the history.. Unfortunately. For example. if in doubt. (causes of ST depression) Use the concept of "patterns of leads". especially if MI occurs in electrically silent areas of the heart. etc.e. and T wave inversion begins. look at the other inferior lead (which is • • • • .
Mobitz I is common with inferior MI (the RCA supplies the AV nodal artery). Sudden occlusion of the Left Main coronary artery leads to sudden death (from massive infarction). Treatment Goals: Since the cause of Acute MI is most often sudden total occlusion of a major coronary artery. . Sudden occlusion of the LAD (Left Anterior Descending) artery leads to anterior infarction. In about 10% of patients this artery (rather than the RCA) also supplies the inferior and posterior walls of the left ventricle. bundle branch block/Mobitz II 2° AV block may be seen. Coronary Anatomy: Relation to the Site of Infarct The most common cause of Acute MI is sudden total occlusion of a major coronary artery. the goal of treatment should be to attempt to restore flow as soon as possible to the IRA (Infarct-Related Artery). • Sudden total occlusion of the RCA (Right Coronary Artery) causes acute inferior MI and/or posterior or right ventricular MI (ST elevation in lead V4R helps diagnose RV infarction. • • • Note .lead II) to see if these changes are also present (review normal variant Q waves/T inversion).).Collateral development changes the above patterns. Sudden occlusion of the Circumflex artery leads to lateral infarction.
12-LEAD ECG's . Who Benefits Most? Those seen earlier (ideally within 4 hours) & those with larger infarcts (i. As a result..A "Web Brain" for Easy Interpretation The Mirror Test / Tall R in Lead V1 . Regarding Thrombolytic Therapy: Who Qualifies? Ideally patients < 75 years old with chest pain and ST elevation who are seen less than 6 hours after symptom onset and who have no contraindications to thrombolysis. anterior location/more ST elevation with more reciprocal depression). Patients who have not yet formed Q waves (or with only small Q waves) are also more likely to benefit (greater chance of reversibility). thrombolytic therapy is the most commonly used method for attempting reperfusion.Acute angioplasty (with or without stenting) may be preferable if available (only about 20% of US hospitals have this on an emergency basis).A "Web Brain" for Easy Interpretation 12-LEAD ECG's .e. Criteria for thrombolysis have been expanded in selected cases to include older patients and those who are seen more than 6 hours after symptom onset.
Finding a "Tall" R wave in lead V1 (i. the purpose of the Mirror Test is to facilitate recognition of ECG changes that might represent acute posterior MI. the QRS complex in lead V1 is predominantly negative (review Precordial Lead Appearance). Thus. ECG changes that occur in the posterior wall must therefore be inferred from indirect observation (leads V1. Causes of Anterior ST Depression in the Setting of Acute Inferior MI • • • Reciprocal changes Concomitant anterior ischemia Posterior infarction (any combination of these) The Mirror Test None of the standard precordial leads directly view the posterior wall of the left ventricle. ST segment depression is commonly seen in the anterior leads (V1. If this was an actual paper ECG tracing. and V3). V2 & V3). V2. you would flip the page over.e.In the setting of acute inferior infarction. V3) provide a mirror. look like Q waves and coved ST elevation when the Mirror Test is performed (second figure). Application of the Mirror Test The anterior precordial leads (V1. that is seen in V1. The Tall R Wave in Lead V1 Under normal circumstances. Thus. WPW o QRS widening &Short PR interval. an R wave that equals or exceeds the S wave in this lead) is distinctly unusual & should prompt consideration of the following: Common Causes of a Tall R Wavein Lead V1 (#s correspond to diagram): 1. V3 of the first figure on the left. V2.. V2. which may be done via the Mirror Test. rotate it 180° & hold it up to the light. There are 3 principal causes. . the tall R waves and ST depression.image view of the posterior wall of the left ventricle.
11 second.. terminal S wave in leads I and V6. QRS widening to > .A "Web Brain" for Easy Interpretation 12-LEAD ECG's .A "Web Brain" for Easy Interpretation .e.o Delta waves (which may be positive or negative). RVH o o o o 4. rSR' (or RBBB equivalent pattern) in lead V1. RBBB o o o 3. Persistent precordial S waves. RVH. 2. after ruling out WPW. Wide. Right ventricular strain. Normal QRS duration & RAA. & posterior infarction) o Often found in otherwise healthy young adult 12-LEAD ECG's . Posterior Infarction -Normal QRS duration o Evidence of inferior infarction o Positive "mirror test" 5. RAD or indeterminate axis/Low voltage. Normal Variant o Normal QRS duration o Diagnosed by exclusion (i. RBBB.
peaked. Contrast with the T wave that is sometimes seen in healthy individuals as a normal variant (shaded box) in which the T wave is rounded. and the QRS widens (K+ >8 mEq/L). Hypokalemia Although the ECG is a fairly good indicator of hyperkalemia. its sides are not symmetric. when ECG changes are seen they tend to be those that are shown in this figure. However. and it has a broad base. . especially for hyperkalemia (in which a fairly good correlation does exist between ECG findings and the serum potassium [K+] level). A normal B shows peaking of the T wave. which is the earliest change (K+ about 6-7 mEq/L) C The T wave becomes taller and more peaked (K+ about 7-8 mEq/L). V Fib usually follows. E P waves disappear (sino. with a narrow base).ventricular rhythm) and the QRS becomes sinusoid (K+ >10 mEq/L). D P wave amplitude decreases.Electrolyte Disturbances Hyperkalemia An ECG should be obtained when electrolyte disturbance is suspected. it almost looks like the Empire State building (tall. the PR interval lengthens. it is not reliable for detecting hypokalemia.
acute MI. potassium.A "Web Brain" for Easy Interpretation 12-LEAD ECG's . 12-LEAD ECG's . which is the earliest change C and D A "U wave" then develops.A normal B shows flattening of the T wave. E and F ST depression is more noticeable and the U wave increases in amplitude until ultimately the U wave overtakes the T wave. calcium. digoxin or diuretic therapy. renal impairment. Hypomagnesemia is often seen in association with other electrolyte abnormalities (low sodium. cardiac arrest. or phosphorus).A "Web Brain" for Easy Interpretation Pericarditis . Note .The ECG changes of hypomagnesemia are identical to those of hypokalemia. At this point distinguishing between the T wave and U wave may be almost impossible ("Q-U" prolongation). associated with ST-T wave flattening and sometimes slight ST depression. A "pseudo P-pulmonale" pattern may be seen. alcohol abuse.
see below) Stage II Transition ( i.e. Recognition of acute pericarditis can be facilitated by thinking of diagnosis as a 3 part process: 1.. ST elevation in almost all leads . Note how. 2.e. Physical exam o Hearing a pericardial friction rub is the most diagnostic sign! 3. III). Stage IV Normalization. ECG findings o These are divided into 4 stages. with elevation being seen in virtually all leads except those "far away" (shaded leads aVR. Stage III Everything is DOWN (inverted T waves). V1. "pseudonormalization").Pericarditis is often a difficult clinical entity to detect. the ST segment elevation is diffuse ("everything up" stage). in the tracing of Stage I pericarditis (figure right). The easiest way to remember these sequential changes is to conceptualize the four stages as follows: Stage I everything is UP (i. Early Repolarization .. History o Inquire about preceding viral illness.
A "Web Brain" for Easy Interpretation . that which is seen in early repolarization. In contrast. chest pain more constant and severe). ST elevation is usually localized to one (or at most two) areas of the heart. Acute MI Acute MI is usually suggested by the history (older patient with risk factors. and acute MI can usually be made because early repolarization is most often seen in otherwise healthy young adults. The ECG may show Q waves.A "Web Brain" for Easy Interpretation 12-LEAD ECG's . while the ST segment is still elevated. 12-LEAD ECG's . with pericarditis the T wave typically does not invert until after the ST segment has returned to the baseline. reciprocal ST depression and T wave inversion.The distinction between the ST elevation of Stage I pericarditis.
Rhythm • • • Are there P waves? Are P waves "married" to the QRS? P waves should always be upright in lead II if there is sinus rhythm (unless there is lead reversal or dextrocardia) Remember: for Rhythm.12-LEAD ECG's . & the 3 R's . be systematic)! Rate • Divide 300 by the number of boxes in the R-R Interval (review). Whenever possible. WRITE OUT your findings (even when time is short. then formulate your clinical impression.A "Web Brain" for Easy Interpretation Analyze an ECG Applying the Systematic Approach Use the following as a guide for your descriptive analysis. you must watch your P's & Q's.
The axis is indeterminate if net QRS deflection is negative in I and aVF.21 second (if clearly more than a LARGE box in duration). • • KEY Point . (if more than half a large box). The QT Interval is prolonged if clearly more than half the R-R interval (provided that heart rate is not more than 100 beats/ minute). There is pathologic LAD (LAHB) if net QRS is more negative than positive in lead II. The QRS Complex is wide if >0. IVCD. but negative in aVF. STOP and find out why (i.20-0. or WPW) before proceeding further. LBBB.Intervals • • Be sure to look at intervals early in the process! The PR Interval is prolonged if >0. There is LAD if the net QRS is positive in lead I. RBBB.e. (review of Axis determination) • • • • . (review causes of wide QRS) Axis • • Axis is determined by looking at lead I (at 0°) and lead aVF (at +90°) The axis is normal if net QRS deflection is positive in leads I and aVF. There is RAD if net QRS deflection is negative in lead I. but positive in aVF.10 sec.If the QRS complex is wide..
. concentrate on shape ("smiley" or "frowny") of the ST segment. • • • . aVF. aVL. and V1.5 mm tall) and peaked (i. T Waves . or persistent precordial S waves. • • • • Infarct (QRST changes) Look at all leads (except aVR) for the following: • Q Waves .Small (normal septal Q waves) are commonly seen in lateral leads (I. "uncomfortable to sit on") in the pulmonary leads (II. and aVF). Consider RVH if there is also a tall R wave in V1 and right ventricular "strain". moderate or large.sized Q waves are normal (as an isolated finding) in leads III. and V1. III. in a patient at least 35 years of age) and 12 (for the R in lead aVL).e. aVL. True chamber enlargement is much more likely if "strain" is also present! There is RAA (P Pulmonale) if P waves are prominent (> 2. II.Does transition occur from V2-V4? Is there a tall R wave in V1? Is there a rSR' pattern in V1? ST Segments . low voltage.shaped) in mitral leads (I.More than the amount of ST segment deviation. Consider pulmonary disease if there is RAA. V4. V5.May normally be inverted in leads III. RAD (or indeterminate axis). aVF. V6). or aVL) or if the P in V1 has a deep terminal negative component.Hypertrophy • The "magic numbers" for LVH are 35 (deepest S in V1 or V2 plus tallest R in V5 or V6. R Wave Progression . incomplete RBBB (or rSr' pattern in lead V1). aVL. There is LAA (P Mitrale) if P waves are notched ("m".
A "Web Brain" for Easy Interpretation .12-LEAD ECG's .
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