Your SlideShare is downloading. ×
0
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
12 LEAD
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

12 LEAD

1,165

Published on

Published in: Education
0 Comments
5 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
1,165
On Slideshare
0
From Embeds
0
Number of Embeds
1
Actions
Shares
0
Downloads
0
Comments
0
Likes
5
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide
  • This information will aid in understanding the ECG subsets in the next section. Define ischemia, injury and infarct. Note that the definitions are correlated with specific ECG criteria. Note that “injury” is also ischemia and does not imply any permanent damage or death to tissue. The term injury simply means ischemia identified by ST segment elevation.
  • While it is not always possible to identify which of the ACS a patient is experiencing, it is possible to determine if a patient can benefit from acute reperfusion therapy. The indication for acute reperfusion therapy is ST segment on the 12-lead ECG. For EMS to identify this subset of patients, a diagnostic 12-lead must be obtained . “ The 12-lead ECG stands at the center of the decision making pathway in the management of patients with ischemic chest pain, and delays in obtaining the 12-lead ECG must be eliminated.” AHA, ACLS Textbook, 1997, 9-13
  • Whether tissue necrosis occurs as in AMI or does not occur resulting in unstable angina is determined by the interplay of several factors. This underscores why it is usually impossible to determine which syndrome is present and why we should instead concentrate on identifying the the presence of any ACS. The issue of suspecting ACS will be addressed after a brief explanation of the terms ischemia, injury and infarction.
  • Thrombolytics are pharmacological agents administered IV that dissolve a coronary thrombus. PTCA is an intervention that utilizes a balloon or other device, inserted through a large artery, to create a larger lumen in the offending coronary artery. Atherectomy procedures remove the occlusion by laser or cutting mechanisims.
  • The typical “3-lead” ECG was never designed to capture QRS-ST-T waveforms with complete accuracy. The 3-lead was designed to provide enough information for the user to determine cardiac rate and rhythm. Because artifact makes interpretation difficult, the 3-lead is set to “filter out” artifact by reducing the spectrum of cardiac electrical activity that it “sees”. This strategy significantly reduces artifact and still renders waveforms of sufficient quality for rate and rhythm determination. However, in doing so, the QRS-ST-T may not always be accurately represented. Therefore, do not use monitor quality for ST analysis.
  • The 12-lead is designed to accurately reproduce the QRS-ST-T waveforms. In order to do so the 12-lead must “look” at a broader spectrum of cardiac electrical activity. This spectrum is referred to as “frequency response” This broader spectrum is referred to as “diagnostic quality”. A diagnostic quality ECG is necessary for accurate ST segment analysis. Unfortunately, when in diagnostic quality, all 12-lead ECGs are more susceptible to more artifact than are 3-lead ECGs.
  • The frequency response is printed on the ECG paper. The frequency response for diagnostic quality is 0.05Hz - 150Hz. There may be some slight variation among manufacturers and ECG models. The low end for monitor quality is often 0.5 Hz (not 0.05Hz), while the high end often is in the range of 20-50Hz.
  • The frequency response is printed on the ECG paper. The frequency response for diagnostic quality is 0.05Hz - 150Hz. There may be some slight variation among manufacturers and ECG models. The low end for monitor quality is often 0.5 Hz (not 0.05Hz), while the high end often is in the range of 20-50Hz.
  • Because of the increased “window” to electrical signals, additional steps must be taken to reduce the amount of artifact produced. Removing excess hair and prepping the skin allows the electrode gel to better penetrate the skin, thus receiving a stronger signal with less artifact. First we will discuss the techniques themselves, later in the module we will look at strategies to accomplish these additional tasks quickly.
  • Excess hair presents two problems: • First, hair may prevent the electrode from adhering well. • Second, hair may inhibit gel contact and skin penetration. Some thrombolytic manufacturers recommend that clippers be used to remove chest hair. The intent is to minimize the potential for bleed sites in a patient who may receive a thrombolytic.
  • Simply rubbing the skin with a gauze pad can have a noticeable effect on ECG clarity by: • Reducing skin oil • Removing part of the stratum corneum
  • When measured from the patient ’s skin, the heart’s electrical signal is extremely small, about 0.0001 to 0.003 volts. That ’s as small as one-ten thousandth of a volt. Compare this with energy from a nine volt battery. Good skin prep will make the ECG signal as strong as possible, and make the artifact signals as small as possible.
  • Once the skin has been prepped and the electrodes applied, there are still other sources of artifact to consider.
  • It is important to place the patient in a position of comfort. The reduction in muscle tension will help to prevent artifact. When possible, the patient should be in the supine position for a 12-lead ECG. Sometimes this is not feasible, practical or desirable. If ECG is not recording in supine position, simply note this on ECG.
  • It is important to place the patient in a position of comfort. The reduction in muscle tension will help to prevent artifact. When possible, the patient should be in the supine position for a 12-lead ECG. Sometimes this is not feasible, practical or desirable. If ECG is not recording in supine position, simply note this on ECG.
  • It is important to place the patient in a position of comfort. The reduction in muscle tension will help to prevent artifact. When possible, the patient should be in the supine position for a 12-lead ECG. Sometimes this is not feasible, practical or desirable. If ECG is not recording in supine position, simply note this on ECG.
  • Note how the baseline straightened out by simply repositioning the patient cables and clipping them onto the sheet. What technique(s) would you consider in order to resolve the muscle artifact?
  • All of the techniques discussed to this point have related to ECG clarity. We now need to look at what is necessary to ensure ECG accuracy.
  • Limb leads should be placed on the limbs. The traditional placement is near the ankles and wrists.
  • V1 fourth intercostal space to the right of the sternum V2 fourth intercostal space to the left of the sternum V3 directly between leads V2 and V4 V4 fifth intercostal space at left midclavicular line V5 level with lead V4 at left anterior axillary line V6 level with lead V5 at left midaxillary line
  • Here is what lead placement looks like on a patient.
  • Once a clear ECG has been obtained (free of excess artifact and has a steady baseline), it may then quickly be examined to confirm accuracy. Listed here are five items that relate the the accuracy of the ECG.
  • It is important to note that the display screen in 12-lead monitors is not in diagnostic quality. Usually a 12-lead must be printed out for accurate ST analysis. Check the 12-lead printout and confirm the correct frequency response.
  • It is important to note that the display screen in 12-lead monitors is not in diagnostic quality. Usually a 12-lead must be printed out for accurate ST analysis. Check the 12-lead printout and confirm the correct frequency response.
  • It is important to note that the display screen in 12-lead monitors is not in diagnostic quality. Usually a 12-lead must be printed out for accurate ST analysis. Check the 12-lead printout and confirm the correct frequency response.
  • These tracings show how much the ECG can change in a short time. Note the times on these ECGs.
  • This excerpt from an American Heart Association algorithm shows the initial 12-lead acquisition along with the vital signs. Note treatment is concomitant and is not inordinately delayed. In later modules we will further develop the concepts relating to the dynamic nature of AMI and the 12-lead ECG. At that time it will be very apparent why early ECGs are critical. Accepting that fact necessitates a strategy for QUICK 12-lead acquisition
  • Exposing the chest before obtaining the 12-lead is probably the single most important factor to reduce time and effort. If a gown is not available a sheet may be used, however, the gown is preferable.
  • ST segments are iso-electric.
  • Define ischemia
  • Note widespread ST depression and T waves inverted in several leads.
  • Define injury. Ischemia affecting the epicardium represented by ST elevation.
  • Ask group to look for ST elevation.
  • Death of tissue.
  • Pathologic Q waves present in II, III and aVF suggest necrosis has occurred in the inferior region of the left ventricle.
  • A normal ECG does NOT rule out any Acute Coronary Syndrome.
  • EXERCISE: approximately 2 minutes Instructions: Review the 12-lead ECG. Go lead by lead, and pick one good complex in each lead. Find the J-point and ST segment. Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now). Place a checkmark next to any lead with 1mm of ST segment elevation. Review findings with group, pointing out every J-point and ST segment. Note leads II, III and aVF display elevation. Remember ST segment elevation is presumptive evidence for AMI. Knowing which part of the heart leads II, III and aVF “sees” would tell you where the infarct is located.
  • This represents the 3x4 format of the 12-lead ECG. Each box represents one lead, and the viewpoint of that lead is indicated.
  • Each box represents one lead, and the viewpoint of that lead is indicated. NOTE: Refer participants to their pocket card where this information is summarized as well.
  • The three subdivisions of the LCA.
  • Note the change and locate the anatomical territory affected, correlate to the suspected coronary artery. This involves the septal and anterior leads. Commonly called antero-septal MI.
  • Note the change and locate the anatomical territory effected, correlate to the suspected coronary artery. This involves the lateral leads. Called lateral wall infarct.
  • Note the change and locate the anatomical territory effected, correlate to the suspected coronary artery. This involves septal, anterior and lateral leads. Commonly referred to as extensive anterior.
  • When the proximal LCA (a.k.a. left main) is occluded, the entire left coronary territory is effected. This includes the septal, anterior and lateral walls; this is referred to as an acute extensive anterior MI. Complications such as LVF with pulmonary edema and/or cardiogenic shock are common and expected. Mortality is high.
  • Thrombolytics work well for extensive anterior MI ’s when the BP is elevated or normal. When cardiogenic shock is evident, a trip to a surgical capable cath lab is indicated because these lesions often require emergency bypass surgery.
  • The bundle branches are primarily supplied by the LCA.
  • The right coronary artery includes the proximal RCA and the PDA.
  • This ECG 4 is an IWMI. The RCA is occluded somewhere along its course. From this view you cannot conclude if the lesion is proximal or distal.
  • If the lesion is proximal (high in the RCA), then right ventricular infarct may result. Additional leads are needed to see the right ventricle.
  • Note obvious acute IWMI. The right chest leads (V4R, V5R and V6R) show ST elevation including RVI. The proximal RCA must be occluded .
  • Evidence of acute IWMI is an indication to examine the right precordial leads.
  • These signs are due to failure of the right ventricle during an acute RVI.
  • If normotensive, supinate patient if possible, have fluid line established, consider small (200cc) fluid challenge, then administer NTG via drip and small incremental doses of MS for pain. NTG via spray or tab can be used if drip not available, be ready for hypotension. If hypertensive, significant failure from RVI is unlikely.
  • Posterior wall MI ’s rarely occur alone, they are usually an extension of a lateral or inferior MI. The posterior wall has a dual blood supply. It receives blood from the RCA and LCA.
  • Note acute posterior wall MI.
  • In these cases, when the LCX occludes, the lateral and inferior walls infarct.
  • Note infero-lateral MI.
  • While ST segment elevation is presumptive evidence of an AMI, there is a whole spectrum of ECG changes associated with AMI. If one were to monitor the heart as a coronary artery became occluded, the earliest ECG change suggestive of AMI would be the T wave becoming tall and peaked. This is referred to as a HYPERacute change, because it may occur so early as to actually precede clinical symptoms. Of course hyperacute T waves are seen only in leads “looking” at the infarcting area. Note: True hyperacute T waves are identified not only by their height, but by their shape as well. However, participants often wonder “how tall is tall”? As a rule of thumb T wave height can normally be up to five millimeters in the limb leads and ten millimeters in the chest leads.
  • ST segment elevation is the next probable ECG change. ST segment elevation implies at least three things: 1. Myocardial tissue injury is presently occurring. 2. This injury is probably due to an occluded coronary artery. 3. Unless corrected, this condition will lead to tissue necrosis. Therefore, even though necrosis has not yet occurred, we say that ST segment elevation is “presumptive evidence” of AMI. Final point: when the ST segment is elevated we assume that the infarct is acute rather than old.
  • Note that the ST segment is elevated. We therefore assume that the infarct is acute (occurring right now). However, notice the presence of a Q wave that is at least 40 milliseconds wide. This pathologic Q wave is associated with cellular necrosis. ECG evidence now suggests that some myocardium is only injured and can still be saved (ST elevation) while some other portions of the myocardium may have already become necrotic (Q wave). It is critical to recognize and consider this pattern as acute and target this patient for reperfusion therapy. NOTE: When Q waves first form, the tissue may not yet be necrotic and, with prompt reperfusion, the Q waves may disappear.
  • Note the presence of a wide Q, and the absence of ST segment elevation. This ECG pattern is associated with a previous MI. It is not possible to determine when this infarct may have occurred, so it is described as “age undetermined” rather than “an old MI”. Look for these additional changes associated with AMI as we practice infarct recognition and localization, but remember, the most important finding is ST elevation in two contiguous leads.
  • It is critical to remember that a patient may indeed be experiencing an acute myocardial infarction even though ST segment elevation is not present on the ECG. Never make the mistake of presuming that a single 12-lead rules out AMI.
  • Instructions: Review the 12-lead ECG. Go lead by lead, and pick one good complex in each lead. Find the J-point and ST segment. Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now). Place a check mark next to any lead with 1mm of ST segment elevation. Localize the area of infarction. Antero-septal
  • Instructions: Review the 12-lead ECG. Go lead by lead, and pick one good complex in each lead. Find the J-point and ST segment. Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now). Place a check mark next to any lead with 1mm of ST segment elevation. Localize the area of infarction. Extensive anterior (septal + anterior + lateral)
  • Instructions: Review the 12-lead ECG. Go lead by lead, and pick one good complex in each lead. Find the J-point and ST segment. Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now). Place a check mark next to any lead with 1mm of ST segment elevation. Localize the area of infarction. Inferior wall infarction Note ST depression in I, AVL and V1-V3. Lets talk about one cause of ST depression, known as reciprocal ST depression.
  • We have been looking for infarct based upon the presence of ST elevation. As mentioned, not every lead is elevated when AMI is present, only the leads looking at the infarct site. In fact, those leads which look at the infarct site from the opposite perspective tend to produce the opposite changes. When a lead “sees” the AMI directly, the segment becomes elevated in that lead. However, when a lead “sees” the infarct from the opposite perspective, the ST segment may be depressed in that lead.
  • Because of the way the leads are oriented on the patients body, II, III and aVF are on the bottom looking up. All the other leads are on the top, looking in. Therefore, when AMI produces elevation in II, III, and aVF, it also tends to produce depression in the opposing leads.
  • Instructions: Determine which leads show ST elevation. Which leads show ST depression. Localize the area of infarction. Determine if a reciprocal pattern exists. ST elevation exists in II, III and aVF. ST depression in I and aVL Does it fit the reciprocal pattern? Yes. NOTE: Not every lead on each side of the seesaw must be elevated or depressed in order to assume reciprocal changes. Rather it is more a matter of at least some leads on one end of the seesaw being elevated and some being depressed.
  • Instructions: Determine which leads show ST elevation. Which show ST depression. Localize the area of infarction. Determine if a reciprocal pattern exists. Here the elevation is in leads I, aVL, V1-V5 And the depression is in leads II, III and aVF Extensive anterior infarction, with reciprocal depression
  • Not all AMIs with ST elevation produce reciprocal depression. Quite simply… some do and some don ’t. When reciprocal depression is noted, the likelihood of AMI is dramatically increased.
  • When clinical presentation suggests AMI and the 12-lead shows ST segment elevation, proceed as if the patient were infarcting. However, providers must be aware that there may be ST segment elevations and may not be diagnosed with AMI.
  • Bundle Branch Block (BBB) has a number of potential causes. BBB can be the result of a fibrosis or calcification of the ventricular conduction system. (Lev ’s disease and Lenegre’s disease are examples.) People can live well for many years with the BBB caused by these conditions. Unless there is evidence of worsening conduction (syncope, dropped beats, etc) these conditions are non-emergent. BBB can also be caused by an ACS. When BBB is caused by an ACS, it identifies a very high risk patient!
  • Literally, BBB can both mask and mimic all of the ECG changes associated with ACS!
  • The presence of a new BBB, or presumably new BBB, is an indication for thrombolytic therapy*. At the physician ’s discretion, thrombolytics may be administered to patients whose BBB obscures the diagnosis of AMI on the ECG. *The 1996 ACC/AHA Guidelines for the Management of Patients with Acute Myocardial Infarction ” lists BBB as a Class I indication for thrombolysis. (Definition of Class 1: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is beneficial, useful, and effective)
  • BBB widens the QRS (120ms or more). This widening is due to the fact that the ventricles are forced to contract sequentially, thus requiring more time. Other conditions widen the QRS; a common one would be ventricular rhythms either paced or spontaneous. A differentiating factor between BBB and ventricular rhythms would be the presence of an underlying supraventricular rhythm. Therefore, when a QRS of 120ms or more is produced by a supraventricular rhythm, think BBB. This rule applies in all leads.
  • Example 1 underlying rhythm sinus QRS width 160ms Example 2 underlying rhythm sinus QRS width 120ms
  • Example 1 underlying rhythm sinus QRS width 160ms Example 2 underlying rhythm sinus QRS width 120ms
  • The “classic” pattern for RBBB in V1 is an RSR.
  • The “classic” pattern of LBBB in V1 is a QS complex. There are many variations to these classic patterns, complicating the process of distinguishing RBBB from LBBB. In addition, each form of BBB produces a different set of changes in V6. Fortunately, a simplified approach does exist.
  • After BBB has been determined to exist, look at lead V1. To identify the terminal force, first locate the J-point. From the J-point, back up about 40 ms into the QRS. Now determine if the terminal force (tail end) is pointing up or down.
  • Always remember, the following rules for differentiating RBBB from LBBB apply only to V1. We will learn to identify the terminal force of the QRS in V1, and determine if it is positive or negative. Simply stated, we will look at the tail end of the QRS complex and decide if it points up or down.
  • Have the participants review these four examples of V1 in the course guide and determine if the BBB is LBBB or RBBB.
  • Any rhythm or beat originating in the ventricles can imitate the ECG changes associated with ACS. NOTE: Sometimes caregivers are less likely to make the interpretation of a ventricular rhythm when the heart rate is greater than 60 but less than 150. Ventricular rhythms can and do occur at this “in between” rate and are referred to as accelerated idoventricular rhythms (AIVR).
  • Here is an example of how ventricular rhythms can imitate changes suggestive of ACS. Remember, they can mask the changes as well.
  • There are many causes of LVH. Most are the result of either the left ventricle working harder over a long period of time or the result of chronic overfilling. For ACS management, it is NOT critical to determine the cause of the LVH. Simply suspecting the presence of LVH is sufficient.
  • LVH can both mask and mimic all of the ECG changes associated with ACS!
  • Unlike BBB and ventricular rhythms, LVH does NOT usually widen the QRS to 120ms or more. Instead of abnormally widening the QRS, LVH increases its amplitude. There are many formulas for suspecting the presence of LVH. The three step method described here is one of the simpler means of suspecting LVH. Remember, we are not trying to identify LVH for its own sake. Rather we seek to identify LVH as a potential imitator of ACS.
  • Participants review this tracing in their course guide while instructor describes method of LVH recognition.
  • STEP 1 Compare V1 and V2. Determine which is the deepest negative deflection. In the deepest lead, count the millimeters of negative deflection.
  • Hypertrophy often causes overlapping of ECG leads which may make counting boxes in V1 and V2 difficult.
  • STEP 2 Compare V5 and V6. Determine which is the tallest. In the tallest lead, count the millimeters of positive deflection.
  • STEP 3 Add the two numbers together. If their sum equals 35 or more, suspect LVH is present.
  • Look again at the ECG, look to see which leads show changes suggestive of LVH. (Point out ST elevations, depressions, T wave inversions.) Could all of these changes be due to ACS? (yes) Could all of these changes be due to LVH? (yes) How would you manage such a patient? If the story suggests ACS, that is how the patient is managed.
  • Despite the obvious ECG changes seen here, this ECG was obtained from a patient with a perfectly normal heart! It is an example of a normal variant called “Benign Early Repolarization”.
  • It has been theorized that the cause of BER is due to one region of myocardium repolarizing early. This produces a difference in electrical potential, and thus causes ST and T wave changes.
  • One ECG sign that should make you consider BER is the notched J-point, creating a fish hook like appearance of the ST segment.
  • A notch at the J-point is shown here. NOTE: The presence of “fish hooks” does not rule out ACS. It is not uncommon to see J-point notching as a result of ACS. NOTE: Patients with BER often meet the voltage criteria for LVH. However, no true hypertrophy may exist.
  • This ECG has ST elevations and some similarities to BER. However, in this case, BER is not present. This is an example of pericarditis.
  • There are numerous causes of pericarditis. These patients often complain of chest pain, which is an indication for a 12-lead. Pericarditis is capable of producing ST changes on the ECG.
  • The “classic” pericarditis presentation has some distinguishing features. The purpose of the following description is not to rule out AMI, but to help the care provider suspect the possibility of pericarditis. Classic presentation: • Sharp chest pain (meaning a stabbing nature, not meaning intense) • Pain can often be localized with one finger • Pain may radiate to the base of the neck or between the shoulder blades (trapezius area)
  • The ST elevation of pericarditis is caused by inflammation of the epicardium secondary to inflammation of the pericardium. This process is not related to coronary artery disease and, therefore, ST changes do not tend to follow anatomical groups typically seen with ACS. Like BER, pericarditis may produce a notching of the J-point and a “fish hook” shaped ST and J-point.
  • Certainly medications have the potential to affect the ECG. One of the best documented changes due to a medication is the digitalis effect.
  • Correct categorization of ECG changes can be complicated when an imitator is present. These imitators can lead to erroneous placement of a patient into the ST elevation or ST depression category. The imitators can also mask changes that would have otherwise been present on the ECG.
  • Correct categorization of ECG changes can be complicated when an imitator is present. These imitators can lead to erroneous placement of a patient into the ST elevation or ST depression category. The imitators can also mask changes that would have otherwise been present on the ECG.
  • Transcript

    • 1. Essentials of 12-Lead ECG Interpretation HeartStart Skills Learning Center 826 Brookside Avenue, Suite A, Redlands, CA 92373 (909) 793-4555 www.heartstartskills.com
    • 2. Topics 12-Lead ECG Overview Critical Concepts of Acute Coronary Syndrome Monitoring versus Diagnostic Acquisition and Transmission Axis Determination Waveform Analysis
    • 3. Topics Injury, Ischemia or Infarction Localization of Injury Bundle Branch Blocks and Hemiblocks ST Imposters Differential Diagnosis of Wide Complex Tachycardias
    • 4. What is the purpose of 12-Lead ECGs?• Demonstrated Advantages – Rapid Identification of Infarction/Injury • Diagnosis made sooner in many cases – Decreased Time to Reperfusion Treatment • Speeds preparation of & time to reperfusion therapies – Increased Index of Suspicion • Lowers false-negatives and false-positives – Modification to Therapies • From less invasive (Fibrinolytic) to aggressive (CABG) interventions
    • 5. Critical Concepts in ACS• Ischemia – lack of oxygenation – ST segment depression or T wave inversion• Injury – prolonged ischemia – ST segment elevation• Infarct – prolonged injury results in death of tissue – may or may not show Q wave
    • 6. Critical Concepts in ACS ST elevation - the key to the acute reperfusion therapy subset You can’t see ST elevation without a 12-lead ECG  Perform on every patient suspected of ACS  Obtain early  Repeat frequently
    • 7. Critical Concepts in ACS
    • 8. Critical Concepts in ACS
    • 9. Critical Concepts in ACS Acute Reperfusion Therapies Fibrinolytics  Percutaneous Transluminal Coronary  Retaplase (rPA) Angioplasty (PTCA)  Actiplase (tPA)  Balloon angioplasty  Streptokinase (rarely used  Stent placement today)  Atherectomy
    • 10. Critical Concepts in ACS Pain is Injury Pain-Free is the Goal Time is Muscle Door to Reperfusion Therapy “Time is the Tissue”
    • 11. Monitoring vs Diagnostic ECGs Extra wires  3 wires versus 5 wires• Monitoring Quality 12-Lead ECG – Designed to provide information needed to determine rate and underlying rhythm – Designed to “filter out” artifact • Reduces the amount and degree of electrical activity seen by the ECG monitor
    • 12. Monitoring vs. Diagnostic ECGs Monitor Quality
    • 13. Monitoring vs. Diagnostic ECGs• Diagnostic Quality ECG – Designed to accurately reproduce QRS, ST and T waveforms – Designed to look more broadly at the cardiac electrical activity – Unfortunately, may result in greater artifact being visible
    • 14. Monitoring vs. Diagnostic ECGs Diagnostic Quality
    • 15. Monitoring vs. Diagnostic ECGs Frequency Response  Term used to describe the breadth of the electrical spectrum viewed by the ECG monitor  Diagnostic quality is usually 0.05 Hz to 150 Hz  Monitor quality is usually 0.5 Hz to 20-50 Hz  Usually printed on the ECG recording strip
    • 16. Monitoring vs. Diagnostic ECGs
    • 17. Monitoring vs. Diagnostic ECGs
    • 18. Acquisition & Transmission ECG quality begins with skin preparation and electrodes Hair removal Skin preparation Age & Quality of Electrodes & Cables Electrode Placement
    • 19. Acquisition & Transmission Hair Removal  Clipper over razor Lessens risk of cuts Quicker Disposable blade clippers
    • 20. Acquisition & Transmission
    • 21. Acquisition & TransmissionSkin Preparation  Helps obtain a strong signal  When measured from skin, heart’s electrical signal about 0.0001 - 0.003 volts  Skin oils reduce adhesion of electrode and hinder penetration of electrode gel  Dead, dried skin cells do not conduct well
    • 22. Acquisition & Transmission Other causes of artifact  Patient movement  Cable movement - Electromagnetic Interference (EMI)
    • 23. Acquisition & Transmission Patient Movement  Make patient as comfortable as possible Supine preferred  Look for subtle movement toe tapping, shivering  Look for muscle tension hand grasping rail, head raised to “watch”
    • 24. Acquisition & Transmission Cable Movement  Enough “slack” in cables to avoid tugging on the electrodes  Many cables have clip that can attach to patient’s clothes or bed sheet
    • 25. Acquisition & Transmission• Electromagnetic Interference (EMI) – Can interfere with electronic equipment – 60 cycle interference is a type of EMI – Look for nearby cell phones, radios or electrical devices – No contact between cables & power cords – Turn off or move away from AC devices – Use shielded cables; inspect for cracks
    • 26. Acquisition & Transmission Things to look for  Little or no artifact  Steady baseline
    • 27. Acquisition & Transmission
    • 28. Acquisition & Transmission  ECG Accuracy depends upon  Lead placement  Frequency response  Calibration  Paper speed
    • 29. Limb Lead Placement
    • 30. Chest Lead Placement V1: 4th ICS right of sternum V2: 4th ICS left of sternum V3: between leads V2 and V4 V4: 5th left midclavicular line V5: level with V4 at left anterior axillary line V6: level with V5 at left midaxillary line
    • 31. Chest Lead Placement
    • 32. ECG AccuracyLook for: Negative aVR  if aVR upright, look for reversed leads One complete cardiac cycle in each lead Diagnostic frequency response Proper calibration Appropriate speed
    • 33. ECG Accuracy Frequency Response  Display screen is non-diagnostic  Use the printed ECG for ST segment analysis
    • 34. ECG AccuracyCalibration  Voltage measured vertically  Each 1 mm box = 0.1 mV  1 mV = 10 mm calibration standard  Confirm calibration calibration impulse should be 10 mm (2 big boxes tall) stated calibration should be “x 1.0”
    • 35. CalibrationCalibration
    • 36. ECG Accuracy Paper Speed  Standard is 25 mm/sec Faster paper speed means the rhythm will appear slower and the QRS wider Slower paper speed means the rhythm will appear faster and the QRS narrower
    • 37. Paper SpeedPaper Speed
    • 38. Time Differences
    • 39. When to AcquireAssessment Treatment Vital Signs OxygenOxygen Saturation Aspirin IV Access Nitroglycerin 12-Lead ECG Morphine Brief History Modified from “The Ischemic Chest Pain Algorithm”, ACLS Textbook, American Heart Association, 2005.
    • 40. Exposing the ChestImmediately upon suspecting ACS... Remove all clothing above the waist Or, open shirt/blouse Replace with gown (if possible) Allows for complete exam Minimizes wire entanglement Enhances quick defibrillation if VF occurs
    • 41. Essentials of 12 Lead ECG InterpretationTopics Discussed: 1. Anatomy Revisited 2. The 12 Lead ECG Device 3. The 12 Lead ECG Format 4. Waveform Components 5. Lead Views
    • 42. Anatomy Revisited  RCA  Right Ventricle  Inferior wall of LV  Posterior wall of LV (75%)  SA Node (60%)  AV Node (>80%)  LCA  Septal wall of LV  Anterior wall of LV  Lateral wall of LV  Posterior wall of LV (10%)
    • 43. Anatomy Revisited  SA node  Intra-atrial pathways  AV node  Bundle of His  Left and Right bundle branches  left anterior fascicle  left posterior fascicle  Purkinje fibers
    • 44. The 12 Lead ECG Device Device serves as a voltmeter  Measures the flow of electricity Unipolar versus Bipolar Leads
    • 45. Bipolar Leads • 1 (+) and 1 (-) electrode – RA always (-) – LL always (+) – LA both (+) & (-) • Traditional Limb Leads are examples of these – Lead I – Lead II – Lead III • View from a vertical plane
    • 46. Unipolar Leads  1 positive electrode & 1 negative “reference point”  calculated by using summation of 2 negative leads  Augmented Limb Leads  aVR, aVF, aVL  view from a vertical plane  Precordial or Chest Leads  V1-V6  view from a horizontal plane
    • 47. The 12-Lead ECG Format
    • 48. The 12-Lead ECG Format Device prints out 2.5 sec each of Leads I, II, III then switches to aVR, aVL, aVF then switches to V1, V2, V3 and then to V4, V5, V6 (varies by device) Device computer analyzes all 10 sec of all 12 leads but only prints 2.5 sec of each group
    • 49. The 12-Lead ECG Format Not always accurate The computer IS very accurate at measuring intervals & durations
    • 50. Waveform Components: R WaveFirst positivedeflection; R waveincludes thedownstroke returningto the baseline
    • 51. Waveform Components: Q WaveFirst negativedeflection before Rwave;Q wave includesthe negativedownstroke &return to baseline
    • 52. Waveform Components: S WaveNegative deflectionfollowing the Rwave; S waveincludes departurefrom & return tobaseline
    • 53. Waveform Components: QRS Q waves  Can occur normally in several leads Normal Q waves called physiologic  Physiologic Q waves < .04 sec (40ms)  Pathologic Q >.04 sec (40 ms)
    • 54. Waveform Components: QRS Q wave  Measure width  Pathologic if greater than or equal to 0.04 seconds (1 small box)
    • 55. Waveform Components: QS ComplexEntire complex isnegatively deflected; No Rwave present
    • 56. Waveform Components: J-PointJunction between end of QRSand beginning of ST segment;Where QRS stops & makes asudden sharp change ofdirection
    • 57. Waveform Components: ST SegmentSegment between J-point andbeginning of T wave
    • 58. Waveform Components: ST Segment• Need reference point – Compare to TP segment – DO NOT use PR segment as reference!
    • 59. Waveform Components: Practice Find J-points and ST segments
    • 60. Lead “Views”
    • 61. 12-Lead GroupsI AVR V1 V4II AVL V2 V5III AVF V3 V6Limb Leads Chest Leads
    • 62. Inferior Wall  II, III, aVF  View from Left Leg ⊕  inferior wall of left ventricleI AVR V1 V4II AVL V2 V5III AVF V3 V6
    • 63. Inferior Wall Posterior View – Portion resting on diaphragm – ST elevation suspect inferior injuryI AVR V1 V4II AVL V2 V5III AVF V3 V6 Inferior Wall
    • 64. Lateral Wall I, aVL – View from Left Arm ⊕ – Lateral wall of left ventricleI AVR V1 V4II AVL V2 V5III AVF V3 V6
    • 65. Lateral Wall V5, V6 – Left lateral chest – Lateral wall of left ventricleI AVR V1 V4II AVL V2 V5III AVF V3 V6
    • 66. Lateral Wall I, aVL, V5, V6 – ST elevation at suspect lateral wall injuryI AVR V1 V4II AVL V2 V5 Anterior ViewIII AVF V3 V6 Posterior View
    • 67. Anterior Wall V3, V4 – Left anterior chest – ⊕ electrode on anterior chestI AVR V1 V4II AVL V2 V5III AVF V3 V6
    • 68. Anterior Wall V3, V4 – ST segment elevation with suspect anterior wall injury I AVR V1 V4 II AVL V2 V5 III AVF V3 V6
    • 69. Septal Wall V1, V2 • Along sternal borders • Look through right ventricle & see septal wallI AVR V1 V4II AVL V2 V5III AVF V3 V6
    • 70. SeptalV1, V2 • Septum is left ventricular tissue I AVR V1 V4 II AVL V2 V5 III AVF V3 V6
    • 71. ST Segment AnalysisST segment deviation 1 mm or more from the baseline
    • 72. 12-Lead ECGAMI recognition Two things to know What to look for Where you are looking
    • 73. AMI RecognitionWhat to look for  ST segment elevation One millimeter or more (one small box) Present in two anatomically contiguous leads
    • 74. Axis Determination & Deviation Why Axis Determination? Definitions Axis Quadrants Axis Determination Axis Deviation  Physiologic vs Pathologic
    • 75. Axis Determination & Deviation Why Axis Determination? The ability to identify hemiblocks (“fascicular blocks”) is the main reason you need to be able to determine axis
    • 76. Axis Determination & Deviation“It is my opinion that the inability to determine the presence of a hemiblock has often been the cause of complete heart block when well-intentioned caregivers have improperly administered Lidocaine.” Mike Taigman, “Taigman’s Advanced Cardiology”, Brady, 1995, p. 71
    • 77. Axis Determination & Deviation What is Axis?  “the general (mean vector) direction of electrical impulses as they travel through the heart”  “the sum total of all electrical currents generated by the ventricular myocardium during depolarization”  normally from upper right to lower left
    • 78. Axis Determination & Deviation What do you need to determine the axis of an ECG?  The 12 Lead ECG  Leads CORRECTLY placed on the patient RA on the right arm LA on the left arm LL on the left leg Not on the chest or abdomen  Knowledge of axis deviation
    • 79. Axis Reference • Hexaxial Reference System • The six frontal leads create six poles that intersect at the center of the heart • Each pole has a positive & negative axis • Each + and - end is assigned a value expressed in degrees • Hexaxial then divided into quadrants (easier to use)
    • 80. Axis QuadrantsLeft axis -90° -30 to -90 ° +120° -60° aVLNormal axis aVR No LAD -30° -30 to 90° -150° Man’s LandRight axis +180° 0° I 90 to 180° RAD Normal +150° +30°Extreme Right axis or“No Man’s Land” +120° +60° -90 to 180° III +90° II aVF
    • 81. Axis DeterminationQuick Axis Determination  Determine the net QRS deflection in Leads I and aVF (positive or negative) Lead I aVF Normal axis LAD RAD ERAD
    • 82. Axis DeterminationEstimating Axis QuicklyDetermine the net QRS deflection in leads I and aVF (-/+) If the net QRS in Lead I is nearly the same as aVF, then axis midway between or 45°  We estimate by calling it, “between +40° and +50° If the net QRS in Lead I is positive and is obviously greater than aVF, then axis closer to lead I  Estimate as “Between 0° and 40°” If the net QRS in aVF is positive and greater than Lead I, then axis is +50° and +90°
    • 83. Axis DeviationPathologic versus Physiologic LAD 1. First step a) Do I have LAD? b) If yes, then proceed on 2. Look at Lead II a) If the net QRS deflection is more negative than positive, then the axis must be MORE NEGATIVE than -30°
    • 84. Ischemia, Injury & InfarctionDefinitionsInjury/Infarct RecognitionLocalization & EvolutionReciprocal ChangesThe High Acuity Patient
    • 85. The Three I’s Ischemia  lack of oxygenation  ST segment depression or T wave inversion Injury  prolonged ischemia  ST segment elevation Infarct  death of tissue  may or may not show a Q wave
    • 86. Injury/Infarct Recognition Well Perfused Myocardium Epicardial Coronary ArterySeptum Lateral Wall of LV Positive Electrode Interior Wall of LV
    • 87. Injury/Infarct Recognition Normal ECG
    • 88. Injury/Infarct Recognition Ischemia Epicardial Coronary ArterySeptum Left Lateral Wall of LV Ventricular Cavity Positive Electrode Interior Wall of LV
    • 89. Injury/Infarct Recognition Ischemia  Inadequate oxygen to tissue  Represented by ST depression or T inversion  May or may not result in infarct or Q waves
    • 90. Injury/Infarct Recognition ST Segment Depression
    • 91. Injury/Infarct Recognition Thrombus Injury Ischemia
    • 92. Injury/Infarct Recognition Thrombus Ischemia
    • 93. Injury/Infarct Recognition Injury  Prolonged ischemia  Represented by ST elevation referred to as an “injury pattern”  Usually results in infarct may or may not develop Q wave
    • 94. Injury/Infarct Recognition ST Segment Elevation
    • 95. Injury/Infarct Recognition Thrombus Infarcted Area Electrically Silent IschemiaDepolarization
    • 96. Injury/Infarct Recognition Infarct  Death of tissue  Represented by Q wave  Not all infarcts develop Q waves
    • 97. Injury/Infarct Recognition Q Waves
    • 98. Injury/Infarct Recognition Thrombus Infarcted Area Electrically Silent IschemiaDepolarization
    • 99. Injury/Infarct Recognition ST segment elevation Present in two or more anatomically contiguous leads
    • 100. Injury/Infarct Recognition: Practice
    • 101. LocalizationI AVR V1 V4 Inferior: II, III, AVFII AVL V2 V5 Septal: V1, V2 Anterior: V3, V4III AVF V3 V6 Lateral: I, AVL, V5, V6
    • 102. 12-Lead Localization I Lateral AVR V1 Septal V4 AnteriorII Inferior AVL Lateral V2 Septal V5 LateralIII Inferior AVF Inferior V3 Anterior V6 Lateral
    • 103. Localization: Left Coronary Artery (LCA)  Left Main (proximal LCA) occlusion  Extensive Anterior injury  Left Circumflex (LCX) occlusion  Lateral injury  Left Anterior Descending (LAD) occlusion  Anteroseptal injury
    • 104. Localization Practice ECG
    • 105. Localization Practice ECG
    • 106. Localization Practice ECG
    • 107. Localization: Extensive Anterior MI Evidence in septal, anterior, and lateral leads Often from proximal LCA lesion “Widow Maker” Complications common  Left ventricular failure  CHF / Pulmonary Edema  Cardiogenic Shock
    • 108. Localization: Definitive Therapy for Extensive AWMI Normal blood pressure  Thrombolysis may be indicated Signs of shock  PTCA  CABG
    • 109. Localization: LCA Occlusions Other considerations  Bundle branches supplied by LCA  Serious infranodal heart block may occur
    • 110. Localization: Right Coronary Artery (RCA) Proximal RCA occlusion  Right Ventricle injured  Posterior wall of left ventricle injured  Inferior wall of left ventricle injured Posterior descending artery (PDA) occlusion  Inferior wall of right ventricle injured
    • 111. Localization Practice ECG
    • 112. Localization: Proximal RCA Occlusion Right Ventricular Infarct (RVI)  12-lead ECG does not view right ventricle  Use additional leads V3R - V6R V4R  Right precordial leads same anatomical landmarks as on left for V3 - V6 but placed on the right side
    • 113. Localization Practice ECG Note: “R” designation manually placed on this ECG for teaching purposes
    • 114. Localization: ECG Evidence of RVI Inferior MI (always suspect RVI) Look for ST elevation in right-sided V leads (V3-V6)
    • 115. Localization: Physical Evidence of RVI Dyspnea with clear lungs Jugular vein distension Hypotension  Relative or absolute
    • 116. Localization: Treatment for RVI Use caution with vasodilators  Small incremental doses of MS  NTG by drip Treat hypotension with fluid  One to two liters may be required  Large bore IV lines
    • 117. Localization: Posterior Wall MI (PWMI) Usually extension of an inferior or lateral MI  Posterior wall receives blood from RCA & LCA Common with proximal RCA occlusions Occurs with LCX occlusions Identified by reciprocal changes in V1-V4  May also use Posterior leads to identify V7: posterior axillary line level with V6 V8: mid-scapular line level with V6 V9: left para-vertebral level with V6
    • 118. Localization Practice ECG
    • 119. Localization: Left Coronary Dominance Approximately 10% of population  LCX connects to posterior descending artery and dominates inferior wall perfusion In these cases when LCX is occluded, lateral and inferior walls infarct  Inferolateral MI
    • 120. Localization Practice ECG
    • 121. Localization Summary Left Coronary Artery  Septal  Anterior  Lateral  Possibly Inferior Right Coronary Artery  Inferior  Right Ventricular Infarct  Posterior
    • 122. Evolution of AMI• Hyperacute – Early change suggestive of AMI – Tall & Peaked – May precede clinical symptoms – Only seen in leads looking at infarcting area – Not used as a diagnostic finding
    • 123. Evolution of AMI Acute  ST segment elevation  Implies myocardial injury occurring  Elevated ST segment presumed acute rather than old
    • 124. Evolution of AMI• Acute – ST segment Elevated – Q wave at least 40 ms wide = pathologic – Q wave associated with some cellular necrosis
    • 125. Evolution of AMI Age Undetermined  Wide (pathologic) Q wave  No ST segment elevation  Old or “age undetermined” MI
    • 126. AMI Recognition A normal 12-lead ECG DOES NOTmean the patient is not having acute ischemia, injury or infarction!!!
    • 127. Practice
    • 128. Practice
    • 129. Practice
    • 130. Reciprocal Changes+ +
    • 131. Reciprocal ChangesII, III, AVF I, AVL, V Leads
    • 132. Reciprocal Changes: Practice
    • 133. Reciprocal Changes: Practice
    • 134. AMI Recognition Reciprocal changes  Not necessary to presume infarction  Strong confirming evidence when present  Not all AMIs result in reciprocal changes
    • 135. Summary ST segment elevation is presumptive evidence for Acute Myocardial Infarction Other conditions may also cause ST elevation  Known as Imposters
    • 136. Practice Case 1
    • 137. Practice Case 2
    • 138. Hemiblocks & Bundle Branch Blocks Value  Help to identify patients at high risk for complete heart block Hemiblocks, Bundle branch blocks and AV blocks are precursors to complete heart block  You are Alert & Better Prepared!!!
    • 139. Anatomy Review Anatomy  Bundle of His  Left Bundle Branch Anterior fascicle  long, thin; only blood supply from LAD Posterior fascicle  shorter, thick; blood supply from RCA and LCX  Right Bundle Branch
    • 140. Definitions Hemiblock  Also called fascicular blocks  block in one of the two fascicles of the left bundle branch Bundle Branch Block  block of the entire left or right bundle branch
    • 141. Hemiblocks Posterior fascicle  Much more difficult to have block  greater disease  Less common but more concerning  Supplies majority of inferior wall of LV  If blocked, results in right axis deviation
    • 142. Hemiblocks Anterior fascicle  Easier to have block; More common  Supplies superior wall of LV  If blocked, results in pathologic left axis deviation
    • 143. Hemiblock Identification Left Anterior Hemiblock  Left Posterior Hemiblock  Pathologic Left Axis Deviation  Right Axis Deviation small q wave in lead I small r wave in lead I small r wave in lead III small q wave in lead III  Normal QRS or RBBB  Normal QRS or RBBB usually does have RBBB “absence of right ventricular hypertrophy
    • 144. Precursors to Complete Heart Block Any Type II AV Block Anyone with disease of both bundles Anyone with two or more of any blocks Examples:  Prolonged P-R & anterior hemiblock  RBBB & anterior hemiblock  RBBB & posterior hemiblock  Prolonged P-R with anterior hemiblock & RBBB
    • 145. Precursors to Complete Heart Block If recognize precursors to CHB, then:  Have high index of suspicion for CHB  Have TCP ready (standby mode)  Patient may need a pacemaker  Administration of Lidocaine and other ventricular anti-Arhythmics may result in CHB Lidocaine contraindicated in patients with precursors to CHB unless TCP in place and ready
    • 146. Bundle Branch Block (BBB) Can be pre-existing condition Can be caused by ACS If AMI caused  60-70% associated with pump failure  40-60% mortality w/o reperfusion
    • 147. Bundle Branch BlockCan Mimic or Hide Evidence Needed to Identify AMI  May Produce  May Hide  ST elevation  ST elevation  ST depression  ST depression  Tall T waves  Tall T waves  Inverted T waves  Inverted T waves  Wide Q waves  Wide Q waves
    • 148. BBB Problem BBB Problem  Critical to reperfuse patients with BBB produced by ACS  ACS “harder” to identify on ECG when BBB present  New or presumably new BBB is an indication for thrombolytic therapy
    • 149. BBB Recognition Fundamental Criteria Wide QRS > 100 ms (or, 0.10 sec) Supraventricular rhythm
    • 150. BBB Recognition
    • 151. BBB Recognition
    • 152. Normal Ventricular Conduction Normal Conduction  fibers of LBB begin conduction  impulse travels across interventricular septum from left to right  towards + electrode creates small r wave  travels across ventricles causing depolarization of both simultaneously  LV contributes most to complex  impulse travels away from + electrode creates primarily negative complex
    • 153. RBBB RBBB in V1  no change in initial impulse travel  small r wave  impulse depolarizes LV by itself since RBBB  RV depolarized by impulse thru muscle  it now contributes to complex  travels toward + electrode creating positive deflection
    • 154.  LBBB in V1  initial deflection altered LBBB since travels right to left now  Q wave or small q wave  RV depolarizes unopposed  may produce small r wave  travels across septum to depolarize LV  deep S wave
    • 155. BBB RecognitionTerminal Force in V1  direction of deflection prior to J point
    • 156. BBB Recognition• Use V1• Find Terminal force• Identify direction of terminal force – Downward  LBBB – Upward  RBBB• Picture a Steering Wheel – Right turn  turn signal goes up – Left turn  turn signal goes down
    • 157. BBB Recognition Practice
    • 158. BBB Recognition Practice
    • 159. Injury/Infarct Imposters Some Common Examples (not all inclusive list)  Ventricular & Paced Rhythms  LBBB Conditions that make the identification of acute injury/infarction DIFFICULT or IMPOSSIBLE  LVH  Benign Early Repolarization  Pericarditis
    • 160. Injury/Infarct Imposters Imposters can incorrectly place an ECG into any of the three categoriesST Elevation ST Depression NormalBBB T wave inversion Non-diagnostic
    • 161. Ventricular & Paced Rhythms Can mask or mimic every ECG change suggestive of ischemia/injury Paced rhythms Idioventricular rhythms V-Tach PVCs
    • 162. Ventricular & Paced Rhythms
    • 163. Differential Diagnosis of Wide Complex Tachycardias  Necessary for appropriate treatment  Identify factors that favor one rhythm  Possibilities:  VT, SVT with aberrant conduction, Afib/Aflutter with aberrant conduction
    • 164. Differential Diagnosis of Wide Complex Tachycardias Top 10 List for Imposters  1. Ventricular Tachycardia  6. VT  2. Ventricular Tach  7. VT  3. VT  8. VT  4. VT  9. SVT with preexisting BBB  5. VT  10. SVT with aberrant conduction
    • 165. Differential Diagnosis of Wide Complex Tachycardias Factors Favoring VT  Concordance across all V leads (+/-)  ERAD axis deviation (“no man’s land”)  QRS > .14 sec  AV dissociation  Suggestive QRS morphology
    • 166. Differential Diagnosis of Wide Complex Tachycardias
    • 167. Differential Diagnosis of Wide Complex Tachycardias
    • 168. Left Ventricular Hypertrophy (LVH)  Enlarged left ventricle  Pumping against increased resistance  Chronic overfilling
    • 169. LVHMay Produce May Hide ST elevation ST elevation ST depression ST depression Tall T waves Tall T waves Inverted T waves Inverted T waves
    • 170. LVH Does not abnormally widen QRS Increases height and depth of QRS  Recognized by this increase  Three step recognition formula
    • 171. LVH
    • 172. LVH Recognition• Step 1 – Look in V1 and V2 – Pick the deepest negative deflection (S wave) – Count small boxes of negative deflection in that lead – Remember that number
    • 173. LVH Recognition
    • 174. LVH Recognition• Step 2 – Look in V5 and V6 – Pick the tallest positive deflection (R wave) – Count small boxes of positive deflection – Remember that number
    • 175. LVH Recognition
    • 176. LVH Recognition• Step 3 – Add the two numbers together – Suspect LVH if the sum is > 35 (> 35 mm)
    • 177. LVH Recognition
    • 178. LVH Recognition
    • 179. Benign Early Repolarization
    • 180. Benign Early Repolarization Normal variant; Difficult to identify Produces  ST elevation  Tall T waves Changes usually seen in anterior & lateral leads Most often seen in males ages 20-40  More common in African-American males  Thin, young persons
    • 181. Benign Early Repolarization Look for notch at J-point  ST segment and J-point create a “fish hook” appearance
    • 182. Benign Early Repolarization
    • 183. Pericarditis
    • 184. Pericarditis May be viral, bacterial or metabolic  Secondary to recent cardiac surgery  Post MI  IV Drug abuse Clinical presentation may include CP Often produces diffuse ST elevation on ECG plus clinical presentation
    • 185. Pericarditis Correlate Diffuse ST segment elevation with Clinical Presentation  Sharp, “Stabbing” chest pain  Can be localized  May be relieved by movement, respiration, position, swallowing  May radiate to base of neck, between shoulder blades
    • 186. Pericarditis May produce ST elevation in any lead May be in all leads May not be anatomically grouped J-point notching often present  Fish hook
    • 187. Medications Some medications affect the ECG Digitalis ST depression Characteristic sag
    • 188. Summary Imitators can produce ST elevation or depression Imitators can eliminate ST elevation or depression Most frequent imitators LVH BBB Paced rhythms
    • 189. Summary Imitators can produce ST elevation or depression Imitators can eliminate ST elevation or depression Most frequent imitators  LVH  BBB  Paced rhythms
    • 190. Summary• If QRS is wide – Consider BBB – Consider ventricular rhythm (or paced)• If QRS is narrow – Consider LVH – Consider pericarditis – Consider early repolarization
    • 191. Summary “Fish hooks” often seen with:  Pericarditis  BER “Fish hooks” can also be seen with ACS
    • 192. Summary The presence of a potential imposter DOES NOT ALWAYSmake it impossible to identify injury/infarction

    ×