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This presentation will briefly cover ECG basics. It has been created with the assumption that the reader will have a solid basic knowledge of ECG interpretation. If you are not comfortable with interpreting standard three lead ECGs, it is recommended that you review that material before moving on to 12 lead ECG.
Program Outline
Bioelectricity
Action Potentials
Precordial lead placement Precordial lead localization Reflecting leads Reciprocal leads Injury & Infarct The 12 lead ECG
J point
otherwise known as the Isoelectric line Upright, rounded and normally present prior to every QRS complex. <0.20s < 0.12s (or <0.10s depending on text book reference) location where the ST segment and QRS complex meet. This is the location that will provide the ST elevation / depression criteria. Normally at the same level as the TP segment and PR interval. Normally upright and rounded, should be asymmetrical.
ST segment: T wave:
Ions
The main positively charged ion in the body is sodium (Na+). The main negatively charged ion in the body is chloride (Cl-). Other common ions in the body include:
Bioelectricity
Bioelectricity is created by the movement of ions through a semi-permeable membrane. The main extracellular ion is sodium (Na+). The main intracellular ion is Potassium (K+).
Movement of sodium and potassium through the cellular membrane generates electricity.
ACTION POTENTIALS
Action Potential
Phase 4: The semi permeable cell membrane has sodium (Na+) leeching in and Potassium (K+) leaking out. The Sodium / Potassium pumps work to push out two Sodium ions and bring in one Potassium ion. At this point the cell is considered net negative. The number of positively charged ions outside the cell membrane is larger than the positive ions inside the membrane. As time passes the Sodium leeching in to the cell offsets the Na+ / K+ pump and the cell becomes more positively charged.
Action Potential
Phase 0:
The increasing Na+ entering the cell has caused the cell to become more positively charged. This is the Threshold Potential, which causes the fast sodium channels to open. This is a one way valve. Since the most abundant extracellular ion is Na+ there is a rush of positive ions into the cell creating a more positive charge. This continues until the cell is no longer polarized. The net charge is isoelectric on both sides of the cell membrane.
Action Potential
Phase 1: This phase is when the cell is at its peak positive charge. At this point negatively charged Chloride (Cl-) ions enter the cell and cause the fast acting Na+ channels to close.
Action Potential
Phase 2: Two different channels open up at this point, the slow Sodium channels and the Calcium (Ca++) channels. This plateau segment begins. Calcium is a double positive ion. CA++ influx with the slowed influx of Sodium allow the cell to stay in a depolarized state for a longer period. Calcium is crucial for cardiac muscle contraction, being the key for Actin / Myosin activation.
Action Potential
Phase 3: Potassium channels now open and allow K+ to leave the cell. This exiting of positively charged ions now returns the inside of the cell to a net negative and the cell is repolarized, allowing the whole process to begin again.
Action Potentials
Action Potentials in different myocytes reach their threshold at different rates. Why is this?
Action Potentials
This is part of a protective mechanism. The SA node reaches action potential at the fastest rate. This will depolarize the other pacemaker sites as electrical depolarization travels down the heart. If the SA node does not send the impulse then the AV node is the next pacemaker to fire, then the ventricles
Pacemaker Sites
Starting with the R.A. and L.A. leads being placed on the lateral to anterior aspects of the shoulders.
The R.L. and L.L. leads being placed on, or below the waist in the pelvic area. More commonly on the anterior distal tibia. The only critical criteria for these leads is that they be a minimum of 10 cm from the heart.
The Limb electrodes (RA, LA, RL, LL) give us six actual leads.
These are part of the HEXAXIAL system.
I / II / III / aVR / aVL / aVF Leads are named where the view is from the positive electrode placement. The ECG monitor will automatically adjust the polarity of the leads for different lead view. These leads look at the heart in two dimensionally (coronal cut) as if under a plate of glass.
Hexaxial System
Precordial Leads
Locate the fourth intercostal space. This is done by identifying the Angle of Louis the small ridge on the top third of the sternum, slightly inferior to the sternal notch. This is the location of the second rib / second intercostal space. Locate the second intercostal space and count down to the fourth intercostal space.
On the right lateral aspect of the sternum place lead V1 on the left lateral aspect of the sternum place lead V2.
Precordial V1 V2
Next slide your finger down to the fifth intercostal space at the left midclavicular line. This is where you will place V4.
Locate the left midaxillary line at the fifth intercostal space. This is the placement point for V6.
V5 is placed at the fifth intercostal space between V4 and V6 at the anterior axillary line
Now that the precordial leads are in place, we have a three dimensional look at the majority of the cardiac conduction system.
12 lead ECG
With the 12 lead ECG, practitioners have the ability to obtain more detailed information in regards to cardiac conduction and function. A few of these are
Electrical Axis & Axis deviation Cardiac Hypertrophy Ischemia & Injury Infarction Pericarditis Drug toxicity
12 Lead ECG
For this presentation we will focusing on: Location of Injury and Infarct
Including RV + Posterior
Lead II Inferior
Lead III Inferior
aVL Lateral
aFV Inferior
V2 Septal
V3 Anterior
V5 Lateral
V6 Lateral
Reciprocal Leads
Reciprocal Leads
M. I. Location Reflecting Leads Reciprocal Leads Blood Supply
Inferior Septal
Anterior Lateral Posterior
RCA LCA
LAD Circumflex
Note ST elevation in II, III & aVF. There is ST depression in reciprocal leads I, aVL. We do not see Reciprocal depression in V5, V6 leads as this ECG is a high inferolateral and has RV involvement (more on RV later).
12 Lead ECG
Looking again a the lead diagram we can see the views of the heart based on the precordial and Hexaxial system.
ST elevation myocardial infarctions (STEMI). Non ST elevation MI (NSTEMI). Ischemia (ST depression). Pathologic Q waves
J-point: the point where the QRS and ST segment join. ST segment: normal or abnormal.
T wave: normal or pathologic
The ST segment represents the time between ventricular depolarization and repolarization. Together the ST segment and the T wave are the area that best reflects Infarct and Ischemic insult to the Myocardium. ST changes are measured from the J-point.
J Point
The J point is the point 1mm behind where the QRS joins the ST Segment. This point can be sharp (easy to define) or slurred (more difficult to identify).
After identifying the baseline, extrapolate where the ST segment would have returned to the isoelectric line.
ST Segment
The main thing to note in looking at the ST segment is its relation to the baseline. In correlation with the baseline and J point we will be better able to identify ST elevation or depression. Aside from depression and elevation there are some ST segment shapes we need to be familiar with.
ST segment shapes
T waves
In speaking to T waves in ischemia and infarct what we are looking for are pathologic T waves. Normal T waves are Asymmetrical.
T Waves
However, these symmetrical T waves may be a normal electrical variant within a small segment of the population.
T waves
T Waves
Symmetrical T waves should be considered pathological until ruled out.
When evaluating the ST segment and T wave we are looking for Elevation or Depression. We are also looking for a regional distribution (contiguous leads)
The Following slides will show examples, which are pathological ST changes and which are normal variants.
While this is not normal this is a tracing of LV strain. Note that the T waves are asymmetrical. While the Ts are inverted there is no real ST depression.
This tracing is indicative of an inferior MI. Note the ST elevation in II / III / aVF with reciprocal depression in I / aVL. Also, in III this may be considered a pathological Q wave
As these progress through the transition zone note the notching and slurred j point, as well as high, peaked Ts. This may be a Minimal pericarditis or early repolarization.
Note the ST depression in V1- V3 with reciprocal changes in II, V4 V5 & V6. this may be an inferolateral infarct with some posterior involvement.
This is another example of LV strain. There is a bit of ST elevation in V1-V2. Note however that the T waves are still asymmetrical.
This ECG is showing marked ST depression in V1 V6 as well as II. This, with the elevation in V1 may be an indicator of diffuse subendocardial ischemia, injury or infarction.
ST Changes
This is an example of a left bundle branch block. Wide QRS, Monomorphic S in V1 Monomorphic R in V6. Diagnosing ST in LBB is problematic.
Note the diffuse ST elevation and flipped Ts in V1- V5. This tracing is indicative of an anteroseptal MI with lateral involvement.
Right Ventricular Involvement can certainly complicate STEMI or AMI treatment.this presentation will not cover the specific treatment modalities, only recognition of the RV Involvement. Please follow local guidelines or protocols for all Patient care.
When placing Right sided leads or posterior leads, please follow manufacturer instructions, guidelines or your local institutional practices. Certain machines have all the leads available, others require alternate placements of standard leads and documentation on the tracing of lead changes
RV Involvement
Lets look at right sided electrode placement!!. V4R, V5R, V6R.same criteria for placing V4, V5, V6 only on the right side instead of the left side.
RV Lead Placement
RV Involvement
Can you see the RV criteria? Other than the obvious V4R lead.lets break it down.
RV Involvement
There are several criteria for identification of RV involvement, lets cover these, remembering that not all of these are a requirement for RV involvement. We will rarely see all of these in a tracing, only a couple will usually be identifiable.
RV Involvement Criteria
1.
2. 3.
4.
ST depression in V2
(unless elevation extends as in #3)
5.
6.
ST depression in V2 can not be more than half the ST elevation in aVF More than one mm elevation in Right sided leads (V4R V6R)
RV Involvement
1.
Approximately 97% of RVI occur with IWMI due to the involvement of the Right Coronary Artery. Whenever you see an inferior MI, check for RVI. These can also occur from a blockage in the circumflex, but this is rare at approximately 3%
RV Involvement
2.
This energy (vector) is directed anteriorly and inferior to the right, and lead III is directly in its path. As this is lead is closer to the vector it shows a higher ST elevation. The infarct here allows for the energy to travel unopposed through the interventricular septum.
RV Involvement
3.
ST elevation in V1
The ST segment will be elevated in V1, this is as mention previously as the energy is travelling unopposed through the interventricular septum. This will most often elevate V1 and depress V2 as it passes these lead areas. Remember, although uncommon that this can cause elevation through V5 V6. If you see ST elevation in II / III / aVF and V1 this is most likely an MI with RVI.
RV Involvement
4.
ST depression in V2
This is due to the vector (energy) passing away from V2. As previously mentioned, the energy is directed more closely to V1, and away from V2, therefore creating ST depression.
RV Involvement
5.
This one is a critical criteria as it points to either a simple RVI or a massive amount of myocardium at risk. If the depression is more than half the height of the elevation in aVF then this points to a possible Inferior-posterior-RV infarct. This is a massive amount of at risk myocaridum.
RV Involvement
6.
Well, since these are directly looking at the RV it is the most specific sign of an RVI. Most cases will show ST elevation in V4R, but some only show in V6R. Make it a habit to collect all three Right sided leads.
RV Involvement
15-25
Rarely do we have isolated RV infarcts, so many of these will have other MI areas associated. What do you note?
Here we see ST elevation in II / III / aFV with lateral reciprocation making this an inferior AMI. What do you see for RV involvement if any?
RV Involvement
ST elevation in III greater than II ST elevation in V1 Elevation greater than 1mm in V4R.
RV Involvement
Elevation in V1
RV Involvement
15-26
RV Involvement
In the tracing, we see Inferior ST elevation and lateral depression making this an IWMI. Looking at our RV Criteria we note
Elevation in III > II Elevation in V1, slight depression in V2 Elevation in V4R V2 depression < half height of aVF
RV Involvement
RV Involvement
15-27
RV Involvement
In this 12 Lead we note ST elevation in III / aVF with reciprocal depression in I / aVL Looking at RV criteria we see
RV Involvement
Elevation in V1
RV Involvement
Why is it critical to diagnose the RVI?
RV Involvement
Most AMI treatments affect preload, and the RV is filled mainly through venous pressure, passive filling. If we drop preload with standard treatments (nitrates, beta blockers) we effectively drop BP through increasing venous system capacitance (venodilation) and cause a decrease in RV filling. In-turn, this decreases flow to the lungs for exchange, then decreased return to the LV, most likely causing a sub-optimal outcome.
Posterior Wall MI
Posterior MI
A posterior wall myocardial infarction (PWMI) is not directly visualized on the standard 12 lead.
We can see posterior MI through reciprocal leads, but require additional leads to view the posterior wall.
V6, V7, V8, V9, V10
Posterior MI
Posterior MI
PWMI, as mentioned are initially observed on a standard 12 lead through reciprocal leads.
These are leads V1, V2
Posterior MI
What we see on this ECG is V1, V2 flattened ST depression, this should prompt you to place the Posterior leads.
Posterior MI
Again, we see ST depression in V1, V2 which should prompt Posterior lead placement. PWMI are not usually isolated events and often occur with IWMI and RVI. This is due to these areas being commonly perfused by the same arteries. RCA, Posterior Descending, or the LCX
Pericarditis
ST Changes (Pericarditis)
PR depression Diffuse ST elevation Scooping, upwardly concave ST segments Notching at the end of the QRS
ST Changes (Pericarditis)
ST Changes (Pericarditis)
ST elevation can be as high as 4mm to 5mm. ST segment elevation is diffuse, not localized to contiguous leads as in AMI. Why is this?
The entire pericardium is irritated, this irritation causes a net positivity of the epicardium. This is electrically displayed as diffuse ST elevation.
ST Changes (Pericarditis)
Note the PR depression in II, III as well as ST elevation in II / III / aVF / V2 V6. The ST elevation is diffuse and not limited to contiguous leads. Also, note there is no reciprocal depression as with AMI. Lastly, there is notching post QRS in V4 V5.
ST Changes (Pericarditis)
The PR depression in this example is not very deep, but note the marked ST elevation in I, II, aVF and all precordial leads. V3 has a great look at notching after the QRS complex.
ST Changes (Pericarditis)
During care of the patient, you may note the amplitude of the ECG diminishing. Fluid build up in the pericardial sac may cause amplitude drops.
Now that we have covered the basics of 12 lead ECG in consideration of ACS and pericarditis, interpret the following ECGs.
Practice Interpretation 1
Anteroseptal AMI
Practice Interpretation 2
Inferolateral MI
Practice Interpretation 3
Lateral MI
Practice Interpretation 4
Anteroseptal MI
Practice Interpretation 5
Practice Interpretation 6
Anteroseptal MI
Practice Interpretation 7
Practice Interpretation 8
Practice Interpretation 9
Pericarditis
Practice Interpretation 10
12 lead ECG
12 lead ECGs are an important diagnostic tool. Remember that this is only a tool to assist your clinical assessment. Provide treatment as per local protocols and with sound medical judgement. Questions, Comments or Concerns? Please contact me at rgjones@abcmeducation.ca