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12 Lead EKG 101

A Basic Overview of How to Interpret 12 Lead EKGs and Treat a Cardiac Patient
Region IV Pre-Hospital Systems Coordination Committee

Purpose:
The purpose of this course is to provide pre-hospital clinicians with the tools necessary to identify the basic A&P of the heart, interpret 12 Lead EKGs, localize and treat AMIs as well as recognize imposters and potential complications.

Basic Cardiac Anatomy & Physiology


Muscular pump about the size of your fist primary function is to pump oxygenated blood to the rest of the body. Made up of four chambers, right and left atria right and left ventricles The septum is a thin muscular wall that separates the right and left sides of the heart. Each contraction of the heart occurs in response to an electrical impulse that starts in the upper portion of the heart. Blood is moved in a closed circuit through the body by the pumping of the heart.

Basic Cardiac Anatomy & Physiology


The heart contracts and pumps blood out to the body (systole) and relaxes to fill with more blood (diastole). The heart muscle itself is like all other organs in the body and requires oxygen to function. The oxygen-rich blood is circulated to the heart muscle through the coronary arteries. There are two main arteries: Right coronary artery Left main coronary artery both start at the aorta

These vessels then branch off into smaller and smaller vessels along the surface of the heart.

In order to perform work, the heart needs oxygen and nutrients. There are two main arteries: Right coronary artery (RCA) Left coronary artery (LCA). The left coronary artery divides into: Left anterior descending (LAD) branch Left circumflex branch(LCX) The right coronary artery and the branches of the left coronary artery provide numerous smaller branches which penetrate the heart muscle, supplying it with blood.

Both coronary arteries originate from the aorta and run along the surface of the heart. In the majority of human hearts, coronary circulation follows a predictable pattern.

Left Main Coronary Artery Branches quickly into the LAD & LCX. Involves almost 2/3 of the heart muscle
Right Coronary Artery (RCA) The RCA supplies blood to the bottom (inferior) portion and part of the back (posterior) portion of the left ventricle. The posterior portion of the septum is also supplied with blood from the RCA. SA Node 55% AV Node 90% AV Blocks Left Anterior Descending Branch (LAD) The LAD supplies blood to the front (anterior) portion of the left ventricle, apical including most of the anterior portion of the septum separating the ventricles. Bundle Branch Block, AMI, CHF Left Circumflux Branch (LCX) The LCX supplies blood to the left side (lateral) portion and the back (posterior) portion of the left ventricle. SA Node 45% AV Node 10% Lateral & posterior MI

Sino-Atrial (SA) Node: natural cardiac pacemaker. The heartbeat starts here and spreads throughout the network of conduction fibers in the two atria causing them to contract.
Normally, the heartbeat can only reach the ventricles (the two lower chambers), after it has passed through the atrioventricular (AV) node. Atrioventricular (AV) Node: slows down the electrical signal so that the atrial contractions can finish filling the ventricles completely. The AV node also prevents the lower chambers from beating too fast if the atria develops a fast rhythm (tachyarrhythmia).

His Bundle, bundle branches, and the Purkinje system : The electrical signal finally passes to the ventricles causing the ventricles to contract

Anatomy of an EKG
The EKG, or a measure of this electrical activity of the heart, is comprised of 3 primary parts...

1. P wave---electrical depolarization of the atria...contraction follows...


2. QRS COMPLEX---electrical depolarization of the ventricles...contraction follows... 3. T wave---electrical repolarization of the ventricles...and thus, relaxation...

P wave: Represents positive and negative deflections of atrial contraction and relaxation PR Interval: Distance between the P wave and the R wave. Should be consistent QRS Complex Q wave: First negative deflection Normal in I, aVL, V1, V6 Significant or pathologic is one box wide and/or 1/3 the height of the R wave R Wave: First positive deflection

S Wave: Next negative deflection

ST Segment: Essentially isoelectric, slopes gentely upward J point: the point at which the ST Segment takes off from the QRS complex T Wave: Upright always in leads I, II, V2-V6. aVR is always negative. Leads III, aVL, aVF, and V1 can be positive or negative U Wave: Seen best in V3, same polarity as T wave, sign of hypokalemia QT Interval: One complete ventricular cycle. None are > the preceding R-R

Putting the A&P with the EKG

Einthovens Triangle
Lead I
extends from the right to the left arm

+ Lead III
extends from the left arm to the left foot

Lead II
extends from the right arm to the left foot

Anatomy of a 12-Lead EKG

This is an example a 12-lead EKG.

Anatomy of a 12-Lead EKG (cont.)


At the bottom of this 12lead are rhythm strips (highlighted). Any of the 12-leads can be shown as rhythm strips. You can configure the device to show you any of the six limb leads on the rhythm strip (I, II, III, aVR, aVL or aVF).

Anatomy of a 12 Lead EKG (cont.)


The format of the 12-lead EKG is very standard. While there are a few exceptions, the format you see here is typical of what you will see in most 12-lead EKGs done in North America.

Anatomy of a 12-Lead EKG (cont.)


The 12-lead can provide a computer generated interpretation.

When you see ACUTE MI SUSPECTED the machine is right about 98% of the time.
In order to attain specificity, if the computer isnt absolutely sure that an AMI is present, it will not say anything about it.

In other words YOU are the primary interpreter, the computer is your backup.

Anatomy of a 12-Lead EKG (cont.)


The 12-Lead is very good at measuring intervals and durations. It is better at measuring the PR-interval and the QRS width. We express these intervals and durations in seconds 12-lead expresses them in milliseconds. It is simple to convert milliseconds to seconds.

Anatomy of a 12-Lead EKG (cont.)


When you use an EKG to determine the cardiac rate and rhythm, certain sampling time is required. 12-lead interpretation: Only one beat from each lead is needed to make an interpretation.

Anatomy of a 12-Lead EKG (cont.)


There are six positive electrodes on the chest, yielding six leads. There are four electrodes on the limbs from which the EKG machine makes another six leads. Each lead has one positive electrode. Positive electrode is a camera. view is from the positive electrode toward the negative electrode.

The portion of the left ventricle that each leads sees is determined by the location of that positive electrode.
Different placements of the electrodes will yield different viewpoints.

Anatomy of a 12-Lead EKG (cont.)


Types of Leads
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Limb Leads

Chest Leads

Anatomy of a 12-Lead EKG (cont.)


View of Posterior Heart Wall
Leads V1 & V2
-Tall R
-ST Depression -Upright T-Wave

Anatomy of a 12-Lead EKG (cont.)


View of Inferior Heart Wall
Leads II, III, aVF
- Looks at inferior heart wall -Looks from the left leg up

Anatomy of a 12-Lead EKG (cont.)


View of Lateral Heart Wall
Leads I and aVL
Looks at lateral heart wall Looks from the left arm toward heart *Sometimes known as High Lateral*

Anatomy of a 12-Lead EKG (cont.)


View of Lateral Heart Wall
Leads V5 & V6
Looks at lateral heart wall Looks from the left lateral chest toward heart

*Sometimes referred to as Low Lateral or Apical view*

Anatomy of a 12-Lead EKG (cont.)


View of Entire Lateral Heart Wall
Leads I, aVL, V5, V6 - Looks at the lateral wall of the
heart from two different perspectives

Lateral Wall

Anatomy of a 12-Lead EKG (cont.)


View of Anterior Heart Wall
Leads V3, V4
Looks at anterior heart wall Looks from the left anterior chest

Anatomy of a 12-Lead EKG (cont.)


View of Septal Heart Wall
Leads V1, V2
- Looks at septal heart wall - Looks along sternal borders

Anatomy of a 12-Lead EKG (cont.)

I Lateral II Inferior III Inferior

aVR aVL Lateral aVF Inferior

V1 Septal

V4 Anterior

V2 Septal

V5 Lateral

V3 Anterior

V6 Lateral

Anatomy of a 12-Lead EKG ST Segment


The ST segment is normally isoelectric (baseline) neither elevated or depressed.
May slope upward toward a relatively tall T wave The ST segment is probably the single most important element to identify on the ECG when looking for evidence of AMI.

The Three Is

Ischemia
Injury

lack of oxygenation ST depression or T inversion

prolonged ischemia ST elevation death of tissue may or may not show in Q wave

Infarct

CARDIAC ISCHEMIA
( Myocardial ischemia, Ischemic heart disease, Ischemia, Myocardium ischemia, Silent ischemia )

Cardiac ischemia is a situation in which the blood flow within a coronary artery is limited to the point where the oxygen needs of the heart muscle cannot be met (hypoxia).

CARDIAC ISCHEMIA
Minor episodes of cardiac ischemia tend to cause little long-term damage to the heart, but these episodes can sometimes cause serious effects in some patients: They can cause arrhythmias, which can lead to either syncope or cardiac arrest and sudden cardiac death. Severe or lengthy episodes can trigger a result in myocardial infarction. The collective effects of minor episodes of cardiac ischemia can potentially lead to cardiomyopathy.

Symptoms of Cardiac Ischemia


May be painful symptoms of cardiac ischemia, Pain, pressure or discomfort from cardiac ischemia is angina. Angina may feel like a squeezing vise or crushing pressure deep in the chest behind the sternum. May also be felt in the shoulders, arms, back, neck or jaw.

EKG in Acute Ischemia

Tracing taken during an episode of anginal pain that occurred while the patient was at rest. Marked ST elevation in leads V2-5 with some ST depression in aVF.

EKG after Acute Ischemia

This tracing was taken 30 minutes after the initial. The patient was pain-free and asymptomatic. The ST segments are isoelectric, and the ECG is normal

Evaluation after Acute Ischemia

Subsequent clinical evaluation


serial ECGs enzyme determinations, revealed no evidence of acute myocardial infarction. Disappearance of the ST elevation and the absence of clinical and electrocardiographic evidence of infarction on subsequent examinations indicate that initial ECG is representative of severe, acute, and reversible ischemia.

Well Perfused Myocardium


Epicardial Coronary Artery
Lateral Wall of LV Left Ventricular Cavity

Septum

Positive Electrode Interior Wall of LV

Normal ECG

Ischemia
Epicardial Coronary Artery
Lateral Wall of LV Left Ventricular Cavity

Septum

Positive Electrode
Interior Wall of LV

Ischemia

Inadequate oxygen to tissue Subendocardial Represented by ST depression or T inversion

May or may not result in infarct

ST depression

Injury

Prolonged ischemia
Transmural

Represented by ST elevation
Usually results in infarct

ST elevation

Injury
Thrombus

Ischemia

Infarct

Death of tissue
Represented by Q wave Not all infarcts develop Q waves

Infarction
Infarcted Area Electrically Silent

Depolarization

Many infarcts do not develop Q waves

Q Waves

Thrombus Infarcted Area Electrically Silent

Ischemia

Depolarization

Summary
A normal ECG does NOT rule out ACS ST segment depression represents ischemia
Possible infarct

ST segment elevation is evidence of AMI Q wave MI may follow ST elevation or depression

Pathophysiology of the AMI


Chronic accumulation of atherosclerotic plaque in coronary vessels around the heart Fibrous plaque prone to rupture, lead to thrombytic blockage Clots form due to damaged tissue and platelets Both release chemicals causing a clot to form Forms a substance called fibren that traps cells and platelets eventually blocking and narrowing Tissue damage in AMI results from rupture of plaque on vessel walls creating a chain reaction that forms a clot in the coronary artery.

Process of an AMI
Impaired blood flow: Produces varying degrees of myocardial injury Damage dependent on flow reduction and duration Tissue death progress quickly in a wave pattern Begins with endocardium Ends with epicardium Infarction becomes larger toward the surface of the heart. Ischemia Shortage of oxygen at cellular level Injury Diminishing supply of oxygen Infarct cardiac cells die of anoxia.

EKG Changes from Infarction


First Detectable Change in EKG
Tall T-waves
increase in height more symmetric may occur in the first few minutes

*Known as hyper acute phase*

EKG Changes from Infarction The Acute Phase


Signs of Myocardial Injury
ST Segment Elevation Primary indication of injury Occurs in first hour to hours ST Segment Elevation in Leads 1mm or greater in limb leads 2 mm or greater in chest leads Hallmark indication of AMI

*Known as Acute Phase*

EKG Changes of Infarction Reciprocal Changes


ST elevation in contiguous leads most often represents acute infarction ST depression in contiguous leads may represent acute ischemia In acute infarction, ST elevation in contiguous leads coupled with reciprocal ST depression in noninfarcting leads is added evidence of an AMI.

Reciprocal ST segment depression

Acute ST segment elevation

EKG Changes from Infarction T Wave Inversion


Signs of Myocardial Injury

T wave inversion
presence of ischemia May precede ST elevation

Prominent in precordial chest leads Inversion in limb leads is pathologic


T wave inversion can be caused by

other things than ischemia

EKG Changes from Infarction The Indeterminate Phase


Signs of Myocardial Infarction Pathologic Q-wave
First indication of tissue death First few to several hours Q-wave size of QRS suggests infarct Represent current or past events Determine timing through ST elevation and T-wave inversion

Natural Progression of EKG in Infarction


Over time:
T-wave regains normal contour ST-segment returns to isometric line

Q-wave remains as evidence of infarct


Indicates presence of previous MI

*ST segment elevation provides the strongest evidence of early recognition of AMI*

EKG Changes from Infarction (cont.)


All of the changes in the previous slides are: Indicative

Changes
ST segment elevation is helpful in detecting an MI in its early stages

Hyperacute (Tall) T-waves alone are specific enough to diagnose an MI


T-wave inversion can occur with simple angina and is therefore not specific

Pathological Q-wave is the most accurate recognition of an MI


Not in the first few hours ST segment elevation provides the strongest evidence for early recognition of an MI

ECG Variants

Coronary Spasm: Printzmetals angina Injury pattern that resolves w/ rest, NTG,O2 etc.

Early Repolarization: elevated J point seen best in V3,4. Key to Dx pts are usually young & asymptomatic

Pericarditis: ST elevation usually global associated w/ fever, pleuritic c/p.

ECG Variants due to Drugs or Electrolytes Imbalances


Hypokalemia: lg U waves ( usually taller than T) seen best in precordial leads. <2.7 Hyperkalemia:
Tall peaked T waves > 6.0

PR prolongs, QRS widens


P waves disappear > 8.0

Hypocalcemia:
Prolonged QT interval

Hypercalcemia:

Shortened QT interval
ST depression- downsloping, curved ST segments. scooping, sagging, flat or inverted Ts in lateral leads PR prolonged QT shortened

Digitalis effect:

Bundle Branch Blocks


Turn Signal Rule
This is a simple method for differentiating right bundle branch block from left bundle branch block. V1 will be the only lead you need to view
1. Locate the terminal (last) force of the QRS complex 2. Determine if it is pointing up or down. 3. Compare to the turn signal in your car:
Up is for a right turn & RBBB Down is for a left turn and LBBB

Clinical significance:
Bundle branch is a significant complication of infarction. Since the left anterior descending artery is the primary supplier of the bundle branches, BBB is considered a complication of anterior septal infarcts. When BBB is the result of MI, the incidence of pump failure is 65-70% and the in-hospital mortality rate is 40%-60%. The BBB itself is not dangerous, but the high mortality rate is due to the extensive amount of tissue death occurring when an infarct is serious enough to cause a BBB. Another manifestation of BBB is in the form of AV Block. This is why infranodal AV blocks are more serious and have wide QRS complexes.

Localizing the Area of Infarction


Indicative changes are not found in every lead
Only present in leads looking at the infarct Indicative changes in two or more leads looking at the same portion of the heart are anatomically contiguous leads Suspect AMI ST segment elevation in two or more leads that are not contiguous AMI not the suspected cause

Recognition & Localization


Recognizing infarct: Know which part of the heart each lead

looks at Localizing Infarct: Note which lead is displaying evidence and which portions of heart they are looking at
Leads Displaying Indicative Changes II, III, aVF V1 & V2 V3 & V4 V5, V6, I, and aVL Location of Infarct Site Inferior Septal Anterior Lateral

*Simply knowing the changes to look for and which part of the heart each lead looks at*

Anterior Wall MI
Anterior Wall infarct: Occlusion of the Left Anterior
Descending Artery (LAD) 2mm ST segment elevation in two or more of leads V1-V4 Reciprocal changes in leads II, III, aVF Lethal due to large myocardium involvement Possible conduction defects: Bundle Branch Block 2nd Degree Block Type II CHB

Anterior Wall MI

Inferior Wall MI
Inferior Wall MI: Occlusion of Right Coronary Artery (RCA)
At least 1mm ST segment elevation in leads II, III, aVF Reciprocal ST depression in leads I & aVL or precordial leads Conduction defects: Sinus bradycardia

Sinus arrest
1st degree block Accelerated Idoventricular rhythm Complications: Bradyarrhythmias protective mechanism, 90% of blood supply for SA & AV nodes from the RCA Hypotension treated with fluids, consider right side involvement

Inferior Wall MI

Lateral Wall MI
Lateral Wall MI: results from occlusion of the Left
Circumflex Artery At least 1 mm ST segment elevation in leads I, aVL, V5 & V6 and /or 2 mm ST segment elevation in V5 & V6

Reciprocal ST depression in V1
Sometimes an extension of an Anterior or Inferior MI Conduction defects are rare

Anterior/Lateral Wall MI

Posterior Wall MI
Posterior Wall MI: Occlusion of the Right Coronary Artery
(RCA) or the Posterior Descending Artery

No leads that look at the posterior wall


Leads look at the infarct site from the opposite side(backwards)

ST depression in V1 & V2
Tall R waves in V1 and/or V2 Most often associated with Inferior MI

*Associated with dangerous conduction disturbances*

Posterior Wall MI

Right Ventricular MI
Right Ventricular MI: caused by proximal occlusion of the
Right Coronary Artery (RCA)

Associated with Inferior Wall MI Can happen independently Standard 12-Lead does not assess right side of heart Infarction is significant Indicates large infarction Indicates involvement of both ventricles If the possibility of RVI exists a set of chest leads can be applied to the right side of the chest V1-6R leads look at right ventricle Lead V4R most accurate

Right Ventricular MI

Septal Wall MI
Septal Wall MI: caused by septal perforation involving the
LAD or the Posterior Descending Most often in the setting of an Anterior MI Loss of R-wave in leads V1, V2 or V3 May have ST segment elevation in V1 & V2 No reciprocal changes

Overview of Infarcts
Location of Infarct
Anterior Inferior Lateral Posterior

Arterial Supply
LAD RCA Circumflex Posterior Descending (RCA)

Indicative Changes
V1-V4 II, III, aVF I, aVL, V5, V6 None

Reciprocal Changes
II, III, aVF I, aVL V1 V1, V2

Septal

Septal Perforating Loss of R wave in None (LAD) V1, V2, or V3 Posterior Descending (RCA

Overview of Infarcts
Suspect infarction when there are indicative changes in at least two anatomically contiguous leads

Indicative changes in many leads suggests larger infarct


With Inferior Wall MI suspect Right Ventricular Wall Infarct Signs of possible Right Ventricular Wall Infarct: Hypotension JVD Clear lung sounds Causes of ST segment depression include digitalis, ischemia and reciprocal changes Suspect Posterior Wall Infarctions when an Inferior Wall Infarction has ST depression in Leads V1-V3

Complications of Myocardial Infarction


Chest Pain: Most common complication
Treatment: Oxygen and ASA (162 to 325)mg NTG initially with Morphine if pain persists Usually very effective

Right Ventricular Wall Infarct:


Reduces output of right ventricle decreasing left ventricular filling (decreased preload)

NTG and Morphine can worsen conditions


Decrease in blood pressure will worsen area of injury Presence of Inferior Wall Infarction with no EKG or clinical evidence of right side infarct does not merit any extra caution when using NTG and Morphine

Complications of Myocardial Infarction


AV Block Location: indicates electrical impulse from atrium is blocked from depolarizing the ventricles Most common block is in the AV Node (nodal block) Second most common block is in the Bundle Branches (infranodal)

Infarct frequently produces AV Block due to increase in parasympathetic tone


Local ischemia around node can produce the block

Less serious than block caused by tissue injury or death


Blocks in AV node produce narrow QRS complex Bundle Branches produce wide complexes

Complications of Myocardial Infarction


Determining the type of QRS presented with is a useful tool in determining the location of the block
Nodal Block Coronary Supply QR Width Right Coronary Artery Narrow Infranodal Block Left Coronary Artery Wide

Stability

Generally Stable

Often Unstable
Often does not respond

Atropine Response Usually improves

Complications of Myocardial Infarction


Hypotension: A common treatment for hypotension which is secondary to the infarct is to administer fluid boluses and inotropic drugs (dopamine) Hypotension in the setting of an inferior wall infarction is most likely secondary to right ventricular involvement.

Although RV Infarcts may require significant boluses to offset loss of preload, continuously monitor the patient for signs and symptoms of developing left sided failure. Hypotension in the setting of an anterior wall infarction may not tolerate fluid boluses and may require a dopamine infusion.

Complications of Myocardial Infarction


Left Coronary Artery Occlusions Leads Showing Indicative Changes Localization Pain Control V1-V6, I, aVL Septal, Anterior, Lateral, Posterior NTG & Morphine as appropriate Infrequent, usually wide ORS, often unstable, Atropine may be ineffective, use standby pacing 200-250 cc fluid bolus, inotropic medications Right Coronary Artery Occlusions II, III, aVF, V4R-V6R Inferior, Posterior, Right Ventricular NTG & Morphine used with caution if RVI present Frequent, usually narrow QRS, Generally stable, Atropine often effective, May not require treatment Vigorous fluid therapy if RVI present, inotropic medications

AV Block

Hypotension

Clinical Pearls
Suspect infarction when there are indicative changes in at least two anatomically contiguous leads Indicative changes in a greater number of contiguous leads suggests a more extensive infarction RV or Posterior infarcts should be considered in setting of Inferior Wall MI

RV: ST segment elevation in rV4


Posterior: ST depression +/or Tall Rwave in V1 & V2 Other clinical signs of RV Infarct may include: Hypotension and JVD in the setting of clear lung sounds Other causes of ST segment depression besides ischemia include digitalis effects and ventricular hypertrophy Suspect Posterior Wall Infarctions when an Inferior Wall Infarction has ST depression in Leads V1-V3

Questions

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