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

12 Lead EKG 10112 Lead EKG 101

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.

Purpose:Purpose:

Basic Cardiac Anatomy & Basic Cardiac Anatomy & PhysiologyPhysiology

•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.

•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.

Basic Cardiac Anatomy & Basic Cardiac Anatomy & PhysiologyPhysiology

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 ArteryBranches 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 EKGAnatomy of an EKGThe 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 > ½ the preceding R-R

Putting the A&P with the EKGPutting the A&P with the EKG

Lead Iextends from the right to the left arm

Lead IIextends from the right arm to the left foot

Lead IIIextends from the left arm to the left foot

Einthoven’s TriangleEinthoven’s Triangle

+-

+

-

This is an example a 12-lead EKG.

Anatomy of a 12-Lead EKGAnatomy of a 12-Lead EKG

•At the bottom of this 12-lead 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 Anatomy of a 12-Lead EKG (cont.)(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 Anatomy of a 12 Lead EKG (cont.)(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 isn’t 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.

•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.)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.


•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.


•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.


Limb Leads Chest Leads

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Types of Leads


View of Posterior Heart Wall

•Leads V1 & V2

-Tall R

-ST Depression

-Upright T-Wave

• Leads II, III, aVFLeads II, III, aVF- Looks at inferior heart wallLooks at inferior heart wall


View of Inferior Heart Wall

-Looks from the left leg upLooks from the left leg up

• Leads I and aVLLeads I and aVL– Looks at lateral heart Looks at lateral heart

wall wall – Looks from the left arm Looks from the left arm

toward hearttoward heart


View of Lateral Heart Wall

*Sometimes known as High Lateral*

• Leads V5 & V6Leads V5 & V6– Looks at lateral heart wallLooks at lateral heart wall– Looks from the left lateral Looks from the left lateral

chest toward heartchest toward heart


View of Lateral Heart Wall

*Sometimes referred to as Low Lateral or Apical view*

• Leads I, aVL, V5, V6Leads I, aVL, V5, V6

- - Looks at the lateral wall of the Looks at the lateral wall of the heart from two different perspectivesheart from two different perspectives


View of Entire Lateral Heart Wall

Lateral Wall

• Leads V3, V4Leads V3, V4– Looks at anterior heart wallLooks at anterior heart wall– Looks from the left anterior Looks from the left anterior

chestchest


View of Anterior Heart Wall

• Leads V1, V2Leads V1, V2- Looks at septal heart wallLooks at septal heart wall- Looks along sternal bordersLooks along sternal borders


View of Septal Heart Wall

I Lateral

II Inferior

III Inferior

aVR

aVL Lateral

V1 Septal

aVF Inferior

V2 Septal

V3 Anterior

V4 Anterior

V5 Lateral

V6 Lateral


•The ST segment is normally iso-electric (baseline) neither elevated or depressed.

•May slope upward toward a relatively tall T wave

Anatomy of a 12-Lead EKG - Anatomy of a 12-Lead EKG - ST SegmentST Segment

•The ST segment is probably the single most important element to identify on the ECG when looking for evidence of AMI.

The Three I’sThe Three I’s

IschemiaIschemia– lack of oxygenation lack of oxygenation – ST depression or T inversionST depression or T inversion

Injury Injury – prolonged ischemia prolonged ischemia – ST elevationST elevation

Infarct Infarct – death of tissuedeath of tissue– may or may not show in Q wavemay or may not show in Q wave

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).

( Myocardial ischemia, Ischemic heart disease, Ischemia, Myocardium ischemia,

Silent ischemia )

CARDIAC ISCHEMIA

CARDIAC ISCHEMIA

Minor episodes of cardiac ischemia tend to cause Minor episodes of cardiac ischemia tend to cause little long-term damage to the heart, but these little long-term damage to the heart, but these episodes can sometimes cause serious effects in episodes can sometimes cause serious effects in some patients: some patients:

They can cause They can cause arrhythmias, which can lead to which can lead to either either syncope or cardiac arrest and and sudden cardiac death.

Severe or lengthy episodes can trigger a Severe or lengthy episodes can trigger a result in in myocardial infarction. myocardial infarction.

The collective effects of minor episodes of The collective effects of minor episodes of cardiac ischemia can potentially lead to cardiac ischemia can potentially lead to cardiomyopathy.

Symptoms of Cardiac Ischemia

May be painful symptoms May be painful symptoms of cardiac ischemia, 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 IschemiaEKG 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 IschemiaEKG 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 Evaluation after Acute IschemiaIschemia

Subsequent clinical evaluationSubsequent clinical evaluation– serial ECGsserial ECGs– enzyme determinations, enzyme determinations,

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

Epicardial Coronary Artery

Lateral Wall of LV

Positive Electrode

Septum

Left Ventricular

Cavity

Interior Wall of LV

Well Perfused Myocardium

Normal ECGNormal ECG

Epicardial Coronary Artery

Lateral Wall of LV

Positive Electrode

Septum

Left Ventricular

Cavity

Interior Wall of LV

Ischemia

IschemiaIschemia

Inadequate oxygen to tissueInadequate oxygen to tissue

SubendocardialSubendocardial

Represented by ST Represented by ST depression or T inversiondepression or T inversion

May or may not result in May or may not result in infarctinfarct

ST depressionST depression

InjuryInjury

Prolonged ischemiaProlonged ischemia

TransmuralTransmural

Represented by ST Represented by ST elevationelevation

Usually results in infarctUsually results in infarct

ST elevationST elevation

Thrombus

Ischemia

InjuryInjury

InfarctInfarct

Death of tissueDeath of tissue

Represented by Q waveRepresented by Q wave

Not all infarcts develop Q wavesNot all infarcts develop Q waves

Infarcted AreaElectrically Silent

Depolarization

Many infarcts do not develop Q waves

InfarctionInfarction

Q WavesQ Waves

Infarcted Area Electrically Silent

Thrombus

Depolarization

Ischemia

SummarySummary A normal ECG does NOT rule out A normal ECG does NOT rule out

ACSACS ST segment depression represents ST segment depression represents

ischemiaischemia– Possible infarctPossible infarct

ST segment elevation is evidence of ST segment elevation is evidence of AMIAMI

Q wave MI may follow ST elevation or Q wave MI may follow ST elevation or depression depression

Pathophysiology of the AMIPathophysiology 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 AMIProcess 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 levelInjury – Diminishing supply of oxygenInfarct – cardiac cells die of anoxia.

EKG Changes from InfarctionEKG 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 EKG Changes from Infarction “The Acute Phase”“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 InfarctionEKG Changes of Infarction“Reciprocal Changes”“Reciprocal Changes”

ST elevation in contiguous leads most ST elevation in contiguous leads most often represents acute infarctionoften represents acute infarction

ST depression in contiguous leads may ST depression in contiguous leads may represent acute ischemiarepresent acute ischemia

In acute infarction, ST elevation in In acute infarction, ST elevation in contiguous leads coupled with contiguous leads coupled with reciprocal ST depression in non-reciprocal ST depression in non-infarcting leads is added evidence of an infarcting leads is added evidence of an AMI.AMI.

Acute ST segment elevation

Reciprocal ST segment depression

EKG Changes from Infarction EKG Changes from Infarction “T Wave Inversion”“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 EKG Changes from Infarction “The Indeterminate Phase”“The Indeterminate Phase”

Signs of Myocardial Infarction

Pathologic Q-wave•First indication of tissue death•First few to several hours

•Q-wave ¼ size of QRS suggests

infarct•Represent current or past events

•Determine timing through ST elevation

and T-wave inversion

Natural Progression of EKG in Natural Progression of EKG in InfarctionInfarction

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 EKG Changes from Infarction (cont.)(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 VariantsECG Variants Coronary Spasm: Coronary Spasm:

“Printzmetals angina”“Printzmetals angina”Injury pattern that Injury pattern that resolves w/ rest, NTG,O2 resolves w/ rest, NTG,O2 etc.etc.

Early Repolarization: Early Repolarization: elevated “J” point seen elevated “J” point seen best in V3,4. Key to Dx best in V3,4. Key to Dx pt’s are usually young & pt’s are usually young & asymptomaticasymptomatic

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

ECG Variants due to Drugs or ECG Variants due to Drugs or Electrolytes ImbalancesElectrolytes Imbalances

Hypokalemia: lg U waves Hypokalemia: lg U waves ( usually taller than T) seen best ( usually taller than T) seen best in precordial leads. <2.7in precordial leads. <2.7

Hyperkalemia:Hyperkalemia:– Tall peaked T waves Tall peaked T waves > > 6.06.0

– PR prolongs, QRS widensPR prolongs, QRS widens– P waves disappear P waves disappear >> 8.0 8.0

Hypocalcemia:Hypocalcemia:– Prolonged QT intervalProlonged QT interval

Hypercalcemia:Hypercalcemia:– Shortened QT intervalShortened QT interval

Digitalis effect:Digitalis effect:– ST depression- downsloping, ST depression- downsloping,

curved ST segments.curved ST segments.– ““scooping”, “sagging”, flat or scooping”, “sagging”, flat or

inverted T’s in inverted T’s in lateral leadslateral leads– PR prolongedPR prolonged– QT shortenedQT shortened

Bundle Branch BlocksBundle Branch Blocks

““Turn Signal Rule”Turn Signal Rule”This is a simple method for differentiating right bundle branch block from left 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 viewbundle branch block. V1 will be the only lead you need to view1. Locate the terminal (last) force of the QRS complex1. Locate the terminal (last) force of the QRS complex2. Determine if it is pointing up or down.2. Determine if it is pointing up or down.3. Compare to the turn signal in your car:3. Compare to the turn signal in your car:

» Up is for a right turn & Up is for a right turn & RBBBRBBB» Down is for a left turn and Down is for a left turn and LBBBLBBB

Clinical significance:Clinical significance: Bundle branch is a significant complication of infarction. Since the left anterior descending artery is the 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.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 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 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 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 BBB is in the form of AV Block. This is why infranodal AV blocks are more serious and have wide QRS complexes.complexes.

Localizing the Area of Localizing the Area of InfarctionInfarction

•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

•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

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

Recognition & LocalizationRecognition & Localization

Leads Displaying Leads Displaying Indicative ChangesIndicative Changes

II, III, aVFII, III, aVF

V1 & V2V1 & V2

V3 & V4V3 & V4

V5, V6, I, and aVLV5, V6, I, and aVL

Location of Infarct SiteLocation of Infarct Site

InferiorInferior

SeptalSeptal

AnteriorAnterior

LateralLateral

Anterior Wall MIAnterior 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 MIAnterior Wall MI

Inferior Wall MIInferior Wall MIInferior 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 MIInferior Wall MI

Lateral Wall MILateral 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 MIAnterior/Lateral Wall MI

Posterior Wall MIPosterior Wall MIPosterior 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 MIPosterior Wall MI

Right Ventricular MIRight Ventricular MIRight 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 MIRight Ventricular MI

Septal Wall MISeptal 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 InfarctsOverview of Infarcts

Location of Location of InfarctInfarct

Arterial Arterial SupplySupply

Indicative Indicative ChangesChanges

Reciprocal Reciprocal ChangesChanges

AnteriorAnterior LADLAD V1-V4V1-V4 II, III, aVFII, III, aVF

InferiorInferior RCARCA II, III, aVFII, III, aVF I, aVLI, aVL

LateralLateral CircumflexCircumflex I, aVL, V5, V6I, aVL, V5, V6 V1V1

PosteriorPosterior Posterior Posterior Descending Descending (RCA)(RCA)

NoneNone V1, V2V1, V2

SeptalSeptal Septal Perforating Septal Perforating (LAD)(LAD)

Posterior Posterior Descending (RCADescending (RCA

Loss of R wave in Loss of R wave in V1, V2, or V3V1, V2, or V3

NoneNone

Overview of InfarctsOverview 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 Complications of Myocardial InfarctionInfarction

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


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


Determining the type of QRS presented with is a useful tool in determining the location of the block

Nodal BlockNodal Block Infranodal BlockInfranodal Block

Coronary SupplyCoronary Supply Right Coronary Right Coronary ArteryArtery

Left Coronary ArteryLeft Coronary Artery

QR WidthQR Width NarrowNarrow WideWide

StabilityStability Generally StableGenerally Stable Often UnstableOften Unstable

Atropine ResponseAtropine Response Usually improvesUsually improves Often does not Often does not respondrespond


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.


Left Coronary Artery Left Coronary Artery OcclusionsOcclusions

Right Coronary Artery Right Coronary Artery OcclusionsOcclusions

Leads Showing Leads Showing Indicative ChangesIndicative Changes

V1-V6, I, aVLV1-V6, I, aVL II, III, aVF, V4R-V6RII, III, aVF, V4R-V6R

LocalizationLocalization Septal, Anterior, Lateral, Septal, Anterior, Lateral, PosteriorPosterior

Inferior, Posterior, Right Inferior, Posterior, Right VentricularVentricular

Pain ControlPain Control NTG & Morphine as NTG & Morphine as appropriateappropriate

NTG & Morphine used NTG & Morphine used with caution if RVI with caution if RVI presentpresent

AV BlockAV Block Infrequent, usually wide Infrequent, usually wide ORS, often unstable, ORS, often unstable, Atropine may be Atropine may be ineffective, use standby ineffective, use standby pacingpacing

Frequent, usually Frequent, usually narrow QRS, Generally narrow QRS, Generally stable, Atropine often stable, Atropine often effective, May not effective, May not require treatmentrequire treatment

HypotensionHypotension 200-250 cc fluid bolus, 200-250 cc fluid bolus, inotropic medicationsinotropic medications

Vigorous fluid therapy if Vigorous fluid therapy if RVI present, inotropic RVI present, inotropic medicationsmedications

Clinical PearlsClinical 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

QuestionsQuestions

12 lead ekg 101

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left coronary artery

coronary arteries

left atriaright

left sides

heart contracts

coronary circulation

coronary artery lca

anterior portion