Contiguous and reciprocal lead charts

Prehospital 12 Lead ECG: Contiguous and reciprocal lead charts

See this site for great 12 lead info…(reproduced below)

Here are some charts to help you identify and localize acute STEMI on the 12 lead ECG.
Contiguous leads

What do we mean when we say leads are “contiguous”?

Contiguous leads are “next” to one another anatomically speaking. They view the same general area of the heart (specifically the left ventricle).
For example, these states in the upper-midwest are contiguous, because they are all touching and in the same region of the country.
The “inferior” leads (II, III and aVF) view the inferior wall of the left ventricle. Remember that the inerior leads make up the lower-left corner of the 12 lead ECG.
The “septal” leads (V1 and V2) view the septal wall of the left ventricle. They are sometimes grouped together with the anterior leads.
The “anterior” leads (V3 and V4) view the anterior wall of the left ventricle.
The “lateral” leads (I, aVL, V5 and V6) view the lateral wall of the left ventricle. Leads I and aVL are sometimes referred to as the “high lateral” leads, because their positive electrode is on the left shoulder. Leads V5 and V6 are sometimes referred to as the “low lateral” leads because their positive electrodes are on the lateral left chest.

In addition, any two precordial leads that a next to one another are contiguous. In other words, V4 and V5 are contiguous, even though V4 is an anterior lead and V5 is a lateral lead. This makes sense when you consider that leads V4 and V5 are next to each other on the patient’s chest.
It’s worth mentioning that the standard 12 lead ECG does a relatively poor job examining the lateral wall of the left ventricle, and does not directly examine the posterior wall of the left ventricle. That’s the reason we sometimes miss acute STEMI in the distribution of the circumflex artery.
This image from Rescue One EMS Prehospital Program © 1999 Centric Medical Communications, Inc. illustrates the point nicely. This was from a class sponsored by Centocor (makers of the drug Retavase) that was taught by a Miami-Dade Fire Captain. In case you weren’t aware, Miami-Dade was the largest enroller in ER-TIMI-19 which was a clinical trial involving prehospital administration of thrombolytic therapy.

Think of it this way. There are 3 main epicardial coronary arteries, the right coronary artery (RCA), left anterior descending (LAD) and the circumflex (LCX).
It stands to reason that approximately 33% of documented acute STEMIs should occur in the distribution of each of the 3 main arteries. But that’s not what we find. Most acute STEMIs are documented in the distribution of the right coronary artery or the left anterior descending.
In other words, the standard 12 lead ECG does a relatively poor job examining the lateral and posterior walls of the left ventricle, so there’s a danger of missing STEMI in the distribution of the circumflex artery.
That’s the main reason it’s so important to carefully analyze the right precordial leads (V1-V3) for reciprocal changes that may indicate posterior STEMI. You can also consider using modified leads V7, V8 and V9 to increase the sensitivity.
Right ventricular infarction is another issue that will have to be addressed another time.
Reciprocal leads

What do we mean when we say that a lead is reciprocal? It means that during an acute STEMI, when ST segment elevation is present in leads that face the acute injury, ST segment depression will often be present in leads that face the “ischemic boundary”.
Many theories have been advanced to help explain reciprocal changes. I can’t go into all of them here, but consider this diagram modified from A Mechanism for ST Depression Associated with Contiguous Subendocardial Ischemia by Bruce Hopenfeld. Jeroen Stinstra, and Rob MacLeod. J. Cardiovasc. Electrophys, 15(10), 1200–1206, 2004.

Computer modeling has shown that as the ischemic zone extends from the endocardium to the epicardium, it creates a relatively positive area above the ischemic zone, and a relatively negative area at the ischemic boundaries.
This computer model helps explain why reciprocal changes may appear prior to ST segment elevation. Some authors have suggested that the first sign of acute inferior STEMI is a downsloping ST segment in lead aVL, and I have seen this happen many times.
Regardless of why reciprocal changes occur, clinical experience shows that the most important reciprocal changes can be viewed between the high lateral leads (I and aVL) and the inferior leads (II, III and aVF).
Keep in mind that reciprocal changes can be subtle, and may present as nothing more than a flattening of the ST segment in the reciprocal leads.
*** Update 01/15/09 ***
Check out this case at Dr. Smith’s ECG blog to see just how subtle reciprocal changes can be! And how they can prevent you from discharging a patient home to experience cardiac arrest!
*** End update ***
You will sometimes notice reciprocal changes in the anterior leads (V1, V2, V3 and V4). These usually represent reciprocal changes associated with injury of the posterior wall of the left ventricle. Since we don’t usually view modified chest leads V7, V8 and V9, we most often see these changes associated with acute inferior STEMI, because the posterior descending artery branches off the right coronary artery (RCA), which also supplies the inferior wall of the left ventricle.
With anterior STEMI, the occlusion is often in the left anterior descending artery (LAD) which branches off the left main coronary artery. Depending on the patient’s coronary vasculature, the culprit artery, and the location of the occlusion, the blood supply may also effect the lateral wall of the left ventricle, which can create reciprocal changes in the inferior leads (sometimes very subtle depending on the stage of the infarct).
Reciprocal changes may not always be present, but when they are present, it is very strong supporting evidence that the patient is experiencing actue STEMI.
See also:
12 lead ECG – lead placement diagrams
The problem of ST segment elevation

Dr Bonaris – 12 Lead EKG

The three Is

Ischemia

• Lack of oxygenation to myocardium
• ST Depression or T wave inversion
• may or may not result in infarct or Q wave

Injury

• Prolonged ischemia
• ST elevations (injury pattern)
• usually results in an infarct may or may not result in a Q wave

Infarction

• Death of tissue
• May throw pathological Q waves (.04 wide and greater than 1/3 of height of R wave)

T to P is the baseline you compare to for comparing ST segment, do not use the the PRI!

T wave inversions may be normal in some leads, but think cardiac.

What to look for

• ST elevations in two or more anatomically contiguous leads
• T wave – tall and round – Tombstone pattern

12 lead EKG Injury Patterns

Evolution of MI

• Hyperacute T waves – Tall Peaked- Suggestive of MI (Also hyperkalemia)
• Tombstone appearance – ominous sign, severe

Reciprocal changes

A change detected electrocardiographically in a wall of the heart opposite the site of a myocardial infarction. In acute inferior wall infarction, reciprocal changes are considered a sign of more extensive myocardial damage. Not always present.

(Electrical alternans – seen in cardiac tamponade)

Some more from http://medinfo.ufl.edu/~ekg/Infarct%20&%20Ischemia.html

Coronary Anatomy: Relation to the Site of Infarct

• The most common cause of Acute MI is sudden total occlusion of a major coronary artery.
• Sudden total occlusion of the RCA (Right Coronary Artery) causes acute inferior MI and/or posterior or right ventricular MI (ST elevation in lead V4R helps diagnose RV infarction.). Mobitz I is common with inferior MI (the RCA supplies the AV nodal artery).
• Sudden occlusion of the Left Main coronary artery leads to sudden death (from massive infarction).
• Sudden occlusion of the LAD (Left Anterior Descending) artery leads to anterior infarction; bundle branch block/Mobitz II 2° AV block may be seen.
• Sudden occlusion of the Circumflex artery leads to lateral infarction.  In about 10% of patients this artery (rather than the RCA) also supplies the inferior and posterior walls of the left ventricle.
• Note -  Collateral development changes the above patterns.

Andy Rodriguez

First Degree Heart Block

• Not a true block
• Conduction delay at AV node
• All impulses are conducted to ventricles
• PRI will be >0.20 consistently across the strip

Second Degree Heart Block

• Intermittent
• Some get through and some don’t
• pathology can be in AV node or below in Bundle of His
• pathology is often blended with other blocks
• Mobitz Type I (Wenckebach)
• Impulses encounter progressive delays at the AV node until one impulse is blocked completely
• PRI starts getting progressively longer and then dropped QRS
• All conducted QRSs present are tight, <0.12 and preceded by a P wave
• Mobitz Type II
• Can be regular or irregular, depending on conduction ratio
• Usually a Brady rhythm
• More than one P wave for every QRS
• PRI constant on conducted beats can be >0.20
• QRS <0.12
• Conduction Ratios
• 2:1, 3:1, etc. two P waves for every conducted QRS

Third Degree Heart Block (Complete Heart Block)

• All impulses generated by Sinus node are being blocked by AV node
• Separate Sinus and Ventricular Pacemakers –
• Complete disassociation between P waves and QRSs
• Regular
• Rate depends on whether its junctional or ventricular
• P waves, normal and upright, more P waves than QRS
• PRI – no relationship between P waves and QRS , occasional superimposed on QRS
• QRS width depends on whether its junctional or ventricular

Heart blocks are best diagnosed using a 12 Lead EKG Machine. This and other used medical equipment can be found easily online.

Download Excel Version Here

UPDATED 6/15/09

Sinus Blocks, Pauses and Arrest

• In all cases, no P, QRS or T wave present – Impulse is blocked a SA node and Atria are never depolarized.
• Sinus Block – Always a multiple of underlying P-P interval. can be more than one missing complex
• Sinus Pause – Not a multiple of P-P interval. Shorter than three times the P-P
• Sinus Arrest – Same as pause but more than 2 missing complexes (consecutive)

Andy Rodriguez

Ventricular Rhythms

• Impulse is generated in the ventricles. Generally recognized by wide QRS complex, >0.12

Premature Ventricular Contraction (PVC)

• Regular – ectopics will interrupt
• Rate – depending on underlying rhythm
• No P wave before PVC
• Wide QRS >0.12
• 
• 
•  

Compensatory Pause

• Allows for heart pick up its rhythm again after a PVC, resumes normal rhythm as was before PVC
• 2x R-R
•  

Interpolated

• R-R stays the same and PVC is between normal R-R
•  

Types of PVCs

• Unifocal – One focus generating the extra beat, generates PVCs that look exactly the same
• Multifocal – Multiple foci generating extra impulses. generates PVCs that look different

R on T Phenomenon

• PVC hits during or end of T wave, can cause Vfib if hits just right
• 

PVC Couplets

• Two PVCs in a row
• May be unifocal or multifocal

PVCs in a run or Run of PVCs

• More than three PVCs in a row
• Also called a “run of vtach”

PVC Groupings

• 1:1 Ratio – Bigeminy (every other is a PVC)
• 2:1 Ratio – Trigeminy (every third is a PVC)
• 4:1 Ratio – Quadgeminy (every fourth is a PVC)

Ventricular Tachycardia

• Usually Regular – can be slightly irregular
• Rate of 150 – 250 (Less than 150 is slow VT, greater than 250 V flutter)
• No P waves
• PRI – None
• QRS- wide and bizarre >0.12
• 

Ventricular Fibrillation

• Multiple foci firing in an uncoordinated fashion
• Grossly irregular
• Wide QRS – Fibrillating
• No pulse
• Shockable Rhythm
• Most lethal rhythm
• 

Idioventricular Rhythm

• Regular rate at 20-40 BPM (above 40 -120 called an accelerated idioventricular rhythm)
• No P waves
• No PI
• QRS wide and bizarre
•  

Asystole

• Absence of any electrical activity

More on EKGs… Andy Rodriguez

Escape Mechanism – normal pacemaker slows down or fails and a lower pacing site assumes pacemaking responsibility.

Sympathetic – both Atria & ventricles
Parasympathic – Only Atria

Analyzing the rhythm

• Regularity – Rhythm
  • regular
  • irregular
  • pattern to irregularity
  • ectopic beats
• Rate
• P Waves
  • present
  • regular, one for every QRS
  • before QRS or after
  • deflection – normal and upright in lead II
  • all P waves look alike
  • are irregular P waves associated by ectopic beats
• PR Intervals (PRI)
• QRS Complex
  • equal duration
  • measurement
  • normal limits
  • all look alike?
  • are unusual QRS complexes associated with ectopic beats?

Sinus Rhythms

Normal Sinus Rhythm – Regular, 60-100 BPM, P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12

Sinus Bradycardia - Regular, Rate <60 BPM, P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12

Sinus Tachyardia - Regular, Rate >100 BPM (usually 100-160), P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12

Sinus Arrhythmia – sinus node fires faster during inspiration and slower during expiration. rate is still normal, and still normal QRS –
Irregular, 60-100 BPM, P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12

Atrial Rhythms

Wandering Pacemaker – pacemaker site wanders between SA node, atria and AV node. rate is usually normal and will conduct normally to ventricles
Slightly Irregular, 60-100 BPM, P wave morphology changes from beat to beat, one before every QRS, PRI 0.12-0.20 but may vary, and QRS <0.12

Premature Atrial Contraction (PAC) – irritable focus within atrium that fires prematurely and produces a single ectopic beat. impulses are conducted normally.
Usually regular (depending on underlying rhythm) except for PAC, 60-100 BPM, P wave changes – one that comes early looks different than normal sinus P waves, one before every QRS, PRI 0.12-0.20 but may be longer, and QRS <0.12

Atrial Tachycardia (or SVT)– Single atrial site fires repetitively at a very high rate. impulses conducted normally
Regular 150-250 BPM, P wave looks different than sinus p wave if visible at all, one before every QRS, PRI not measurable, QRS <0.12

Atrial Flutter -  single focus initiates rapid repetitive impulses, AV node protects ventricles by blocking conduction of some impulses. Atrial Rhythm- regular, several flutter waves (saw tooth)before each QRS (F waves), PRI unable to determine, atrial rate 250-350 bpm

Atrial Fibrillation – multiple foci initiate rapid repetitive impulses, AV node protects ventricles by blocking conduction of some impulses.
Grossly irregular, atrial rate >350 bpm, ventricular rate varies greatly, no discernable P waves, no PRI, QRS <.12

Steve Kanarian

Some cardiology review:

• Location of Heart: Retrosternal
• Point of maximal impulse, Left 5th intercostal, midclavicular line, above mitral valve as well.
• Pericardium contains approx 30cc of fluid
• CO= SV x HR
• Frank Starling Law – (use fluid challenge to increase CO, increase in volume = increase in stretch therefore increase CO)
• S1 – closing of mitral and tricuspid valves
• s2 – closing of pulmonic and aortic valves
• s3 – murmur, caused by ventricular filling, caused by left sided CHF
• s4 – sign of CHF
• Coronary Vessels come off base of aorta and come back via the coronary sinus
  • right coronary artery (RCA) (right atrium and ventricle)
  • left coronary artery (LCA) splits; (mostly left ventricle and atrium)
    • left anterior descending
    • circumflex coronary
• Preload; pressure in ventricle at diastole
• Afterload; pressure against which heart has to pump

Depolarization causes contraction.(Na+ rushes in) Repolarization is the refractory state. (K+ left in the cell)

Cardiac Physiology

(Bundle of Kent – Wolf Parkinson’s White –WPW)

EKG Lead Placement

• Bipolar (Limb) Leads – impulses traveling towards positive lead, upright wave, going towards negative lead, points down
• Augmented (Unipolar) Leads – Boosted Electrically)
• Precordial (Chest) Leads- V1-V6 (Septal 1,2, Anterior 3,4 Lateral 5,6 Inferior 2,3, aVF) SALI

Electrical Conductivity and the EKG

‘Monitoring’ leads are not diagnostic, 12 Lead EKG Machines are diagnostic quality

ECG Paper

• Speed (horizontal Boxes smallest= .04 sec, big box is .20 sec)
• Amplitude – Vertical box = 0.1mV height  (1mm)

Normal Electrocardiogram

• P-R Interval (PRI) – 0.12 – .20 sec (Prolonged PRI indicates Heart block)
• QRS – <0.12 sec – wider indicates rhythm below AV node
• QT interval – Q wave to repolarization – prolonged means heart is at risk for ventricular dysrythmias (poisoning, overdoses)

5 points to look for

• Rate
• Rhythm
• P waves
• PRI
• QRS