Everything Electrical and Cardiac:An EKG Treatise

By Michael GarciaAugust 18, 2001

Note: You will need the notes to look at the EKGs. I believe that Campbell will test us from those patterns. There is also a ton of great sites with classic EKG patterns on them. Just search www.Google.com, EKG and you will find all the resources you need.

The Basics – First things First

Cardiac Electrophyisiology – a very brief overview The heart is depolarized by a wave of positive charges traveling down the heart from their origin in the SA node in the right atrium until their endpoint at the end of the left and right bundle branches in the atrium. The myocytes of the heart depolarize from the endocardium to the epicardium (in to out) and repolarize in the opposite direction (out to in). As the heart depolarizes the muscles contract. It is the movement of this electrical charge that creates the deflections known as EKGs. I know this is all review but it makes EKGs so much easier to understand with these few basic facts.

The conduction system through the heart SA AV Bundle of His Left and Right Bundle Branches

The SA node controls the rate and rhythm of the heart. It acts as the conductor and orchestrates a proper heartbeat. The conduction system is set up in such a way that it includes back up “pacemakers” present at every level, so each part of the conduction system provides a back up for the pacemaker above. If the Sinus node goes out the AV node will pick up the pacemaking responsibilities all be it at a slower inherent rate (more on that slowly). And so on and so forth.

Some important features of the conducting system –

The SA node is located in the RV and is supplied by the right main arteryThe AV node is located between the two AV valves and is supplied by the Right main as well. Because of this right-sided infarcts can cause severe life threatening arrhythmias.The AV valves act as an insulator separating the electricity of the atria from the ventricles allowing the wave of stimulation to only pass through the AV node. Conduction slows through the AV node allowing the atria to completely contract before the ventricles receive stimulation to do the same. Important distinction conduction speed versus inherent rate - inherent rate decreases the farther you get from the SA node (SA fastest ventricles slowest) conduction speed varies through the heart (e.g. the speed at which the wave of depolarization moves through the heart…AV slowest ventricles fastest)

EKG dynamics - the basics

*******A positive charge moving at a positive electrode produces a positive deflection*********

The WavesP wave – atrial depolarizationQRS – ventricular depolarizationT wave – ventricular repolarization (a negative moving away from a positive – positive deflection) U wave – final phase of purkinge repol. may mean hypokalemia or quinidine toxicity

The Intervals/Segments

The difference between a segment and an interval is the interval contains the wave discussed, segments don’t.

PR interval – start of the P wave to the R waveQT interval – from the start of the QRS to the end of the T waveST segment – from the end of S wave to the start of the T wave

The Lead System – see pg 335, its really important to understand the location and charge of the leads

The Limb leads – I, II, IIIThe Augmented limb leads – avR, avL, avF (R stands for right arm, L for left arm, F for foot)

The Precordial leads – V1-V6

The Limb leads divide the heart in a coronal plane (looking through the heart)The precordial leads divide the heart in a horizontal plane (look around the heart)By using all the leads – we can “see” the function of the entire heart.

Each lead is part of a grouping of leads that display the function of a certain section of the heart.

Limb leads grouping - I and avL are the lateral leads (positive charge placed at the lateral aspect of heart. see p. 335II, III, and avF are the inferior limb leads

Precordial lead grouping – V1 and V2 are the septal leadsV2, V3, and V4 are the anterior leadsV4, V5, and V6 are the lateral leads

The limb leads are at different angles (degrees) I – 0, II – 60, III – 120avF – 90, avR - -150, avL - -30 Review the orientation of the heart in the chest How many boxes? –

One big box - .2 sec long 1 V highOne little box is a millimeter – used to determine the significance of waves.

Lines are placed on the top of the sheet every 3 seconds – two of these together are known as six-second strips.

The Method – see notes pg 333

It is very important to have a standard method that you go though on every EKG.Don’t jump straight to Infarct/Ischemia or you will miss something. Everyone that I have ever heard speak of EKGs has emphasized this.

Rate Rhythym Axis Blocks Hypertrophy Infarction Weird Shit

Use this system and you will cover everything. The most important concept!!!!!!!!!

1. Rate – very easy

300,150,100,75,60,50 just memorize this the formula takes to long to do, anyways most modern EKG machines calculate this for us anyway. Method – find an QRS on a line at the start of a big box, then count the number of big boxes until the next QRS. One box the rate is 300, 2 the rate 150, etc.

The formula – 300/number of big boxes between QRS

If rate is irregular use the six second strip – simply count the number of QRS complexes in the interval per six-second strip and multiply by ten. Easy

Some rate memorization facts – SA node inherent rate – 60 to 80 beats per minuteAV node “ “ - 40 to 60Ventricular “ “ - 20 to 40Tachycardia > 100 b/minBradycardia < 60 b/min

2. Rhythm –

First ask if the rhythm is regular (looks appealing to the eye)If it is then it is Sinus Rhythm and you can move on to the next stepUse the “Rhythm strip” to determine this – usually a reprint of lead II at the bottom of the EKG If it isn’t regular it becomes a real pain in the ass.

Arrhythmias-Atrial – The only benign arrhythmia is sinus arrythmia – usually seen in young healthy atheletes, the RR

interval decreases (heart speeds up) with insipration

Irregular Rhythms –

Wandering pacemaker – multiple areas of the heart are becoming the pacemaker P waves show different morphology in each complex atrial rates are less than 100 irregular ventricular rhythmMultifocal Atrial Tach (MFAT) –

Wandering pacemaker but the atria are beating faster than 100

Atrial Flutter – sawtooth atrial rate 250-350

Atrial Fibrillation – chaotic atrial electrical activityImportant to determine ventricular response (ventricular rate)

Junctional Rhythms – AV node has become the pacemaker QRS is normal duration, rate is usually decreased

40-60 (can be increased to sinus rate 60-80 in accelerated junctional rhythm variations – no p waves normal qrs,

the AV node depolarization subsequently depolarizes the Sinus node effecting the morphology of the p wave (inverted, either preceding directly before the qrs with short pr interval or within the complex, p. 342)

note: these rhythms are also called escape rhythms because a new pacemaker has “escaped” the control of the SA node and is now running the show. By examining QRS morphology (wide, irregular or normal) and the rate of the heart and determine the location of the pacemaker. Use junctional rhythms as a model and apply this to atrial escape rhythms – normal qrs, new p wave morphology (another location in the atria is the new pacemaker), and a atrial rate 60-80

PVCs, PACs – this is a pattern thing, if you don’t know what they look like look them up in an EKG book, once you see them you will never forget them.Mitral Valve Prolapse can cause PVCs – Barlow Syndrome

Supravetricular Tachycardia (SVT) – a new automaticity focus above the ventricles has become very pissed off (not the sinus node, either

an atrial focus or the AV node) and is rapidly conducting down the tree causing a very rapid heartbeat. Typically the rate is > 100 and no p waves are seen.

Vtach/Vfib – this is bad news. p 343 These rhythms are very recognizable – look at them

remember Vfib is just a quivering heart (no pulses, no flow) and indicates imminent death unless the patient is cardioverted.

Torsades de Pointes – is Vtach with changing voltages seen in the EKG, looks like a party streamer. Quick name all the drugs from Pharm that cause this.

WPW – delta waves and shortened PRLook for pacer spikes to see if a pacemaker is installed

3. AXIS Really easy – just look at lead I and avF if they are both mostly positive then the axis is correct. Otherwise look at the diagram on p345. If avF is mostly negative it is above the the horizontal axis, if avF is mostly positive then it is below the horizontal. etc. This is easier when drawn out. Use the diagram and remember the quadrants definitions. Any problems find me and I will explain.

To determine the degrees of the axis look for the most isoelectric limb lead, the one that is a s positive as it is negative or the one that is closest to flat, and add 90 to the degree value assigned to that lead (see above).

4. BLOCKSAV Blocks – First Degree - PR interval longer than one big box (.2 secs) Second Degree - Mobitz Type 1 (Wenkebach) PR internval increases with each cycle until a beat is dropped Mobitz Type 2 – PR interval is regular, a beat is dropped every once in a whileThird Degree – complete AV nodal block – P waves doing there thing (P to P interval regular) QRS doing there things (R to R interval is regular) but the two are not associated

Bundle Brach Blocks – Widened QRS > 120 ms or three little boxesLook for terminal forces in leads V1 and V6 to determine which bundle is blocked

V1 and V2 show rt ventricle (bunny ears (R-R’) are good to look for but if QRS is widened and there are no Bunny ears in V1 or V2 it does not mean that you do not have a right bundle)V5 and V6 show left ventricle, rememberTerminal forces ex. - If the last bit of the QRS is positive in V6 and negative in V1 the terminal forces are going away from rt ventricle and towards the left ventricle meaning the left is delayed in depolarization therefore left BBB.

5. Hypertrophy

See pg 333, 354-357 for definintions of hypertrophy, this is really just a memorization thing that doesn’t really need explanation.

The most important and widely used criteria is the sum of the V5,V6 R wave and the V1,V2 S wave.

Strain pattern is the presence of a sloping ST depression in the precordial leads and T wave inversion – again a typical pattern that is easily recognized. This coupled with left atrial enlargement can indicate LVH.P waves are best visualized in lead II or V1

6. Infarctions/Ischemia

T wave abnormalities (inversions) - ischemiaT wave inversion is the first EKG change seen during AMI and during acute ischemia. It indicates

ischemic areas of the heart and is most worrisome if the inversion is symmetric (looks like the letter U stretched out)

ST elevations – InjuryIndicate present or past injury to the myocardium. Is very troublesome and is the earliest consistent

sign of infarction. Must be at least 1mm high to be considered significant. Look to elevation if present with depression to locate the area of acute injury.

ST depressions – often reciprocal in the leads opposite those showing ST elevation. More of an artifact. Can indicate a universal subendocardial ischemia/infarction. The key element of EKG changes in positive stress tests. Digitalis toxicity causes this as well.

Q Waves – NecrosisQ waves indicate a necrotic area of myocardium. Diagnositc of infarction. Must be at least 2/3 of R

wave or 1mm deep and 1mm wide. Q waves (insignificant) can be normal so comparison to old EKGs is important. Any Q waves meeting the pathological standards of significance must be considered indicative of infarct. Q waves can be seen in the limb leads and in V5,V6 due to initial septal depolarization and not infarct (usually very tiny)

Poterior infarcts may be silent on EKGs look reciprocal changes in the antero-septal leadsi.e. large R waves, ST depression.

See pg. 358 for examples of these patterns7. Weird Shit –

Hyperkalemia – peaked T waves, Give Ca2+ for txHypokalemia – developing U waves, ST depressionSevere hypokalemia – above plus prolonged QTDetermining QT prolongation – If the QT interval is longer than ½ the R-R interval then it is prolonged. This can lead to Torsades. p. 366 for causesDigitalis effect – ST depression with upright T waves. Looks like ½ of Salvaldor Dali’s mustache. Really it looks like the ST segment has a downward curve instead of being flat.Hypercalcemia – short QTHypocalcemia – long QTQuinidine – notched P wave, Long QT, U waves, episodic Torsades, wide QRSPacemakers – look for weird narrow waves, sometimes they are very small.

Lead misplacement is also mentioned but I cannot find any info on the subject. If anyone knows this please email the class, thanks.

This sums up EKGs pretty well, it is pretty in depth but I think that if you can understand the stuff then you will be able to apply this to heart pathology and not just look for patterns. This translates to correct test questions. Hope this helps. Any questions, call me at 835-6444 at anytime or hunt me down.

Mike

 

Axis

 

The Basics Of Electrical Axis: The electrical axis tells us the direction of depolarization through the heart. When the axis deviates from the norm, you are alerted to look for a pathologic problem such as LAFB, LPFB, infarction, or hypertrophy as discussed in other sections. There are four main quadrants that the axis can fall into: normal range, left axis deviation (LAD), right axis deviation (RAD), or extreme RAD. Here is an easy way to determine which quadrant the axis is in:

      Check QRS orientation in lead I       Check the QRS in aVF

      Use the chart below

I aVF AXIS Degrees

› › Normal -30 to +90

› Ø LAD -30 to -90

Ø › RAD +90 to+270

Ø Ø Extreme RAD  

With a quick check to I and aVF you can assess, if upright in both, that there is a normal axis.

 

Axis Determination in Degrees: The quadrant determination can help flag an abnormality early in your reading, but you should still continue and figure the axis in degrees. Although there is a variety of ways to do this, the one I find most helpful involves using the isoelectric limb lead. Leads in degrees: I=0°, II=60°, III=120°, aVF=90°, aVL=-30°, aVR=-150°

      Scan all the limb leads to find the one that is closest to the baseline or has equal parts up and down (isoelectric)

      The axis is at 90° (perpendicular) to this lead (example: if I is isoelectric, than the axis is either +90° or -90°)

      Look to the lead(s) that these axes refer to (in our example that would be aVF)

      The direction of the QRS determines the negativity or positivity of the axis (if up in aVF then the axis would be +90°, if down -90°)

See diagram below

 

Determination of Axis Rotation: Another element to axis is it’s rotation in the horizontal plane. Unlikely axis deviation, axis rotation is figured using the precordial leads.

      Again, look for the isoelectric lead- here this is called transition; this should be found in V3 and V4. Transition is the point in the precordial leads where the R wave becomes larger than the S wave.

      If the isoelectric lead is in V1 or V2, than the rotation is to the right

      If in V5 and V6, rotation is to the left

This is important to know as rotation is always away from infarction and towards hypertrophy

 

Axis Abnormalities:

Low voltage: R and S waves in all limb leads are less than 6mm and less than 11mm in precordial leads. Typically seen with COPD, chronic constrictive pericarditis,

pericardial effusion, multiple MI’s, myxedema, amyloidosis, marked obesity, or hypothyroidism.

Poor R wave progression: Typically, R waves get larger and S waves get smaller as you move from V1 to V6. If the R wave is ≤3mm in V3 than it is considered poor R wave progression. Cannot diagnose low voltage, LBBB, or WPW when present. Causes of poor R wave progression include: LVH, RVH, pulmonary disease, anterior or anteroseptal infarct, conduction defects such as LBBB, cardiomyopathy, chest wall deformity, lead misplacement, and (if all else rules out) a normal variant compare old EKGs.

Electrical Alternans: Consistent alteration of amplitude of the P wave, QRS complex, or T wave signifying changing of axis with each beat (see EKG below); see with SVT or pericardial tamponade.

EKG 

1) 1)    The P wave is the first bump and represents atrial depolarization. The P-R interval is the P wave plus the flat line leading to the small depression. The P-R interval represents the electrical activity in the atria including the time delay at the AV Node. The slight depression followed by the large up and down spike is called the QRS wave and represents the depolarization of the ventricles. The last bump is the T wave and it represents ventricular repolarization. The Q-T interval is the distance from the beginning of the Q to the end of the T and represents the total electrical activity occurring in the ventricles. The EKG is produced as a result of moving electricity in the heart, i.e. when ions move across membranes during action potentials.

2) 2)    The sinoatrial node is the first spot, located in the upper right part of the right atrium. The atrioventricular node is the spot of tissue located in the center of the four chambers. Attached to the AV Node is the AV bundle which then breaks into the left and right bundle branches which, in turn, lead to the branching Purkinje Fibers.

3) 3)    The SA Node generates action potentials on its own. This is called auto-rhythmicity. All heart cells have this ability but the SA Node depolarizes more frequently than any other cell in the heart so it sets the pace. It does this by either having leakier ion channels or a lower threshold for depolarization.

4) 4)    The conduction system transmits the action potential more quickly than would occur in its absence and, more importantly, it times the contraction of the atria and ventricles so that they each have adequate time for filling and no blood gets backed up.

5) 5)    To allow the ventricles to fill with blood both before, and as a result of, contraction of the atria.6) 6)    Normocardia means a heart rate between 60 and 100 beats per minute and is normal. Tachycardia

indicates a heart rate of greater than 100 beats per minute and is normal during exercise or times of severe stress but is otherwise abnormal. Bradycardia indicates a heart rate of less than 60 beats per minute and is normal for athletes at rest but is otherwise abnormal.

7) 7)    The abnormality is a prolonged P-R interval. The problem is located in the AV node. The problem is that the AV Node is transmitting the signal to the ventricles even more slowly than usual.

8) 8)    Ventricular fibrillation is fatal. The reason is that the ventricles are not contracting in a coordinated fashion so they are not strong enough to pump blood throughout the body so the body doesn’t get enough oxygen. Atrial fibrillation is not fatal (unless you die of a blood clot from the slow moving blood in the auricle of the atria) because most of the blood gets to the ventricles without the aid of the atria anyway.

9) 9)    PVC occurs when a cell in the ventricles depolarizes on its own rather than waiting to receive the signal by way of the conduction system. When this occurs adjacent cells also depolarize and spread the signal throughout the ventricles. A contraction follows depolarization so what you end up with is a relatively normal contraction at an unusual time (because it didn’t result from the conduction system). Generally the next heart beat is skipped because all the cells are in the refractory period when the next impulse is sent along the AV Node. The next contraction can be stronger than normal because the ventricles have had more time than normal to fill; the extra filling has stretched the ventricular muscle. After the PVC episode, the normal pattern resumes.

10) 10) There are several ways to do this but they all rely on the fact that a contraction will follow each QRS wave, so knowing that you can count QRS waves as heart beats and knowing the speed of the chart paper you can calculate heart rate. One simple way is to count the number of QRS waves in 5 seconds worth of chart paper and then convert that to beats per minute.

11) 11) Mean electrical axis is the average directional flow of electricity in the heart. It usually goes from the upper right (where the SA Node is) to the lower left so that it is pointing from the center of the chest toward the left leg. It is used as a measure of the electrical activity on each side of the heart. If

there is growth of cells on one side of the heart the MEA will deviate toward that side. If there is death of cells on one side the MEA will deviate toward the other side. The MEA is calculated from three leads of the EKG because each lead sees a different angle of the heart’s electrical activity. Two possible causes of left axis deviation are death of cells on the right side of the heart (right sided myocardial infarction) and growth of cells on the left (many causes, blood doping and hypertension among them).

12) 12) B. left ventricular hypertrophy

PRECORDIAL LEADS: V1 thru V6 are placed to specific places on the chest, for advanced ECG diagnostics. V1 is right-most, near the SA-Node, while V6 is leftmost, past the apex of the heart.

MEAN ELECTRICAL AXIS OF THE HEART:

Two ways to graphically determine mean electrical axis: o SHORT WAY: This is only accurate when there is a net QRS-Deflection of virtually zero

(i.e. the R deflection is equal and opposite to the S deflection). Determine the lead that has a net zero QRS-Deflection. On the hexaxial system, the mean electrical axis points in the direction that is

perpendicular to that lead. o LONG WAY: This is longer but more accurate.

Consider any two of the six hexaxial leads. Determine again the Net QRS-Deflection for each lead.

Plot that deflection along the appropriate axis on a hexaxial chart. Draw a dotted line perpendicular to each of the above plots, and extend the two lines

until the intersect each other. The Mean Electrical Axis is the vector that points from the center to the intersection

of those two lines. LAB: Different physiological effects on the mean electrical axis:

o INSPIRATION: The diaphragm moves down ------> It pulls the apex of the heart toward the right (i.e. in a more vertical direction) ------> the mean electrical axis is more positive (+ more degrees).

o FORCED EXPIRATION: The exact opposite of above. The apex of the heart gets pushed upward and toward the left horizontal axis ------> the mean electrical axis is less positive or even negative.

o PREGNANCY: The mean electrical axis would deviate to the left, within normal limits. The physical presence of the fetus would push up the diaphragm ------> heart leans toward left.

o LEFT VENTRICULAR HYPERTROPHY: Mean axis deviation toward the left. o Pulmonary Valve Stenosis: If we assume that it leads to Right Ventricular Hypertrophy ------

> Then we get (potentially severe) right axis deviation. o INFANCY: Right Axis Deviation, because the infant's right ventricle and left ventricle

musculature are about the same size at birth. Left ventricle becomes larger within a couple months.

NORMAL MEAN AXIS: Anywhere between -30 and +110. o Anything negative of -30 is left axis deviation, as occurs from left ventricular hypertrophy.

o Anything positive of +110 is right axis deviation, as occurs from right ventricular hypertrophy.

ECG ABNORMALITIES:

SINUS BRADYCARDIA: A heart rate slower than 60 SA-Nodal depolarizations per minute. "Sinus" indicates that the cardiac impulse is originating from the SA-Node as normal.

SINUS TACHYCARDIA: Heart rate faster than 100 bpm, originating as normal from the SA-Node.

o Tachycardia generally means you'll see a shorter RR-Interval (i.e. faster heart rate). SINUS ARREST: No SA-Node depolarization.

o This can be artificially induced by carotid massage, which results in overstimulation of the Vagus ------> SA-Node hyperpolarized.

ATRIAL PAROXYSMAL TACHYCARDIA: Faster heart rate resulting from an ectopic pacemaker in the atrial muscle.

o In the example the P-Wave points downward because the atrial depolarization starts in the LA, because that is where the tissue is leaky.

BUNDLE-BRANCH BLOCKS: There is some conduction block in the Bundle of His (Left or Right Bundle branches), with results as below:

o 1 BLOCK: Partial block. The PR-Interval is longer than normal because it takes longer to conduct the impulse from SA-Node to AV-Node.

o 2 BLOCK: A QRS-Complex occurs only after every other P-Wave. In other words, it takes two P-Waves to sufficiently excite the AV-Node to conduct the impulse to the ventricles.

o 3 BLOCK: There is no temporal relationship between the P-Wave and QRS-Complex. Atrial and ventricular depolarizations are being controlled by their own independent pacemakers (the SA-Node and AV-Node respectively).

AV-NODAL TACHYCARDIA: Tachycardia, plus the P-Wave is insignificant or absent. o This is tachycardia, where the impulse originates from the AV-Node. The inherent

pacemaker of the AV-Node is faster than the SA-Node. PREMATURE VENTRICULAR CONTRACTION (PVC): A premature QRS-Complex, or one

that occurs without being preceded by a P-Wave. o That means that the P-Wave didn't start the impulse, but it started somewhere else. o Ectopic Pacemaker: With PVC, the impulse originates in the ventricular muscle itself, due

to leaky membranes in the muscle. VENTRICULAR FIBRILLATION: Waves of depolarization traveling in multiple directions all

over the ventricular muscle. The pacemaker activity is lost. ATRIAL FIBRILLATION: Fibrillation in the atria is not serious in children, but it is serious in old

people. o That's because in old people, atrial systole contributes a greater relative blood volume to

cardiac output than in children.

CLINICAL LECTURE: WOLF-PARKINSON-WHITE SYNDROME

Normally, the AV-Node is the only pathway for conduction of the impulse from the atria to the ventricles.

o Bachman's Bundle: Normally conducts the impulse from Right Atrium to Left Atrium during atrial systole.

o Moderator Band: Normally conducts the impulse from the right ventricular septal wall to the right free wall during ventricular systole.

Lupus Erythematosus: Rare condition associated with pediatric bradycardia. Usually pediatric heart problems result in Tachycardia -- not bradycardia.

PEDIATRIC TACHYCARDIAS: They are divided into two types o Supraventricular Tachycardia (SVT): One where the problem originates somewhere in the

AV-System. o Ventricular Tachycardia (VT): Problem originates in the ventricular system.

Wolf-Parkinson-White Syndrome: Extra conductive tissue in the myocardium, creating an accessory pathway for conduction from atria to ventricles.

o This accessory pathway ultimately results in a Reentry Tachycardia, or a conduction loop between the normal and accessory pathways.

o The Wolf-Parkinson-White ECG: Shorter PR-Interval due to rapid conduction of signal to ventricles through accessory pathway.

This is the ECG when the patient is healthy and no problems are going on. The P-Wave and the QRS-Complex are scrunched together, creating the appearance

of a delta-wave (hump right before QRS), and a longer overall QRS Complex. Reentry Tachycardia: You get it from a unidirectional block in one pathway, coupled with slowed

conduction of an alternative pathway. This results in continuous impulse conduction, or circus dysrhythmia.

o With WPW, the accessory pathway can get blocked because it hasn't had the time to repolarize, then the normal pathway provides a mean for retrograde conduction of depolarization.

o This results in a conduction loop and severe tachycardia. TREATMENT: Slow down the conduction through one pathway or the other.

o Use Ca+2-Channel Blockers (such as Verapamil) o Use Digoxin to increase AV-Nodal sensitivity to ACh. o Use beta-Blockers to block the normal NorE sympathetic receptors on the AV-Node and

cardiac muscle. o In severe cases, surgically remove the conductive tissue from the myocardium.