ECG

6 limb leads: look at the heart @ a different 30 degree interval the limb leads: BIPOLAR I< II< III Unipolar limb leads aVR>aVL>aVF -reference point is in the centre of the ?

CHEST Leads V1-V6 unipolar leads looking into the heart

-sum of all the electrical activity of all the cardiomyocytes

atrial depolarization -Abnormal axis indicates ectopic atrial pacemaker - Abnormal morphology or duration indicate RA or LA pathology

The PR interval represents the time from the start of atrial depolarization to the start of ventricular depolarization. It includes the delay in conduction that occurs at the AV node. The PR interval P.50 normally lasts from 0.12 to 0.2 seconds -Short PR interval indicates accessory AV pathway - Long pathway indicates conducting tissue disease (AV node/His) FLAT LINE: but really its not flat but because we cant reach the AV node with electrodes (small structure)

septal depolarization left-right direction -Pathological (large) q wave indicates myocardial damage - usually old infarct

Usually from left side to right side that's why the Q wave is negative

Ventricular Depolarization Too large, or wrong axis: may indicate hypertrophy. Too small: may indicate damage Big R wave as the impulse moves from the back to the front of the heart (towards electrodes) The amplitude of the QRS complex is much greater than that of the P wave because the ventricles, having so much more muscle mass than the atria, can generate a much greater electrical potential.

remaining ventricular depolarization Prolongation of QRS complex indicates delay in conduction within ventricle, including bundle branch block

ventricular systole: usually horizontal or gently up-sloping in all leads. It represents the time from the end of ventricular depolarization to the start of ventricular repolarization ST elevation may indicate myocardial infarction or pericarditis. ST depression may indicate ischaemia.

ventricular repolarisation: Unlike depolarization, which is largely passive, repolarization requires the expenditure of a great deal of cellular energy the membrane pump) Twave is highly susceptible to all kinds of influences, both cardiac and noncardiac (e.g., hormonal, neurologic), and is therefore variable in its appearance. The amplitude, or height, of a normal T wave is one third to two thirds that of the corresponding R wave. Inverted T wave seen in myocardial infarction and ischaemia. Prolonged T wave indicates delayed repolarization

a wave on the cardiac cycle that indicates an immature cardiovascular system or an electrolyte imbalance little blip

PR: from P to Q (some machines dont have a Q wave)

1. Rate 2. QRS axis (I, aVF) 3. Rhythm: PR relationship 4. QRS width (BBB), voltage (LVH) 5. Ischaemia: Q, ST, TWI 6. QT interval 7. Previous ECG fro comparison

1. Amplitude (1mV/cm) 2. Time 25mm/sec 3. Small boxes= 40msec X 0.1mV 4. Large box= 0.2sec x 0.5mV

HR= 300/(# of large boxes"

The frontal plane is a coronal plane. The limb leads view electrical forces moving up and down and left and right on the frontal plane

for each lead a line from -ve to +ve and the angle superimposing on the 360 circle of the frontal plane

is created by making the left arm positive and the right arm negative. Its angle of orientation is 0°.

is created by making the legs positive and the right arm negative. Its angle of orientation is 60°.

is created by making the legs positive and the left arm negative. Its angle of orientation is 120°.

-A single lead is chosen to be positive, and all the others are made negative, with their average essentially serving as the negative electrode -called augmented because the EKG machinery must amplify the tracings to get an adequate recording In AUGMENTED one lead is compared with the mean of all the others

is created by making the left arm positive and the other limbs negative. Its angle of orientation is -30°.

is created by making the right arm positive and the other limbs negative. Its angle of orientation is -150°.

is created by making the legs positive and the other limbs negative. Its angle of orientation is +90°

Leads II, III, and AVF most effectively view the inferior surface of the heart. The inferior surface, or wall, of the heart is an anatomic term for the bottom of the heart, the portion that rests on the diaphragm. This is the region suppplied by the right coronary artery

Leads I and AVL -V5 V6 too

is a loner called whatever

chest leads -horizontal plane from anterior to posterior -the chest electrode is made +ve and the whole body is made common ground

V1 is placed in the fourth intercostal space to the right of the sternum. V2 is placed in the fourth intercostal space to the left of the sternum. V3 is placed between V2 and V4. V4 is placed in the fifth intercostal space in the midclavicular line. V5 is placed between V4 and V6. V6 is placed in the fifth intercostal space in the midaxillary line.

-right ventricle lies anteriorly and medially within the body cavity, and the left ventricle lies posteriorly and laterally. -Leads V1 and V2 lie directly over the right ventricle, -V3 and V4 over the interventricular septum -V5 and V6 over the left ventricle.

V1-V4

-the chaos of the heart impulses is averaged to produce an average vector direction (goalie in a soccer game)

The vector of atrial depolarization points leftward and inferiorly. -Any lead that views the wave of atrial depolarization as moving toward it will record a positive deflection on the EKG paper Therefore, lead I records a positive wave, AVR records a negative wave lead III records a biphasic wave: lies perpendicular to the atrial current

-V5 and V6 record a positive deflection -V1, lying over the right heart, is oriented perpendicularly to the direction of current flow and records a biphasic wave -V2 through V4 are variable.

Because the atria are small, the voltage they can generate is also small. The amplitude of the P wave does not normally exceed 0.25 mV (2.5 mm, or two and one half small squares) in any lead. The P wave amplitude is usually most positive in lead II and most negative in lead AVR.

Rotation of the heart within the chest cavity redirects the perceived direction of current flow. Lead III is normally oriented perpendicularly to atrial depolarization. With the apex of the heart turned leftward, lead III will view atrial depolarization as receding and will record a wave that is largely negative.

The PR segment represents the time from the end of atrial depolarization to the beginning of ventricular depolarization. The PR segment is usually horizontal and runs along the same baseline as the start of the P wave.

a tiny negative deflection in one or several of the left lateral leads. This initial negative deflection, or Q wave, may therefore be seen in leads I, AVL, V5, and V6. Sometimes, small Q waves may also be seen in the inferior leads and in V3 and V4. -Normal septal Q waves have an amplitude of not greater than 0.1 mV.

QRS dominated by LV (due to size) so average vector swings left (normal 0 to +90) -therefore, large positive deflections (R waves) may be seen in many of the left lateral and inferior leads. -Lead AVR, lying rightward, records a deep negative deflection (S wave).

-V1, V2 record deep S waves because current moving left away from them -V5, V6 tall R waves -V3, V4 is the transitional zone (usually one of these is biphasic; Rwave= Swave amplitude)

pattern of progressively increasing R-wave amplitude moving right to left in the precordial leads -Lead V1 has the smallest R wave; lead V5, the largest (the R wave in lead V6 is usually a little smaller than that in lead V5)

duration of the QRS complex, is 0.06 to 0.1 seconds in duration

usually horizontal or gently up-sloping in all leads. It represents the time from the end of ventricular depolarization to the start of ventricular repolarization NORMALLY flat as all myocytes are depolarised at this time

repolarization usually begins in the last area of the heart to have been depolarized, and then travels backward, in a direction opposite that of the wave of depolarization - Because both an approaching wave of depolarization and a receding wave of repolarization generate a positive deflection on the EKG, the same electrodes that recorded a positive deflection during depolarization (appearing as a tall R wave) will also generally record a positive deflection during repolarization

beginning of ventricular depolarization to the end of ventricular repolarization -electrical events of the ventricals -repolarisation time> depolarisation -QT is proportionate to HR. Faster HR need to repolarise quicker -QT interval composes about 40% of the normal cardiac cycle

<50

>120

+120 to -30 -calcualted using 2 leads @ right angles to each other -Eg 1 and aVF -If QRS is +ve in lead 1 then its heading towards that direction -If the QRS is +ve in aVF (then add the 2 vectors to...) using the diagram

PR- elongated AVN disease First degree heart block

2:1 P wave supperimposed by T wave not followed by a QRS complex -every second impulse isnt conducted to by the AV node - mobitz type 2

a) conduction delay -1st degree Heart block -2nd degree heart block -Mobitz type 1 or 2 -3rd degree heart block b) extra beats -junctional -atrial -ventricular c) tachycardias -atrial fibrillation -atrial flutter -SVT -VT -VF

2nd degree AV block Progressive lengthening of PR interval until beat is dropped. Usually asymp almost always impaired conduction of AV (can be normal in young people)

aburpt failure of AV conduction no PR interval prolongation prior to "dropped QRS" usually due to block below the AV node usually associated w/ a wide, abnormal QRS PM is always required; always worsens w/ time -> P wave makes it through AV node, but fails infra-nodally. this is failure in the his-P tree. pt can have syncope wide QRS is associated w/ BBB 3:2 sequence. every 3rd P wave is dropped

P wave have no relationship to the QRS complex

-junctional -atrial -ventricular

term for when escape beats come from near the AV node or Bundle of His and the QRS morphology may look relatively normal

P wave comes early

produces enormous QRS complex, caused by burst of parasympathetic activity that depresses SA node and atrial and junctional foci

-atrial fibrillation -atrial flutter -SVT -VT -VF

occurs when the normal rhythmic contractions of the atria are replaced by rapid irregular twitching of the muscular heart wall -waving atria no obvious P wave

Characterized by a "saw-toothed" wave formation with a slower ventricular rate. The atrial rate generally ranges form 220 to 350 beats/min. Cardioversion may be used. IMAGE: 4:1

i think there is always one atrial blip buried in the QRS

• Tachycardia originating above the ventricle • Usually difficuft to find P waves because rate is too high. — If present superimposed on T — Unable to determine if originating from sinus, atria or AV node • Normal QRST • Paroxysmal Supraventricu lar Tachycardia (PSVT)

a rapid heart rhythm in which the electrical impulse begins in the ventricle (instead of the atrium), which may result in inadequate blood flow and eventually deteriorate into cardiac arrest. -leads to death

the rapid, irregular, and useless contractions of the ventricles -disorganised, no patterns

-hypertrophy -BBB

LBB activates septum RBB activates RV LBB activates LV

-Conduction Delay

LV activation

RV activation

If the QRS looks like W in V1 and M in V6 it is LBBB. (WiLLiaM) If the QRS looks like M in V1 and W in V6 it is RBBB. (MoRRoW)

>120ms in block

small first R because the muscle in the right is much less than the left

large R wave

any of the 4 chambers can develop hypertrophy increased muscle mass means increased voltage find the lead(s) that sample the chamber of interest

tall P wave in II

long notched or biphasic Pwave in I, II, or V1 impulse has to travel across and delay activation of the big left atrium

increased voltage in V4-6 with strain ST pattern RV tall R wave in V1; RV will contribute to more of the QRS complex and V1 sits right over the RV so hypertrophy is a big wave in V1

increased voltage in V1-3 R in V5/6 > 5 large boxes OR R in V5/6 + S in V1/2 >7 large boxes

IHD affects -Q wave -ST segment -T wave depending on timing & severity of ischemia

ST segment elevation is usually attributed to impending infarction, but can also be due to pericarditis or vasospastic (variant) angina. In some healthy young adults, a form of ST elevation can be normal. The height of the ST segment is measured at a point 2 boxes after the end of the QRS complex. ST segment elevation is considered significant if it exceeds 1 mm in a limb lead or 2 mm in a precordial lead.

subendocardial ischemia (e.g., classical angina pectoris)

Death of tissue that extends through the full thickness of the myocardial wall

inner half, multifocal/patchy, circumferential, coronary thrombosis rare, result of shock, no epicarditis, do not form aneurysms

T wave inversion means either ischemia or evolving changes after infarction

significant Q waves are greater than 0.04 sec in duration and/or deeper tahn 25% of the height of the accompanying R wave in amplitude. (in I, aVL, V5, and V6 as normal septal depolarization) -imply completed transmural infarction

Gives global Saddle shaped ST-elevation and PR elevation (in all leads), means infaraction everywhere which is less likely (you'ld be dead)

Use slope-intercept method Define isoelectric line (may be in PR segment) Then, find segment with maximum slope on downward T wave segment, and see where it intersects isoelectric line

R -R interval

Rate: Use your 300/150/100/75/60 ... rule for each large box Count boxes for RR interval Rhythm: Is there a p wave preceding each QRS complex? Is there a QRS for each P wave? Is it regular or irregular? Is the QRS wide or narrow? Axis: Positive in I and AVF (which quadrant)? Or use I and AVF for X and Y amplitudes Intervals pr interval, QRS duration Waveforms P wave (left or right atrial abnormality) QRS (pathologic Q waves, ST shift, ventricular hypertrophy) QT interval

Look at the electrical depolarisation of the limb leads and the one with the biggest R wave wins so the axis is closest to it -Why is the axis helpful? -Range of normal is huge -30 to +90 (that's why it doesn't matter that we are measuring it to the nearest 30 degrees) -Physical position of the heart varies a lot depending on the size and shape of the patient

II, III, aVF

V1,2,3,4 anterior leads and septal leads of the ventricles

aVL, V5,6, I

II - easiest to see P wave

S (V1) + R (V6 or V5) > 35mm then the patient has LVH high probability of underlying LVH +ve predictive value 90% -ve predictive value 46%

Voltage of 1mV should make 2 box 1mV = 10mm and also 0.2sec width (large square)

- atherosclerotic plaque busts - clot completely blocks coronary artery - Myocardium supplied by that section becomes ischaemic - @ t=20min the endocardium dies and then the death moves towards the outside till by ?12 hrs full thickness death

- assymetrical in shape - less than 50% of the height of the R wave - longer and broader (because slower conduction)

<5mins of MI the Twaves rise (>50%) - mechanism is unknown

ST elevation (hallmark of complete occlusion) - mechanism is unknown (injury current)

in the leads that the QRS ends with an R wave, the R wave rises in amplitude in the leads were the QRS ends in an S wave then the S wave may be obliterated Reflect worsening crisis in the mycocardial wall (death in the purkinje fibres which are more resistant than myocardium)

if Tx then can reverse the damage unTx the muscle will die in that region

Pathological Q waves (late marker and stays for ever) - due to the death in muscle the Q wave becomes deeper and prolonged (it is normally quickly overwhelmed by the LV depolarisation) Pathological Q waves: >2ss tall and 1 ss wide

- timing in this is unclear - inverted T waves possibly due to re-vascularisation (and then they return to normal after a week or so)

if they occur early they can be transient if treated quick enough so that the muscle is still viable

it gives time for the ventricels to fill with blood

-pericardium repolarise first - thus the wave of repolarisation spreads in the oposite direction (important)

prolonged QT can cause fatal arrhytmias while using some drugs this changes with HR - i.e high HR may miss a long QT uses V1, V2 or aVL or aVR (because it can be difficult to determine the end of the T-wave in some leads)

QTc = QT interval / ?RR interval RR interval = 60/HR

is the earliest QRS in any lead and the latest in any lead - as a comprimise we normally chose the lead with the widest QRS complex

goes from inverted to upright between leads V3 to V4 represents healthy LV

Normal negative T wave in children and blacks (leads V1 and V2) normal in healthy adults

- moves from left to right also moves upwards - therefore moves away from the inferior leads (II, III, aVF)

Differences in newborns The right ventricle is dominant S waves in V6 120degrees

The axis is swinging around (90degrees)

Axis now 80 degrees

45 degrees Left ventricular dominant heart This is a 15 lead ECG

HR increases from birth, peaks at 1-2 months of age, then slowly declines

Shape Duration ( lead II) < 3yo 0.03-0.09sec > 3yo 0.05-0.1sec Amplitude; < 2.5 mm Axis

Start of P to start of QRS complex Measured in lead II Increases with age Decreases with heart rate SNS: allows the SA node to INC. firing and also AV node conduction too

Duration Beginning to end Measure in lead V5 Increases with increasing muscle mass Increases with age < 7yo ?< 0.08 sec >7yo ?<0.09 sec Axis Deflection of QRS in I and avF Isoelectric method: axis is perpendicular to the limb lead where the QRS voltage is closest to isoelectric Morphology Amplitude

End of the S wave to start of T wave ST depression > 1mm ST elevation > 0.5 mm Early repolarisation may occur in adolescence Up to 4 mm in mid praecordial leads

A. Amplitude Very variable Low voltage or flattening in several leads > 2mm in I,II, V6 < 7 mm in limb leads and 10 mm in praecordial leads B. Direction > 5 days to adolescence: inverted in V1 and V3R <5 days and in adults: may normally be upright in V1 and V3R

Start of the QRS to the end of the T Using the longest interval in any lead Correct for heart rate by Bazett's formula QTc = QT (sec)/?RR (sec) QTc> 0.45 seconds prolonged (>0.46s in female) Standardised for 60bpm - machine pretty good at the calculation but sometimes can get the QT interval wrong (thus have to check this manually)

1. QR pattern in the right chest leads - Moderate ?RVP 2. Upright T wave in lead V1 - Moderate ? RVP but may become asymmetric inversion in severe PHT 3. Tall R wave in lead V1 4. Deep S wave in lead V6 5. Abnormally large R/S in lead 1 6. Right axis deviation IMAGE- progressive worsening of RVH

Asymmetric T wave inversion in leads V5 or V6 - Most reliable ECG sign ST depression V6 R + V1 S > 98th percentile Usually not found alone IMAGE- progressive worsening of LVH (last one is LVH with strain)

• Caused by a muscle bridge between the atria and ventricles • Allows a "short circuit" to be set up • Usually travels down the His system, and from the V to the A up the pathway

- His is very efficent thus narrow QRS but here the extra impulse through muscle extends the impulse - At risk of SVT and re-entry circuits and also INC. risk of sudden death

short PR (when kids get this with re-entry circuits called wolfe- parkinsons syndrome)

pre-excitation, early right to left conduction pathway blockage evidenced by short PR interval with normal P wave; delta wave on upstroke of R wave

- difficult to pick up (they cancel each other) - if you can see LVH then look for RVH and vice versa

- 1st degree (slowed AV node conduction) -2nd degree -type 1 -type 2 3rd Degree

2nd Degree; mobitiz type 1 - common in adolescents that are asleep

more worring this child had a pacemaker implanted

narrow QRS means its a good escape rhythm thus still using the His (wider QRS complexes means its coming somewhere form the ventriclesa nd is less realiable)