Module 8 : ECG and Rhythm Recognition Flashcards
12 lead ECG
- measurement of the electricity produced from the heart is sensed by 10 different electrodes over the body
- electricity is organized into leads that can tell the reader what area the heart signal is coming from
Electrocardiogram ECG
- measuring electricity of the heart
parts of the ECG waveform
- P wave
- T wave
- QRS complex
- PR interval
- PR segment
- QT interval
- ST interval
The ECG - 2 electrical planes
- ECG electrodes on 12 lead ECG senses the electricity of the heart in 2 planes
1) frontal plane
2) horizontal plane
Frontal Plane / Vertical Axis
- the LIMB LEADS (right arm left arm left leg) (I II III) and the AUGMENTED VECTOR LEADS (aVR, aVL, aVF) produce signal in the frontal plane
horizontal plane
- the V leads (chest, V1-V6) produce the signal in the horizontal plane
the limb leads in the frontal plane
Lead I
Lead II
Lead III
frontal plane limb leads - Lead I
- Right arm (RA) (-)
- Left arm (LA) (+)
frontal plane limb leads - Lead II
- Right Arm (-)
- left foot (LF) (+)
frontal plane limb leads - Lead III
- left arm (-)
- left foot (+)
leads
the path between the electrodes on the chest
einthovens triangle
- the triangle formed by the leads and electrodes
The P wave
- represents atrial depolarization (NOT CONTRACTION)
- ATRIAL CONTRACTION OCCURS DURING PR SEGMENT
- SA (sinotrial) node passes the signal through the inter–nodal tracts to the LA and RA muscle
- may be totally absent or very disorganized in some arrhythmias (atrial fibrillation)
- must have pause after the P wave to allow the atria to contract and eject its contents into the ventricle (PR INTERVAL)
LENGTH OF THE PR INTERVAL
LESS THAN 200ms
stages of the ECG wave - Stage 1
- depolarization of atrial contractile fibres produce P wave
stages of the ECG wave - stage 2
- atrial systole
- in the PR segment
stages of the ECG wave - stage 3
- depolarization of the ventricular contractile fibres produces QRS complex
stages of the ECG wave - stage 4
- ventricular systole ( contraction )
- ST segment
stages of the ECG wave - stage 5
- repolarization of ventricular contractile fibres produces the T wave
stages of the ECG wave - stage 6
- ventricular diastole (relaxation)
P wave reacted to hemodynamics
- the P wave corresponds to the late filling portion of the cardiac cycle
The PR interval
- covers the time from when the beginning of the P wave to the end of the PR sement / beginning of QRS complec
- covers atrial depolarization and contraction
the PR segment
- the atria are now contracting (mechanical) while the signal is sitting at the bundle of His (electrical)
+ waiting to go into bundle branches
The Atrioventricular Node (AV Node)
- the AV node and Bundle of His slow the conduction speed considerably
- slowing conduction allows the atria to have time to contract
- once atria contract and fill the ventricles then the signal gets the green light to go into the left and right bundle branches and on the ventricles
the QRS complex
- involves the depolarization of different parts of both ventricles in sequence
- REPRESETNS VENTRICULAR DEPOLARIZATION
- NOT WHEN VENTRICLE CONTRACTS
- combination between conduction through bundle branches, purkinjie fibres
and ventricle muscle cells - each segment of the QRS represents a different segment (of the heart) of conduction
left bundle branch (LBB)
- has 2 fascicles
+ left anterior and left posterior fascicle - fascicles are like wires
- left has more fascicles because left ventricle more complex and thicker
right bundle branch (RBB)
- only has 1 fascicle
speed of impulse in bundle branches
- the speed of travel through the BB impact the QRS duration
- if signal is blocked the QRS duration gets wider
normal QRS duration
< 100ms
Abnormal QRS duration
> 120ms
Left Bundle Branch Block (LBBB)
- impulse normally travels very fast through the BB’s
- get blocked by dead tissue
- usually wider and below the line in V1 (-)
- very negative
Right Bundle Branch Block (RBBB)
- (+) in V1
- makes lead V1 had Rabbit ears
QRS amplitude
- voltage/height of QRS complex
QRS amplitude - influencing factors
- muscle thickness
- body habitus
- pericardium
muscle thickness affecting QRS amplitude
more muscle = more QRS amplitude
body habitus affecting QRS amplitude
- impedance of electricity
- obese = small amplitude signal, fat tissue acts as an insulator so it can’t get through
- small = large amplitude signal
pericardium habitus affecting QRS amplitude
- excess pericardial fluid or thickened pericardium may shrink the QRS amplitude
+ inflamed, fibroised muffles ECG
the ST segment
- represents the gap between ventricular depolarization and repolarization
- period of time when the ventricles start to contract
- ST segment is isoelectric and should be same level as PR segment
- if it changes up or down compared to PR segment something is wrong
ST segment decreased
- indicates myocardial ischemia
- tissue not dead but not enough blood flow
ST segment increased
- indicates myocardial infarction
- blocked artery
- having a heart attack
- not always symptomatic
the T wave
- represents
+ electrically = ventricular repolarization
+ mechanically = coincides with ventricular systole - may be merged with ST segment
- may have positive or negative polarity
- negative T wave may be caused by ischemia, digoxin (given for atrial fib), electrolyte imbalance
Normal Sinus Rhythm (NSR)
- ## impulse is originating from the sinus node travels through NORMAL CONDUCTION PATHWAY through the heart
NSR rate
60-90 bpm
bradycardia
50-60 bpm
tachycardia
90-100 bpm
5 step method for diagnosing rhythms
1) heart rate
2) rhythm (regular and irregular)
3) P waves (before QRS, identical?)
4) PR interval (long or short)
5) QRS (wide or normal)
step 1 - heart rate
- between 60-90 bpm normal
- regular
step 2 - rhythm
R-R interval should be regular
- same beat to beat
step 3 - P waves
- one P wave for every QRS complex
step 4 - PR interval
- normal PR interval
- 170 ms
260 is prolonged
step 5 - QRS complex width
- needs to be narrow too wide may be LBBB
first degree AV block
- long PR interval
- p waves before each QRS complex but AV node holding the impulse too long
- don’t need a pace maker
atrial fibrillation
- no detectable P waves
- disorganized atrial contraction
- baseline undulates with no defined P waves
- ventricles contract when they can
- irregular R-R intervals
premature atrial contraction (PAC)
- MOST BENIGN ARRHYTHMIAS
- atrial tissue produces its own impulse leading ti atrial contraction followed by ventricular contraction
- may be result of too much catecholamines (stress hormones or caffeine)
- ectopic focus
PAC on ECG
- during a compensatory pause pause the timing is reset with the SA node takin over rhythm again
- biphasic P wave
premature ventricular contration (PVC)
- similar causes as the PAC
+ catecholamines, stress - however may also be caused by PARTIALLY BLACKED ARTERY CAUSING ZONE OF ISCHEMIA
zone of ischemia
- has altered ions within it which alters the impulse formation and propagation properties leading to PVCs
- usually follows by compensatory pause
PVC on ECG
- no P wave
- PVC usually has higher voltage than normal beats
- repolarization is messed up because depolarization is messed up
atrial flutter
- atrial contraction is semi-organized so P waves look similar to normal P waves
- electrical re-entry loop through the atrial tissue which allow it to depolarize repeatedly
ventricle response to atrial flutter
2: 1 3:1 4:1
- for every 2,3,4 P waves one QRS complex occurs
atrial rate in atrial flutter
- 250-300 bpm
atrial flutter on ECG
- SAW TOOTH
- atrial and ventricles do not talk to each other very well each do their own thing
- the atria contract all crazy and the ventricle contract with the bundle of his allows a impulse to them
atrial fibrillation ( af, afib)
- caused by very disorganized atrial contraction
- many ectopic electrical atrial foci competing to pace the heart
- R-R interval always changing
- LV outflow always changes as preload changes
- patient lose atrial kick
- early ventricular filling okay but loss of late filling
- atria QUIVERING not CONTRACTING
atrial fibrillation factors
- congestive heart failure (CHF)
- atrial enlargement (ALMOST ALWAYS)
afib characteristics
- in PLAX the MV appears to bounce many times before the LV contracts
- ventricles respond to atrial stimuli from the his bundle whenever it can leading to conduction down the bundle branches soit can contract
atrio-venricular blocks
first degree AV block
second degree AV block
third degree AV block
second degree AV block
- points of non contracting P waves
- some QRS beats are dropped
third degree AV block
- atrio-ventricular dissociation
- atria not speaking to ventricle at all
- prolonged P waves without QRS complex until QRS comes back
- lead II is the best lead to see P waves
multiple PVC’s
- can occur in 2’s 3’s or 4’s
- these are unifocal (from one focus) the mechanism is a re entry loop in the ventricles
- the ectopic focus where the impulse originates may be in a zone of ischemia
multifocal PVC’s
- impulse originates from more than one focus within the ventricles
- the shape of the QRS complex looks different beat to beat
ventricular tachycardia
- no blood to brain
- no blood to heart
- coronaries aren’t filling
- very rapid ventricular beats
- re entry loops through ventricles only
- very bad need the shock
ventricular fibrillation (vfib)
- very bad the absolute worst
- can sshock but not good outcome
- ventricles just fluttering not contracting at all
