Introduction to the ECG Flashcards
What is the heart
a functional syncytium with gap junctions electrically coupling cells
what is a functional syncytium and a syncytium
Syncytium = one large cell having many nuclei that are not separated by cell membrane (eg skeletal muscle cells)
Functional syncytium = many cells functioning as one
what the 3 types of cardiac myocyte cells
Pacemaker cells – settle heart rhythm
Conducting cells – transmitting rhythm throughout heart
Contractile cells – contracting heart to the rhythm
how does speed of propagation vary
contractile – atrial and ventricular myocytes 0.3-0.5 m/s
Conducting system (modified cardiomyocytes) eg Purkinje fibres – up to 5m/s (compared fastest neurons about 100 m/s)
AV nodes 0.05 m/s slow
how is electrical impulse conducted through the heart
Signal starts in SA node
Travels to av bundles in atrium
Fibrous skeleton doesn’t allow for electrical signal to pass so has to pass through av node
Travels in conducting system (bundle of his, branches) to ventricles
how does impulse spread through the antra
Internodal bundles conduct impulse form SA node to AV node
4 specialised bundles in the atria (contain purkinje like cells – cardiomyocytes modified to conduct) in direct contact with atrial muscle
what do internodal bundles ensure in the atria
Bundles ensure synchronous contraction of the atria
Conducting via atrial muscle would be slow (0.3-0.5m/s) so conducts faster via bundles (1 m/s)
what happens to the impulse at the av node
only point where the wave of depolarisation passes from atria to ventricles (ventricles insulated by connective tissues from atria)
AV node delays wave of excitation from A to V by 1-2 s (V contract after, permit longer and more effective filling)
AP is conducted very slowly in AV node (composed of small modified cardiomyocytes, electrical conduction between adjoining cells is weaker)
how does the av node conduct action potential slowly
AP is conducted very slowly in AV node (as its composed of small modified cardiomyocytes and electrical conduction between adjoining cells is weaker)
how does ventricular propagation occur
AV nodes connects directly to bundle of his followed by purkinje fibres
Purkinje are very large myocytes – transmit the impulse faster (bigger diameter cells conduct faster)
Transmit the impulse rapidly to the main mass of ventricles (from there slower conduction between contractile myocytes can occur)
First part of v wall depolarised is septum apex and av groove
what is an ECG
Is a gross electrical measurement of the hearts electrical activity
How does an ECG work
The individual currents of cardiac myocytes are tiny (few nano amps)
Currents can be detected from wrist and ankle, nearly 1 metre from heart
Possible due to heart being functional syncytium so large groups of cells all make electrical changes simultaneously
what can an ECG diagnose
Excellent for rate (so is pulse, holter monitor (ECG) allows 24/7 rate det), esp useful when atrial is different to ventricular rate
Many subtleties (not a one stop diagnosis, patient history essential for interpretation)
Diagnosis req other techniques (but ecg fast and affordable)
what are leads
Seen on ecg depends on placement of electrodes
A lead is a configuration of the electrodes (usually a positive, negative and sometimes ground)
what is a standard 12 lead ECG
A standard 12-lead ECG looks at heart from 12 different angles, creating measurements for 12 leads with 10 electrodes
Lead II is a positive electrode on left leg, negative on right arm and ground on right leg (ground could be almost anywhere)
Lead II most shown/used in teaching
what are the 12 standard leads
3 bipolar leads I,II,III seen frontal plane (positive and negative opposite sides of heart)
3 augmented leads
6 precordial leads
what are the elements of a 12 lead ECG
Normal 12 lead ECG has
Switching leads shown by vertical lines (and small citations)
Bottom tracing (aqua) shows a long reading from a single lead (II) – consistency of rhythm in bottom strip
what is the P-wave
depolarisation of atria in response to SA node triggering
first bump
what is the PR segment
delay of AV node to allow ventricular filling (Start of P to start of QRS complex)
what is the QRS complex
depolarisation of ventricles, triggers main pumping contractions
Tall peak with two dips either side (Q R S)
What is the ST segment
beginning of ventricle depolarisation, should be flat
end of QRS to start of t wave
what is the t wave
ventricular depolarisation, last bump
what is indicated with a wide and misshaped QRS complex
V conduction is abnormal eg ectopic pacemaker or bundle branch block
More cells give a bigger contribution – almost no conduction from His and conduction system
Large (deep) waves are a sign of dead tissue (old MI)
what is sinus rhythm
When the heart rhythm is generated from SA node
Each P wave is followed by QRS complex (and vice versa)
When the PR interval must be normal (3-5 little boxes)
Sinus tachycardia – specifically driven by SA node beating too quickly
It has normal pr intervals, each p matched with a QRS
what causes sinus tachycardia
specifically driven by SA node beating too quickly
It has normal pr intervals, each p matched with a QRS
what is the QT interval
start of the QRS to end of T wave
what are the boxies used on an ECG
Small - 0.04 sec and 0.1 mv
Large (5x5 small boxes)
what are the normal durations of the PR interval
3-5 boxies (120-200 ms)
what are the normal durations of the QRS complex
2-3 boxies (80-120 ms)
what is the normal duration of the QT interval
9-11.5 boxies (360-460 ms)
how is rate calculated on an ECG
Horizontal scale is 2.5cm/sec
To calculate rate count how many boxes between two P waves
how is ventricular rate calculated on an ECG
count between R waves Rate = 300/big boxes or 1 big box = 300 bpm 2 boxes = 150 bpm 3 =100 4=75 5=60 6=50 10=30
How is CVS rate and contractility controlled autonomically
The heart – parasympathetic input via vagus nerve (muscarinic stimulation decreases heart rate, contractility and conduction velocity Sympathetic input (sympathetic stimulation increases above)
what is the effect of sympathetic/parasympathetic withdrawal
Parasympathetic withdrawal increases heart rate, contractility and conduction velocity
Can be caused by Atropine – muscarinic agonist
Vasculature not innervated by PS system
Sympathetic input to heart via Stellate nerves,
beta agonists increase rate and beta blockers decrease
what are heart blocks
type of dysrhythmia, any kind of impulse conduction blocked (includes AV block, bundle branch block etc)
what are AV heart blocks
A delay of failure of atrial signalling stimulating ventricle
what are the causes of heart blocks
Ischaemia of av node/bundle Compression of AV bundle by scar or calcified tissue Inflammation of av node or bundle Symptoms Asymptomatic Palpitations Hypotension-like: dizziness, malaise, syncope Risk of sudden death
what is first degree heart block
When pr interval is greater than 5 little boxes (200ms) But all p’s followed by QRS Almost always asymptomatic Often young people Delayed av node transmission Rarely treated
what is mobitz type 1
Second degree heart block some p waves blocked and not followed by QRS – some QRS missing
Mobitz type 1 (Wenckebach)
Pr interval gets longer until QRS wave fails to follow p wave
Likely cause is av node damage
Usually no treatment given
what is mobitz type 2
Some P waves are blocked and not followed by QRS but Pr intervals always remain same
aka Hay
Likely bundle of His
High risk – can progress to 3rd degree HB
Treatment implant pacemaker
what is 3rd degree heart block
Atrial systoles consistently fail to arrive at ventricles
V rate is consistent
Time between a beats and v beats is variable
Pr intervals varies radically – sometimes greater than 12 boxes (p and qrs very inconsistent)
Intrinsic v rate is slow (less than 60 bpm, eg 40)
A beats consistent (not always visible)
what are ectopic beats
Escape beats and premature beats
Individual abnormal beats
These beats often triggered by ventricular tissue (or av node)
what are premature beats
Premature beats triggered by irritable tissue
what are escape beats
Escape beats (late) triggered by natural rhythmicity of non-atrial tissue, occur when signal is very delayed (wait for SA node but only so long)
how is premature ventricular contraction characterised
Unusually wide (width determined by slow conduction velocity) and weird looking electrical activity
No S wave, instead a wide negative dip where t wave should be
Often beat triggered in middle of myocardium
The two ventricles electrically unsynchronised so delayed and ineffective conduction (non-purkinje)
what is atrial fibrillation
Disorganised electrical activity in atria (no P wave, instead a flat or wiggly line)
Ventricular rate is fast and irregular (many signals reach AV node)
Very common in the elderly
Can lead to thrombus formation in atrium due to slow blood flow (stroke risk, need anti-coagulants)
what is respiratory sinus arrhythmia
beat is slightly faster during inspiration, slightly slower during expiration
Normal: sign of healthy heart
Usually only in children and athletes
Caused by respiratory centres in medulla
Observe ventricular rate : inverse of RR interval
what is is an interval and segment
Interval= duration of start from one marker to end of another marker Segment= the wave form between 2 other waves
what is a ST segment elevation
is a sign of acute MI
Iso-electric baseline is from end of T to next P wave
ST elevation means ST segment doesn’t go back down to iso-electric baseline
