Arrhythmology
Cardiomyocytes
Heart muscle consists of
different types of
cardiomyocytes:
1) „Fast cells“ of working myocardium that
make a contraction as a response to
electric signal created in pacemaker
cells – most common type
2) „Slow cells“ which participate in
conduction through SA and AV node
3) „Pacemaker cells“ that create the
electric signal – ability of all the „slow“
cells and some „fast“ cells as well
Connection between two cells is
maintained by desmosomes and
connexin channels
Mechanism of cardiomyocyte activity 1
Three cations present in both extra- and intracelular fluid participate
in electrical activity of heart muscle: Na+, K+ and Ca2+. Na+ and Ca2+
are present mainly in ECF (Ca2+ also in endoplasmic reticulum), K+
in ICF
During fast depolarisation of a cardiomyocyte (phase 0), voltagegated
sodium channels (INa) open at -65 mV. Subsequent influx of
Na+ leads to depolarisation up to +40 mV and closing of Na+
channels.
Phase 1 means partial repolarisation carried by diffusion of K+
through specific ion channels (Ito – „transient outward“) K+ ions
diffuse according to both electrical and chemical gradient. In the
same time, Ca2+ „long-lasting“ (ICa-L) channels are opened. During
phase 0 to 2, heart muscle cell doesn‘t respond to any new electrical
signal – absolute refractory period
Mechanism of cardiomyocyte activity 2
In phase 2 („plateau“), prolonged depolarisation is maintained by
the influx of Ca2+ through ICa-L channels. Unlike INa or Ito, ICa-L
channel is gated both by voltage and receptor mechanism, that
responds to vegetative nervous signalisation. Ca2+ binds to
ryanodin receptor of sarcoplasmic reticulum, where it enhances the
release of more Ca2+ into the cytoplasm. Ca2+ then binds troponin
which changes its conformation and stops blocking the actin-myosin
interaction. Contraction of muscle fibre follows as in other types of
muscles. Another, delayed K+ channel (IK) is open.
Finally, with closing of Ca2+ channel, efflux of K+ lowers the voltage
inside the cardiomyocyte to the values during diastole (phase 3)
Before next repolarisation, Na+ ions are pumped outside the cell in
exchange for K+ by Na/K ATP-ase (3:2). Some Na+ ions return
inside the cell in change for Ca2+ through specific exchanger. Ca2+
is also pumped into sarcoplasmic reticulum.The heart muscle gets
to diastole
Pacemaker cells
In pacemaker cells, sympathicus- and parasympathicuscontrolled
sodium, potassium and calcium channels remain
open during the diastole, leading into continual loss of
negative voltage up to -65mV, when fast depolarisation
begins.
Pacemaker cells are present in SA node, AV node and
Purkinje fibres
Slow cells do not contain fast sodium channels, their depolarisation is
then mediated by Ca2+. The Ca2+ ion channels are influenced by the
sympathicus and the parasympathicus.
• Unlike in healthy fast cells, the amplitude of action potentials
decreases during consequent depolarization of the slow cells
population (decrement)
• Under some circumstances (e.g. repeated stimulation in a short time
period), depolarization of the neighbouring cell may become
subthreshold, and the depolarization wave stops
Slow cells
VC
SA node
AV node
Bundle of His
Purkinje fibre
SA node
Atrial myocardium
AV node
Bundle of His
Purk. fibre
ECG
ventricle
QRS
0.60.2 0.4
M /1
1
Aorta
Time (s)
P
T
U
According to Katzung's Basic & Clinical Pharmacology.
McGraw-Hill Medical; 9 edition (December 15, 2003)
Normal conduction within the heart
Sinoatrial (SA) node
Group of pacemaker cells located in the right atrium
Under normal circumstances it serves as primary
pacemaker of the heart
It spontaneously generates electrical impulses at a
rate of 60-90/min
The SA node is richly
innervated by both sympaticus
and parasympaticus, which
modify the SA node rate and
thus heart frequency
Atrial conduction system
Bachmann‘s bundle – conducts action potentials
to the left atrium
Internodal tracts (anterior, middle and posterior) –
run from SA node to AV node, converging near
the coronary sinus. Atrial automacity foci are
present within the atrial conduction system
Atrioventricular (AV) node
Area of specialized tissue located between atria and ventricles,
near the coronary sinus and tricuspid valve. It serves as
secondary pacemaker and is the only way of electric
connection between the atria and the ventricles under normal
circumstances.
AV node consists of 3 zones: AN (atria-nodus), N (nodus) and
NH (nodus-His).
In AN zone, the conduction gets slower, as there is less sodium
channels and slower depolarisation
N zone is formed by nodal cells with low voltage (-50mV) –
„slow cells“. In NH zone, the nuber of sodium
channels increase again. The cells of
NH zone can take over the function
of pacemaker, in the case if no signal from
upper parts of the conduction system is
present. Its rate is slower than that
of SA node: 40-60/min
Bundle of His
Part of cardiac tissue specialized for fast electrical
conduction that leads the signal from AV-node to
working myocardium of the ventricles.
After its short course, the Bundle of His branches ito
right and left bundle branch (Tawara branches). Right
bundle branch is long and thin, thus more vulnerable
than the left one
Left bundle branch is then
divided into the left
anterior and left posterior
fascicle
Purkinje fibres
Terminal part of the conduction system
Tertiary pacemaker – idioventricular rhythm (20-40/min), without
innervation
Jan Evangelista Purkyně (1787-1869),
Czech physiologist
Recording of action potentials
Action potentials in various parts of the heart can be registered using
electrodes
Besides the electrodes and a recorder, signal amplifier is also a part of the
device
For recording the ECG curve, potential difference between two electrodes
is used.
Thus a dipole with its dipole moment (vector) appears – leading from
negatively to positively charged electrode
The voltage difference generates a deviation from the isoelectric line (=
condition, when the potential at both electrodes is equal)
Leads
• The direction of the deviation depends on the
comparison of the electrode pair (lead), to which a
conventional direction is assigned (usually, it points
from right, up and back to left, down and forward), and
recorded dipole moment vector
• Standardly, 12 leads are defined using 10
electrodesEach possible position (lead) matches one
ECG curve
• The direction and the magnitude of deviation on the
record (for a given lead) depends on:
A) character of voltage change (depolarization or
repolarization
B) direction of voltage change spreading (in comparison
with a dipole moment vector)
12-leads ECG (uses 10 electrodes)
Electrode placement:
RA: On the right arm, avoiding bony prominences.
LA: In the same location that RA was placed, but on the left arm this time.
RL: On the right leg, avoiding bony prominences – it‘s used as a ground.
LL: In the same location that RL was placed, but on the left leg this time.
V1: In the fourth intercostal space (between ribs 4 & 5) just to the right of the
sternum (breastbone).
V2: In the fourth intercostal space (between ribs 4 & 5) just to the left of the
sternum.
V3: Between leads V2 and V4.
V4: In the fifth intercostal space (between ribs 5 & 6) in the mid-clavicular line
(the imaginary line that extends down from the midpoint of the clavicle
(collarbone).
V5: Horizontally even with V4, but in the anterior axillary line. (The anterior
axillary line is the imaginary line that runs down from the point midway between
the middle of the clavicle and the lateral end of the clavicle; the lateral end of
the collarbone is the end closer to the arm.)
V6: Horizontally even with V4 and V5 in the midaxillary line. (The midaxillary
line is the imaginary line that extends down from the middle of the patient’s
armpit.)
12-leads ECG – electrode placement
Orientation of the leads
Einthoven‘s leads
– A reference electrode is on one limb,
an active one on another
Wilson‘s leads
– Reference electrode is constructed as
the Wilson‘s terminal, an active one is
placed on a chest
Goldberger‘s leads
– One electrode is detached from the
Wilson‘s terminal and serves as an
active one, the remaining two together
as a reference one
Choose the right answer
An ectopic focus in the apex generates
depolarizing current towards the AV
node. Given the normal heart orientation
(apex on the left and down), following
finding is visible on the ECG:
A. Positive deviation in the lead I
B. No deviation in V5
C. Negative deviation in aVR
D. Negative deviation in II
E. Positive deviation in aVF
Electric potential changes – summation of vectors (ECG
curve in the leads I, II, III)
Summation of vectors (ECG curve in the leads I, II, III)
Slowing the potassium current
in phase 3 leads into...
A. P-wave widening
B. T-wave widening
C. ST-segment shortening
D. QRS-complex widening
E. PQ (PR) interval lengthening
Normal ECG curve
Description of ECG
• rhythm
• sinus
– 60-90/min
– other
• junctional
– 40-60/min
• idioventricular
– 30-40/min
• atrial fibrilation
• atrial flutter
• heart rate
– normal
• 60 – 100/min
– tachycardia
• >100/min
– bradycardia
• <60/min
• description of waves and intervals
• electrical axis of the heart
Normal Sinus Rhythm
Implies normal sequence of conduction, originating in the sinus node and
proceeding to the ventricles via the AV node and His-Purkinje system.
ECG Characteristics: Regular narrow-complex rhythm
Rate 60-100 bpm
Each QRS complex is preceded by a P wave
P wave is upright in lead II & downgoing in lead aVR
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Normal 12-lead ECG
Arrhythmias:
Electrophysiological abnormalities arising from the
impairment of the electric signal
Arrhythmias are defined by exclusion - i.e., any rhythm that is not
a normal sinus rhythm is an arrhythmia
With respect to the
– Frequency – bradyarrythmias vs. tachyarrhythmias
– Localization – supraventricular (SV), ventricular (V)
– Mechanism – abnormal signal formation / conduction
Possible causes of arrhytmia
Myocardial ischaemia, hypoxia and reperfusion, pH disorders
Disorders of myocardium – hypertrophy, dilatation, amyloidosis, scar aftar acute myocardial infarction
Inflammation (myocarditis)
Aberrant conduction – pre-excitation syndromes
Vegetative nervous system disorder (nervous lability, compensation of heart failure, shock, anxiety)
Disorders of ion balance
Drugs (β-blockers, digitalis, antiarrhytmics)
General state (trauma, endokrinopathy..)
Genetic causes (ion channel mutations)
Brady- and tachyarrhythmias:
1. Bradyarrhythmias
- SA block
- sick-sinus syndrome
- AV block
2. Tachyarrhythmias
a) Supraventricular (SV)
- SV premature beat – atrial, junction
- atrial tachycardia, flutter, fibrillation
- AV node re-entry tachycardia (AVNRT)
- AV re-entry tachycardia (Wolf-Parkinson-White syndrome)
b) Ventricular
- ventricular extrasystoles
- ventricular tachycardia
- flutter/fibrillation…
Badyarrhythmias
Mechanism of Arrhythmia
1. Pacemaker activity disorder
(enhanced, depressed, ectopic)
2. Re-entry
3. Triggered activity
(early afterdepolarisations, delayed
afterdepolarisations)
4. Conduct block
Recognizing altered automaticity on ECG
Gradual onset and termination of the arrhythmia.
The P wave of the first beat of the arrhythmia is typically the same
as the remaining beats of the arrhythmia (if a P wave is present at
all).
Mechanism of Re-entry
• The two pathways may be defined both morphologically and functionally
• Substrate:
- different conduction velocities
- different refraktory periods
- unidirectional blocks
- premature depolarizations
Mechanism of Re-entry 2
Prior to re-entry formation, new electric impulse is required
immediately after the preceding one (e.g. ectopic pacemaker)
Only the α pathway is depolarized, β is in the refractory period
If the conduction through α pathway is slow, the signal gets to the
second “crossroads“ just after the cells of β pathway are ready for a
new depolarisation
Signal might then return through the β pathway (backwards). A reentry
circuit is formed which depolarizes the surrounding tissue – a
high-frequency ectopic focus is formed
Signal in the re-entry circuit goes down through the slow pathway (!)
Recognizing reentry on ECG
Abrupt onset and termination of the arrhythmia.
The P wave of the first beat of the arrhythmia is
different from the remaining beats of the
arrhythmia (if a P wave is present at all).
Reentrant Rhythms
AV nodal reentrant tachycardia (AVNRT)
AV reentrant tachycardia (AVRT)
– Orthodromic
– Antidromic
Atrial flutter
Atrial fibrillation
Ventricular tachycardia
Triggered activity
Early afterdepolarization (EAD)
Under certain circumstances, the action potential can be much
longer than absolute refractory period (usually factors lengthening
the phase 3 – hypokalemia, genetic causes, some drugs) → long
QT
Such cells can be easily depolarized by local currents
Their depolarization then induce the depolarization wave in the
whole myocardium
Delayed afterdepolarization (DAD)
Whenever there is high level of
Ca2+ in the cytoplasm, ryanodin
receptors might be activated,
which leads into spilling of Ca2+
ions from sarcoplasmic
reticulum into the cytoplasm
The Ca2+ ions are then
exchanged for Na+ via their
exchanger in a ratio 1:3 (positive
charge 2:3)
This leads into lower membrane
voltage, which can result in the
opening of Na+ channels and
new depolarization
Sinus bradycardia
HR< 60 bpm; every QRS narrow, preceded by p wave
Can be normal in well-conditioned athletes
HR can be 30 bpm in children, young adults during
sleep, with up to 2 sec pauses
Sinus arrhythmia
Usually respiratory--Increase in heart rate during inspiration
Exaggerated in children, young adults and athletes—decreases with age
Usually asymptomatic, no treatment or referral
Can be non-respiratory, often in normal or diseased heart, seen in digitalis toxicity
Referral may be necessary if not clearly respiratory, history of heart disease
SA arrest with compensatory AV activity
When the activity of SA node is stopped, AV node takes over the role of pacemaker
If the pause is > 3 sec, it can lead into syncope
Very similar type of arrhythmia is SA block: pacing in SA node is generated, but not conducted
to the myocardium
Increased/Abnormal Automaticity
Sinus tachycardia (normal sequence and shape
of P and QRS)
• stress reaction, fever, physical effort,
hyperthyreoidism, reaction to hypotension
Junctional tachycardia (P wave either follows
QRS, or is hidden behind it, or goes
immediately before QRS and is bizzare)
Ectopic atrial tachycardia (P wave is bizzare)
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Sick Sinus Syndrome
Altered function of SA node in older age (fibrosis) or following ischemia
Other causes: amyloidosis, hypothyreoidism, hypothermia, medication
Manifests by alternating types of arrhythmia:
- Sinus bradycardia
- Wandering pacemaker (ectopic atrial foci)
- SA arrest or SA block
- atrial fibriation (brady-tachy) or flutter
Supraventricular premature beats
(supraventricular extrasystoles)
Narrow QRS complexes.
In case of premature atrial contractions
(PAC), the origin is an ectopic focus in
the atria. The QRS is preceded by a
bizarre P wave
In case of premature junctional
contraction (PJC), P wave is usually
hidden behind the narrow QRS
Both ectopic automaticity and microreentry
can lead into PAC and PJC
Supreventricular extrasystoles are
usually benign, often present in healthy
people
Atrial Flutter
Most cases of atrial flutter are caused by a large re-entrant circuit in the wall of the right atrium („typical
flutter“ – see below)
ECG Characteristics: Biphasic “sawtooth” flutter waves at a rate of ~ 300 bpm
Flutter waves have constant amplitude, duration, and
morphology through the cardiac cycle
There is usually either a 2:1 or 4:1 block at the AV node
(thanks to its decrement), resulting in
ventricular rates of either 150 or 75 bpm – regular
rhythm (1:1 AV conduction→ circulatory failure)
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Unmasking of Flutter Waves
In the presence of 2:1 AV block, the flutter waves may not be immediately
apparent. These can be brought out by administration of adenosine
(increases the K+ efflux, which leads into hyperpolarization and disabling the
AV node depolarization).
Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed., 2005.
Atrial Fibrillation
Atrial fibrillation is caused by numerous wavelets of depolarization spreading throughout the atria
simultaneously, leading to an absence of coordinated atrial contraction.
Mild tachycardia usually < 150 bpm, when controlled by rate-slowing treatment, it may oscillate
between tachy- and bradycardia (tachy-brady syndrome)
This kind of rhythm is present in up to 5% of adult population, mostly in older age. It is often
connected with other diseases of the heart (ischaemic haert disease, heart failure, valvular disease.
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Atrial Fibrillation
ECG Characteristics: Absent P waves
Presence of fine “fibrillatory” waves which vary in
amplitude and morphology
Irregularly irregular ventricular response
Complications:
Missing atrial systole (may constitute a problem in failing heart
Systemic embolization (thrombus is usually localized in the left atrial
appendage)
Symptoms of tachycardia
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AV nodal re-entry tachycardia (AVNRT)
• Most common regular supraventricular
tachyarytmia, indistinguishable from escaped
junctional rhythm (enhanced AV automaticity),
AVNRT has usually higher heart rate (>140/min).
• AVNRT is based on re-entry between slower and
faster pathways in the AV node.
Mechanism of AVNRT
AV re-entry tachycardia (AVRT)
Re-entry between AV node and an accessory pathway
There are several type of accessory pathway
1. Kent: adjacent atrial and ventricular
2. Mahaim: adjacent lower part of the AVN and ventricular (with decrement)
Usually no structure heart disease, occur in any age individual
Pre-excitation of ventricular myocardium manifests by δ-wave
Δ-wave
Wolff-Parkinson-White
Syndrome (WPW) is a
condition in which the heart
beats too fast due to
abnormal, extra electrical
pathway between the heart’s
atrium and ventricle – bundle
of Kent (orthodromic AVRT).
AV re-entry tachycardia (AVRT)
- AVRT can be orthodromic (i.e. antegrade conduction through AV node – more often): δ-wave
appears during the steady state but disappears during the arrhythmia; or antidromic (i.e.
antegrade conduction through accessory pathway): δ-wave is present during the arhythmia
Atrioventricular Block
AV block is a delay or failure in
transmission of the cardiac impulse
from atrium to ventricle.
Three degrees:
– 1) all the depolarization waves are
transmitted to ventricles, but with a delay
– 2) some signals are transmitted, some not
– 3) no signals are transmitted
1st Degree AV Block
ECG Characteristics: Prolongation of the PR interval (over 0.22s), which
is constant
All P waves are conducted
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/
2nd Degree AV Block
Mobitz 1
(Wenckebach)
ECG Characteristics: Progressive prolongation of the PR interval until a P
wave is not conducted (increasing decrement)
As the PR interval prolongs, the RR interval actually
shortens
Usually caused by vegetative dysbalance
ECG Characteristics: Constant PR interval with intermittent failure to conduct
Usually caused by structural disease
Mobitz 2
(Hay; or only Mobitz)
3rd Degree (Complete) AV Block
ECG Characteristics: No relationship between P waves and QRS complexes
Relatively constant PP intervals and RR intervals
Greater number of P waves than QRS complexes
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QRS complexes are usually narrow with HR 40-60 bpm (junctional rhythm). When
the pacemaker cells in NH zone are destroyed, there might be idioventricular
rhythm with wide QRS and HR 20-40 bpm
Intraventricular Block
(Bundle Branch Block, BBB)
Right bundle branch block, RBBB (complete,
incomplete)
Left bundle branch block, LBBB (complete)
Incomplete LBBB: left anterior hemiblock
(LAH), left posterior hemiblock (LPH)
Trifascicular block
• Usually asymptomatic
• Severe bradycardia in trifascicular block
• Risk of re-entry (Bundle Branch Re-entry
Tachycardia)
• Asynchrony of the ventricles (may worsen
hemodynamic compromise in heart failure) –
may be treated by biventricular pacemaker
implantation
Intraventricular block - ECG
Widening of QRS (iRBBB, LPH, LAH: 100-120 ms; RBBB,
LBBB: ≥120 ms)
In complete left- or right bundle block, there are also
changes in plateau and repolarization synchronization,
leading into changes of ST segment and T wave (esp.
LBBB)
In RBBB, most striking changes are in V1 (dipole moment
pointing to the right); in LBBB, in V6 (dipole moment pointing
to the left)
In LAH, the axis is deviated into extreme negative values (<-
45°); in LPH, into extreme positive values (>120°)
Trifascicular block leads into complete atrio-ventricular
dissociation as in 3rd degree AV block (with idioventricular
rhythm)
Name the arrhythmia
A. SA block
B. 2nd degree AV block, Mobitz I
C. 2nd degree AV block, Mobitz I
D. 3rd degree AV block
E. Transient trifascicular blockage
Ventricular Premature contractions (VPC)
Syn. ventricular extrasystoles (VES)
Is caused by either reentrant signaling or enhanced automaticity in some
ectopic focus or by triggered activity
The QRS complex is enlarged (>120ms) and has different shape, it is
accompanied by changes in ST, T wave and compensation pause (SA
node is „decharged“)
Coupling of VES
Isolated VES are usually benign
Premature ventricular beats occurring after every normal beat are termed ventricular
bigeminy, if 2 normal QRS complexes are followed by VES, we speak of ventricular
trigeminy (caused by ectopic pacemaker focus)
Two VES grouped together are called a couplet, three a triplet. Runs longer than 3 VES is
referred as non-sustained ventricular tachycardia (nonsustained if <30 sec) - re-entry
What is this arrhythmia?
Monomorphic ventricular tachycardia
Monomorphic = fixed re-entry circuit
Monomorphic ventricular tachycardia is usually caused by re-entry, and most commonly
seen in patients following myocardial infarction.
Sometimes, it is called „ventricular flutter“
In rarer cases, ventricular tachycardia may be polymorphic – alternating, but stable re-entry
circuits, or torsades de pointes
Ventricular or supraventricular?
While narrow QRS is typical for supraventricular arrhythmias (i.e. origin in
SA node, atria, AV node), wide QRS can be caused by ventricular
arrhythmia -80% of cases, as well as by supraventricular arrhythmia
combined with conduction block or by AVRT -20% of cases
An older (non-arythmic) ECG of the same person might be checked, if
available
If we don‘t know, it is better to treat the arrhythmia as ventricular
Polymorfní komorová tachykardie – torsades de pointes
“Twisting of the points“
Is connected with the long QT interval – early afterdepolarization (triggered
activity)
Unstable cardiomyocytes may be influenced by local currents that induce
new depolarization, while the former action potential is still not finished (Ron-T
phenomenon). Tachyarhythmia with unstable, rotating circuit may be
triggered
Torsades de pointes - ECG
The rotation of the circuit leads into changing shape of QRS in a given lead
Causes: hypokalemia, pharmacological/genetic block of K+ or Na+ channels
Ventricular fibrillation
• Uncoordinated electric currents and contractions in the ventricles with the frequency of >300bpm
• Lethal arrhythmia, which causes most of the total number of cardiac arrests
• Leads into asystolia (straight line on ECG) when untreated
• It may complicate myocardial infarction or be a result of other ventricular tachyarrhythmia
• VF might be induced by strong electric current or by contrast matter during cardiac catheterization
Defibrillation
• Electric action of the heart can be recoordinated
by electric discharge (with the
energy of 200 – 360 J).
• One electrode is put at upper sternum, the
other above the apex of the heart.
• If a defibrillator is unavailable, a precordial
thump may be tried (up to 30 sec from the
arrest) – limited efficiency.
At public places, automatized external defibrillators
(AED) are available. They are capable of automatic
analysis of cardiac electric activity in 10-20 sec, and
performing discharge, when necessary
ICD
Patients at risk may
undergo the
implantntation of
defibrillator (ICD =
implantable cardioverter-
defibrillator).
The device will
automatically discharge
during ventricular
fibrillation
ICD is usually implanted
below left clavicle
Cardiac stimulation (arteficial pacemaker - PM)
PMs are used in manifesting bradyarrhythmia
(SA and AV blocks, trifascicular block; in tachybrady
atrial fibrillation and sick sinus syndrom it
is used together with pharmacological treatment
lowering the HR)
Usually implanted below right clavicle
Most often, „on demand“ PMs are used, that
register the HR and start discharging only when
it is lower than the threshold previously set up
Combined devices (PM+ICD) also exist
ECG in cardiac stimulation
The stimulating electrodes are installed in stimulated parts of the heart
– Atria
– Right ventricle
– Both ventricles (biventricular)
– Sequential – atria + ventricles
– Atrial triggered ventricular stimulation
The waves on ECG curve are preceded by narrow „spikes“ (according to
stimulated part of the heart)
Wide QRS appears during the
stimulation of...
A. Atria
B. AV node
C. One ventricle
D. Both ventricles
E. Atria and both ventricles
ECG in cardiac stimulation - examples
Sequential stimulation of atria
and ventricles with a drop out
“On demand“ ventricular stimulation
Ineffective stimulation
Thank you for your attention