cardiovascular physiology electrocardiogram … 2 and 3...electrodes are connected to (+)/(–) side...
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CARDIOVASCULAR PHYSIOLOGY
Electrocardiogram (ECG)
Part 1 and 2
Dr. Ana-Maria Zagrean
Electrocardiogram (ECG)
ECG is a non-invasive method to record time-dependent electrical
vectors of the heart representing the sum of the extracellular signals
produced by the movement of action potentials through cardiac
myocytes, using electrodes attached to the skin.
ECG detects the dynamic of electro-mechanic events
- the rate and regularity of heartbeats,
- the size and position of the chambers,
- the presence of any damage to the heart,
- the effects of drugs etc.
Electrodes are connected to (+)/(–) side of a
voltmeter.
A standard 12-lead ECG is obtained using
2 electrodes on the upper extremities, 2 on the
lower extremities, and 6 on standard locations
across the chest.
Fluctuations of extracellular voltage recorded by
one lead, between one (+) and one (–) electrode,
are called waves.
The electrodes on the extremities generate the
6 limb leads (3 standard and 3 augmented), and
the chest electrodes produce the 6 precordial
leads.
ECG machine has amplifiers and filters to
reduce the electrical noise/artifacts.
Electrocardiogram (ECG)
Instantaneous potentials develop on the surface of a cardiac
muscle mass that has been depolarized in its center.
Voltmeter
Myocardium extracellular surface
In a lead, one electrode is
treated as the positive side of a
voltmeter and one or more
electrodes as the negative side
a lead records the fluctuation
in voltage difference between (+)
and (-) electrodes.
From AP to ECG
+ + + + + + + +
-o
+
- - - + + + + + +
- - - - - + + + +
- - - - - - - - - - -
depolarization
-o
+
- - - - - - - - - - -
+ + + - - - - - - -
+ + + + - - - - -
repolarization
+ + + + + + + +
Recordings of electrical activity in isolated muscular fibers
+/- Deflections correspond to the recorded +/- waves
(+) wave when the depolarization moves towards the positive/exploratory electrode
Extracellular side of
the cell membrane
1
2
3
4
5
6
7
8
Recordings of electrical activity in isolated muscular fibers
Electrocardiogram trace recorded
simultaneously with AP in the heart.
QRS complex voltage (from the top of the R
wave to the bottom of the S wave)
1 - 1.5 mV, when ECGs recorded from
electrodes on the two arms or on one arm
and one leg (standard leads).
3 - 4 mV, when ECGs recorded with one
electrode placed on the thorax directly over
the ventricles and a second electrode is
placed elsewhere on the body, remote from
the heart (precordial leads)
Monophasic AP 110 mV recorded
directly at the heart muscle membrane
during normal cardiac function, showing
rapid depolarization and then repolarization
ECG traces show the sum of all the electrical potentials
generated by all the cells of the heart at any moment
Tissue fluids conduct electricity…
heart
skin
Action Potentials in the Heart
AV
Purkinje
Ventricle
Aortic artery
Left atrium
Descending aortaInferior
vena cava
Ventricluar
Atrial muscle
Pulmonary
veins
Superior
vena cava
Pulmonary artery
Tricuspid valve
Mitral valve
Interventricular
septum
AV node
SA node
ECG
QTPR
0.12-0.2 s approx. 0.44 s
SA
Atria
Purkinje
fibers
muscle
Specialized
conducting
tissue
The different waveforms for each of the specialized cells found in the heart are shown. The latency shown approximates that normally found in the healthy heart.
Action Potentials in the Heart
Electrical conduction in the heart
The movement of charge/the spreading wave of electrical activity in the heart has
both a three-dimensional direction and a magnitude the signal measured on
an ECG is a vector.
Standard 12-lead ECG
ECG leads classification
- polarity
- bipolar: - 3 Bipolar Limb Leads I, II, III (Standard Leads): LI, LII, LIII
utilize a positive and a negative electrode between which electrical
potentials are measured.
- unipolar: - 6 Chest Leads (Precordial Leads): V1 V6
the positive recording electrode is placed on the anterior
surface of the chest directly over the heart, and the negative
electrode (indifferent electrode), is connected through equal
electrical resistances to the right arm, left arm, and left leg all
at the same time
- 3 Augmented Limb Leads (aVL, aVR, aVF)
two of the limbs are connected through electrical resistances
to the negative terminal of the electrocardiograph, and the
third limb is connected to the positive terminal.
- direction
-frontal plane – 6 limb leads: 3 standard bipolar leads, 3 augmented leads
-horizontal plane - 6 chest leads: precordial leads
The ECG recording from a single lead shows how that lead views the
time-dependent changes in voltage of the heart.
The projections of the lead
vectors of the 12-lead ECG
system in three orthogonal
planes when one assumes the
volume conductor to be spherical
homogeneous and the cardiac
source centrally located.
ECG Leads
Conventions / Rules, for recording and interpreting an ECG
Rules:
Left leg
II
+
Right arm Left arm+I-
III
-
standard bipolar limb leads I, II and III
Rules: standard bipolar & augmented unipolar limb leads
Einthoven triangle
I-
-+-
II III+ +
aV
F
Bipolar Standard Leads:
• Lead I - from the right arm to the left arm
• Lead II - from the right arm to the left leg
• Lead III - from the left arm to the left leg
Augmented Unipolar Limb Leads:
aVR lead - the positive terminal is on the right arm; inverted !
aVL lead - the positive terminal is on the left arm;
aVF lead - the positive terminal is on the left leg.
Each of the 6 frontal plane
leads has a negative '-’ and
positive '+' orientation.
Lead I (and to a lesser extent
Leads aVR and aVL) are right
left in orientation.
Lead aVF (and to a lesser
extent Leads II and III) are
superior inferior in
orientation.
Frontal plane leads - Einthoven's Triangle
Frontal Leads
0
-120
180
-60
120 60
+150
-30
+30
90
aV
F
Precordial / chest leads
in transverse plane (Wilson)
Unipolar Precordial Leads:
• V1 - 4th intercostal space to the right of sternum
• V2 - 4th intercostal space to the left of sternum
• V3 - halfway between V2 and V4
• V4 - 5th intercostal space in the left mid-clavicular line
• V5 - 5th intercostal space in the left anterior axillary line
• V6 - 5th intercostal space in the left mid axillary line
When the wave of depolarization moves toward the positive lead, there is a positive deflection in the extracellular voltage difference.
When a lead is perpendicular to
the wave of depolarization, the
measured deflection on that lead
is isoelectric.
When the wave of depolarization
moves away from the positive
electrode, a negative deflection is
recorded.
Two-cell model of the ECG demonstrates that the wave of depolarization
behaves like a vector, with both magnitude and direction
ECG - a direct measurement of the rate, rhythm, and time-dependent electrical
vector of the heart
- provides fundamental information about the origin and conduction of the
cardiac action potential within the heart.
The normal electrocardiogram
P
Q
R
S
T
Right Arm
Left Leg
QTPR
0.12-0.2s 0.35 - 0.44 s
Atrial muscledepolarization
Ventricular muscledepolarization
Ventricularmusclerepolarization
“Lead II”
• ECG normally, consists of 3 waves:
– P wave = Represents atrial depolarization
• Atria begin to contract about 0.1 sec after P wave begins
– QRS complex = Represents ventricular depolarization
• Why is it a larger signal than the P wave?
• Ventricular contraction shortly after the peak of the R wave
– T wave = Indicates ventricular repolarization
• Why do we not see a wave corresponding to atrial repolarization?
The normal electrocardiogram
Waves:
P wave – A depolarization
QRS complex– V depolarization
q or Q – first negative wave
R or r – first positive wave
s – second negative wave
R’ – if second positive wave
Segments: PR, ST, TP
Intervals: PR, QT, ST
Nomenclature and durations of ECG
The various waves of the ECG are named P, Q, R, S, T, and U:
• P wave: a small, usually positive, deflection before the QRS complex
• QRS complex: a group of waves that may include a Q wave, an R wave,
and an S wave; not every QRS complex consists of all three waves
• Q wave: the initial negative wave of the QRS complex
• R wave: the first positive wave of the QRS complex, or the single wave if the
entire complex is positive
• S wave: the negative wave following the R wave
• QS wave: the single wave if the entire complex is negative
• R’ wave: extra positive wave, if the entire complex contains more than two
or three deflections
• S’ wave: extra negative wave, if the entire complex contains more than two
or three deflections
• T wave: a deflection that occurs after the QRS complex and the following
isoelectric segment (i.e., the ST segment that we define later)
• U wave: a small deflection sometimes seen after the T wave (usually of same sign
as the T wave)
We use upper- and lower-case letters as an estimate of the amplitude of Q, R, and S
waves:
Capital letters Q, R, S are used for deflections of relatively large amplitude.
Lowercase letters q, r, s are used for deflections of relatively small amplitude. For
instance: an rS complex indicates a small R wave followed by a large S wave.
Nomenclature and durations of ECG
(from www.ecgwaves.com)
The various intervals are
PR interval: measured from the beginning of the P wave to the
beginning of the QRS complex; normal duration is 0.12 - 0.2 s (three to
five small boxes on the recording)
QRS interval: measured from the beginning to the end of the QRS
complex, as defined previously; normal duration is <0.12 s
QT interval: measured from the beginning of the QRS complex to the
end of the T wave; the QT interval is an index of the length of the overall
ventricular action potential; duration depends on heart rate because the
AP shortens with increased heart rate
RR interval: the interval between two consecutive QRS complexes;
duration is equal to the duration of the cardiac cycle
ST segment: from the end of QRS complex to the beginning of T wave
Nomenclature and durations of ECG
The two major components of the ECG are waves and segments.
Atrial
depolarization
Atrial contraction
Ventricular
depolarization
Ventricles contract
Ventricular
repolarization
Lead I
HR
HR
Conduction pathways through the heart.Spreading wave of depolarization.
Correlation between the ECG and the electrical events in the heart
Wave of repolarization (the ventricular myocytes
that depolarize last are
the first to repolarize)
Spreading wave of depolarization
Start of ECG Cycle
Different parts of the heart activate sequentially the time-dependent changes
in the electrical vector of the heart in different regions generate ECG waves.
Early P Wave
Dark red - depolarization
Later in P Wave
Dark red - depolarization
The P wave reflects the atrial depolarization.
Early QRS
Dark red - depolarization
Light blue - repolarization
Later in QRS
Dark red - depolarization
Light blue - repolarization
The QRS complex corresponds
to ventricular depolarization.
S-T Segment
Dark red - depolarization
Early T Wave
Dark red - depolarization
Light blue - repolarization
Later in T-Wave
Dark red - depolarization
Light blue - repolarization
T wave reflects ventricular
repolarization.
Back to where it started
Q
P
R
S
T
ECG paper has a grid of small 1-mm square
boxes and larger 5-mm square boxes.
The vertical axis is calibrated at 0.1 mV/mm;
the horizontal (time) axis, at 0.04 s/mm
(small box) or 0.2 s/5 mm (large box) five
large boxes correspond to 1.0 second.
Lead I
Lead II
aVR
ECG
The generation of the ECG signal in the Einthoven limb leads.
The generation of the ECG signal in the Einthoven limb leads.
Einthoven's triangle, illustrating
the voltmeter connections for
standard limb leads I, II, and III.
Magnitude and direction of the QRS
complexes in limb leads I, II, and III
when the mean electrical axis (Q) is
60 degrees (A), 120 degrees (B), and
0 degrees (C).
Leads and electrical vectors of the heart
• The inferior leads (leads II, III and aVF) show the electrical activity
from the inferior region (wall) of the heart - the apex of the left ventricle.
• The lateral leads (I, aVL, V5 and V6) look at the electrical activity
from the lateral wall of the heart.
• The anterior leads, V1 through V6, and represent the anterior wall
of the heart.
The lateral and anterior leads record events from the left wall and front
walls of the left ventricle, respectively.
aVR is rarely used for diagnostic information, but indicates if the ECG leads
were placed correctly on the patient.
The right ventricle has very little muscle mass it leaves only a small
imprint on the ECG, making it more difficult to diagnose changes in the right
ventricle.
Normal ECG
ECG Analysis
1. Check ECG calibration
2. Frequency (heart rate)
3. Rhythm of the heart: "normal sinus rhythm"
4. Electrical axis of the heart
5. Measurement of waves, segments, intervals
- the sizes of the voltage changes
- the duration and temporal relationships of the various components
6. Conduction analysis (PR interval, QRS duration, QT interval)
Analysis of Normal ECG
1. Check ECG calibration
2. Frequency (heart rate)
3. Rhythm of the heart: "normal sinus rhythm"
4. Electrical axis of the heart
5. Measurement of waves, segments, intervals
- the sizes of the voltage changes
- the duration and temporal relationships of the various components
6. Conduction analysis (PR interval, QRS duration, QT interval)
How to record an ECG? Calibration.• Put electrodes on the skin, on arms, legs and chest in order to record
in different leads (don’t forget the ground electrode)
• Standardization of the recording:
calibration lines on the recording paper:horizontal lines: 10 small divisions upward/downward =+/-1 mV vertical lines: 0.04 sec = 1 smaller interval
for a paper speed of 25 mm/sec
Calibration
Analysis of Normal ECG
1. Check ECG calibration
2. Frequency (heart rate)
3. Rhythm of the heart: "normal sinus rhythm"
4. Electrical axis of the heart
5. Measurement of waves, segments, intervals
- the sizes of the voltage changes
- the duration and temporal relationships of the various components
6. Conduction analysis (PR interval, QRS duration, QT interval)
Frequency/Heart rate (HR)
• HR – reciprocal of the time interval between 2 successive
heartbeats/QRS complexes
• If the normal interval between 2 successive QRS complexes
(RR interval) is 0.83 sec, then HR = 60/0.83=72 beats/min
• Normal HR ~ 60-100 beats/min
• Method of determination…
75 b/m
Frequency determination – Method 1
25mm/s
a) If 60s = 1500 div. of 0,04 s HR = 1500 div./ no. of div. for R-R
(1 s = 25 divisions (small squares) of 0.04 s for a recording at 25 mm/s )
R-R interval = duration of the cardiac cycle
b) 60 s / R-R (s) = 60 / 0.04 x no. of div. for R-R
Frequency determination – Method 2
0.04 s, for 25 mm/sec
R R
Measure the number of large boxes that form the R-R interval.
HR of 300, 150, 100, 75, 60, 50, corresponds to an interval of one, two, three, four,
five, or six large boxes.
Rate = 300/(number of large boxes)
Ex: four large boxes separate the R waves, the heart rate is 75 beats/min.
Analysis of Normal ECG
1. Check ECG calibration
2. Frequency (heart rate)
3. Rhythm of the heart: "normal sinus rhythm"
4. Electrical axis of the heart
5. Measurement of waves, segments, intervals
- the sizes of the voltage changes
- the duration and temporal relationships of the various components
6. Conduction analysis (PR interval, QRS duration, QT interval)
Heart Rhythm
• Normal Sinusal Rhythm (SR):
Impulses originate at S-A node at normal rate
all complexes normal, evenly spaced:
1. P wave (in Lead II: < 2.5 mm; < 0.11 sec)
2. P-R Interval ~ 0,12-0,21s
3. Frequency ~ 60-100 beats/min, regulated (var.<10%)
4. P wave electrical axis ~ 0º ÷ +75º (close to +45º ÷ +60º)
• Nodal rhythm: superior / middle / inferior part of AV node
• Ventricular rhythm: in A-V dissociation
Analysis of Normal ECG
1. Check ECG calibration
2. Frequency (heart rate)
3. Rhythm of the heart: "normal sinus rhythm"
4. Electrical axis of the heart
5. Measurement of waves, segments, intervals
- the sizes of the voltage changes
- the duration and temporal relationships of the various components
6. Conduction analysis (PR interval, QRS duration, QT interval)
Electrical axis of the heart
Electrical axis for a given electrical potential is
represented as a vector:
– vector = an arrow that points in the direction of the
electrical potential generated by the current flow, with
the arrowhead in the positive direction.
– by convention, the length of the arrow is drawn
proportional to the voltage of the potential
– the summated vector of the generated potential at
any particular instant is called instantaneous mean
vector
Electrical axis of the heart: QRS axis
• QRS electric axis (mean vector) denotes the average direction of the electric activity throughout ventricular activation:- the direction of the electric axis denote the instantaneous direction of the electric heart vector.
• The normal range of the electric axis lies between -30° and +90° in the frontal plane and between +30° and -30° in the transverse plane.
QRS axis
Left axis
deviation (LAD)
Right axis
deviation
(RAD)
Extreme
RAD
Normal
Small LAD
Small RAD
Important LAD
Extreme LAD
Extreme RAD
Electrical axis in the frontal plane
Definition, relation with anatomical axis, deviations
QRS Axis
The direction of the electric axis may be approximated from the
12-lead ECG by finding the lead in the frontal plane, where the QRS-
complex has largest positive deflection. The direction of the electric
axis is in the direction of this lead vector.
QRS Axis
- inspection method (qualitative) -
First find the isoelectric lead if there is one; i.e., the lead with equal forces in the positive and negative direction. Often this is the lead with the smallest QRS.
The QRS axis is perpendicular to that lead's orientation.
Since there are two perpendiculars (+ and -) to each isoelectric lead, chose the perpendicular that best fits the direction of the other ECG leads.
Occasionally each of the 6 frontal plane leads is small and/or isoelectric. The axis cannot be determined and is called indeterminate. This is a normal variant.
Qualitative inspection method.
When the wave is isoelectric (i.e., no deflection, or equal positive and negative
deflections), then the electrical vector responsible for that projection must be
perpendicular to the isoelectric lead.
Step 1:
Identify a lead in which the wave of interest is isoelectric (or nearly isoelectric).
The vector must be perpendicular (or nearly perpendicular) to that lead Because the
leads in the frontal plane define axes every 30 degrees, every lead has another lead
to which it is perpendicular.
Step 2:
Identify a lead in which the wave is largely positive.
The vector must lie roughly in the same direction as the orientation of that lead.
If the wave of interest is not isoelectric in any lead, then find two leads onto which the
projections are of similar magnitude and sign.
The vector has an axis halfway between those two leads.
Geometric method
Measurement of the magnitude of the wave projected onto at least two leads in
the frontal plane
Step 1: Measure the height of the wave on the ECG records in two leads (number of
boxes). A positive deflection is one that rises above the baseline, and a negative
deflection is one that falls below the baseline.
Step 2: Mark the height of the measured deflections on the corresponding lead lines on
a circle of axes. Starting at the center of the circle, mark a positive deflection toward the
arrowhead and a negative deflection toward the tail of the arrow.
Step 3: Draw lines perpendicular to the lead axes through each of your two marks.
Step 4: Connect the center of the circle of axes (tail of the vector) to the intersection of
the two perpendicular lines (head of the vector).
Step 5: Estimate the axis of the vector that corresponds to the R wave, using the
“angle” scale of the circle of axes
In a normal heart, the average direction of the vector
during spread of the depolarization wave through the
ventricles (mean QRS vector) is about +59 degrees.
Axis in the normal range
Lead aVF is the isoelectric lead.
The two perpendiculars to aVF are
0o and 180o.
Lead I is positive (i.e., oriented to
the left).
Therefore, the axis has to be 0o.
To determine how much of the voltage in vector A will be recorded in
lead I, a line perpendicular to the axis of lead I is drawn from the tip of
vector A to the lead I axis projected vector (B) along the lead I axis,
with the arrow toward the positive end of the lead I axis, which means
that the record momentarily being recorded in the electrocardiogram of
lead I is positive.
C – projected vector along the L II axis
D – projected vector along the L III axis
The ventricular vectors and QRS complexes: 0.01 second after onset of ventricular depolarization (A); 0.02
second after onset of depolarization (B); 0.035 second after onset of depolarization (C); 0.05 second after onset
of depolarization (D); and after depolarization of the ventricles is complete, 0.06 second after onset (E).
Einthoven’s law: If the three standard limb leads (I,II,III) are placed correctly, the sum of
the voltages in leads I and III equals the voltage in lead II
LI + LIII = LII
QRS axis in the horizontal plane
T wave – ventricles repolarization
T wave duration ~ 0.15 sec.; axis: +30 , +60 degrees)
T wave axis
QRS and T vectorcardiograms:
- vector increases and decreases in length because of increasing and
decreasing voltage of the vector.
- vector changes direction because of changes in the average direction of the
electrical potential from the heart.
P wave axis
P wave - depolarization of the atria
Spread of depolarization through the atrial muscle is much slower than in the
ventricles (atria have no Purkinje system for fast conduction of the depolarization
signal).
Repolarization begins in SA node atrial repolarization vector is backward to
the vector of depolarization, and it is almost always totally obscured by the
large ventricular QRS complex.
Analysis of Normal ECG
1. Check ECG calibration
2. Frequency (heart rate)
3. Rhythm of the heart: "normal sinus rhythm"
4. Electrical axis of the heart
5. Measurement of waves, segments, intervals
- the sizes of the voltage changes
- the duration and temporal relationships of the various components
6. Conduction analysis (PR interval, QRS duration, QT interval)
Waves: P, QRS, T, U
Segments – isoelectric lines on ECG:
no potentials are recorded when the ventricular muscle is either completely polarized or completely depolarized.
PQ(R), ST, TP
Intervals – segments + waves
PQ(R), ST, QT
ECG Measurement of waves, segments, intervals
ECG Measurement of waves, segments, intervals
P wave: atrial depolarization wave
- amplitude < 2.5 mm in lead II
- duration < 0.11 s in lead II (atrial depolarization duration)
- axis: between 0 – +75 (+45 and +60) degrees
-morphology: rounded, symmetrical, usually positive wave, except aVR
- abnormal P waves: right atrial hypertrophy, left atrial hypertrophy…
QRS
• Ventricular depolarization wave
• QRS duration ~ 0.06 - 0.10 s (how long it takes for the wave of
depolarization to spread throughout the ventricles)
• q <0.04s, <25% R, reflects normal septal activation in the
lateral leads (LI, aVL, V5, V6).
Intrinsecoid Deflection in precordial leads
– definition:
– up to 0,02 sec for V1,2
– up to 0,05 sec for V4-6
T wave: ventricular repolarization
- amplitude:
~ 1/3 R, but it is considered normal within the ¼ R – ½ R interval
- duration ~ 0.15 s
- axis: +30 ÷ +60 degrees
- morphology: rounded, asymmetrical wave.
Wave U
• Amplitude usually < 1/3 T wave amplitude in same lead
• direction - the same as T wave direction in the same lead
• more prominent at slow HR, best seen in the right precordial leads.
• origin of the U wave
- related to afterdepolarizations which interrupt or follow repolarization
- also possible due to delayed repolarization of papillary muscles
Analysis of Normal ECG
1. Check ECG calibration
2. Frequency (heart rate)
3. Rhythm of the heart: "normal sinus rhythm"
4. Electrical axis of the heart
5. Measurement of waves, segments, intervals
- the sizes of the voltage changes
- the duration and temporal relationships of the various components
6. Conduction analysis (PR interval, QRS duration, QT interval)
Conduction Analysis
"Normal" conduction implies normal sino-atrial (SA), atrio-
ventricular (AV), and intraventricular (IV) conduction:
• PR interval= 0.12 - 0.20 s (how long it takes the AP to
conduct through the AV node before activating the ventricles)
• QRS complex ~ 0.06 – 0.1 s
• QT segment - gets shorter as the heart rate increases, which reflects
the shorter AP that are observed at high rates.
• QT interval (how long the ventricles remain depolarized; rough measure
of the duration of the overall “ventricular” AP).
~ 45% RR
0.33 s ÷ 0.46 s
depends on HR
+90
+75
+50
+150
+90
+30
+15
0
-15
-45
-75
+120
-45
-40
Indeterminable!
Pathologic ECG
Vector analysis - Axis determination
Normal axis
Left axis deviation
Right axis deviation
Abnormal Voltages of the QRS complex
Increased voltage (att to electrode location)
Decreased voltage
Prolonged QRS
Cardiac rhythms – cardiac arrhythmias
TachycardiaBradycardiaSinus arrhythmia
Deviation of the electric axis
• to the right = increased electric activity in the RV due to increased RV mass (e.g. severe pulmonary hypertension).
• to the left = increased electric activity in the LV due to increased LV mass (e.g. hypertension, aortic stenosis, etc.).
Axis in the left axis deviation (LAD) range
Lead aVR is the smallest and
isoelectric lead.
The two perpendiculars are -
60o and +120o.
Leads II and III are mostly
negative (i.e., moving away
from the + left leg)
The axis, therefore, is -60o.
Axis deviation – left ventricle hypertrophy
Axis in the right axis deviation (RAD) range
Lead aVR is closest to being
isoelectric (slightly more
positive than negative)
The two perpendiculars are -
60o and +120o.
Lead I is mostly negative; lead
III is mostly positive.
Therefore the axis is close to
+120o. Because aVR is slightly
more positive, the axis is
slightly beyond +120o (i.e.,
closer to the positive right arm
for aVR).
Axis deviation – right ventricle hypertrophy
Pathologic ECG
Vector analysis - Axis determination
Normal axis
Left axis deviation
Right axis deviation
Abnormal Voltages of the QRS complex
Increased voltage (attention to electrode location)
Decreased voltage
Prolonged QRS
Cardiac rhythms
TachycardiaBradycardiaSinus arrhythmia
Abnormal Voltages of QRS
• Increases:
- If sum of the voltages of QRS [S-R] of the 3 standard leads
> 4 mV high voltage ECG
- ex. cardiac muscle hypertrophy
• Decreases:
- cardiac myopathies
- diminished muscle mass – ex. after myocardial infarctions
(delay of impulse conduction and reduced voltages)
-‘short-circuits’ of the heart electrical potentials through
pericardial fluid, pleural effusions
- pulmonary emphysema
Pathologic ECG
Vector analysis - Axis determination
Normal axis
Left axis deviation
Right axis deviation
Abnormal Voltages of the QRS complex
Increased voltage (att to electrode location)
Decreased voltage
Prolonged QRS
Cardiac rhythms
TachycardiaBradycardiaSinus arrhythmia
Cardiac Arrhythmias
Any change in cardiac rhythm from the normal sinus rhythm
is defined as an arrhythmia.
Can be normal/adaptive or pathological
Causes of the cardiac arrhythmias
1. Abnormal rhythmicity of the pacemaker
2. Shift of the pacemaker from the sinus node to another place in
the heart
3. Blocks at different points in the spread of the impulse through
the heart
4. Abnormal pathways of impulse transmission through the heart
5. Spontaneous generation of impulses in almost any part of the
heart
Abnormal Sinus Rhythms
• Sinus tachycardia (fast heart rate driven by the sinus node, in an adult
person >100 beats /min) is determined by increased body temperature (18
beats/°C, up to 40.5°C), stimulation of the heart by the sympathetic nerves (in
frightened or startled individuals, during normal exercise);
rarely, can be pathological – ex. in patients with acute hyperthyroidism
• Bradycardia (slow heart rate, def. as fewer than 60 beats/minute:
- in athletes; after vagal stimulation
• Sinus arrhythmia with respiratory cycle results from cyclic variations in the
sympathetic and parasympathetic tone, that influence the SA node
- results mainly from "spillover" of signals from the medullary respiratory center
into the adjacent vasomotor center during inspiratory and expiratory cycles of
respiration
alternate increase and decrease in the number of impulses transmitted
through the sympathetic and vagus nerves to the heart
increased HR during inspiration and decreased HR during expiration: 5% for
normal/quiet respiration, up to 30% for deep respiration.
- when loss, is a sign of autonomic system dysfunction, as in diabetes.
Conduction abnormalities are a major cause
of arrhythmias
-can occur at any point in the conduction pathway
-partial or complete.
-multiple causes
1) abnormal depolarization
2) abnormal anatomy.
1) If a tissue is injured (stretch, anoxia), an altered balance of ionic currents can lead to
a depolarization that partially inactivates INa and ICa, slowing the spread of current
slowing conduction
the tissue may become less excitable (partial conduction block)
or completely inexcitable (complete conduction block).
2) The presence of an aberrant conduction pathway, reflecting abnormal
anatomy - an accessory conduction pathway that rapidly transmits AP from the
atria to the ventricles, bypassing the AV node, which normally imposes a conduction
delay.
Patients with the common Wolff-Parkinson-White syndrome have a bypass pathway
called the bundle of Kent.
The existence of a second pathway between the atria and ventricles predisposes to
supraventricular arrhythmias.
Abnormal conduction – accessory pathways (Wolff-
Parkinson-White)
Kent pathway - NSA to the ventricle base
James pathways - NSA. to Hiss bundle
Mahaim pathway - Hiss b. to the ventricle base
Partial or Incomplete Conduction Block
1) slowed conduction
- the tissue conducts all the impulses, but more slowly than normal, unusually long PR
interval
2) intermittent block, in which the tissue conducts some impulses but not others.
First-degree AV block reflects a slowing of conduction through the AV node.
Second-degree AV block: incomplete (i.e., intermittent) coupling of the atria to the ventricles.
-2 types:
Mobitz type I block (or Wenckebach block), the PR interval gradually lengthens from one cycle
to the next until the AV node fails completely, skipping a ventricular depolarization; every third or
fourth atrial beat fail to conduct to the ventricles.
Mobitz type II block, the PR interval is constant from beat to beat, but every nth ventricular
depolarization is missing.
Rate-dependent block - bundle branches
- a form of intermittent conduction block, in the large branches of the His-Purkinje
fiber system.
When the heart rate exceeds a critical level, the ventricular conduction system
fails, presumably because a part of the conducting system lacks sufficient time to
repolarize the impulse is left to spread slowly and inefficiently through the
ventricles by conducting from one myocyte to the next the resulting contraction
loses some efficiency.
Such a failure, intermittent or continuous, is known as a bundle branch block
and appears on the ECG as an intermittently wide QRS complex.
3) unidirectional block
Partial or Incomplete Conduction Block
Right bundle branch
block is visible in the
V1 or V2 precordial
leads
Left bundle branch block
is visible in the V5 or V6
leads.
Bundle branch Blocks
Right Left
Complete Conduction Block or third degree AV block – medical emergency!
- complete block at the AV node stops any supraventricular electrical impulse from
triggering a ventricular contraction atria and ventricles beat under control of its
own pacemakers = AV dissociation.
The only ventricular pacemakers that are available to initiate cardiac contraction are
the Purkinje fiber cells (unreliable and slow.) fall of cardiac output and blood
pressure.
Treatment: placement of an artificial ventricular pacemaker.
On an ECG, complete block appears as regularly spaced P waves (SA node properly
triggers the atria) and as irregularly spaced QRS and T waves that have a low
frequency and no fixed relationship to the P waves
Unidirectional block
- a conduction defect that is essential for re-entry
- a type of partial conduction block: impulses travel in one direction but
not in the opposite one.
- may arise as a result of a local depolarization or may be due to
pathological changes in functional anatomy, as an asymmetric
anatomical lesion
Re-Entry- re-entrant excitation or circus movement, a major causes of clinical arrhythmias
It occurs when a wave of depolarization travels in an apparently endless circle.
Re-entry has three requirements:
(1) a closed conduction loop,
(2) a region of unidirectional block (at least briefly),
(3) a sufficiently slow conduction of action potentials around the loop.
Normal cardiac tissue can
conduct impulses in both
directions.
If this re-entrant movement (steps 2 → 5 → 2,
and so on) continues, the frequency of re-
entry will generally outpace the SA nodal
pacemaker (frequency of step 1) and is often
responsible for diverse tachyarrhythmias
because the fastest pacemaker sets the heart
rate.
Re-entry excitation may be responsible for
atrial and ventricular tachycardia, atrial
and ventricular fibrillation, and many other
arrhythmias.
Re-entry can occur in big loops or in small
loops consisting entirely of myocardial cells.
Accessory Conduction Pathways - Wolff-Parkinson-White (WPW) syndrome
- an accessory conduction pathway provides a short circuit (i.e., bundle of Kent)
around the delay in the AV node.
- the fast accessory pathway is composed of muscle cells.
- it conducts the AP directly from the atria to the ventricular septum, depolarizing
some of the septal muscle earlier than if the depolarization had reached it via the
normal, slower AV nodal pathway ventricular depolarization is more spread out in
time than is normal, giving rise to a wider QRS complex.
- the general direction of ventricular depolarization is reversed the events normally
underlying the Q wave of the QRS complex have an axis opposite to normal one
early depolarization / pre-excitation, appears as a small, positive delta wave at
the beginning of the QRS complex
WPW syndrome + re-entry supraventricular tachycardia
Paroxysmal supraventricular tachycardia (PSVT)- a regular tachycardia; ventricular rate usually exceeding 150 beats/min.
- because ventricular depolarization still occurs via the normal conducting pathways,
the QRS complex appears normal.
- if, during an episode of PSVT, the conduction direction for re-entry is in the reverse
direction (i.e., down the accessory pathway and back up through the AV node), the
QRS shape may be unusual wide and bizarre QRS complexes
- a small number of people with WPW syndrome have more than one accessory
pathway, so that multiple re-entry loops are possible
Fibrillation: many regions of re-entrant electrical activity are present electrical chaos
that is not associated with useful contraction.
Atrial fibrillation
- an wandering re-entry loop within the atria moves wildly and rapidly, generating a rapid
succession of APs (500 per minute) the fastest pacemaker in the heart, outpacing
the SA node and bombarding the AV node.
- AV node cannot repolarize fast enough to pass along all of these impulses irregular
appearance of QRS complexes without any detectable P waves, still the ventricular
rate can be quite high.
- the baseline between QRS may appear straight or show small, rapid fluctuations.
- atrial fibrillation is well tolerated as the atria function mainly as a booster pump.
- attempts to convert the rhythm back to normal sinus rhythm: electrical or chemical
means, or, when not possible, to slow conduction through the AV node:
-digitalis: increase PS and decrease S stimulation to the AV node, decreasing
the speed of AV conduction and thus reducing the ventricular rate.
-β-adrenergic blockers or Ca2+ channel blockers are also used to control
ventricular rate.
Ventricular fibrillation is a life-threatening medical emergency.
The heart cannot generate cardiac output because the ventricles are not able
to pump blood without a coordinated ventricular depolarization.
Depolarization-Dependent Triggered Activity
- a positive shift in the maximum diastolic potential brings Vm closer to the threshold for an AP
induce automaticity (otherwise with no pacemaker activity).
- depends on the interaction of the Ca2+ current (ICa) and the repolarizing K+ current (IK). an
accelerated pacemaker depolarization in the SA or AV nodal cells
- it can also increase the intrinsic pacemaker rate in Purkinje fiber cells, which normally have a very
slow pacemaker.
-is particularly dramatic in nonpacemaker tissues (e.g., ventricular muscle),
which normally exhibit no diastolic depolarization.
During the repolarization phase, INa remains inactivated because the
cell is so depolarized. On the other hand, Ica has had enough time to recover from inactivation and
because the cell is still depolarized, triggers a slow, positive
deflection in Vm known as an early afterdepolarization (EAD).
Eventually, IK increases and returns Vm toward the resting potential. Such EADs may trigger an
extrasystole.
Isolated ventricular extrasystoles (premature ventricular contractions -PVCs) may occur in normal
individuals.
Alterations in cellular Ca2+ metabolism may increase the tendency of a prolonged AP to produce
an extrasystole.
! Drugs used to treat arrhythmias can become arrhythmogenic by producing EADs (quinidine by
inhibiting Na+ channels and some K+ channels prolongs the ventricular muscle AP)
Altered automaticity can originate from the sinus node or from an ectopic locus
Altered automaticity can originate from the sinus node or from an ectopic locus
Abnormal automaticity in ventricular muscle.
The prolonged AP keeps INa inactivated but permits ICa and IK to interact and
thereby produce a spontaneous depolarization - the early afterdepolarization.
Altered automaticity can originate from the sinus node or from an ectopic locus
The afterdepolarization reaches threshold,
triggering a sequence of several slow pacemaker-
like APs that generate extrasystoles.
More than one extrasystole, a run of
extrasystoles, is pathological.
A run of three or more ventricular
extrasystoles is the minimal
requirement for diagnosis of
ventricular tachycardia (120-150
beats/min or faster).
This arrhythmia is life-threatening
(can degenerate into ventricular
fibrillation, the heart cannot
pump blood effectively).
Long QT Syndrome (LQTS)
- prolonged ventricular AP
- patients prone to ventricular arrhythmias, susceptible to a form of ventricular
tachycardia called torsades de pointes (“twisting of the points”) in which the QRS
complexes appear to spiral around the baseline, constantly changing their axes and
amplitude.
- can be
-congenital (mutations of cardiac Na+ or K+ channels.
-acquired (more common)
electrolyte disturbances, especially hypokalemia and hypocalcemia
prescribed or over-the-counter medications (antiarrhythmic drugs,
tricyclic antidepressants, some nonsedating antihistamines
when they are taken together with certain antibiotics,
notably erythromycin).
Ca2+ overload and metabolic changes can cause arrhythmias
Ca2+ Overload
Causes: digitalis intoxication; injury-related cellular depolarization.
When [Ca2+]i increases, causes the SR to sequester too much Ca2+ overloaded
SR begins to cyclically and spontaneously dump Ca2+ and then take it back up.
The Ca2+ release may be large enough to stimulate a Ca2+-activated nonselective
cation channel and the Na-Ca exchanger.
These current sources combine to produce Iti, a transient inward current that
produces a delayed afterdepolarization (DAD).
When it is large enough, Iti can depolarize the cell beyond threshold and produce a
spontaneous action potential.
Metabolism-Dependent Conduction Changes
During ischemia and anoxia fall in [ATP]i activates the ATP-sensitive K+ channel
(KATP), which is plentiful in cardiac myocytes.
When [ATP]i falls sufficiently, KATP is less inhibited, K+ goes out and the cells tend to
become less excitable.
The activation of this channel may explain, in part, the slowing or blocking of
conduction that may occur during ischemia or in the periinfarction period.
Electromechanical Dissociation
Rarely, patients being resuscitated from cardiac arrest exhibit electromechanical
dissociation in which the heart’s ECG activity is not accompanied by the pumping
of blood (absence of detectable pulse).
Causes frequently not understood, or known (ex. a large pericardial effusion may
manifest normal electrical activity, but the fluid between the heart and the
pericardium may press in on the heart (cardiac tamponade) and prevent effective
pumping).