CARDIOVASCULAR PHYSIOLOGY Electrocardiogram … 2 and 3...Electrodes are connected to (+)/(–) side...

CARDIOVASCULAR PHYSIOLOGY

Electrocardiogram (ECG)

Part 1 and 2

Dr. Ana-Maria Zagrean


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.


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

http://butler.cc.tut.fi/~malmivuo/bem/bembook/06/06x/conducti/0607a.htm

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

http://butler.cc.tut.fi/~malmivuo/bem/bembook/15/15x/1508x.htm

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

http://butler.cc.tut.fi/~malmivuo/bem/bembook/15/15x/1504x.htm

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.


(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


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


The P wave reflects the atrial depolarization.

Early QRS


Light blue - repolarization

Later in QRS



The QRS complex corresponds

to ventricular depolarization.

S-T Segment


Early T Wave



Later in T-Wave



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









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










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.










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










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.










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










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


Normal axis

Left axis deviation



Increased voltage (attention to electrode location)

Decreased voltage

Prolonged QRS

Cardiac rhythms


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


Normal axis

Left axis deviation



Increased voltage (att to electrode location)

Decreased voltage

Prolonged QRS

Cardiac rhythms


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


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.


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).

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