cvs lecture 02

7/27/2019 CVS lecture 02

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Dr CO LarsonDr CO Larson

20122012

Electrical activity of the heartElectrical activity of the heart

Diagrams: ADAM: Thomas Nosek 2000;

Martini and Nath:Anatomy and Physiology. 2009

MIS264MIS264Learning outcomes

I. Clinical importance ofECG.

II. Features (elements) of normal electrocardiogram and their relationship to electrical

events in heart.

Assessment criteria:

1. Cardiac electrical conduction system.

2. Functions of components of cardiac electrical conduction system.

3. Differences inaction potential between slow and fast fibres.

4. Influence of autonomic nervous system on heart.

5. Terms "electrocardiogram" and "electrocardiograph".

6. Annotated diagram ofa normal lead ECG.

7. Features of normal electrocardiogram and their relationship to electrical events in

heart, with the normal time parameters.

8. Calculate electricalaxis ofheart.

9. Main elements of ECGinterpretation.

10.Terms "lead" and "axis of a lead".

11.12 different ECG leads: 6 precordial (chest)/unipolar leads and 6 frontal/bipolar

leads(3 standard and 3 augmented leads)

Heart: mechanical pump

under electrical control,

that requires adequate

blood supply itself.

CVS function: transport (gases, hormones, nutrients, wastes).

Cardiovascular disorders: leading cause of morbidity and

mortality in developed world.

I. ECG: clinical importanceI. ECG: clinical importance

Assists in diagnosis (and follow-up evaluation) of:

1. Abnormal cardiac excitation2. Arrhythmias

3. Conduction defects

4. Myocardial damage (e.g. due to myocardialischaemia or necrosis)

5. Cardiac enlargement

Clinical disorders where an ECGmay be of diagnostic value:

1.Acute chest pain at rest

Acute coronary syndrome:

ECGwith up- or downward ST deflection

ECGwith T wave inversion

Normal ECG

2. Heart palpitations Ectopic beats (supra-ventricular/ventricular)

Tachycardia

Atrial fibrillation

3. Extreme tiredness or syncope

Heart block: first, second or third degree; bundle branch block

4. Cardiovascular collapse

Asystole (cardiac arrest)

Ventricular fibrillation


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1 and 2: Cardiac electrical conduction

system and functions of components

After stimulation sudden increase in

membrane permeability (depolarization)

positive ions, mainly sodium enter the cell

depolarized tissue with a relatively negative

external field next to polarized muscle. A

potential difference now exists between theareas.

An electrical current is created that flows from

the positive to the negatively charged fibre.

The dynamic boundary between the polarized

and depolarized muscle moves along the fibre

from the point of excitation.

Inherently excitable tissue: cellmembranes semi-permeable to ions.Contractile cells are polarized duringcardiac diastole. (Anions andcations on opposite sides of themembrane and an electrodeimmersed in this polarized volumeconductor will register a flat or iso-electric line)

Certain

specialized

cardiomyocytes

("pacemakers")

can initiate

impulses.

Others conduct

impulses.AV

node

Posterior wall of RAbelow opening of SVC

Spread of depolarization

Begins in SA node P wave

(upright in II; inverted in aVR)

AV node (delay)

His bundle

Septum

Ventricles (QRS complex)

SA node overdrive suppresses all

foci:

Atrial foci (inherent rate: 60-80/min)

Junctional foci (inherent rate: 40-

60/min)

Ventricular foci (inherent rate: 20-

40/min)


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AV junction: part or all of

region comprising

atrioventricular node and

bundle of His (excluding

bundle branches).

Contains potential automaticity

foci.

Conduction

slows down in

AV node, but

accelerates

again through

His bundle andPurkinje system

What are the

functions of the

other

components?

3. Slow and fast fibres: differences in

action potential

Distinction: slope of depolarization phase

Ordinary (fast type) myocytes (like myocytes elsewhere in body):

resting voltage potential difference across plasmalemma is

approximately -90 mV. Include parts of conducting tissues. At

rest very few sodium ion channels are open, although many

potassium ion channels are open. The few open sodium ion

channels allow a slow leak of sodium, but sodium potassium

ATPase pump counteracts this, so that resting membrane potential

is stable.

Fast fibres: absolute and relative refractory

periods


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Slow fibres (in SA and AV nodes): resting membrane

potential is -50 to -60 mV. Intrinsic rate of impulse

generation of SA node ("primary pacemaker") is

approximately 60/min compared to that of AV node

("secondary pacemaker"): 25 to 55 /min

4. Influence of ANS on heart

Sympathetic stimulation makes slope of

depolarization phase steeper (mainly due to an

increase in sodium ion influx in slow fibres)

Parasympathetic nervous stimulation makes slope of

depolarization more gradual in slow fibres, by mainly

increasing potassium ion efflux.

LeadsDr Willem

Einthoven assigned

certain polarities to

the attachments of

three leads, which

form the sides of anequilateral triangle.

Most ECG

information is

provided by these

three standard limb

leads.


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Chest (precordial)

leads mainly

provide

information

regardinglocalization of

cardiac

abnormalities (e.g.

ischaemia, necrosis

or calcification).

The frontal plane leads (I, II, and III and aVF,

aVR and aVL) register the magnitude,

direction and duration of voltage changes in a

frontal plane.

Horizontal plane leads (V1 to V6)

Electrical wave spreads throughseptum from left to right.Then from right to left through LVand simultaneously through rightventricle from left to right.Repolarization (T wave:asymmetric; is normally inverted inIII, aVR and V1)

5. Terms "electrocardiogram" and

"electrocardiograph".

Electrocardiogram:

standardized two

dimensional

representation of

vectors, that differs

from lead to lead due

to orientation

(perspective) of leads.

Electrocardiograph

Volt- / galvanometer

(electrical apparatus)

that registers

electrocardiograms

Electrocardiogram

Graphic registration of electrical potentials

generated by heart.

Registers immediate differences in electricalpotential between electrodes.

Represents a complex spatial summation of

electrical potentials from many myocardial

cells that are conducted from surface of heart.


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Electrocardiograph:

galvanometer/electromagnet that detects thechanging potential of the electrical field aroundthe heart.

Has positive and negative poles to whichelectrodes are connected.The two electrodes constitute a lead which isplaced in any three dimensional relationship tothe heart.The lead detects changes in electrical potentialbetween the electrodes.

Net electromagnetic force directed toward

positive electrode of a lead: ECG records a

positive deflection.

A negative deflection recorded when the net

force is deflected away from positive pole.

Electromagnetic force is a vector, i.e. has

magnitude and direction.

6, 7 and 9: normal electrocardiogram: features

and their relationship to electrical events in heart,

with normal time parameters.

The electrocardiogram (ECG)The electrocardiogram (ECG)

Martini andMartini and NathNath

FigureFigure 202014b14b

ECG characteristic

P wave

QRS complex

T wave

P-R (P-Q) interval (PR because

Q wave may be absent)

R-R interval

Q-T interval

ST segment

U wave

Electrical activity

Atrial depolarization

Ventricular depolarization

Late ventricular repolarization

AV conduction time

Time between successive QRS

complexes (cardiac cycle length)

Ventricular depolarization and

repolarization

Plateau phase (Phase 2 of action

potential)

Repolarization of ventricular

papillary muscle

8. Calculate cardiac (mean ventricular)

electrical axis

(Guyton pages 134-135)


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Determination of mean ventricular electrical

axis

The dominant direction of the sum of all the

instantaneous QRS vectorsNormal: 0 to +90 (must establish cause if it

lies outside these boundaries)

Left and right deviation

Left deviation: endomorphs, obesity and

ascites

9. ECG interpretation: main elements

Rhythm and rate

PR interval

P wave abnormalities

Rhythm abnormalities

QRS complex

Duration

Mean QRS vector (mean electrical axis)

Abnormalities

ST segment and T wave

J point

Abnormalities

QT interval

ECG standardization

ECG paper: each small block = 0,04 seconds

2 vertical big blocks = 10 mm = 1 mV

Determination of heart rate

300 divided by the number of large blocks

between 2 QRS complexes

Sinus rhythm: criteria

Sinus rhythm

1. P wave before every QRS complex and everyQRS complex preceded by a P wave and they arerelated

P waves must be upright in I, II and aVF; if theyare absent or abnormal: supra-ventriculararrhythmiaSome books: upright P waves in I and aVF or Iand II3. Normal and constant PR interval (regardingtime)4. Rate constant between 60 and 100 beats

Criteria: P waves constant and upright in leads I, II and AVF

Each P wave followed by a QRS complex and each QRS

complex preceded by a P wave.

Normal, constant PR interval

Regular rate between 60 (50 in fit persons) and 100 beats/min


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10. Terms "lead" and "axis of a lead" 11. 12 ECG leads:

6 precordial (chest) /unipolar leads (registerelectrical potential differences in horizontal

plane)

6 frontal leads (3 standard bipolar and 3augmented unipolar leads that register potentialdifferences in frontal plane)

(Refer to Guyton and ECG practical notes)

MIS264 Session 3MIS264 Session 3

Diagrams: ADAM: Thomas Nosek 2000;

Martini and Nath:Anatomy and Physiology.

2009

Learning outcomes:

1. Terms "sinus arrhythmia, "extrasystole" ,"ventricular escape" ,"current ofinjury" and"re-entry phenomenon" anda fewcommoncauses thereof.

2. Mechanisms by whichcommon cardiacarrythmias occur.

3. ECGchanges dueto sinus tachycardia, sinus bradycardia, a sino-atrial block;atrial, AV nodal, AV bundle, and ventricular premature beats, atrio-ventricularconduction blocks, acute and chronic myocardial ischaemia and myocardialinfarction, atrial flutter and atrial fibrillation, ventricular tachycardia andventricular fibrillation, a cardiac arrest.

4. Physiological factors and/ or medicaldisordersthatinfluence :

duration (length) of PR interval

height (voltage) of QRS complexes.

duration (length) of QRS complexes

shape(conformation/configuration)of QRS complexes

cardiac rate

cardiac rhythm

size andconfiguration of T wave

positionof J point andST segment

directionof mean ventricular axis

5. Causes of atrial fibrillation or flutter, ventricular fibrillation and cardiacarrest.

1. Terms "Sinus arrhythmia"

= misnomer

Inspiration: increase in heart rate Expiration: decrease in heart rate

Postulated mechanisms: circulatorymechanisms that alter strengths of sympatheticand parasympathetic nerve signals to sinusnode e.g. respiratory type (see Guyton andHall)


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"Extrasystole"

Premature contraction / beat or ectopic beat

Most premature contractions caused by ectopicfoci

Common causes of ectopic foci: ischaemia,

calcified plaques, toxins (drugs, nicotine,

caffeine)

"Ventricular escape"

Response of an atrial, junctional (AV junction) orventricular automaticity focus to a pause inpacemaker activity.

Automaticity focus escapes overdrive suppressiontransiently to cause one beat or for long periods tocause an escape rhythm.

If SA node pacing stops, automaticity focusescapes to pace at its intrinsic rate, causing anescape rhythm.

"Current of injury" (Guyton and Hall p. 138)

Part of heart remains partially or totally

depolarized) all the time (because potassium ion

channels most susceptible to ischaemic injury)

so that current flows between pathologically

depolarized and normally polarized areas, even

between heart beats

Common causes: trauma, infections, coronary

ischaemia

"Re-entry phenomenon" and predisposingconditions (Guyton and Hall page 149)

Prerequisites:

Central inexcitable region around which re-entrantimpulse can circulate

Impulse delayed at one point so that tissues infront of impulse can recover fromrefractoriness

A zone ofunidirectional block: conduction stillpossible in another direction


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2. Mechanisms by which common cardiac

arrythmias occur.

ArrhythmiasArrhythmias

Abnormal impulse formation

(abnormal automaticity) and/or

conduction (re-entry)

All parts of conduction system:

spontaneous phase 4 depolarization,

therefore are latent pacemakers

Impulse conduction disorders include:

Three degrees of AV conduction block

WPW syndrome

Some arrhythmias can occur due to

abnormal impulse formation or

conduction

Sino-atrial node paces heart at highest frequency

(60/70 -80 beats/min) therefore it causes overdrive

suppression of pacemaking by AV node (40/50-60

beats/min) or Purkinje fibres (20/30 to 40 beats/min).

Ischaemia, hypokalaemia, fibre stretch or local

catecholamine release can increase automaticity in

these latent pacemakers, which can override SA nodal

pacemaking.

If their membrane potential is sufficiently depolarized

(e.g. due to ischaemia), atrial and ventricular muscle

cells can initiate impulses.

Atrial or junctional foci become irritable due to

Adrenaline released by adrenal medullae

Increased sympathetic nervous stimulation

Caffeine, amphetamines, cocaine or other beta 1

adrenergic receptor stimulants Excess digitalis, some toxins, occasionally ethanol

Hyperthyroidism

Stretch

Hypoxia

(Source: Dale Dubin:Rapid Interpretation of EKG's, 2000 page123)


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Triggered automaticityTriggered automaticity

Caused by afterdepolarizations which occur during

repolarization (early afterdepolarizations) or afterrepolarization (delayed afterdepolarizations).

Potentials that reach threshold initiate premature action

potentials and heart beats.

Afterdepolarization magnitude is influenced by changes

in heart rate, catecholamines and decrease in

parasympathetic input.

Early afterdepolarizations

During terminal plateau or repolarization phase

Purkinje fibres most susceptible

Predisposing factors

Agents that prolong action potential and

increase inward sodium ion movement or block

potassium ion outflow.

HypokalaemiaBradycardia

Delayed afterdepolarizations

Caused by excessive increase in [Ca++] in

myocytes e.g. digitalis toxicity or

catecholamines that increase Ca++ influx

through L-type Ca++ channels.

Abnormal impulse conduction (re-entry)

An impulse delayed in one region re-excites adjacent

areas more than once.

Prerequisites:

1. Central (anatomical/functional) inexcitable region

around which re-entrant impulse can circulate

2. Impulse delayed at one point so that tissues in

front of impulse can recover from refractoriness

3. A zone of unidirectional block: conduction still

possible in another direction

Slowed conduction

Slope of phase 0 depolarization more gradual


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Important abnormal ECG patterns that you mustrecognize:

Four main types of atrial tachycardia:

sinus tachycardia, PAT

atrial flutter, atrial fibrillation

Sinus bradycardia

Ventricular tachycardia

Ventricular fibrillation

Premature cardiac beats - atrial, nodal and ventricular

Conduction blocks: Atrioventricular (three degrees)

Intraventricular LBBB en RBBB

Fascicular block

Myocardial ischaemia and -infarct

Tachycardia

I. 4 main types of atrial tachycardia

1. Sinus tachycardia (due to sympathetic

nervous stimulation)

2. Paroxysmal atrial tachycardia

(Cause: an ectopic atrial pacemaker due to inter

alia caffeine, nicotine, excessive alcohol)

Treatment: carotid sinus massage ( Vagal tone) Sinus tachycardia

Absent or inverted P waves, because

atria activated in an abnormal way,

usually due to an atrial ectopic

pacemaker

3. Atrial flutter

(Cause: single re-entry/ectopic focus in atrium

(usually R.A): usually regular pulse rate

4. Atrial fibrillation

(Cause: multiple atrial re-entry circuits/ectopic

foci usually in L.A.). Often triggered by mitral

stenosis, hyperthyroidism or IHD.

Irregular pulse rate, -rhythm or force

Prolonged atrial fibrillation HF and atrial

thrombosis with pulmonary/systemic emboli


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Normal SA nodal impulses reach AV node while

it is refractory after it is depolarized by the

premature impulse from the ventricle.

Long compensatory pause, because normalimpulse is not conducted to the ventricles.

Cause: especially IHD, which increases the

excitability of the conduction system and

myocardium.A single random ectopic ventricular

pacemaker

Conduction block

Sites:

1. Rare: SA node (= sick sinus syndrome)

Loses one entire cardiac beats. Heart starts to

pump again after an interval of less than two

complete cardiac cycles

2. AV node/ His bundle: three degrees

3. R/LBBB: prolonged QRS time (see later in

course: semester five)

Prolonged, but constant PR interval,

usually due to myocardial ischaemia

or drugs.

Mobitz type II block: PR interval

lengthened but of equal length and some

QRS complexes missing


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cvs lecture 02

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