CORONARY CARE 1

HCPT 2013
Session 1
ECG Interpretation made Incredibly
Easy 5th edition
chapters 1-4
1

Course Expectations
4 hours of pre-class learning
assignment
4 weeks of in class learning, 8 hour
days
There will be an assignment due at the
beginning of each class.
Week 5 will include an in class review
and then a comprehensive
examination.
You will have 3 hours to complete the
exam.

Course Objectives
The student will be able to;
Describe the normal cardiac anatomy and
physiology of the heart, including electrical, blood
flow and coronary perfusion.
Identify the waveforms of the cardiac cycle.
Identify different lead placements.
Utilize the 8 step ECG interpretation approach for
interpretation.
Identify normal and deviations of an ECG
Recognize sinus, atrial, junctional, atrioventricular
blocks and ventricular dysrhythmias.
Understand the significance of the dysrhthmia,
related symptoms and treatment
Recognize and troubleshoot pacemaker
malfunctions

Week 1

Anatomy and physiology of the heart

Coronary blood supply
Electrical system of the heart
The heart as a pump
Pulmonary and systemic circulation
Cardiac output, preload, afterload, contractility
and heart rate.
Autonomic nervous system
Renal regulation
Introduction to ECG rhythm analysis

The Cardiovascular System

The primary purpose of the cardiovascular
system is to supply an adequate amount of blood
to peripheral tissues to meet their metabolic
demands at all times.
The arterial system supplies tissues and organs
throughout the body with oxygen, nutrients,
hormones, and immunologic substances.
Through venous return it removes wastes from
tissues, routing deoxygenated blood through the
lungs for excretion of metabolic wastes.

ANATOMY AND PHYSIOLOGY

OF THE HEART

Aorta

Pulmonary Artery
Left Atrium

Superior Vena Cava

Mitral Valve

Pulmonary Valve

Aortic valve
Tricuspid valve
Left Ventricle
Right Atrium
Coronary Sinus
Inferior Vena Cava
Right Ventricle

3 SYSTEMS OF THE HEART

BLOOD SUPPLY
ELECTRICAL STIMULATION
MECHANICAL PUMP

BLOOD SUPPLY

ANTERIOR CORONARY
VESSELS
LEFT MAIN
CORONARY ARTERY
LEFT CIRCUMFLEX
LEFT ANTERIOR
DESCENDING
LEFT MARGINAL
DIAGONAL
ARTERIES
RIGHT CORONARY
ARTERY
RIGHT MARGINAL
ARTERY
THE BLOOD IS FED
TO THESE VESSELS
THROUGH THE
CORONARY OSTIUM
FROM THE AORTA

10

11

Coronary Arteries
Right Coronary Artery

supplies;
the right atrium, right
anterior wall and the posterior
and papillary muscles
Posterior septum
Electrical structures;Sinus and
AV nodes
The inferior wall of the left
ventricle

Left Circumflex Artery

Supplies;
the left atrium
Posterior wall of left ventricle
Posterior septum

Left Coronary Artery

Supplies:
Left anterior descending
(LAD)
Anterior left ventricle
Anterior interventricular
septum
Bundle of HIS
Left Bundle branches
Anterior left papillary muscle

12

ELECTRICAL STIMULATION

13

The Sino-Atrial Node is the

main pacemaker of the
heart.
It has an intrinsic rate of 60100 beats per minute.
The atrial conduction fibres
called the Bachmans Bundle
connect the right to the left
atrium so that they
depolarize simultaneously.

14

The Atrio-ventricular
Node lies at the bottom of
the Atria and sends the
conduction through to the
ventricles.
It has an intrinsic rate of
40-60 beats per minute.
The bundle of HIS is the
next structure.
It relays the conduction
to the right and left
bundle branch.

15

The next structure after the

bundle branches are the
Purkinji Fibres, they thread
through the Apex and outer
walls of the ventricles.
Any structure within the
ventricular conduction
system has an intrinsic rate
of 20-40

16

Electrical properties of cardiac cells

Cardiac cells are
unique from other
cells in the body.
They have the ability
to initiate, respond &
conduct an electrical
impulse.
The cardiac cell also
contracts after
receiving that
impulse.

17

Cardiac Cell Properties'

18

Automaticity
Automaticity is the ability to
spontaneously initiate and electrical
impulse
All cells in the heart have this ability
but the Pacemaker cells fire at a
higher rate and therefore set the pace
for the others.
SA node- 60-100
AV node- 40-60
Ventricles- 20-40

19

Excitability
Is the ability the cardiac cell has
to respond to an impulse
recieved.
The ions shift across the cell
membranes
Na+, K+, Ca++
It is important to maintain
electrolyte balance for cardiac
stability

20

Conductivity
The ability to conduct the impulse received
to the next cell. Relay the impulse

21

Contractility
Ability of the cell to contract after
receiving the impulse
this occurs after depolarization and
depends on the stretch of the muscle
fibers.

22

Ion transport
The cardiac cell has a semi
permeable membrane that
allows the exchange of ions
. This flow of ions in and
out of the cells is the key to
all four of the properties of
cardiac cells previously
discussed.
Automaticity
Excitability
Conductivity
Contractility

23

Ions
Potassium (K+) is a key intracellular ion.
Sodium (Na+) is a key extracellular ion.
The cell membrane becomes permeable to Na+ when it
receives an electrical impulse
Na+ moves into the cell and K+ moves out this causes
the inside of the cell to more positively charged.
The loss of the cells internal negative charge to a
positive charge is the phase of Depolarization.
Depolarization moves cell to cell through the heart
sending the impulse quickly in order to pump the
blood out of the ventricle at a rate of 60-100bpm.

The Cardiac Cycle

Depolarization

Polarized cells are at rest

there is no electrical activity
At rest the cell is negatively
charged inside of the cell
This is called the resting
potential
After a stimulus occurs the
ions cross the membranes
causing an action potential
(cell depolarization)

text p.14

Repolarization

The cell returns to its

state of rest after
depolarization
The ions reverse and
move out of the cell
leaving it negatively
charged once again
The action potential of
the cell has 5 phases

24

25

Action potential of the cardiac cell

26

ACTION POTENTIAL
Phase 0 (A) the cell receives the impulse and
depolarizes. Na+ influx
Phase 1 ( at the point) is early
repolarizatioin
Phase 2 (B) also called plateau phase and is
a slow repolarization
Phase 3 (C) is the rapid repolarization
phase, the cell returns to its original state
Phase 4(E) Is the resting phase and by the
end of the phase it can receive another
stimulus
Absolute refractory period is considered
phase 1,2 and the beginning of phase 3.
During this time the cell cannot be excited
no matter how strong the stimulus.

27

MECHANICAL PUMP

28

The Pump
It works as a pump by expanding and
contracting without placing added stress
on the cardiac muscle and without
developing muscle fatigue.
The heart pumps 4 to 8 liters per minute.
This is equivalent to 6,000 liters per day.
It has an inherent capability to generate
electrical impulses that maintain proper
rhythm regardless of other factors

29

THE EFFICIENT
PUMP
Bringing deoxygenated
blood back from the
circulation into the right
side of the heart.
Into the pulmonary system
for oxygenation.
Through the left side of the
heart and out to the body
and coronary sinus with
oxygenated blood.

30

STRUCTURES OF THE HEART

The heart consists of four hollow

chambers,
the upper chambers are called
atria, they have a thin muscular
wall.
The bottom 2 structures are the
ventricles.
The ventricular walls are thick and
muscular.
The left ventricle wall is
approximately 3 times thicker than
the right side.
The septum divides the right and
left sides of the heart .

31

CHAMBERS
The Atria
There are 2 atria, right and left
upper chambers of the heart.
they are divided by the intra-atrial
septum.
The atrial walls are muscular but
thin. Filling of the ventricle is mostly
passive (approximately 70%).
Atrial contraction or kick
contributes approximately 20-25%
of the volume inside the ventricle
prior to contraction.

32

The Ventricles
These 2 chambers are
much thicker and
stronger than the
atrium. The left
ventricle is 3 times
thicker. The chambers
are divided by the
intra-ventricular
septum.

33

CIRCULATION THROUGH THE HEART

The heart receives deoxygenated blood from the body
through the superior& inferior vena cava & the
coronary sinus into the right atrium.
It then passes through the tricuspid valve into the right
ventricle. The right ventricle contracts, sending the blood
into lungs through the pulmonic valve into the
pulmonary arteries to receive oxygen.
The left atrium then is filled with oxygenated blood from
the pulmonary veins which travels through the mitral
valve into the left ventricle.
The left ventricle contracts sending the oxygenated blood
through the aortic valve into the systemic circulation
and then at repolarization into the coronary ostium to
feed the heart circulation .

34

CIRCULATORY PATHWAY

35

36

37

CARDIAC OUTPUT

38

CARDIAC OUTPUT
Cardiac Output is the amount of blood pumped
into the aorta every minute
Normal volume is 4-8 liters/min

CO=HRxSV
Stroke Volume is the amount of blood ejected
by the ventricle with each contraction
Stroke volume is affected by PRELOAD AND
AFTERLOAD

39

THE PRESSURES
Preload is the force exerted on the ventricle at the end of
diastole (just before ejection). Also known as LVEDP (left
ventricle end diastolic pressure) It is influenced by the
volume of blood and the stretch of the ventricle. (Starlings
Law)

Afterload is the pressure that the ventricle is pushing

against. It is influenced by arterial BP and arterial
resistance, including embolus, valve stenosis, volume
overload, vasoconstriction.

40

STARLINGS LAW
states that the greater the
volume of blood entering the
heart during diastole (enddiastolic volume), the greater
the volume of blood ejected
during systolic contraction
(stroke volume).

www.wikipedia.org

41

FACTORS AFFECTING
CARDIAC OUTPUT

42

FACTORS AFFECTING PRELOAD

43

FACTORS AFFECTING AFTERLOAD

44

AUTONOMIC NERVOUS
SYSTEM
The Autonomic Nervous System is in
constant control of involuntary
bodily functions.
CARDIAC CONTROL
Heart rate and stroke volume
BLOOD PRESSURE
Regulating blood vessel tone

Autonomic Nervous System

Sympathetic or adrenergic

Stimulates cardiac activity

Increase HR
Increase CO
Increase BP
bronchodilation

Para sympathetic or
cholinergic or vagal

Depresses cardiac
activity
Slowing of the HR
Decreased CO
Decreased blood
pressure
Nausea & vomiting
Fainting
bronchoconstriction
45

46

BARORECEPTORS

PRESSURE RECEPTORS IN THE AORTIC ARCH

AND CAROTID SINUS DETECT CHANGES IN
BLOOD PRESSURE AND INCREASE OR DECREASE
THE STIMULATION OF THE PARASYMPATHETIC
RESPONSE
47

48

BARORECEPTORS

49

SYMPATHETIC OR STRESS
RESPONSE

ACTIVATED BY PHYSICAL OR EMOTIONAL STRESS

(exercise, fever, trauma, hypoxia, fear, pain)
CHEMORECEPTORS IN THE AORTIC ARCH AND
CAROTID SINUS DETECT SUBTLE CHANGES IN pH, O2,
Co2
RELEASE CHEMICALS TO ACTIVATE THE
SYMPATHETIC NERVOUS SYSTEM
50

51

STRESS RESPONSE

Renal Regulation
The role of the kidneys in cardiac
health

52

53

ADRENAL GLANDS
The Adrenal Gland sits on top of each
kidney.
The gland stores and releases
hormones to maintain fluid and
pressure balance in the body.
The Adrenal Gland consists of two
portions; the Adrenal Cortex and the
Adrenal Medulla.

54

ADRENAL CORTEX
The Adrenal Cortex responds directly to the
ACTH hormone released from the Pituitary
Gland.
Aldosterone is released from Adrenal
Cortex it acts on the renal tubules
promoting reabsorption of Na+ & Cl- and
excretion of K+
this helps to conserve the fluid volume in
the intravascular space.

55

RENIN-ANGIOTENSIN ALDOSTERONE
SYSTEM

The Adrenal Medulla responds directly to

impulses from the Sympathetic Nervous System.
It secretes Catecholamine hormones Epinephrine
and Norepinephrine.

ADRENAL MEDULLA

56

57

ADRENAL MEDULLA

Coronary Care 1
Session 1
ECG Interpretation
Arrhythmia Assessment and
Management

58

59

Wilhelm Einthoven 1903

Inventor of the EKG

60

TELEMETRY

Quick detection of cardiac changes

Assessment tool
Noting specifically:
Fast or slow rhythms
Premature or extra beats
Atrial/ ventricular relationship
Dysrhthmias
Lethal rhythms

61

The Electrocardiogram as an
Assessment tool
An essential part of the cardiac assessment
A recorded strip should be added to your
progress notes along with vital signs, respiratory
assessment and full general assessment.
Any changes from previous cardiac rhythm, rate
or ectopic beats should be noted.
Chest pain and activity tolerance are also
important observations

62

The ECG Monitor

3 lead placement:
Depolarization wave moving
toward a positive lead will be
upright.
Depolarization wave moving
toward a negative lead will
inverted.
Depolarization wave moving
between negative and positive
leads will have both upright
and inverted components.

63

Einthovens Triangle

64

The Five Lead Monitor

Five lead placement allows
viewing of all leads within the
limits of the monitor.
V1 lead is the best lead to view
ventricular activity and
differentiate between right
and left bundle branch
blocks.
V1 cannot be monitored in a 3 lead
system
White is right
Black is left
Red to the heart
Brown to the sternum
Green to right lower ribs

65

Lead II
Lead II is the same as
standard lead two on a
12 lead EKG.
It is the most common
monitoring lead.

For the purposes of the

this course we will be
using Lead II for our
rhythm interpretation.

66

ECG Recordings
EKG paper is a grid
where time is
measured along the
horizontal axis.
Each small square is
1 mm in length and
represents 0.04
seconds.
Each larger square is
5 mm in length and
represents 0.2
seconds.
The paper represents
25mm/sec

67

Determining Heart Rate

When the rhythm is regular, the
heart rate is 300 divided by the
number of large squares between
the QRS complexes.
For example, if there are 4
large squares between regular
QRS complexes, the heart rate
is 75 (300/4=75).
The second method can be used
with an irregular rhythm to
estimate the rate. Count the
number of R waves in a 6 second
strip and multiply by 10.
For example, if there are 7 R
waves in a 6 second strip, the
heart rate is 70 (7x10=70).

68

The Components of the ECG Complex

The isoelectric line
is the baseline on the
ECG recording where
electrical activity is
resting.
It becomes important
later on in
determining if there
has been ischemia or
damage to the cardiac
muscle

69

Components of an ECG
P wave
Indicates atrial depolarization,
or contraction of the atrium.
Normal duration is not longer
than 0.12 seconds (3 small
squares)
Amplitude (height) is no more
than 3 mm

70

ECG Components
QRS complex
Indicates ventricular
depolarization, or contraction
of the ventricles.
Normally not longer than .10
seconds in duration
In Lead ll, R waves are
deflected positively and the Q
and S waves are negative

71

ECG Components
T wave
Indicates ventricular
repolarization or resting state
Not more that 5 mm in
amplitude
Rounded and asymmetrical

72

ECG Components
ST segment
Indicates early ventricular
repolarization (first phase of
the resting state)
Normally not depressed more
than 0.5 mm
May be elevated slightly in
some leads (no more than 1
mm)

73

ECG Components
PR interval
Indicates AV
conduction time
Duration time is 0.12
to 0.20 seconds

74

QT interval

ECG Components

Measured from the Q to the end of the T.

Represents ventricular depolarization and
repolarization (sodium influx and potassium
efflux)

QT usually less than half the R-R interval

0.32-0.40 seconds when rate is 65-90/minute)
QT varies with rate.

Prolonged QT may be inherited or

acquired

(predisposes to long QT syndrome and torsades

de pointe)
Inherited - defective sodium or potassium
channels
Acquired - drugs, electrolyte imbalance or MI
Atleast, 50 drugs known to affect QT
(including: quinidine, amiodarone)

75

The Normal Measurements

P wave = or <0.01 sec
PR Interval = 0.12-0.20 sec
Q wave significant if 0.04 wide
and 1mm high
QRS complex = 0.08-0.12 sec
T wave = upright
QT interval = 0.36-0.44 is heart
rate dependant

76

Analyzing an ECG Rhythm Strip

5 STEP PROCESS

Regular or Irregular?
What is the Heart Rate?
P wave present and upright?
PR Interval
QRS related to P wave? Measurement?

77

STEP BY STEP

78

Normal Sinus Rhythm

Regular
Heart rate 80 bpm
P wave upright
PRI = 0.20
QRS = 0.06

79

WHY DO ABNORMAL RHYTHMS OCCUR?

Abnormal heart rhythms occur for several
reasons.
The vagal stimulation of the parasympathetic
nervous system can cause a decrease in the rate
at the SA node and can also decrease the
excitability of the AV junction fibers. This causes
a slowing of the heart rate, and in severe cases a
complete blockage of the impulse through the
AV junction.

80

SYMPATHETIC ALTERATIONS
Sympathetic stimulation also effects cardiac
rhythm and conduction. It increases the rate at
the SA node and increases the rate of conduction
and excitability throughout the heart. It also
increases the force of myocardial contraction.
Subsequently, the overall workload on the heart
is increased.

81

EXTRA BEATS
A small area of the heart can become more
excitable than normal, which causes abnormal
heart beats called ectopy. Ectopic foci are usually
caused by an irritable area in the heart. This
irritability can be caused by ischemia, stimulants
such as nicotine and caffeine, lack of sleep or
anxiety (Guyton, 1982).

82

WRONG PATHWAY
Aberrant conduction pathways can cause
arrhythmias by providing an alternate route for
the wave of depolarization.
Normally, atrial and ventricular tissues are
isolated by nonconductive fat and connective
tissue.
Aberrant pathways form a short circuit bridge
across the nonconductive tissue.
Hence, tissue can be depolarized prematurely or
out of sync.

83

CHANGES IN THE ACTION POTENTIAL

Inherited or acquired channelopathy can
predispose an individual to dangerous
arrhythmias, notably torsades de pointes.
Faulty ion channels may result in prolonged
repolarization, lengthening the QT interval.
The heart is most vulnerable during
repolarization. Channelopathies can be due to
"leaky" or slow closing sodium channels,
ineffective potassium channels or drugs and
toxins which can affect the transport of ions
across these channels.

84

ST segment changes
The ST segment represents the end of ventricular
conduction and the beginning of ventricular recovery or
repolarization.
The point the marks the end of the QRS complex and the
beginning of the ST segment is the
J point
The normal ST segment:
Is from the S wave to the beginning of the T wave
Should be on the baseline (isoelectric) or -0.5-1.0mm
Any change may indicate a myocardial injury or ischemia

85

ST segment changes
ST segment depression- -0.5mm below the
baseline, may indicate myocardial ischemia or
digoxin toxicity
ST segment elevation- 1mm or more above the
baseline may indicate myocardial injury

86

The T wave abnormalities

The T waves peak represents the relative
refractory period of benricular repolarization
The cells are at the peak of vulnerability to extra
stimuli (relative refractory period)
Bumps on T wave may indicate a P wave hidden
Tall, peaked or tented T waves may indicate
myocardial injury or electrolyte imbalances such
as hyperkalemia
Inverted T waves may indicate myocardial
ischemia

87

The U wave
Is not normally seen on a rhythm strip
It is a small symmetrical wave following the T
wave
If it is pronounced it may indicate digoxin
toxicity, hypokalemia or hypercalcemia

88

89

SINUS BRADYCARDIA

Rate

<59 bpm

P wave

sinus

QRS

normal (.06-.12)

Conduction

P-R normal or slightly prolonged at

slower rates

Rhythm

regular or slightly irregular

90

SINUS BRADYCARDIA
This rhythm is often seen as a normal variation in
athletes, during sleep, or in response to a vagal
maneuver. If the bradycardia becomes slower than
the SA node pacemaker, a junctional rhythm may
occur.
Treatment includes:
treat the underlying cause,
atropine,
artificial pacing if patient is hemodynamically
compromised.

91

SINUS TACHYCARDIA

Rate

101-160/min

P wave

sinus

QRS

normal

Conduction

normal

Rhythm

regular or slightly irregular

92

SINUS TACHYCARDIA
The clinical significance of this dysrhythmia depends
on the underlying cause. It may be normal.
Underlying causes include:
increased circulating catecholamines
CHF
hypoxia
PE
increased temperature
stress
PAIN
Treatment includes identification of the underlying
cause and correction.

93

SINUS ARRHYTHMIA

Rate

45-100/bpm
Within normal limits

P wave

sinus

QRS

normal

Rhythm

regularly irregular

Conduction

normal

94

SINUS ARRHYTHMIA
The rate usually increases with inspiration and
decreases with expiration.
This rhythm is most commonly seen with
breathing due to fluctuations in parasympathetic
vagal tone. During inspiration stretch receptors
in the lungs stimulate the cardioinhibitory
centers in the medulla via fibers in the vagus
nerve.
The non respiratory form is present in diseased
hearts and sometimes with an increase in ICP
Treatment is not usually required unless
symptomatic bradycardia is present.

95

SINUS ARREST/PAUSE

Rate

normal

P wave

those that are present are normal

QRS

normal

Conduction

normal

Rhythm

The basic rhythm is regular. The length

of the pause is not a multiple of the
sinus interval.

96

SINUS ARREST/PAUSE
This may occur in individuals with healthy
hearts. It may also occur with increased vagal
tone, myocarditis, MI, and digitalis toxicity.
If the pause is prolonged, escape beats may
occur.
The treatment of this dysrhythmia depends on
the underlying cause.
If the cause is due to increased vagal tone and
the patient is symptomatic, atropine may be
indicated.
the pause is an unknown length and not a P-P
distance

97

SINOATRIAL BLOCK

Rate

normal or bradycardia

P wave

those present are normal

QRS

normal

Conduction

normal

Rhythm

basic rhythm is regular*.

98

Sinoatrial Exit block

This results from the sinus node initiating an
impulse that is blocked from conducting through
the atria
The block is an indefinite period of time but
ends with a sinus rhythm complex
The pause will be a multiple of the P-P interval
Meaning that exact complexes are missing

99

Sick Sinus Syndrome (tachy/brady)

Malfunctioning sinus node. Several arrhythmias can result from this:
Sinus Bradycardia in the absence of medication
Sinus Arrest or sinoexit block
Brady-tachycardia syndrome (can include Atrialfibrillation, Atrial flutter)

100

Sick Sinus Syndrome

Disturbance in the way the SA node generates
impulses and the way that they are conducted
Also refered as brady-tachy syndrome
The condition is progressive and chronic
Irregular rhythm with sinus pauses

Lets Practice
In-class hand out for
Sinus Arrhythmias

101

102

REFERENCES
WWW.fotofolio.com
www.heart-vessel.com
www.wikipedia.org
www.rnceus.com
Husczar, Robert J,Basic Dysrhythmias, Mosby,
Newyork,2002.
Wolters Klumwer, ECG Interpretation Made
Incredibly Easy, Lippincott Williams & Williams,
Philadelphia, 2008.