TUTOR’S GUIDE

CARDIOVASCULAR SYSTEM

CASE 2
Arrhythmias

Faculty of Medicine
Universitas Padjadjaran
Bandung
2014 - 2015
Year Academic : 2014-2015
Semester :5
System : Cardiovascular
Week theme (B.3) : Cardiac conduction
Trigger case (B.5) : arrhythmias : SVT, VT, VF, AF (SKDI competency level
3B)
Differential diagnoses (B.6): -
Differential causes of palpitations : Cardiac, thyroid disease, drugs, anxiety

Specific learning objectives from each Department related to the theme (A.3):
At the end of the week the student should be able to :
1. Explain about conducting system of the heart (C3)
2. Explain about the innervation of the heart (C3)
3. Explain about histology of conducting system of the heart (C3)
4. Explain the cardiac conduction system and relate it to mechanical functioning of the
heart, cardiac action potential, fast and slow responses (C3)
● explain the mechanism of rhythmical excitation of the heart
● explain the specialized excitatory and conductive system of the heart
● explain the control of excitation and conduction in the heart.
● Sketch the normal ECG Characteristic of the normal Electro Cardio Grams.
● explain the method for recording electrocardiograms.
● explain the electrocardiographic leads.
5. Drug used in arrhytmia (amiodaron, digoksin, disopiramid, epinephrine, lidocain,
propanolol, verapamil) :
● Concept of mechanism of Action of certain drugs (amiodaron, digoksin,
disopiramid, epinephrinee (resucitation), lidokain, propanolol,
verapamil(supraventricular arrhytmia))
● Adverse Effect of amiodaron (bradycardia, heart block), digoxin(severe
arrhytmias), disopiramid (urinary retention), epinephrinee, lidokain (neurologic
syndrome), propanolol (asthma, AV blockade, acute heart failure), verapamil
(constipation);
● Contraindication disopiramid (Heart failure)
● Good prescription for drugs used in cardiovascular diseases (C3)
6. Explain all about arrhythmias (tachyarrythmias : SVT, VT, VF and AF.
Bradyarrithmias/heart block) : the definition, pathogenesis, pathophysiology,
diagnosis and treatment (C2)
7. Formulate research problems of the case. (How to build a good research
background)
8. Evaluate the issue of losing rights due to health
Concept map

Sequence and Pacing

Three meetings
First meeting : Page 1 – Page 4
Second meeting : Discussion and Epilogue
Third meeting : Discussion

Scenario and Student’s case

PAGE 1

Ms. Agnes, 21-year-old female was admitted to the emergency room of Dr. Hasan
Sadikin Hospital with palpitation. Two days ago she got diarrhea. This was her fourth
time admission to this hospital for palpitation.

The palpitation started 3 hours before admission, which was felt as rapid and regular of
heart beats.

She was hospitalized two months ago, due to palpitation with documented ECG
abnormality. She was discharged a day after and was told that she had heart beat
disturbance. The doctor gave her medicine. He urged her to take the medication
regularly but for the last week she never consumed it because she felt better. She
often felt palpitation but recovered to normal immediately before seeing any doctor.

She once applied to get a driver’s license but the authority declined her application
because of her condition.

Question:
1. Generate the problems and list the hypothesis of this patient!
2. What further information do you need?
3. What is your opinion of the declining of driver’s license application?
4. Does patients with heart disease history entitled to have driver’s license? Would you
give recommendation for such patient to have a driver’s license?
5. Discuss this issue through the perspective of ethical and professional values: Non
maleficent versus Non discrimination

PAGE 2
 The physical examination:
● Showed a fatigue patient.
● The BP was 100/60 mmHg. The pulse was regular, equal, with a rate of 164 BPM.
● The respiration rate was 28 x/min.
● The temperature was 36.70C.
● HEENT was normal without bruit at carotid.
● The heart was normal, S1 and S2 normal and no visible cardiac murmur. The heart
beat was regular with a rate of 164 BPM.
● No rales were heard.
● Abdomen was normal.
● Extremities were normal.

Laboratory examination was performed, which revealed normal CBC, RBS, liver
function normal, but ureum 130 mg/dl and creatinin 2.2 mg/dl. The electrolytes showed
sodium concentration of 130 mEq/L and potassium concentration of 2.5 mEq/L.

The chest X-Ray showed normal.

The rhythm on the ECG showed an SVT
The echocardiography normal

Questions
1. What is the patient’s problem?
2. Do you change your hypothesis?
3. What further information do you need?
4. What are the managements for the patient?

PAGE 3

Patient was admitted to the ICCU. Cardiac monitor was hooked on; O2 3 l/min was
given through binasal catheter. NaCl 0.9% was given 500 cc/24 hours. The doctor
wanted to give verapamil injection but not available, so digoxin bullous was given.

Question:
1. Why this patient admitted to the ICCU?
2. How the mechanism of action of this drug?
3. How the preparation of this drugs?
4. How the doctor should write the prescription for the patient?
5. What is the principle of this drug should doctor know before give this drug?

Page 4
 One hour after admitted to ICCU, her ECG monitor showed bigeminal and couplet
PVCs. The doctor in charged planned to give her an amiodarone. But suddenly
seizure occurred, and the ECG monitor showed sustained VT degenerating into VF.
Cardiac resuscitation was immediately performed. The Ventricular Fibrilation
transformed into atrial fibrillation after defibrillation. Amiodarone was given to prevent
further recurrence of the arrhythmia.

Question:
1. What are the patient’s problems?
2. What are the causes and contributing factors that lead to cardiac arrest?
3. How the mechanism of action of this drug?,
4. How the preparation of this drugs?
5. How the doctor should write the prescription for the patient?
6. What is the principle of this drug should doctor know before give this drug?
7. Which the Indonesian Medical Oath point was neglected by the doctor in charge?
8. What is known about the topic? Why is research question important? What kind of
answer will the study provide?

Epilogue
She was discharge after a week of hospitalization in ICCU. She was advised to have
regularly check up to her physician, and given bisoprolol 2,5 mg once daily for
maintenance.

Guiding Question
Page 1 Guiding Question:
1. What can trigger arrhythmia?
2. How a bad adherence can trigger the arrhythmia?
3. Is there any relationship between the diarrhea and the arrhythmia? Is it because the
diarrhea or because the drugs she might had due to the diarrhea? What do you
think?
4. She told that the palpitation sometimes recovered to normal without any specific
medication from the doctor. Is it possible? How can it possible?
5. What type of arrhythmia that usually occurs in young adult population?
6. Is arrhythmia a life threatening condition? Can she die suddenly?
7. If one of your friends that have a history of SVT is having palpitation, what can you
suggest? (Valsava maneuver) How can this maneuver can lighten the symptom?

The students are supposed to discuss the problems of:

● Palpitations:
● Type of palpitation
● Specific cardiac arrhythmia and specific clinical features
● Pathogenesis and pathophysiology of cardiac arrhythmia
● Discussion on the possible role of precipitating/predisposing factors for
the occurrence of arrhythmias.

Page 2 Guiding Question:

1. Which electrolyte involved in heart conduction (action potential)?

2. What is the most important electrolyte due to heart conduction?
3. What cause hyponatremia and hypokalemia in this patient?
4. Can electrolyte imbalance cause arrhythmia?
5. Discussion of the particular specific arrhythmia in this case (physical findings,
correlated with the ECG features)
 6. What is the hemodynamic consequences of arrhythmias in general, and in particular
the specific arrhythmia in this patient
7. How arrhythmia can cause hemodynamic consequences?
8. The patient looked fatigue. Why can these happen since she hardly does anything
except lying in bed?
9. Why it is important to identify that there was no bruit at the carotid?
10. Since some type of arrhythmia can cause life threatening condition, where should
she be treated (ICU)?
11. How is the epidemiology of arrhythmia?
12. How is the primary and secondary prevention of arrhythmia?

Page 3 Guiding question:

1. What is the drug of choice of SVT?
2. What should we be aware of while we give the drugs to the patient?
3. How soon can we expect the drug effects?

Page 4 Guiding Question:

1. Why did the seizure happen? Is there any relationship between seizure and
arrhythmia? Can seizure cause arrhythmia? Or is it the arrhythmia that causes
seizure? Why can this happen?

Brief explanation of each specific learning objective

 Anatomy

Conducting system of the heart

The conducting system of the heart is the system that coordinates the cardiac
cycle. consisting of cardiac muscle cells and highly specialized conducting fibers
for initiating impulses, and conduct them rapidly throughout the heart called
the nodal tissue.

The Sinoatrial node (SA node)

- located anterolaterally, deep to epicaridium at the junction of SVC and RA.

Near the superior end of sulcus terminalis
- Is small collection of nodal tissue. act as the pacemaker of the heart. It initiates
and regulates impulses for contraction. Approximately 70 times per minute in
most people
- The SA node is supplied by the sinuatrial nodal artery, usually arises as an atrial
branch of the RCA (in 60% of people), but it may arise from the LCA (in 40%).
- The SA node is stimulated by the sympathetic division of the autonomic
nervous system to accelerate the heart rate and
- Inhibited by the parasympathetic division to return to or toward its basal rate

The atrioventricular node (AV Node)

- Smaller collection of nodal tissue compared to SA Node.

- Located in the posteroinferior region of interatrial septum, near the opening of
coronary sinus.
- The signal generated by the SA node passes through the walls of the right
atrium, propagated by the cardiac muscle (myogenic conduction), transmits
the signal rapidly from the SA node to the AV node.
- AV node distributes the signal to the ventricles through the AV bundle
- The AV node is supplied by the AV nodal artery, the largest and usually the first
IV septal branch of posterior IV artery, a branch of the RCA in 80% of people.
- The arterial suppy to both SA and AV nodes usually derived from the RCA.
- Sympathetic stimulation speeds up conduction
- Parasympathetic stimulation slows it down

The AV bundle

- The only bridge between the atrial and ventricular myocardium, passes from
the AV node through the insulating fibrous skeleton of the heart, along the
membranous part of the IVS
- Divides into right and left bundles at the junction of the membranous and
muscular parts of the ventricular septum.
- These branches proceed on each side of the muscular IVS deep to the
endocardium and ramify into subendocardial branches (Purkinje fibers)
- The AV bundle in the anterior two thirds supplied by the IVS branches of the
anterior IV branch of the LCA

Purkinje fibers

- The subendocardial branches of the right bundle stimulate the muscle of the
IVS, the anterior papillary muscle through the septomarginal trabecula
(moderator band), and the wall of the right bentricle.
- The left bundle divides near its origin into approximately six smaller tracts,
which give rise to subendocardial branches that stimulate the IVS, the anterior
and poterior papillary muscles, and the wall of the left ventricle.

Impulse generation and conduction summary

- The SA node initiates an impulse that is rapidly conducted to cardiac muscle

fibers in the atria, causing them to contract
- The impulse spreads by myogenic conduction, which rapidly transmits the
impulse from the SA node to the AV node.
- The signal is distributed from the AV node through the AV bundle and its
branches (the right and left bundles), which pass on each side of the IVS to
supply subendocardial branches to the papillary muscles and the walls of the
ventricles
Physiolog
CARDIAC CONDUCTION SYSTEM AND RELATE IT TO MECHANICAL
FUNCTIONING OF THE HEART, CARDIAC ACTION POTENTIAL, FAST AND SLOW
RESPONSES

Physiologic Anatomy of Cardiac Muscle

Figure 9–2 shows a typical histological picture of cardiac muscle, demonstrating cardiac muscle fibers
arranged in a latticework, with the fibers dividing, recombining, and then spreading again. One also notes
immediately from this figure that cardiac muscle is striated in the same manner as in typical skeletal
muscle. Further, cardiac muscle has typical myofibrils that contain actin and myosin filaments almost
identical to those found in skeletal muscle; these filaments lie side by side and slide along one another
during contraction in the same manner as occurs in skeletal muscle (. But in other ways, cardiac muscle is
quite different from skeletal muscle, as we shall see.

Cardiac Muscle as a Syncytium. The dark areas crossing the cardiac muscle
fibers in Figure 9–2 are called intercalated discs; they are actually cell
membranes that separate individual cardiac muscle cells from one another.
That is, cardiac muscle fibers are made up of many individual cells connected
in series and in parallel with one another
The heart actually is composed of two syncytiums: the atrial syncytium that
constitutes the walls of the two atria, and the ventricular syncytium that
consti- tutes the walls of the two ventricles. The atria are sepa- rated from the
ventricles by fibrous tissue that surrounds the atrioventricular (A-V) valvular
open- ings between the atria and ventricles. Normally, poten- tials are not
conducted from the atrial syncytium into the ventricular syncytium directly
through this fibrous tissue. Instead, they are conducted only by way of a
specialized conductive system called the A-V bundle, a bundle of conductive
fibers several millimeters in diameter.
This division of the muscle of the heart into two functional syncytiums allows
the atria to contract a short time ahead of ventricular contraction, which is
important for effectiveness of heart pumping.

Action Potentials in Cardiac Muscle

The action potential recorded in a ventricular muscle fiber, shown in Figure
9–3, averages about 105 milli- volts, which means that the intracellular
potential rises from a very negative value, about -85 millivolts, between beats
to a slightly positive value, about +20 millivolts, during each beat. After the
initial spike, the membrane remains depolarized for about 0.2 second,
exhibiting a plateau as shown in the figure, followed at the end of the plateau
by abrupt repolarization. The presence of this plateau in the action potential
causes ventricular contraction to last as much as 15 times as long in cardiac
muscle as in skeletal muscle.
In cardiac muscle, the action potential is caused by opening of two types of
channels: (1) the same fast sodium channels as those in skeletal muscle and
(2) another entirely different population of slow calcium channels, which are
also called calcium-sodium channels. This second population of channels
differs from the fast sodium channels in that they are slower to open and, even
more important, remain open for several tenths of a second. During this time,
a large quantity of both calcium and sodium ions flows through these channels
to the interior of the cardiac muscle fiber, and this maintains a prolonged
period of depolarization, causing the plateau in the action potential. Further,
the calcium ions that enter during this plateau phase activate the muscle
contractile process, while the calcium ions that cause skeletal muscle con-
traction are derived from the intracellular sarcoplasmic reticulum.
The second major functional difference between cardiac muscle and skeletal
muscle that helps account for both the prolonged action potential and its
plateau is this: Immediately after the onset of the action potential, the
permeability of the cardiac muscle membrane for potassium ions decreases
about fivefold, an effect that does not occur in skeletal muscle. This decreased
potassium permeability may result from the excess calcium influx through the
calcium channels just noted. Regardless of the cause, the decreased potassium
permeability greatly decreases the outflux of positively charged potassium ions
during the action potential plateau and thereby prevents early return of the
action potential voltage to its resting level. When the slow calcium-sodium
channels do close at the end of 0.2 to 0.3 second and the influx of calcium and
sodium ions ceases, the membrane permeability for potassium ions also
increases rapidly; this rapid loss of potassium from the fiber immediately
returns the membrane potential to its resting level, thus ending the action
potential.

RHYTHMICAL EXCITATION OF THE HEART

The heart is endowed with a special system for

(1) generating rhythmical electrical impulses to cause rhythmical contraction of
the heart muscle and
(2) conducting these impulses rapidly through the heart
Automatic Electrical Rhythmicity of the Sinus Fibers
Some cardiac fibers have the capability of self-excitation, a process that can
cause automatic rhythmical discharge and contraction. This is especially true of
the fibers of the heart’s specialized conducting system, including the fibers of
the sinus node. For this reason, the sinus node ordinarily controls the rate of
beat of the entire heart, as discussed in detail later in this chapter. First, let us
describe this automatic rhythmicity.

Mechanism of Sinus Nodal Rhythmicity. Figure 10–2 shows action potentials

recorded from inside a sinus nodal fiber for three heartbeats and, by
comparison, a single ventricular muscle fiber action potential. Note that the
“resting membrane potential” of the sinus nodal fiber between discharges has
a negativity of about -55 to -60 millivolts, in comparison with -85 to -90
millivolts for the ventricular muscle fiber. The cause of this lesser negativity is
that the cell membranes of the sinus fibers are naturally leaky to sodium and
calcium ions, and positive charges of the entering sodium and calcium ions
neutralize much of the intracellular negativity.
Before attempting to explain the rhythmicity of the sinus nodal fibers,.
They are
(1) fast sodium channels,
(2) slow sodium- calcium channels, and
(3) potassium channels. Opening of the fast sodium channels for a few
10,000ths of a second is responsible for the rapid upstroke spike of the action
potential observed in ventricular muscle, because of rapid influx of positive
sodium ions to the interior of the fiber. Then the “plateau” of the ventricular
action potential is caused primarily by slower opening of the slow
sodium-calcium channels, which lasts for about 0.3 second. Finally, opening of
potassium channels allows diffusion of large amounts of positive potassium
ions in the outward direction through the fiber membrane and returns the
membrane potential to its resting level.
But there is a difference in the function of these channels in the sinus nodal
fiber because the “resting” potential is much less negative—only -55 millivolts
in the nodal fiber instead of the -90 millivolts in the ven- tricular muscle fiber.
At this level of -55 millivolts, the fast sodium channels mainly have already
become “inactivated,” which means that they have become blocked. The cause
of this is that any time the mem- brane potential remains less negative than
about -55 millivolts for more than a few milliseconds, the inacti- vation gates
on the inside of the cell membrane that close the fast sodium channels
become closed and remain so. Therefore, only the slow sodium-calcium
channels can open (i.e., can become “activated”) and thereby cause the action
potential. As a result, the atrial nodal action potential is slower to develop than
the action potential of the ventricular muscle. Also, after the action potential
does occur, return of the potential to its negative state occurs slowly as well,
rather than the abrupt return that occurs for the ventricular fiber.

Internodal Pathways and Transmission of the Cardiac Impulse Through the

Atria
Summary of the Spread of the Cardiac Impulse Through the Heart
Figure 10–4 shows in summary form the transmission of the cardiac impulse through the
human heart. The numbers on the figure represent the intervals of time, in fractions of a
second, that lapse between the origin of the cardiac impulse in the sinus node and its
appearance at each respective point in the heart. Note that the impulse spreads at moderate
velocity through the atria but is delayed more than 0.1 second in the A-V nodal region before
appearing in the ventricular septal A-V bundle. Once it has entered this bundle, it spreads very
rapidly through the Purkinje fibers to the entire endocardial surfaces of the ventricles. Then
the impulse once again spreads slightly less rapidly through the ventricular muscle to the
epicardial surfaces.
It is extremely important that the student learn in detail the course of the cardiac impulse
through the heart and the precise times of its appearance in each separate part of the heart,
because a thorough quantitative knowledge of this process is essential to the understanding of
electrocardiography.

Control of Heart Rhythmicity and Impulse Conduction by the Cardiac Nerves:

The Sympathetic and Parasympathetic Nerves
The heart is supplied with both sympathetic and parasympathetic nerves. The
parasympathetic nerves (the vagi) are distributed mainly to the S-A and A-V
nodes, to a lesser extent to the muscle of the two atria, and very little directly
to the ventricular muscle. The sympa- thetic nerves, conversely, are distributed
to all parts of the heart, with strong representation to the ventricular muscle
as well as to all the other areas.
Parasympathetic (Vagal) Stimulation Can Slow or Even Block Cardiac Rhythm
and Conduction—“Ventricular Escape.” Stimulation of the parasympathetic
nerves to the heart (the vagi) causes the hormone acetylcholine to be released
at the vagal endings. This hormone has two major effects on the heart. First, it
decreases the rate of rhythm of the sinus node, and second, it decreases the
excitability of the A-V junctional fibers between the atrial musculature and the
A-V node, thereby slowing transmission of the cardiac impulse into the
ventricles.
Weak to moderate vagal stimulation slows the rate of heart pumping, often to
as little as one half normal. And strong stimulation of the vagi can stop
completely the rhythmical excitation by the sinus node or block completely
transmission of the cardiac impulse from the atria into the ventricles through
the A-V mode. In either case, rhythmical excitatory signals are no longer
transmitted into the ventricles. The ventricles stop beating for 5 to 20 seconds,
but then some point in the Purkinje fibers, usually in the ventricular septal
portion of the A-V bundle, develops a rhythm of its own and causes ventricular
contraction at a rate of 15 to 40 beats per minute. This phenomenon is called
ventricular escape.

Mechanism of the Vagal Effects. The acetylcholine released at the vagal nerve
endings greatly increases the permeability of the fiber membranes to
potassium ions, which allows rapid leakage of potassium out of the conductive
fibers. This causes increased negativity inside the fibers, an effect called
hyperpolarization, which makes this excitable tissue much less excitable
In the sinus node, the state of hyperpolarization decreases the “resting”
membrane potential of the sinus nodal fibers to a level considerably more
nega- tive than usual, to -65 to -75 millivolts rather than the normal level of -55
to -60 millivolts. Therefore, the initial rise of the sinus nodal membrane
potential caused by inward sodium and calcium leakage requires much longer
to reach the threshold potential for excitation. This greatly slows the rate of
rhythmicity of these nodal fibers. If the vagal stimulation is strong enough, it is
possible to stop entirely the rhythmical self-excitation of this node.
In the A-V node, a state of hyperpolarization caused by vagal stimulation
makes it difficult for the small atrial fibers entering the node to generate
enough electricity to excite the nodal fibers. Therefore, the safety factor for
transmission of the cardiac impulse through the transitional fibers into the A-V
nodal fibers decreases. A moderate decrease simply delays conduction of the
impulse, but a large decrease blocks conduction entirely.

Effect of Sympathetic Stimulation on Cardiac Rhythm and Conduction.

Sympathetic stimulation causes essentially the opposite effects on the heart to
those caused by vagal stimulation, as follows: First, it increases the rate of
sinus nodal discharge. Second, it increases the rate of conduction as well as the
level of excitability in all portions of the heart. Third, it increases greatly the
force of contraction of all the cardiac musculature, both atrial and ventricular,
as discussed in Chapter 9.
In short, sympathetic stimulation increases the overall activity of the heart.
Maximal stimulation can almost triple the frequency of heartbeat and can
increase the strength of heart contraction as much as twofold.
Mechanism of the Sympathetic Effect. Stimulation of the sympathetic nerves
releases the hormone norepi- nephrine at the sympathetic nerve endings. The
precise mechanism by which this hormone acts on cardiac muscle fibers is
somewhat unclear, but the belief is that it increases the permeability of the
fiber mem- brane to sodium and calcium ions. In the sinus node, an increase of
sodium-calcium permeability causes a more positive resting potential and also
causes increased rate of upward drift of the diastolic mem- brane potential
toward the threshold level for self- excitation, thus accelerating self-excitation
and, therefore, increasing the heart rate.
In the A-V node and A-V bundles, increased sodium-calcium permeability
makes it easier for the action potential to excite each succeeding portion of
the conducting fiber bundles, thereby decreasing the conduction time from
the atria to the ventricles.
The increase in permeability to calcium ions is at least partially responsible for
the increase in contrac- tile strength of the cardiac muscle under the influence
of sympathetic stimulation, because calcium ions play a powerful role in
exciting the contractile process of the myofibrils.

Characteristics of the Normal Electrocardiogram

The normal electrocardiogram (see Figure 11–1) is composed of a P wave, a
QRS complex, and a T wave. The QRS complex is often, but not always, three
separate waves: the Q wave, the R wave, and the S wave.
The P wave is caused by electrical potentials generated when the atria
depolarize before atrial contraction begins. The QRS complex is caused by
potentials generated when the ventricles depolarize before contraction, that is,
as the depolarization wave spreads through the ventricles. Therefore, both the
P wave and the components of the QRS complex are depolarization waves.
The T wave is caused by potentials generated as the ventricles recover from
the state of depolarization. This process normally occurs in ventricular muscle
0.25 to 0.35 second after depolarization, and the T wave is known as a
repolarization wave.
Depolarization Waves Versus Repolarization Waves
Figure 11–2 shows a single cardiac muscle fiber in four stages of depolarization
and repolarization, the color red designating depolarization. During
depolarization, the normal negative potential inside the fiber reverses and
becomes slightly positive inside and negative outside.
In Figure 11–2A, depolarization, demonstrated by red positive charges inside
and red negative charges outside, is traveling from left to right. The first half of
the fiber has already depolarized, while the remaining half is still polarized.
Therefore, the left electrode on the outside of the fiber is in an area of
negativity, and the right electrode is in an area of positivity; this causes the
meter to record positively. To the right of the muscle fiber is shown a record of
changes in potential between the two electrodes, as recorded by a high-speed
recording meter. Note that when depolarization has reached the halfway mark
in Figure 11–2A, the record has risen to a maximum positive value.
In Figure 11–2B, depolarization has extended over the entire muscle fiber, and
the recording to the right has returned to the zero baseline because both
electrodes are now in areas of equal negativity. The completed wave is a
depolarization wave because it results from spread of depolarization along the
muscle fiber membrane.
Figure 11–2C shows halfway repolarization of the same muscle fiber, with
positivity returning to the outside of the fiber. At this point, the left electrode
is in an area of positivity, and the right electrode is in an area of negativity. This
is opposite to the polarity in Figure 11–2A. Consequently, the recording, as
shown to the right, becomes negative.
In Figure 11–2D, the muscle fiber has completely repolarized, and both
electrodes are now in areas of positivity, so that no potential difference is
recorded between them. Thus, in the recording to the right, the potential
returns once more to zero. This completed negative wave is a repolarization
wave because it results from spread of repolarization along the muscle fiber
membrane.

Methods for Recording Electrocardiograms

Sometimes the electrical currents generated by the cardiac muscle during each
beat of the heart change electrical potentials and polarities on the respective
sides of the heart in less than 0.01 second.
Flow of Current Around the Heart During the Cardiac Cycle
Recording Electrical Potentials from a Partially Depolarized Mass of Syncytial
Cardiac Muscle
Figure 11–4 shows a syncytial mass of cardiac muscle that has been stimulated
at its centralmost point.
Before stimulation, all the exteriors of the muscle cells had been positive and
the interiors negative. as soon as an area of cardiac syncytium becomes
depolarized, negative charges leak to the outsides of the depolarized muscle
fibers, making this part of the surface electronegative, as rep- resented by the
negative signs in Figure 11–4. The remaining surface of the heart, which is still
polarized, is represented by the positive signs. Therefore, a meter connected
with its negative terminal on the area of depolarization and its positive
terminal on one of the still-polarized areas, as shown to the right in the figure,
records positively.
Two other electrode placements and meter readings are also demonstrated in
Figure 11–4. These should be studied carefully, and the reader should be able
to explain the causes of the respective meter readings. Because the
depolarization spreads in all directions through the heart, the potential
differences shown in the figure persist for only a few thousandths of a second,
and the actual voltage measurements can be accomplished only with a
high-speed recording apparatus.

Flow of Electrical Currents in the Chest Around the Heart

Figure 11–5 shows the ventricular muscle lying within the chest. Even the lungs, although
mostly filled with air, conduct electricity to a surprising extent, and fluids in other tissues
surrounding the heart conduct electricity even more easily. Therefore, the heart is actually
suspended in a conductive medium. When one portion of the ventricles depolarizes and
therefore becomes electronegative with respect to the remainder, electrical current flows from
the depolarized area to the polarized area in large circuitous routes, as noted in the figure.

It should be recalled from the discussion of the Purkinje system in Chapter 10

that the cardiac impulse first arrives in the ventricles in the septum and shortly
thereafter spreads to the inside surfaces of the remainder of the ventricles, as
shown by the red areas and the negative signs in Figure 11–5. This provides
electronegativity on the insides of the ventricles and electropositivity on the
outer walls of the ventricles, with electrical current flowing through the fluids
surrounding the ventricles along elliptical paths, as demonstrated by the
curving arrows in the figure. If one algebraically averages all the lines of
current flow (the elliptical lines), one finds that the average current flow occurs
with negativity toward the base of the heart and with positivity toward the
apex.
During most of the remainder of the depolarization process, current also
continues to flow in this same direction, while depolarization spreads from the
endocardial surface outward through the ventricular muscle mass. Then,
immediately before depolarization has completed its course through the
ventricles, the average direction of current flow reverses for about 0.01
second, flowing from the ventricular apex toward the base, because the last
part of the heart to become depolarized is the outer walls of the ventricles
near the base of the heart.

Electrocardiographic Leads
Three Bipolar Limb Leads

Figure 11–6 shows electrical connections between the patient’s limbs and the
electrocardiograph for recording electrocardiograms from the so-called standard bipolar limb
leads. The term “bipolar” means that the electrocardiogram is recorded from two electrodes
located on different sides of the heart, in this case, on the limbs. Thus, a “lead” is not a single
wire connecting from the body but a combination of two wires and their electrodes to make a
complete circuit between the body and the electrocardiograph. The electrocardiograph in each
instance is represented by an elec- trical meter in the diagram, although the actual
electrocardiograph is a high-speed recording meter with a moving paper.

Lead I. In recording limb lead I, the negative terminal of the electrocardiograph

is connected to the right arm and the positive terminal to the left arm.
Therefore, when the point where the right arm connects to the chest is
electronegative with respect to the point where the left arm connects, the
electrocardiograph records positively, that is, above the zero voltage line in the
electrocardiogram. When the opposite is true, the electrocardiograph records
below the line.
Lead II. To record limb lead II, the negative terminal of the electrocardiograph
is connected to the right arm and the positive terminal to the left leg.
Therefore, when the right arm is negative with respect to the left leg, the
electrocardiograph records positively.
Lead III. To record limb lead III, the negative terminal of the electrocardiograph
is connected to the left arm and the positive terminal to the left leg. This
means that the electrocardiograph records positively when the left arm is
negative with respect to the left leg.

Einthoven’s Triangle.
In Figure 11–6, the triangle, called Einthoven’s triangle, is drawn around the
area of the heart. This illustrates that the two arms and the left leg form apices
of a triangle surrounding the heart. The two apices at the upper part of the
triangle represent the points at which the two arms connect electrically with
the fluids around the heart, and the lower apex is the point at which the left
leg connects with the fluids.

Einthoven’s Law. Einthoven’s law states that if the electrical potentials of any
two of the three bipolar limb electrocardiographic leads are known at any
given instant, the third one can be determined mathematically by simply
summing the first two (but note that the positive and negative signs of the
different leads must be observed when making this summation).
For instance, let us assume that momentarily, as noted in Figure 11–6, the right
arm is -0.2 millivolt (negative) with respect to the average potential in the
body, the left arm is + 0.3 millivolt (positive), and the left leg is +1.0 millivolt
(positive). Observing the meters in the figure, it can be seen that lead I records
a positive potential of +0.5 millivolt, because this is the difference between the
-0.2 millivolt on the right arm and the +0.3 millivolt on the left arm. Similarly,
lead III records a positive potential of +0.7 millivolt, and lead II records a
positive potential of +1.2 millivolts because these are the instantaneous
potential differ- ences between the respective pairs of limbs.
Now, note that the sum of the voltages in leads I and III equals the voltage in
lead II; that is, 0.5 plus 0.7 equals 1.2. Mathematically, this principle, called
Einthoven’s law, holds true at any given instant while the three “standard”
bipolar electrocardiograms are being recorded.

Chest Leads (Precordial Leads)

Often electrocardiograms are recorded with one electrode placed on the
anterior surface of the chest directly over the heart at one of the points shown
in Figure 11–8. This electrode is connected to the positive terminal of the
electrocardiograph, and the negative electrode, called the indifferent
electrode, is connected through equal electrical resistances to the right arm,
left arm, and left leg all at the same time, as also shown in the figure. Usually
six standard chest leads are recorded, one at a time, from the anterior chest
wall, the chest electrode being placed sequentially at the six points shown in
the diagram. The different recordings are known as leads V1, V2, V3, V4, V5,
and V6.
Figure 11–9 illustrates the electrocardiograms of the healthy heart as recorded from these six
standard chest leads. Because the heart surfaces are close to the chest wall, each chest lead
records mainly the electrical potential of the cardiac musculature immediately beneath the
electrode. Therefore, relatively minute abnormalities in the ventricles, particularly in the
anterior ventricular wall, can cause marked changes in the electrocardiograms recorded from
individual chest leads.
In leads V1 and V2, the QRS recordings of the normal heart are mainly negative because, as
shown in Figure 11–8, the chest electrode in these leads is nearer to the base of the heart than
to the apex, and the base of the heart is the direction of electronegativity during most of the
ventricular depolarization process. Conversely, the QRS complexes in leads V4, V5, and V6 are
mainly positive because the chest electrode in these leads is nearer the heart apex, which is
the direction of electropositivity during most of depolarization.

Augmented Unipolar Limb Leads

Another system of leads in wide use is the augmented unipolar limb lead. In
this type of recording, 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 termi- nal. When the positive terminal is on
the right arm, the lead is known as the aVR lead; when on the left arm, the aVL
lead; and when on the left leg, the aVF lead.
Normal recordings of the augmented unipolar limb leads are shown in Figure
11–10. They are all similar to the standard limb lead recordings, except that
the
recording from the aVR lead is inverted

Pharmacology

Mechanisms of Action
Arrhythmias are caused by abnormal pacemaker activity or abnormal impulse
propagation. Thus, the aim of therapy of the arrhythmias is to reduce ectopic
pacemaker activity and modify conduction or refractoriness in reentry circuits
to disable circus movement. The major mechanisms currently available for
accomplishing these goals are (1) sodium channel blockade, (2) blockade of
sympathetic autonomic effects in the heart, (3) prolongation of the effective
refractory period, and (4) calcium channel blockade.
Antiarrhythmic drugs decrease the automaticity of ectopic pacemakers more
than that of the sinoatrial node. They also reduce conduction and excitability
and increase the refractory period to a greater extent in depolarized tissue
than in normally polarized tissue. This is accomplished chiefly by selectively
blocking the sodium or calcium channels of depolarized cells (Figure 14–8).
Therapeutically useful channel-blocking drugs bind readily to activated
channels (ie, during phase 0) or inactivated channels (ie, during phase 2) but
bind poorly or not at all to rested channels. Therefore, these drugs block
electrical activity when there is a fast tachycardia (many channel activations
and inactivations per unit time) or when there is significant loss of resting
potential (many inactivated channels during rest). This type of drug action is
often described as use-dependent or state-dependent; that is, channels that
are being used frequently, or in an inactivated state, are more susceptible to
block. Channels in normal cells that become blocked by a drug during normal
activation-inactivation cycles will rapidly lose the drug from the receptors
during the resting portion of the cycle (Figure 14–8). Channels in myocardium
that is chronically depolarized (ie, has a resting potential more positive than
–75 mV) recover from block very slowly if at all In cells with abnormal
automaticity, most of these drugs reduce the phase 4 slope by blocking either
sodium or calcium channels, thereby reducing the ratio of sodium (or calcium)
permeability to potassium permeability. As a result, the membrane potential
during phase 4 stabilizes closer to the potassium equilibrium potential. In
addition, some agents may increase the threshold (make it more positive).
β-Adrenoceptor–blocking drugs indirectly reduce the phase 4 slope by blocking
the positive chronotropic action of norepinephrine in the heart.
In reentry arrhythmias, which depend on critically depressed conduction, most
antiarrhythmic agents slow conduction further by one or both of two
mechanisms: (1) steady-state reduction in the number of available unblocked
channels, which reduces the excitatory currents to a level below that required
for propagation (Figure 14–4, left); and (2) prolongation of recovery time of the
channels still able to reach the rested and available state, which increases the
effective refractory period (Figure 14–4, right). As a result, early extrasystoles
 are unable to propagate at all; later impulses propagate more slowly and are
subject to bidirectional conduction block.
By these mechanisms, antiarrhythmic drugs can suppress ectopic automaticity
and abnormal conduction occurring in depolarized cells—rendering them
electrically silent—while minimally affecting the electrical activity in normally
polarized parts of the heart. However, as dosage is increased, these agents also
depress conduction in normal tissue, eventually resulting in drug-induced
arrhythmias. Furthermore, a drug concentration that is therapeutic
(antiarrhythmic) under the initial circumstances of treatment may become
"proarrhythmic" (arrhythmogenic) during fast heart rates (more development
of block), acidosis (slower recovery from block for most drugs), hyperkalemia,
or ischemia.

Specific Antiarrhythmic Agents

The most widely used scheme for the classification of antiarrhythmic drug
actions recognizes four classes:
1. Class 1 action is sodium channel blockade. Subclasses of this action reflect
effects on the action potential duration (APD) and the kinetics of sodium
channel blockade. Drugs with class 1A action prolong the APD and dissociate
from the channel with intermediate kinetics; drugs with class 1B action
shorten the APD in some tissues of the heart and dissociate from the channel
with rapid kinetics; and drugs with class 1C action have minimal effects on the
APD and dissociate from the channel with slow kinetics.
2. Class 2 action is sympatholytic. Drugs with this action reduce β-adrenergic
activity in the heart.
3. Class 3 action manifests as prolongation of the APD. Most drugs with this
action block the rapid component of the delayed rectifier potassium current,
IKr.
4. Class 4 action is blockade of the cardiac calcium current. This action slows
conduction in regions where the action potential upstroke is calcium
dependent, eg, the sinoatrial and atrioventricular nodes.

Table 14–3 Clinical Pharmacologic Properties of Antiarrhythmic Drugs.

1
May suppress diseased sinus nodes.
2
Anticholinergic effect and direct depressant action.
3
Especially in Wolff-Parkinson-White syndrome.
4
May be effective in atrial arrhythmias caused by digitalis.
5
Half-life of active metabolites much longer.

Drugs that Prolong Effective Refractory Period by Prolonging the Action

Potential (Class 3)
These drugs prolong action potentials, usually by blocking potassium channels
in cardiac muscle or by enhancing inward current, eg, through sodium
channels. Action potential prolongation by most of these drugs often exhibits
the undesirable property of "reverse use-dependence": action potential
prolongation is least marked at fast rates (where it is desirable) and most
marked at slow rates, where it can contribute to the risk of torsade de pointes.
Although most drugs in the class evoke QT prolongation, there is considerable
variability among drugs in their proarrhythmic potential to cause torsade de
pointes despite significant QT-interval prolongation. Recent studies suggest
that excessive QT prolongation alone may not be the best predictor of
drug-induced torsade de pointes. Other important factors in addition to QT
prolongation include action potential stability and development of a triangular
shape (triangulation), reverse use-dependence, and dispersion of
repolarization.

Amiodarone
In the USA, amiodarone is approved for oral and intravenous use to treat
serious ventricular arrhythmias. However, the drug is also highly effective for
the treatment of supraventricular arrhythmias such as atrial fibrillation. As a
result of its broad spectrum of antiarrhythmic action, it is very extensively used
for a wide variety of arrhythmias. Amiodarone has unusual pharmacokinetics
and important extracardiac adverse effects. Dronedarone, an analog that lacks
iodine atoms, is under investigation.
Cardiac Effects
Amiodarone markedly prolongs the action potential duration (and the QT
interval on the ECG) by blockade of IKr. During chronic administration, IKs is also
blocked. The action potential duration is prolonged uniformly over a wide
range of heart rates; that is, the drug does not have reverse use-dependent
action. In spite of its present classification as a class 3 agent, amiodarone also
significantly blocks inactivated sodium channels. Its action potential-prolonging
action reinforces this effect. Amiodarone also has weak adrenergic and calcium
channel blocking actions. Consequences of these actions include slowing of the
heart rate and atrioventricular node conduction. The broad spectrum of
actions may account for its relatively high efficacy and low incidence of torsade
de pointes despite significant QT-interval prolongation.

Extracardiac Effects
Amiodarone causes peripheral vasodilation. This action is prominent after
intravenous administration and may be related to the action of the vehicle.

Toxicity
Amiodarone may produce symptomatic bradycardia and heart block in patients
with preexisting sinus or atrioventricular node disease. The drug accumulates
in many tissues, including the heart (10–50 times more so than in plasma),
lung, liver, and skin, and is concentrated in tears. Dose-related pulmonary
toxicity is the most important adverse effect. Even on a low dose of 200 mg/d
or less, fatal pulmonary fibrosis may be observed in 1% of patients. Abnormal
liver function tests and hepatitis may develop during amiodarone treatment
and should be monitored regularly. The skin deposits result in a
photodermatitis and a gray-blue skin discoloration in sun-exposed areas, eg,
the malar regions. After a few weeks of treatment, asymptomatic corneal
microdeposits are present in virtually all patients treated with amiodarone.
Halos develop in the peripheral visual fields of some patients. Drug
discontinuation is usually not required. Rarely, an optic neuritis may progress
to blindness.
Amiodarone blocks the peripheral conversion of thyroxine (T4 ) to
triiodothyronine (T3). It is also a potential source of large amounts of inorganic
iodine. Amiodarone may result in hypothyroidism or hyperthyroidism. Thyroid
function should be evaluated before initiating treatment and should be
monitored periodically. Because effects have been described in virtually every
organ system, amiodarone treatment should be reevaluated whenever new
symptoms develop in a patient, including arrhythmia aggravation.

Pharmacokinetics
Amiodarone is variably absorbed with a bioavailability of 35–65%. It undergoes
hepatic metabolism, and the major metabolite, desethylamiodarone, is
bioactive. The elimination half-life is complex, with a rapid component of 3–10
days (50% of the drug) and a slower component of several weeks. After
 discontinuation of the drug, effects are maintained for 1–3 months.
Measurable tissue levels may be observed up to 1 year after discontinuation. A
total loading dose of 10 g is usually achieved with 0.8–1.2 g daily doses. The
maintenance dose is 200–400 mg daily. Pharmacologic effects may be achieved
rapidly by intravenous loading. QT-prolonging effect is modest with this route
of administration, whereas bradycardia and atrioventricular block may be
significant.
Amiodarone has many important drug interactions, and all medications should
be reviewed when the drug is initiated and when the dose is adjusted.
Amiodarone is a substrate for liver cytochrome CYP3A4, and its levels are
increased by drugs that inhibit this enzyme, eg, the histamine H2 blocker
cimetidine. Drugs that induce CYP3A4, eg, rifampin, decrease amiodarone
concentration when coadministered. Amiodarone inhibits the other liver
cytochrome metabolizing enzymes and may result in high levels of drugs that
are substrates for these enzymes, eg, digoxin and warfarin.

Therapeutic Use
Low doses (100–200 mg/d) of amiodarone are effective in maintaining normal
sinus rhythm in patients with atrial fibrillation. The drug is effective in the
prevention of recurrent ventricular tachycardia. It is not associated with an
increase in mortality in patients with coronary artery disease or heart failure.
In many centers, the implanted cardioverter-defibrillator (ICD) has succeeded
drug therapy as the primary treatment modality for ventricular tachycardia,
but amiodarone may be used for ventricular tachycardia as adjuvant therapy to
decrease the frequency of uncomfortable cardioverter-defibrillator discharges.
The drug increases the pacing and defibrillation threshold and these devices
require retesting after a maintenance dose has been achieved.

VERAPAMIL : Slows SA node automaticity and AV nodal conduction velocity -->

Reduce vascular resistance, cardiac rate, and cardiac force --> decreased
oxygen demand, decreases cardiac contractility --> reduces blood pressure.
Toxicity: Atrioventricular block, acute heart failure; Adverse effect :
constipation, edema, lassitude, nervousness.
Preparation available :
Verapamil (generic, Calan, Isoptin) Oral: 40, 80, 120 mg tablets Oral
sustained-release: 100, 120, 180, 240 mg tablets or capsules.
Parenteral: 2.5 mg/mL for injection.

Dept. Cardiology

Tachyarrhythmias
Tachyarrhythmias are broadly characterized as supraventricular tachycardia (SVT), defined
as a tachycardia in which the driving circuit or focus originates, at least in part, in tissue
above the level of the ventricle (i.e., sinus node, atria, AV node, or His bundle), and
ventricular tachycardia (VT), defined as a tachycardia in which the driving circuit or focus
solely originates in ventricular tissue or Purkinje fibers. Because of differences in prognosis
and management, the distinction between SVT and VT is critical early in the acute
management of a tachyarrhythmia.1 In general (with the exception of idiopathic VT,
described later), VT often carries a much graver prognosis, usually implies the presence of
significant heart disease, results in more profound hemodynamic compromise, and
therefore requires immediate attention and measures to revert to sinus rhythm. On the
other hand, SVT is usually not lethal and often does not result in hemodynamic collapse;
therefore, more conservative measures can be applied initially to convert to sinus
rhythm.2-

The distinction between SVT and VT can usually be made on the basis of the
electrocardiogram (ECG) obtained during tachycardia.

Atrial Fibrillation
Atrial fibrillation (AF) is a supraventricular arrhythmia characterized
electrocardiographically by low-amplitude baseline oscillations (fibrillatory or f
waves) and an irregularly irregular ventricular rhythm. The f waves have a rate of 300
to 600 beats/min and are variable in amplitude, shape, and timing. In contrast,
flutter waves have a rate of 250 to 350 beats/min and are constant in timing and
morphology

Classification of Atrial Fibrillation

AF that terminates spontaneously within 7 days is termed paroxysmal, and AF
present continuously for more than 7 days is called persistent. AF persistent for more
than 1 year is termed longstanding, whereas longstanding AF refractory to
cardioversion is termed permanent. However, “permanent AF” is not necessarily
permanent in the literal sense because it may be successfully eliminated by surgical
or catheter ablation.

Clinical Features
The symptoms of AF vary widely between patients, ranging from none to severe and
functionally disabling symptoms. The most common symptoms of AF are
palpitations, fatigue, dyspnea, effort intolerance, and lightheadedness.

The hallmark of AF on physical examination is an irregularly irregular pulse. Short R-R

intervals during AF do not allow adequate time for left ventricular diastolic filling, resulting
in a low stroke volume and the absence of palpable peripheral pulse. This results in a
“pulse deficit,” during which the peripheral pulse is not as rapid as the apical rate. Other
manifestations of AF on the physical examination are irregular jugular venous pulsations
and variable intensity of the first heart sound.
Prevention of Thromboembolic Complications
Risk Stratification
A major goal of therapy in patients with AF is to prevent thromboembolic
complications such as stroke. It is well established that warfarin is more
effective than aspirin for prevention of thromboembolic complications.

Long-Term Management of Atrial Fibrillation

Pharmacologic Rate Control Versus Rhythm Control
Several randomized studies have compared a rate-control strategy with a
rhythm-control strategy in patients with AF. The largest study by far was the
AFFIRM study, which consisted of 4060 patients with a mean age of 70 years
who had AF for 6 hours to 6 months. The authors of the AFFIRM study
concluded that there is no survival advantage of a rhythm-control strategy over
a rate-control strategy and that a rate-control strategy has advantages such as
a lower probability of hospitalization and of adverse drug effects.

Nonpharmacologic Management of Atrial Fibrillation

Pacing to Prevent Atrial Fibrillation, Implanted Atrial Defibrillator, Catheter
Ablation of Atrial Fibrillation

Supraventricular Tachycardia
Diagnostic algorithm
Algorithm for diagnosis of a narrow QRS tachycardia. AVRT = AV reentrant tachycardia; AVNRT = AV nodal
reentrant tachycardia; MAT = multifocal atrial tachycardia; PJRT = permanent form of AV junctional
reciprocating tachycardia.

Differences between SVT and VT

SUPPORTS SVT SUPPORTS VT
Slowing or termination by vagal tone Fusion beats
Onset with premature P wave Capture beats
RP interval ≤100 msec AV dissociation
P and QRS rate and rhythm linked to suggest P and QRS rate and rhythm linked to suggest that atrial
that ventricular activation depends on atrial activation depends on ventricular discharge, e.g., 2 : 1
discharge, e.g., 2 : 1 AV block rSR′ V1 VA block
Long-short cycle sequence “Compensatory” pause

Left-axis deviation; QRS duration >140 msec

Specific QRS contours

Ventricular Tachycardia
VT arises distal to the bifurcation of the His bundle in the specialized conduction
system, ventricular muscle, or combinations of both tissue types. Mechanisms include
disorders of impulse formation (enhanced automaticity or triggered activity) and
conduction (reentry) considered earlier.

Electrocardiograph recognition
The electrocardiographic diagnosis of VT is suggested by the occurrence of a series of
three or more consecutive, abnormally shaped PVCs whose duration exceeds 120
milliseconds, with the ST-T vector pointing opposite the major QRS deflection. The R-R
interval can be exceedingly regular or can vary. Patients can have VTs with multiple
morphologies originating at the same or closely adjacent sites, probably with different
exit paths.
 Algorithm for diagnosis of a wide QRS tachycardia. AP = accessory pathway; AT = atrial tachycardia; AVRT = AV
reentrant tachycardia; LBBB = left bundle branch block; RBBB = right bundle branch block; SVT = supraventricular tachycardia; VT =
ventricular tachycardia.

Algorithm Treatment for Tachyarrhythmia

Bradyarrhythmias
Bradyarrhythmias are arbitrarily defined as a heart rate below 60 beats/min. In some
cases, bradyarrhythmias are physiologic, as in well-conditioned athletes with low resting
heart rates or type I AV block during sleep, and in other cases are pathologic. Like
tachyarrhythmias, bradyarrhythmias can be categorized on the basis of the level of
disturbance in the hierarchy of the normal impulse generation and conduction system
(from sinus node to AV node to His-Purkinje system).

Atrioventricular Block (Heart Block)

Heart block is a disturbance of impulse conduction that can be permanent or transient,
depending on the anatomic or functional impairment. It must be distinguished from
interference, a normal phenomenon that is a disturbance of impulse conduction caused by
physiologic refractoriness resulting from inexcitability caused by a preceding impulse.
Interference or block can occur at any site where impulses are conducted, but they are
recognized most commonly between the sinus node and atrium (SA block), between the
atria and ventricles (AV block), within the atria (intra-atrial block), or within the ventricles
(intraventricular block).

Classification
As the term indicates, dissociated or independent beating of the atria and ventricles
defines AV dissociation. AV dissociation is never a primary disturbance of rhythm but is a
“symptom” of an underlying rhythm disturbance produced by one of three causes or a
combination of causes that prevent the normal transmission of impulses from atrium to
ventricle
TUTOR GUIDE CRP:

Broadly speaking, any question that we want answered and any assumption or assertion that we
want to challenge or investigate can become a research problem or a research topic for our study.
The formulation of research problem is the first and most important step of the research process. It
is like the identification of a destination before undertaking a journey. A research problem is like the
foundation of a building. The type and design of the building is dependent upon the foundation. If
the foundation is well-designed and strong we can expect the building to be also. The research
problem serves as the foundation of a research study, if it is well formulated, we can expect good
study to follow.
Table 1. Sources of research problem (four of ‘P’)
Aspect of a study About Study of
Study Population People Individuals, organization, groups, and communities
Subject area Problem Issues, situations, associations, needs, population
composition, profiles, etc.
Program Contents, structure, outcomes, attributes, satisfaction,
consumers, service providers, etc
Phenomenon Cause and effect relationships, the study of a
phenomenon itself, etc
Most research on a particular ‘P’ may vary from study to study but generally in practice most
research studies are based upon at least a combination of two ‘P’s.
When selecting a research problem/topic there is a number of considerations to keep in mind.
These help to ensure that our study will be manageable and that you will remain motivated. These
considerations are:
Interest : Select a topic that really interests you; this one of the most important
considerations. A research endeavour is usually time-consuming, and
involves hard work and possibly unforeseen problems. If you select a topic
which does not greatly you, it could become extremely difficult to sustain
the required motivation, and hence the completion time could be affected
Magnitude : You should have sufficient knowledge about the research process to be
able to visualize the work involved in completing the proposed study.
Narrow the topic down to something manageable, specific and clear. It is
extremely important to select a topic that you can manage within the time
and resources at your disposal.
Measurement of : If you are using a concept in your study, make sure you are clear about its
concepts indicators and their measurement. For example if you plan to measure the
effectiveness of a health promotion program, you must be clear as to what
determines effectiveness and how it will be measured. Do not use concept
in your research problem that you are not sure how to measure. This does
not mean you cannot develop a measurement procedure as the study
progresses. While most of the developmental work will be done during your
study, it is imperative that your reasonably clear about the measurement of
this concept at this stage.
Level of expertise : Make sure you have an adequate level of expertise for the task you are
proposing. Allow for the fact that you will learn during the study and may
receive help from your research supervisors an others, but remember you
need to do most of the work yourself.
Relevance : Select a topic that is relevance to you as a professional. Ensure that your
study ads to the existing body of knowledge, bridges current gaps or is
useful in policy formulation. This will help you to sustain interest in the
study.
Availability of data : If your topic entail collection of information from secondary sources (office
records, client records, census or other already-published reports, ect.),
before finalising your topic, make sure that these data are available and in
the format you want.
Ethical issues : Another important consideration in formulating a research problem is the
ethical issues involved. In the course of conducting a research study, the
study population may be: adversely affected by some of the question
(directly indirectly); deprived of an intervention; excepted to share sensitive
 and private information; or excepted to be simply experimental ‘guinea
pigs’. How ethical issues can affect the study population and how ethical
problems can be overcome should be thoroughly examined at the problem
formulation stage.

TUTOR GUIDE BHP

DOCTOR’S ROLE IN LICENSURE
There is a tendency to assume that physical impairments of drivers are important in the causation of
accidents, although little evidence has been collected to confirm or deny this assumption. Little is
known about how driver licensure regulations related to health tests relate to the older driver traffic
fatality rate. Medical conditions and medications have been hypothesized as determinants of crash
involvement. For example, a study in Alabama (2000), older drivers with heart disease were more
likely to be involved in at-fault automobile crashes. Not-at-fault drivers involved in crashes were also
more likely to have heart disease, stroke, and arthritis compared with drivers not involved in
crashes. Based on the present state of knowledge, health related driver impairments comprise of
gross physical defects (e.g blindness), chronic disease, and conditions that are not obvious or
frequently temporary, which can be just as incompatible with safe driving (e.g. taking alcohol or
certain kinds of medicine).

There are debates among clinicians about the appropriate role of public policy in regulating older
drivers, in many advanced countries calling on doctors to help reduce traffic accidents safely by
testing motor skills and by regulating medications. The purpose is not only for the person’s safety,
but for public safety. However, regulating the driving licensure for those who have certain physical
impairment, although necessary for community protection, often impose a variety of negative
consequences, which include social, economic, health, and psychological consequences.

Driving is a symbol of status, independence, and autonomy. Driving is an essential part of daily
living. It reduces or eliminates employment opportunities and participation in social activities. It
reduces options, spontaneity, and comfort. Male drivers, in particular, may perceive their inability to
continue driving as a threat to their status as head of the family. To hire a personal driver is not
always an easy option. The ethical values in conflict are autonomy-nondiscriminationvs
responsibility for public safety-nonmaleficent.

Doctor may play a key role in the license revocation or restriction process. In certain countries
doctors may report to the authority, in writing the name, age, and address of any person diagnosed
by him to have any chronic health problem which in the doctor’s judgment will significantly affect the
person’s ability to safely operate a motor vehicle. In certain states in USA, no civil action may be
brought against the commissioner, the department or any of its employees, the board or any if its
members or any doctor for providing any reports, records, examinations, opinions or
recommendations. Any person acting in good faith, shall be immune from liability.

It is suggested that periodic medical updates required by drivers with certain medical conditions
including certain cardiovascular conditions, such as coronary heart disease, angina pectoris,
myocardial infarction, cardiac failure, cardiac arrhythmias, cardiac effects of pulmonary disease, and
hypertension. Other conditions may be applied as well, such as dementia, cerebrovascular
conditions, ocular disease, COPD, Diabetes Mellitus, arthritis, and conditions under medications.
Driving restriction or license revocation may varies in degree depends on the condition.

References

1. Braunwald E, Zipes DP, Libby P. Heart Disease, A Textbook of Cardiovascular

Medicine. 9th Ed,. WB Saunders Coy, Philadelphia, 2011: Chapter 39-40. Specific
arrhytmias: Diagnosis and Treatment; Atrial Fibrillation: Clinical Features,
Mechanism, and Management.
2. Neumar RW, Otto CW, Link MS, et al. Part 8: Adult Advanced Cardiovascular Life
Support: 2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Circulation
2010;122;S729-S767.
3. Gerald McGwin, Jr, Richard V. Sims, LeaVonne Pulley, and Jeffrey M. Roseman
(2000): Relations among Chronic Medical Conditions, Medications, and Automobile
Crashes in the Elderly: A Population-based Case-Control Study. Am J Epidemiol.
152(5):424-431
4. Insurance Institute for Highway Safety. (2007): U.S. driver licensing procedures for
older drivers. www.iihs.org/laws/olderdrivers.aspx. Accessed November 31, 2007.
5. Kumar R. Research Methodology: A Step-by-Step Guide for Beginners. SAGE Publications;
2005.