CARDIOVASCULAR SYSTEM (CVS)

- Dr. Vivek V. Nalgirkar

Section 1 ~ Introduction, Properties of cardiac muscle

Section 2 ~ Conducting system of heart, Origin & spread of cardiac impulse

Section 3 ~ Cardiac cycle:- Events, pressure and volume changes in atria & ventricles; Heart
sounds

Section 4 ~ Electrocardiogram (ECG):- Leads, Waves & intervals, Clinical application

Section 5 ~ Cardiac output:- Introduction, Factors determining cardiac output, Physiological

and Pathological factors that influence cardiac output; methods of measurement. ANS
influence on cardiac function, Heart rate

Section 6 ~ Circulation:- Types of blood vessels, blood flow. Capillary circulation, Starling’s
forces, lymphatics.

Section 7 ~ Blood pressure:- Determinants & factors influencing BP, Regulation of BP

Section 8 ~ Regional circulation, circulatory shock, cardiovascular changes during exercise

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 Section 1

Introduction, properties of cardiac muscle

Learning objectives:

- To understand the basic principles governing the function of heart.

~ Introduction:

Human heart has 2 atria and 2 ventricles. Atria are primer pumps; pumping
blood into ventricles. When it is said that heart pumps out blood, it is the
ventricles that perform this function.

Heart is said to have two sides – Right side receives deoxygenated (venous) blood
coming from all over the body; right ventricle (RV) pumps it into the pulmonary
artery (PA). This blood reaches lungs, picks up oxygen, and then returns to left
side of the heart. Left ventricle (LV) then pumps it into the aorta, for the
oxygenated blood to be distributed throughout the body.

From functional standpoint, heart has the following subsystems –

 The conducting system or specialized junctional tissues of the heart: It is

responsible for the spread of sequential electrical excitation of the heart.
Heart continues to beat rhythmically forever due to the impulse generation
and transmission by the conducting system.
 The myocardium: Heart muscle cells are striated, and not under voluntary
control. The myocardium is composed of separate cardiac muscle cells that
are electrically connected to one another by gap junctions. These
connections are low-resistance pathways. The gap junctions allow free
passage of ions (charges) from one cell to the next. This arrangement is
called “syncytium” (a mass of cytoplasm with numerous nuclei). There is
free passage of ions from one cell to the next. Excitation spreads very
quickly into whole of the myocardium, once it excites one part of it. Hence,
all fibers of a chamber contract together. {Actually, the heart functions as
two syncytia – one being the atria and the other is the ventricles.} Note:
The two atria contract together; the two ventricles contract together.

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 Video link ~ Syncytium; gap junctions

Also note: Another unique feature is presence of the intercalated discs. They
provide for electro-mechanical tethering to the myocardial fibers. This tethering
has important consequence for the direction and strength of contraction of the
heart muscle fibers. If they were just a loose bunch of fibers, it would have
resulted in a haphazard, weak, and directionless contraction of heart chambers.
 The valves: 2 sets of valves – (1) Atrio-ventricular (A.V.) valves: Include
tricuspid valve (between right atrium [RA] and right ventricle [RV]) and
mitral valve (between left atrium [LA] and left ventricle [LV]); and (2)
Semilunar valves: Include pulmonary valve (between the right ventricle and
the pulmonary artery) and aortic valve (between the left ventricle and the
aorta). The function of the valves is to maintain a unidirectional flow of
blood as it moves from atria to ventricles and from ventricles to the vessels.
They prevent a backflow of blood. {Note that: These valves operate on the
basis of “pressure gradients” between the chambers and the vessels. For
instance, the AV valves are open when “ atrial pressures > ventricular
pressures”; this allows blood flow from the atria to the ventricles. And,
when “ventricular pressure > atrial pressure”, the AV valves will be closed so
that blood does not flow back from the ventricles into the atria.}
 The coronary circulation: The entire thickness of the myocardium cannot
derive nutrition from the blood that is contained within its chambers.
Hence, heart has an independent circulation; the coronary vessels running
within musculature of the heart.
 Innervation to the heart: Although heart is a self-excitable tissue, it
receives innervation from the autonomic nervous system (ANS) which can
modify the cardiac activity to suit the bodily needs of circulation.
Parasympathetic supply: Right vagus → SA node; left vagus → AV node.
Vagus innervation is only to the conducting system and to atria, not to
ventricles. Sympathetic supply: Fibers from stellate ganglion; the fibers
innervate SA node, AV node, atria, and ventricles.

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 Video link ~ How do the valves operate?

~ Properties of the cardiac muscle:

(1) Excitability –
Cardiac muscle shows property of excitability. Electrical excitation spreads
sequentially through the heart, resulting in contraction of the chambers.
(2) Contractility –
Cardiac muscle contraction causes pumping of blood out of heart chambers.
As the ventricular muscle contracts, it pumps the blood into the vessels. This
contraction has a certain force, so that blood reaches tissues in adequate
amounts.
(3) Autorhythmicity – (the “pacemaker potential”)
There are two properties in it ~ ‘auto’ and ‘rhythmic’
“Auto” means self; it is the property of ‘self-excitation’ or automaticity.
 The membrane potential reaches threshold by itself, due to the special
types of ionic currents, and completes the depolarization.
 It happens in a rhythmic fashion. At the end of every repolarization,
the membrane potential begins to rise spontaneously again, to reach
the threshold.
It allows the heart to continue to beat independently forever.
o Many parts in the heart inherently possess this property. Normally,
only the pacemaker (SA node) will exhibit autorhythmicity, and other
parts will excite due to the impulse coming from the pacemaker. If
pacemaker fails due to some reason, some other part (like, AV node)
can become the pacemaker as it too has autorhythmicity. Thus, heart
can continue to beat forever.

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[Fig: It shows the AP in cells that exhibit autorhythmicity. At the end of every
repolarization, the membrane potential rises again to threshold. This potential,
which rises automatically to threshold, is termed prepotential or pacemaker
potential.]

(4) Long refractory period – (the “plateau potential”)

Immediately after (every) excitation, there is time during which another
excitation is not possible. This is called refractory period. The tissue can be
excited again only when this period ends.
Cardiac tissue, especially the ventricular fibers, have a long refractory period.
[Compare:- Refractory period ~ (a) for a nerve = 1 msec; (b) for Purkinje fiber
= 200-300 msec.]
Refractory period determines what can be the maximum frequency of
excitation of a tissue.

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[Fig: Action potential in Purkinje fiber. It shows the plateau phase during repolarization. Due
to the plateau phase, the AP duration and the refractory period is much longer.]

Advantage of the long refractory period: [NO TETANUS]

Due to the long refractory period, the heart muscle cannot be stimulated at
very high frequencies.

- Since the refractory period is long, heart muscle can never go into
tetanus. Tetanus is sustained state of contraction of muscle (failure to
relax) caused by high frequency stimulation. Due to the long refractory
period, heart muscle cannot be stimulated at a high frequency; there will
always be sufficient time, between two successive stimuli, for heart to
relax.

- Also, heart muscle will never fatigue. It will always get sufficient time for
recovery, between two successive stimuli.

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  Ionic basis of action potentials in heart:
Under normal circumstances, there are two types of APs (and hence two
types of cells) in heart ~ 1. Slow response type (i.e., slowly depolarizing
cells), and 2. Fast response type (i.e., rapidly depolarizing cells).

Slow response type Fast response type

- SA node, AV node - Purkinje fiber, ventricular

muscle fiber

- RMP is less negative (– 55 - RMP is more negative (– 90

to – 65 mV) mV); hence amplitude of AP
is larger

- Exhibit autorhythmicity - Do not have

autorhythmicity under
normal circumstances

[Fast response type fiber may get converted to slow response type, under some conditions; it
may then develop autorhythmicity.]

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 (1) Slow response type:

[Fig: It shows the AP in the slow response type cells. Note the slow but spontaneous
depolarization reaching threshold, at the end of every repolarization. Refer to text for details.]

In the figure - 1, 2, 3, and 4 represent various ionic currents responsible for

depolarization; and, 5 represents repolarization. To understand how membrane
begins to depolarize automatically at the end of repolarization, let’s start with
phase 5.

5. Repolarization: K+ efflux
1. Membrane begins to depolarize spontaneously: K+ efflux stops; and, K+
starts accumulating inside of the membrane
2. Depolarization continues further: Influx of Na+ through “funny”
channels. (These Na+ channels are hyperpolarization-activated cyclic
nucleotide gated [HCN-gated] channels. The influx of Na + is described
“funny” current.)
3. Reaching of threshold: Influx of Ca++ through Ca++[T] channels. (T =
Transient.)

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 4. Depolarization above threshold: Influx of Ca++ through Ca++[L] channels,
completes the depolarization.

Video link: K+ current; automaticity explained

(2) Fast response type:

[Fig: AP in Purkinje fiber; fast response type. Refer to text for details.]
 Phase 0: Rapid upstroke ~ Na+ influx through ‘fast’ Na+ channels
 Phase 1: Early repolarization ~ K+ efflux starts
 Phase 2: Plateau ~ Influx of Ca++ through slow Ca++ channels.

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  Phase 3: Repolarization ~ K+ efflux continues (Ca++ influx has stopped
already)
 Phase 4: RMP

Due to the presence of plateau phase, the Purkinje fiber has ~

- Long AP duration (200-300 msec)

- Long recovery time (repolarization)
- Long refractory period

Note the end of repolarization; phase 4 is flat. That is, at the end of repolarization,
membrane potential does not rise automatically to threshold. Hence, these fibers
do not exhibit autorhythmicity under normal circumstances.

Video link ~ Increased slope of phase 4; enhanced automaticity and arrhythmias

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 Section 2

CONDUCTING SYSTEM OF THE HEART

SPECIAL JUNCTIONAL TISSUES OF THE HEART

ORIGIN & SPREAD OF CARDIAC IMPULSE

Learning objectives:

- This section deals with sequential excitation in the heart. Why is SA

node the pacemaker of the heart? Why is there a delay between atrial
and ventricular excitation? These questions will be answered in this
section.
- There are different types of action potentials in the heart. They serve
specific purposes to the respective parts of the heart. These APs, their
ionic basis, and their implications will be discussed in this section.

Introduction:

There are the special junctional tissues in the heart, collectively called as
‘conducting system of heart’. They cause sequential spread of electrical excitation
in the heart.

Components of the conducting system:

1. S.A. node
2. Internodal pathways
3. A.V. node
4. Bundle of His
5. Right & left branches of bundle of His
6. Purkinje fibers

{The electrical excitation starts at the S.A. node in the right atrium, and spreads
through these parts of the conducting system into the ventricles. As a result of this
sequential spread of excitation, the heart will contract.}

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