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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Module 1:
CO1 Lecture on
Cardiovascular Physiology

BE104-2P UREAH THEA A. SEVILLA, Ph.D.


Systems Physiology 2 School of Chemical, Biological, and Materials
Engineering and Sciences

Identify the parts and functions of the heart, explain the


Course Outcome 1 Topics: electrical activity and mechanical events of cardiac cycle
and control of cardiac output, and explain how the
circulatory system contribute to homeostasis.

• Overview of the Cardiovascular System


• The anatomy of the heart
• Electrical activity of the heart
• Mechanical events of the cardiac cycle
• Cardiac output and its control
• Contribution to Homeostasis

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

The Cardiovascular System


• Cardiovascular system consists of the heart, the blood vessels
(arteries, veins, and capillaries) and the blood that traverse the whole
human body.
• Heart is the anatomical pump that imparts pressure to the
blood to establish the pressure gradient needed for blood to
flow to the tissues.
• Blood vessels are the passageways through which blood is
directed and distributed from the heart to all parts of the body
and subsequently returned to the heart.
• Blood is the transport medium within which materials being
transported long distances in the body, such as O2, CO2,
nutrients, wastes, electrolytes, and hormones, are dissolved
or suspended.

Location of the Heart in the


Thoracic Cavity

Mediastinum (“midway”) –
central compartment of the
thoracic cavity

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Pulmonary and Systemic


circulations in relation to the Heart

• Pulmonary circulation carries


blood between the heart and
lungs
• Systemic circulation carries blood
between the heart and organ
systems.

Pulmonary and Systemic


circulations in relation to the
Heart
• Each of these loops forms a figure “8”
with the pulmonary circulation
simultaneously supplying the right and
left lungs and the systemic circulation
simultaneously supplying the upper
body and lower body.

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Anatomy of the Heart


• The atria (upper chambers) -
receive blood returning to the
heart and transfer it to the
lower chambers
• The ventricles (lower
chamber) - pump blood from
the heart.
• The vessels that return blood
from the tissues to the atria
are veins, and those that carry
blood away from the
ventricles to the tissues are
arteries.

Anatomy of the Heart

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Anatomy of the Heart


• Aortic and pulmonary – controls the
blood flow from the ventricles
• Pulmonary valve – between the RV
and PA
• Aortic valve –between the LV and
aorta
• Tricuspid valve (right atrioventricular)
valve – located between RA and RV
• Mitral valve (left atrioventricular
valve) – between LA and LV
https://www.mayoclinic.org/diseases-conditions/heart-valve-disease/symptoms-
causes/syc-20353727

Organization of Cardiac Muscles


The heart walls are composed primarily of
spirally arranged cardiac muscle fibers:
• Endocardium (thin inner layer) - a unique
type of epithelial tissue that lines the
chambers of the heart
• Myocardium (middle layer) - composed of
cardiac muscle and constitutes the bulk of
the heart wall. (The myocardium consists of
interlacing bundles of cardiac muscle fibers
arranged spirally around the circumference
of the heart.)
• Epicardium (thin external layer) - covers the
heart.

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Organization of Cardiac Muscles


Two types of membrane junctions
are present within intercalated
disc:
• Gap junctions
• Desmosomes

Organization of Cardiac Muscles


• The heart is enclosed by a
the pericardial sac. The
pericardial sac has two
layers, a serous layer and a
fibrous layer. It encloses the
pericardial cavity which
contains pericardial fluid.
• The pericardium fixes the
heart to the mediastinum,
gives protection against
infection and provides the
lubrication for the heart.

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Pericarditis
• Pericarditis, an inflammation of the pericardial sac that results in
painful friction between the two pericardial layers, occurs
occasionally because of viral or bacterial infection.

Electrical Activity of the Heart


The heart contracts rhythmically as a result of action potentials that it
generates by itself, a property called autorhythmicity (or automaticity).

There are two specialized types of cardiac muscle cells:


• Contractile cells, which are 99% of the cardiac muscle cells, do the
mechanical work of pumping. These working cells normally do not initiate
their action potentials.
• Autorhythmic cells, the small but extremely important remainder of the
cardiac cells, do not contract but instead are specialized for initiating and
conducting the action potentials responsible for contraction of the working
cells.

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Electrical Activity of the Heart


• The heart's pacemaker is in
the sinoatrial node (SA node)
where a group of
autorhythmic cells are located
at the junction of the vena
cava and the right atrium

Electrical Activity of the Heart


The specialized non-contractile cardiac cells capable of autorhythmicity lie in the
following specific sites:
1. The sinoatrial node (SA node) - a small,
specialized region in the right atrial wall
near the opening of the superior (upper)
vena cava.
2. The atrioventricular node (AV node) - a
small bundle of specialized cardiac
muscle cells located at the base of the
right atrium near the septum, just above
the junction of the atria and ventricles.

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Electrical Activity of the Heart


The specialized non-contractile cardiac cells capable of autorhythmicity lie in the
following specific sites:
3. The bundle of His (atrioventricular bundle)
- a tract of specialized cells that originates
at the AV node and enters the septum
between the ventricles. It divides to form
the right and left bundle branches that
travel down the septum, curve around the
tip of the ventricular chambers, and travel
back toward the atria along the outer walls.
4. Purkinje fibers - small terminal fibers that
extend from the bundle of His and spread
throughout the ventricular myocardium,
much like small twigs of a tree branch.

Electrical Activity of the Heart


• An action potential initiated at the
SA node first spreads throughout
both atria (interatrial pathway).
• The AV node is the only point where
an action potential can spread from
the atria to the ventricles
(internodal pathway). From the AV
node, the action potential spreads
rapidly throughout the ventricles,
hastened by a specialized
ventricular conduction system
consisting of the bundle of His and
Purkinje fibers.

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Pacemaker Potential in Autorhythmic Cells


• Cardiac autorhythmic cells do not have a resting potential. Instead,
they display pacemaker activity.
• The most important changes in ion movement that give rise to the
pacemaker potential are:
(1) an increased inward Na+ current,
(2) a decreased outward K+ current,
(3) an increased inward Ca2+ current

Pacemaker Potential in Autorhythmic Cells

The first half of the pacemaker potential is


the result of simultaneous opening of
funny channels, which permits inward Na+
current, and closure of K+ channels, which
reduces outward K+ current.
The second half of the pacemaker
potential is the result of opening of T-type
Ca2+ channels.
Once threshold is reached, the rising
phase of the action potential is the result
of opening of L-type Ca2+ channels,
whereas the falling phase is the result of
opening of K+ channels.

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Action Potential in Skeletal Muscle Cells vs Cardiac


Contractile Cells

Action Potential in Cardiac Contractile Cells

(0) There is rapid rising of action potential in contractile cells as a


result of Na+ entering on open Na+ channels at threshold.
(1) The early, brief repolarization after the potential is reached
its peak is because of limited K+ efflux on opening of transient
K+ channels, coupled with inactivation of the Na+ channels.
(2) The prolonged plateau phase is the result of slow Ca2+ entry
on opening of L-type Ca2+ channels, coupled with reduced K+
efflux on closure of several types of K+ channels.
(3) The rapid falling phase is the result of K+ efflux on opening of
ordinary voltage-gated K+ channels, as in other excitable cells.
(4) Resting potential is maintained by opening of leaky K+
channels.

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Summary of Electrical Activity of the Heart


• Identify the labeled items

Autorhythmic and Contractile Cells

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The Electrocardiogram
• An ECG is a recording of that part of the electrical activity present in
body fluids from the cardiac impulse that reaches the body surface,
not a direct recording of the actual electrical activity of the heart.
• The ECG is a complex recording representing the overall spread of
activity throughout the heart during depolarization and
repolarization.

ECG Waves
A normal ECG has three
distinct wave-forms:
• P wave – atrial
depolarization
• QRS complex –
ventricular
depolarization
• T wave – ventricular
repolarization

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

ECG waves
• P wave – atrial
depolarization
• QRS complex –
ventricular
depolarization
• T wave – ventricular
repolarization

ECG Measurements

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Heart Rhythm and Heart Rate


Normal sinus rhythm:
• Each P wave is followed by a
QRS
• Regular or irregular

Heart Rhythm and Heart Rate

A method to determine the


heart rate:
= 1500/ # of small boxes
between RR

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Heart Rhythm and Heart Rate


Another method to measure rate (BPM):
Rate = 60/0.2=300 (note that per 1 big box = 0.2
sec)
• 1 big box = 300 beats/min (duration = 0.2sec)
• 2 big boxes = 150 beats/min (duration = 0.4sec)
• 3 big boxes = 100 beats/min (duration = 0.6sec)
• 4 big boxes = 75 beats/min (duration = 0.6sec)
• 5 big boxes = 60 beats/min (duration = 1.0sec)

Heart Rhythm and Heart Rate


• P wave rate 60 - 100 bpm with <10%
variation - Normal
• Rate < 60 bpm = Sinus Bradycardia
Rate > 100 bpm = Sinus Tachycardia

Results from
- Pain / anxiety
- Volume depletion
- Pericarditis
- Chronotropic Drugs (Dopamine)

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

ECG Measurements

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ECG Measurements

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

ECG Measurements

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Abnormalities in Heart Rhythm


• Rhythm refers to the regularity or spacing of the ECG waves. Any
variation from the normal rhythm and sequence of excitation of the
heart is termed an Arrhythmia.
• Other abnormalities include the following and can be detected on an
ECG:
• atrial flutter, atrial fibrillation, ventricular fibrillation, and heart block.

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Abnormalities in Heart Rhythm

Mechanical Events of the Cardiac Cycle


Mechanical events of the cardiac cycle include:
• contraction, relaxation, and the resultant changes in blood flow
through the heart

The heart alternately contracts to empty and relaxes to fill.


The cardiac cycle consists of alternate periods:
• Systole - contraction and emptying
• Diastole - relaxation and filling of blood

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

The Cardiac Cycle


• The cardiac cycle can be divided into four stages:
• Filling phase – the ventricles fill during diastole and atrial systole.
• Isovolumetric contraction – the ventricles contract, building up
pressure ready to pump blood into the aorta/pulmonary trunk.
• Outflow phase – the ventricles continue to contract, pushing blood
into the aorta and the pulmonary trunk. This is also known as systole.
• Isovolumetric relaxation – the ventricles relax, ready to re-fill with
blood in the next filling phase.

IVR
IVC

• Atrial Pressure
• Aortic Pressure
• Ventricular Pressure

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Wigger’s Diagram
Wigger’s diagram correlates various events
that occur concurrently during the cardiac
cycle, including ECG features, pressure
changes, volume changes, valve activity, and
heart sounds.

Wigger’s Diagram
(1-2) Mid-ventricular diastole – passive blood
filling
(3-6) Late ventricular diastole
(7) End of ventricular diastole (EDVave = 135mL)
(8-9) Onset of ventricular systole
(10-11) Isovolumetric ventricular contraction
(12-14) Ventricular ejection
(15) End of ventricular systole (ESVave = 65mL)
(16-18) Onset of ventricular diastole
(19-20) Isovolumetric ventricular relaxation
(21-25) Ventricular filling

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Mechanical Events of Cardiac Cycle

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Mechanical Events of Cardiac Cycle


Left-ventricular pressure–volume
loop for a single cardiac cycle

Mechanical Events of Cardiac Cycle


Two normal heart sounds are associated with
valve closures:
• First heart sound “lub” - low-pitched, soft, and
relatively long;
• Second heart sound “dup” - has a higher pitch
and is shorter and sharper

• The first heart sound is associated with closure


of the AV valves
• The second sound is associated with closure of
the semilunar valves

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Heart Murmurs
• Blood normally flows in a laminar fashion—that is, layers of the fluid
slide smoothly over one another (lamina means “layer”).
• Laminar flow does not produce an audible sound. When blood flow
becomes turbulent, however, a sound can be heard, this is called
heart murmurs.

Cardiac Output
• Cardiac output (CO) - the volume of blood pumped by each ventricle
per minute (not the total amount of blood pumped by the heart).
Blood Volume (pulmonary circulation) = Blood Volume (systemic circulation)

• Cardiac output depends on heart rate (HR) and stroke volume (SV).
• The average resting HR is 70 beats per minute (established by SA
node rhythmicity); the average resting SV is 70 mL per beat,
therefore:

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Cardiac Reserve
• Cardiac reserve (CR) - difference between
the cardiac output at rest and the
maximum volume of blood the heart can
pump per minute

• How can CO vary so tremendously,


depending on the demands of the body?
• engaging in strenuous physical activities
where there is a need for increased cardiac CR refers to the heart’s ability to
output thus, regulation of CO depends on adjust the demands/stress place
control of both HR and SV. upon it.

Influence of Autonomic
Nervous System on Heart Rate
Both parasympathetic and
sympathetic NS bring about
their effects on the heart
primarily by altering the activity
of the cyclic adenosine
monophosphate (cAMP)
second-messenger pathway in
the innervated cardiac cells.
Acetylcholine (ACh) released
from the vagus nerve binds to a
muscarinic cholinergic receptor
and is coupled to an inhibitory
G protein that reduces activity
of the cAMP pathway.

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Parasympathetic nervous system’s


influence on the SA node is to
decrease HR

Sympathetic stimulation on the heart:


• improve its effectiveness as a pump by increasing HR,
decreasing the delay between atrial and ventricular
contraction,
• decreasing conduction time throughout the heart,
• increasing the force of contraction,
• speeding up the relaxation process so that more time is
available for filling

Stroke Volume
• Cardiac output is determined also by stroke volume.
• Stroke volume is influenced by:
(1) intrinsic control related to the extent
of venous return
(2) extrinsic control related to the extent
of sympathetic stimulation of the
heart.
Both factors increase SV by increasing the
strength of heart contraction.

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BE104-2P SYSTEMS PHYSIOLOGY 2 – M1-CO1

Intrinsic Control of Stroke Volume (Frank-Starling curve)


Frank–Starling Law of the Heart
“The heart normally pumps out during systole the volume of blood returned to it
during diastole; increased venous return results in increased SV.”
The main determinant of cardiac muscle fiber
length is the degree of diastolic filling.
The greater the diastolic filling, the larger
the EDV, and the more the heart is
stretched. The more the heart is stretched,
the longer the cardiac fibers before
contraction.
The increased length results in a greater
force on the subsequent cardiac contraction
and thus in a greater SV.

Sympathetic Stimulation (Extrinsic control)


• Sympathetic stimulation increases the contractility of the heart.
• SV is subject to extrinsic control by factors originating outside the
heart e.g. epinephrine
Sympathetic stimulation increases SV not only by
strengthening cardiac contractility but also by
enhancing venous return.

Sympathetic stimulation constricts the veins, which


squeezes more blood forward from the veins to the
heart, increasing the EDV and subsequently
increasing SV even further.

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Sympathetic Stimulation
Effect of sympathetic stimulation on stroke volume
Ejection fraction is often used
clinically as indication of contractility.
• It is the ratio of stroke volume to
end-diastolic volume.
• It is the proportion of the blood in
the ventricle that is pumped out.
• A healthy heart normally has an
ejection fraction of 50% to 75%
under resting conditions and may go
as high as 90% during strenuous
exercise, but a failing heart may
pump out 30% or less.

Summary of the Control of Cardiac Output

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Heart Defects
• Heart failure (HF) is the inability of CO to keep pace with the body’s
demands for supplies and removal of wastes.

Nourishing the Heart Muscle


• The heart receives most of its blood
supply through the coronary circulation
during diastole.
Blood contents:
• Oxygen
• Nutrients (As fuel sources, the heart
primarily uses fatty acids and, to a
lesser extent, glucose and lactate,
depending on their availability.)

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Heart Diseases associated with Coronary


circulation (Coronary Artery Disease)
• Vascular spasm is an abnormal spastic constriction that transiently
narrows the coronary vessels.

Vascular spasm

Heart Diseases associated with Coronary


circulation (Coronary Artery Disease)
• Atherosclerosis is a progressive, degenerative arterial disease that
leads to occlusion (gradual blockage) of affected vessels, reducing
blood flow through them. Atherosclerosis is characterized by plaques
forming beneath the vessel lining within arterial walls.

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Heart Diseases associated with Coronary


circulation (Coronary Artery Disease)
• Thromboembolism - formation in a blood vessel of a clot (thrombus)
that breaks loose and is carried by the blood stream to plug another
vessel.

Possible Outcomes of a Heart Attack


Immediate death result from:
• acute systolic heart failure occurring because the heart is too
weakened to pump effectively to support the body tissues
• fatal ventricular fibrillation brought about by damage to the
specialized conducting tissue or induced by O2 deprivation
Delayed death from complications:
• fatal rupture of the dead, degenerating area of the heart wall affected
by the acute infarction
• slowly progressing congestive heart failure because the pumping
ability of the weakened heart is unable to keep up with venous return

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Possible Outcomes of a Heart Attack


• Full functional recovery owing to replacement of the damaged area
with a strong scar, accompanied by hypertrophy (enlargement) of the
remaining normal contractile tissue to compensate for the lost
cardiac musculature
• Recovery with impaired function on account of persistence of
permanent functional defects, such as bradycardia or conduction
blocks, caused by destruction of irreplaceable autorhythmic or
conductive tissues

Contribution to Homeostasis
The circulatory system contributes to homeostasis:
• Body’s transport system - provides a way to rapidly move materials
from one part of the body to another. Without the circulatory system,
materials would not get quickly enough to where they need to be to
support life- sustaining activities.
• Example: O2 would take months to years to diffuse from the body
surface to internal organs, yet through the heart’s swift pumping
action the blood can pick up and deliver O2 and other substances
to all the cells in a few seconds.

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Review Questions:

• Label the peaks.


• What is the heart rate?
• Classify the heart rate.

Review Questions:

• Label the peaks. How would you describe this ECG recording?
• What is the heart rate?
• Classify the heart rhythm.

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Review Questions:

• Label the peaks. How would you describe this ECG recording?
• What is the heart rate?
• Classify the heart rhythm (possible problem).

Review Questions:

• Label the peaks.


• What is the heart rate?
• Classify the heart rhythm.

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Review Questions:

If EDV = 200 and ESV =60

• What is SV?
• What is CO?
• What is the ejection fraction?

References:
Lauralee Sherwood, Human Physiology: From Cells to Systems, 9th
edition. Cengage Learning, 2016.

Bryan H. Derrickson, Human Physiology 2nd edition, Wiley, 2016.

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