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Continuing Medical Education Programs
Dr. Anika Niambi Al-Shura, Lecturer
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Integrative Anatomy and
Patho-Physiology in
TCM Cardiology
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This course is approved by the
following agencies:
National Certification Commission for Acupuncture and
Oriental Medicine (NCCAOM) for 14 PDA points and
Florida State Board of Acupuncture for 15 CEUs.
The companion textbook:
Integrative Anatomy and Patho-Physiology
in TCM Cardiology
must be ordered at www.elsevier.com
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Course Description
This course examines of the structure, function
and pathology of the heart from the western
medicine and Chinese medicine perspectives.
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Course Objectives
• Review the normal anatomy and physiology of
the cardiovascular system.
• Evaluate the disease characteristics found in
sections of the heart sections.
• Analyze the inter-relationship between western
medicine and TCM theory in cardiology.
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Copyright 2014 Niambi Wellness. All rights reserved
Course Modules
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Module 1:
Cardiovascular Anatomy
Module 2:
Physiology
Module 3:
Pathology
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Module 2
Cardiovascular
Physiology
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Contents
Chapter 4:
Cardiac Rhythm
Chapter 5:
Pumping Actions
Chapter 6:
Vascular Function and Circulation
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Contents
Chapter 7:
Humeral Control
Chapter 8:
Nervous System Regulation
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Chapter 4: Cardiac Rhythm
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Contents
Part 1:
Cardiac Muscle Structure
Part 2:
Cardiac Muscle Contractility
Part 3:
Electrical Activity
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Part 1: Cardiac Muscle
Structure
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Cardiac myocyte: Sarcomere
Look in the textbook
and label each
myocyte section.
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Part 2: Cardiac Muscle
Contractility
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Cardiac muscle contractility
Look in the textbook
and label each
section.
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Part 3: Electrical Activity
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Resting potentials
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Nernst equation
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Goldman equation
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Action Potentials
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Chapter Assessment
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According to the textbook
1.
2.
3.
4.
5.
Describe the sarcomere.
Discuss the role of ATP.
Explain Resting potentials.
Explain action potentials.
Describe the site of transmission.
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According to the course
1. What are types of lines and bands of a
sarcomere?
2. What are the three types of troponin in muscle
contractility?
3. Which two ions are crossing the cell membrane
during resting potentials?
4. What does the Nernst equation describe about
ions?
5. Which three ions are part of the Goldman
equation?
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Chapter 5: Pumping Actions
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Contents
Part 1:
Cardiac Cycle
Part 2:
Regulation
Part 3:
Preload on Stroke Volume
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Contents
Part 4:
Inotropy (Contractility)
Part 5:
Afterload on Stroke Volume
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Part 1: Cardiac Cycle
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Wiggers Diagram/ Heart Qi
The cardiac cycle
includes to the events
related to the flow and
pressure of blood
through the heart
from one heartbeat to
the next.
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Phase 1: Atrial Systole
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P wave represents
the atrial electrical
depolarization.This
phase is ventricular
diastole.
Circle this in your
textbook.
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During filling,
pressure within the
right atrium increases,
pushing blood across
the AV valves into the
right ventricle.
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At the end of the
phase the ventricles
are completely filled
to about 140mL. This
is the EDV (end
diastolic volume).
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The S4 (fourth heart
sound) is sound
heard during this
phase.
It’s usually heard in
ventricular
hypertrophy.
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Phase 2: Isovolumetric
Ventricular Systole
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QRS wave represents
the beginning of
systole.
Circle this in your
textbook.
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This phase
represents ventricular
depolarization. The
rise in pressure in the
ventricles exceeds
the pressure in the
atrium causing the AV
valves to close.
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The S1 (first heart
sound) is sound
heard during this
phase.
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Phase 3: Ventricular Ejection
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This section
represents the S and
T wave.
Circle this in your
textbook.
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The pressure in the
ventricle exceeds the
pressure within the
pulmonary arteries
and the aorta. The
pulmonic valves open
to allow blood flow.
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No heart sound is
heard in healthy
valves. A sound heard
at this phase is called
an ejection murmur.
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Phase 4: Ventricular Relaxation
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This section
represents the T wave
after the QRS wave.
Circle this in your
textbook.
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The pressure in the
ventricle decreases
due to emptying.
Atrial pressure is
rising.
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No heart sound is
heard in healthy
valves. A sound heard
at this phase is called
an ejection murmur.
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Phase 5: Isovolumetric Relaxation
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Phase 5: Isovolumetric Relaxation
This section
represents the end of
the T wave.
Circle this in your
textbook.
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The volume of blood
which remains in the
left ventricle which is
= 70mL is called the
ESV (end systolic
volume).
EDV-ESV=SV
(140- 70 =70)
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S2 sound is heard as
the valve closes.
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Phase 6: Diastolic
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This section
represents the end of
the T wave to the
middle of the P
phase.
Circle this in your
textbook.
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The atria fills with
blood, the pressure
causes the AV valves
open to release the
blood into the
ventricles.
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No sound is heard in
healthy AV valves. If
S3 sound is heard, it
is considered normal
in children, but
ventricular dilation in
adults.
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Part 2: Regulation
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The Fick prinicple
CA= arterial blood
CV= venous blood
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In 1870 Adolf Eugen Fick in 1870 calculated the
oxygen consumption rate as it flows through
blood.
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The principle calculates the rate of blood flow
and the rate of oxygen picked up by the red
blood cells.
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The Fick principle involves measuring oxygen
concentration in the veins and arteries, however
this collection and analysis can be difficult to
obtain.
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The Oxygen Content Equation
Record this information
in your textbook.
CaO2=(SaO2xHbx1.34)+
.003(PaO2)
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Physicians consider that the measurement of oxygen
content in hemoglobin is a simpler process. Hemoglobin
carries oxygen and deficiency (anemia) can lead to
hypoxemia.
Each gram of hemoglobin carries 1.34 mL of O2.
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Part 3: Preload
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Frank-Starling mechanism
1
2
3
4
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Part 4: Inotropy (contractility)
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cAMP
(cyclic adenosine monophosphate
ATP is cellular energy
and is used in signal
transduction.
Adenylate cyclase
uses ATP to produce
cyclic AMP.
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cAMP is a second
messenger, as it
regulates the function
of ion channels and
assists the passage
of ions and certain
hormones into cells.
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It is also involved in
glycogen and
adrenaline regulation
and lipid metabolism.
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Part 5: Afterload on
Stroke Volume
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Afterload
Afterload is the
pressure generated in
the ventricles to eject
blood out of the heart.
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The pressure must be
greater than pulmonic
and systemic
pressure for valve
opening.
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As afterload
increases, cardiac
output decreases.
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Chapter Assessment
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According to the textbook
1. Describe heart qi.
2. List the phases of the cardiac cycle on the
Wiggers diagram.
3. Discuss the rule of 70.
4. Discuss how blood volume affects stroke
volume.
5. Describe contractility
6. Describe afterload.
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According to the course
1. Discuss the Fick principle
2. Discuss the oxygen content equation.
3. What 4 factors are described in the FrankStarling mechanism ?
4. What is cAMP?
5. What is afterload?
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Chapter 6: Vascular Function
and Circulation
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Contents
Part 1:
Calcium Channels
Part 2:
Contraction of Smooth Muscle
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Contents
Part 3:
Endothelial Factors
Part 4:
Metabolites
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Part 1: Calcium Channels
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Calcium Channel Blocker
A calcium channel is
a gate on the cell
surface which allows
calcium ions to pass.
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There are 2 kinds of
calcium channels:
high voltage
low voltage
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High voltage
Voltage gated:
L-type
P-type
N-type
R-type
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L-type
Myocytes (ventricle)
Skeletal and smooth
muscle
Osteoblasts
Dendrites
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P-type
Certain neural cells
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N-type
Certain neural cells
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R-type
Certain neural cells
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Low voltage
T-type
Certain neural cells
Pacemaker (SA nodal
cells)
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Part 2: Contraction of
Smooth Muscle
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The pressure in blood vessels can contract and
neurotransmitters can cause more or less
contraction or relaxation.
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ATP can be an important neurotransmitter. It is
released with noradrenaline and neuropeptide
from peri-vascular sympathetic nerves.
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ATP can assist at P2 receptors to cause smooth
muscle contraction in vessels.
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Part 3: Endothelial Factors
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Endothelial cells form the linings of the blood
vessels. Endothelin-1(ET-1) is involved in tissue
production and repair throughout the body.
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ET-1 also repairs and extend capillaries in a
spontaneous process called sprouting. In this
process, endothelial cells may act similarly to
hyphae in fungus.
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Nitric oxide is produced by endothelial cells and
can serve as a neurotransmitter by relaxing
smooth muscle tissue such as in vessels.
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Part 4: Metabolites
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Adenosine regulated by ATP. Also it is involved
with vasodilation. It causes relaxation of smooth
muscle as is found inside the artery walls.
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K+ channel activity is an important determinant
of vascular tone and functioning.
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Endothelial cell dysfunction may be due to
problems with nitric oxide which could also
cause changes in K+ channel activity which will
affect vasodilation.
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Chapter Assessment
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According to the textbook
1. Explain the significance of Ca++ and H+ on smooth
muscle contraction.
2. Describe Ca++ affect on smooth muscle contraction.
3. Which endothelin is associated with vascular
functioning? How?
4. What is the role of prostaglandins in vasodilation?
5. Which four metabolites are involved with increase in
vasodilation?
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According to the course
1.
2.
3.
4.
5.
What are the two kinds of calcium channels?
Which kinds are involved with cardiac functioning?
Describe the role of ATP in vascular contraction.
What is ET-1?
What is the role of nitric oxide (NO) in vascular
functioning?
6. What is the role of adenosine and K+ activity in
vascular functionin
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Chapter 7: Humoral Control
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Contents
Part 1:
Local Hormones
Part 2:
System Hormones
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Part 1: Local Hormones
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Bradykinin
This is a kinin which is part of inflammation, and
is formed in locally around the site of an injury,
which causes vasodilation and edema.
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Serotonin
This is a neurotransmitter which causes
vasoconstriction and smooth muscle contraction.
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Part 2: System Hormones
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Renin-angiotensin-aldosterone
The renin-angiotensin-aldosterone system
(RAAS) is involved in regulating vascular
resistance, blood volume, cardiac output and
arterial pressure.
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Adrenals
Epinephrine causes constriction in many
networks of minute blood vessels but dilates the
arteries and bronchus.
Norepinephrine constricts blood vessels.
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Chapter Assessment
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According to the textbook
1. Explain bradykinin as part of pathogenic
issues.
2. Explain serotonin as part of pathogenic issues.
3. Explain renin-angiotensin.
4. Explain adrenal hormones.
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According to the course
1. Define bradykinin.
2. Define serotonin.
3. Explain the renin-angiotensin-aldosterone
system.
4. Explain the role of epinephrine.
5. Explain the role of norepinephrine.
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Chapter 8: Humoral Control
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Contents
Part 1:
Autonomic Nervous System
Part 2:
Sympathetic Reflexes
Part 3:
Parasympathetic Reflexes
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Part 1: Autonomic
Nervous System
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The sympathetic and parasympathetic are part
of the autonomic nervous system. The
sympathetic reflexes cause vasoconstriction.
The parasympathetic reflexes cause
vasodilation.
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Part 3: Parasympathetic
Reflexes
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The sympathetic
reflexes accelerates
the heart beat.
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The sympathetic
reflexes relaxes the
bronchus.
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Part 2: System Hormones
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The parasympathetic
reflexes slows the
heart beat.
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The parasympathetic
reflexes constricts the
bronchus.
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Module 1 Review
Questions
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Complete the Module 2
review interactive practice quiz.
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Please continue on to Module 3
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