Cardiovascular Physiology

Heart and Circulation

Blood vessels
Key words
Overview of
the circulatory
system
The circulatory system is composed of:

1) the blood (the circulating material)

2) the heart (pump)

3) blood vessels (conduit)

 COMPONENTS OF CIRCULATORY
SYSTEM

 Cardiovascular System (CV):

 Heart:
 Pumping action creates pressure head needed to push blood through
vessels.
 Blood vessels:
 Permits blood flow from heart to cells and back to the heart.
 Arteries, arterioles, capillaries, venules, veins.
 Lymphatic System:
 Lymphatic vessels transport interstitial fluid.
 Lymph nodes cleanse lymph prior to return in venous blood.
The circulatory system
Why is cardiovascular system needed?
Life evolved from oceans.
 Nutrients

cell
 Nutrients

cell
cell
cell
cell
cell
cell
cell
 Nutrients
cell
cell
cell
cell
cell
cell
cell
Internal environment the interstitium

cell H2O
cell
Glucose
cell Lipids
cell Amino acids
cell Vitamins
cell Minerals
cell O2
pH 7.35-7.45
~38° C
280-300 mOsm
External environment
 Goal Constant
(homeostasis)

H2O
cell Glucose
cell Lipids
cell Amino acids
cell Vitamins
cell Minerals
O2
cell
cell pH 7.35-7.45
~38° C
290 mOsm
 External
Environment H2O
Glucose
Lipids
Digestive
Amino acids
Vitamines
Minerals
Respiratory Blood O2
Respiratory
Urinary pH 7.35-7.45
All tissue cells
~38° C
Urinary
290 mOsm
Endocrine
Neural
Interstitium
Primary Functions of the Circulatory System

1) Transportation

Deliver life-supporting materials, i.e., O2, glucose,

amino acid, fatty acids, vitamins, minerals, etc.
Deliver regulating signals, i.e., hormones to tissue
cells

Collect waste products from tissue cells and de-

liver to special organs (kidney, lung) for disposal

Distribute heat throughout the body

Primary Functions of the Circulatory System

2) Protection
Special components of the blood patrol the whole body
and fight against invaded microorganisms and cancer-
ous cells.

H2O
cell Glucose
cell Lipids
cell Amino acids
cell Vitamins
cell Minerals
O2
cell
cell pH 7.35-7.45
~38° C
290 mOsm
 5 types of circulation
 Systemic: blood pumping to body (system)
 Pulmonary: blood pumping to the lungs

 Coronary: blood pumping to the heart itself

 Fetal: circulation of blood to and from the placenta

 Hepatic: blood going through liver to be filtered and

detoxified
PATTERNS OF CICULATION
 Blood moves through the body in a continuous fashion:
 Left ventricle → systemic circulation (body) → right atrium→
right ventricle → pulmonary circulation (lungs) → left
atrium→ left ventricle.
 Deoxygenated blood is pumped from the right ventricle
into the lungs through the pulmonary arteries –
 the only arteries to carry deoxygenated blood.

 Blood returns to the heart through the pulmonary veins,

the only veins to carry oxygenated blood.
PATTERNS OF CICULATION
 The systemic circulation starts at the left ventricle and
ends at the right atrium. It carries blood to and from the
rest of the body.
 The heart itself receives its supply of blood from the two
coronary arteries leading from the aorta. Blood enters
into capillaries that lead to veins through which blood
returns to the right atrium.
PATTERNS OF CICULATION
 There are three parts of the systemic circulation that you
need to know:
 A. coronary circulation - supplying blood to the heart muscle
(coronary artery).
 B. renal circulation – supplying blood to the kidneys (renal
artery).
 Nearly 25% of the blood leaving the heart flows to the kidneys, which
are pressure filters for waste.
 C. hepatic portal circulation- nutrients picked up by capillaries
in the small intestines are transported directly to the liver in
the hepatic portal vein, where excess nutrients are stored.
 This is about 70% of the liver’s blood supply. The liver also receives oxy-
genated blood from the hepatic artery, which branches off the aorta,
and provides 30% of its blood. All blood leaves the liver through the he-
patic vein.
 PULMONARY AND SYSTEMIC
CIRCULATIONS
 Pulmonary circulation:
 Path of blood from right
ventricle through the lungs
and back to the heart.
 Systemic circulation:
 Oxygen-rich blood pumped
to all organ systems to sup-
ply nutrients.
 Rate of blood flow through
systemic circulation = flow
rate through pulmonary
circulation.
Blood Flow Through Heart
Trace the pathway of blood (    )through the body using the following terms:
 Aorta
 Right atrium
 Left atrium
 Right ventricle
 Left ventricle
 Lungs
 Vena Cava
 Venules
 Arterioles
 Capillaries
 Body tissues
 Pulmonary artery
 Pulmonary vein
Blood Supply to Cardiac Muscles
Can cardiac muscles get nutrients from
the blood in heart chambers?
 The cardiac muscles get nutri-
ents from coronary circulation.

Anterior view Posterior view

Coronary arterial anastomosis

endocardium

epicardium
LV

RV
 Coronary venous blood is emptied into the right
atrium through cardiac veins and coronary sinus.

Posterior view

coronary sinus
Blockade of coronary artery causes myocardial
infarction, or heart attack.

endocardium

epicardium
LV

RV
The Heart

30
The Heart
 Functions of the Heart
 Generating blood pressure
 Routing blood
 Heart separates pulmonary and systemic circulations
 Ensuring one-way blood flow
 Heart valves ensure one-way flow
 Regulating blood supply
 Changes in contraction rate and force match blood delivery to
changing metabolic needs
 Cardiovascular System Function
 To create the “pump” we have to examine the Functional
Anatomy
 Cardiac muscle
 Chambers
 Valves
 Intrinsic Conduction System
 Functional Anatomy of the Heart
Cardiac Muscle

 Characteristics
 Striated
 Short branched cells
 Uninucleate
 Intercalated discs
 T-tubules larger and
over z-discs
 Functional Anatomy of the Heart
Chambers

 4 chambers
 2 Atria
 2 Ventricles

 2 systems
 Pulmonary
 Systemic
 Functional Anatomy of the Heart
Valves

 Function is to prevent backflow

 Atrioventricular Valves
 Prevent backflow to the atria
 Prolapse is prevented by the chordae

tendinae
Tensioned by the papillary muscles


 Semilunar Valves
 Prevent backflow into ventricles
 Functional Anatomy of the Heart
Intrinsic Conduction System

 Consists of “pace-
maker” cells and con-
duction pathways
 Coordinate the contrac-
tion of the atria and ven-
tricles
Size, Shape, Location of Heart

 Size of a closed fist

 Shape
 Apex: Blunt rounded point of
cone
 Base: Flat part at opposite of
end of cone
 Located in thoracic cavity in me-
diastinum
External Anatomy
 Four chambers
 2 atria
 2 ventricles
 Major veins
 Superior& Inferior vena
cava
 Pulmonary veins
 Major arteries
 Aorta
 Pulmonary trunk
External Anatomy
External anatomy: anterior
External anatomy: posterior
Coverings of the heart: pericardium

Three layered:
 (1) Fibrous pericardium

 Serous pericardium of layers (2) & (3)

 (2) Parietal layer of serous pericardium
 (3) Visceral layer of serous pericardium = epicardium: on heart and
is part of its wall
(Between the layers is pericardial cavity with pericardium fluid)

43
Pericardium
 Layers of the heart wall
 Muscle of the heart with inner and outer membrane cov-
erings
 Muscle of heart = “myocardium”

 The layers from out to in:

 Epicardium= visceral layer of serous pericardium
 Myocardium = the muscle
 Endocardium lining the chambers

45
 Heart Wall
 Three layers of tissue
 Epicardium: (aka visceral peri-
cardium) This serous membrane of
smooth outer surface of heart
 Myocardium: Middle layer com-
posed of cardiac muscle cell and re-
sponsibility for heart contracting
 Endocardium: Smooth inner surface
of heart chambers
Relative thickness of muscular walls

LV thicker than RV because it forces blood out against more resistance; the sys-
temic circulation is much longer than the pulmonary circulation

Atria are thin because ventricular filling is done by gravity, requiring little atrial effort

47
 Atrioventricular and Semilunar Valves
 Atriaand ventricles are separated into 2 functional units
by a sheet of connective tissue by AV (atrioventricular)
valves.
 One way valves.
 Allow blood to flow from atria into the ventricles.
 At
the origin of the pulmonary artery and aorta are
semilunar valves.
 One way valves.
 Open during ventricular contraction.
 Opening and closing of valves occur as a result of pres-
sure differences.
Atrioventricular and Semilunar Valves
Function of AV valves

50
Function of semilunar valves
(Aortic and pulmonic valves)
 Cardiac Cycle
Coordinating the activity

 Cardiac cycle is the sequence of events as blood enters

the atria, leaves the ventricles and then starts over
 Synchronizing this is the Intrinsic Electrical Conduction
System
 Influencing the rate (chronotropy & dromotropy) is done
by the sympathetic and parasympathetic divisions of the
ANS
 Cardiac Cycle
Coordinating the activity

 Electrical Conduction Pathway

 Initiated by the Sino-Atrial node (SA node) which is myogenic at 70-80 action poten-
tials/minute
 Depolarization is spread through the atria via gap junctions and internodal pathways
to the Atrio-Ventricular node (AV node)
 The fibrous connective tissue matrix of the heart prevents further spread of
APs to the ventricles
 A slight delay at the AV node occurs
 Due to slower formation of action potentials
 Allows further emptying of the atria
 Action potentials travel down the Atrioventricular bundle (Bundle of His) which
splits into left and right atrioventricular bundles (bundle branches) and then into the
conduction myofibers (Purkinje cells)
 Purkinje cells are larger in diameter & conduct impulse very rapidly
 Causes the cells at the apex to contract nearly simultaneously
 Good for ventricular ejection
 Cardiac Cycle
Coordinating the activity

 Electrical Con-
duction Pathway
 Cardiac Cycle
 Refersto the repeating pattern of contraction and
relaxation of the heart.
 Systole:
 Phase of contraction.
 Diastole:
 Phase of relaxation.
 End-diastolic volume (EDV):
 Total volume of blood in the ventricles at the end of diastole.
 Stroke volume (SV):
 Amount of blood ejected from ventricles during systole.
 End-systolic volume (ESV):
 Amount of blood left in the ventricles at the end of systole.
 Cardiac Cycle (CONTINUED)

 Step 1: Isovolumetric contraction:

 QRS just occurred.
 Contraction of the ventricle causes ventricular pressure to rise
above atrial pressure.
 AV valves close.
 Ventricular pressure is less than aortic pressure.
 Semilunar valves are closed.
 Volume of blood in ventricle is EDV.
 Step 2: Ejection:
 Contraction of the ventricle causes ventricular pressure to rise
above aortic pressure.
 Semilunar valves open.
 Ventricular pressure is greater than atrial pressure.
 AV valves are closed.
 Volume of blood ejected: SV.
 Cardiac Cycle (CONTINUED)

 Step 3: T wave occurs:

 Ventricular pressure drops below aortic pressure.
 Step 4: Isovolumetric relaxation:
 Back pressure causes semilunar valves to close.
 AV valves are still closed.
 Volume of blood in the ventricle: ESV.
 Step 5: Rapid filling of ventricles:
 Ventricular pressure decreases below atrial pressure.
 AV valves open.
 Rapid ventricular filling occurs.
 Cardiac Cycle (CONTINUED)

 Step 6: Atrial systole:

 P wave occurs.
 Atrial contraction.
 Push 10-30% more
blood into the ventri-
cle.
 1) Isovolumic
Ventricular Contraction 2) Ventricular Ejection

3) Isovolumic
4) Ventricular Filling 5) Atrial Contraction
Ventricular Relaxation
Can the heart beat by itself ?
Autorhythm
The heart can beat on its own without the need
for exogenous commands.
 Conclusion ?

The heart generates electricity.

Motor nerve
Skeletal muscle
 Heart Sounds
Four heart sounds can be recorded via phono-
cardiography, but normally only two, the first
and the second heart sounds, are audible
through a stethoscope.
 Heart Sounds

 Closing of the AV and

semilunar valves.
 Lub (first sound):
 Produced by closing of the AV
valves during isovolumetric
contraction.
 Dub (second sound):
 Produced by closing of the
semilunar valves when pres-
sure in the ventricles falls be-
low pressure in the arteries.
First heart sound:

- occurs when the atrioven-

tricular (AV) valves close at
the beginning of ventricular
contraction.

- generated by the vibration of

the blood and the ventricular
wall

-is louder, longer, more reso-

nant than the second heart
sound.
 Second heart sound

- occurs when aortic and

pulmonary semilunar
valves close at the begin-
ning of ventricular dilation

- generated by the vibration

of the blood and the aorta

- Aortic valve closes slightly

before pulmonary valve.
 Heart Murmurs
 Abnormal heart sounds produced by abnormal patterns of
blood flow in the heart.
 Defective heart valves:
 Valves become damaged by antibodies made in response to an infec-
tion, or congenital defects.
 Mitral stenosis:
 Mitral valve becomes thickened and calcified.
 Impairs blood flow from left atrium to left ventricle.
 Accumulation of blood in left ventricle may cause pulmonary HTN.

 Incompetent valves:
 Damage to papillary muscles.
 Valves do not close properly.
 Murmurs produced as blood regurgitates through valve flaps.
 Heart Murmurs

 Septal defects:
 Usually congenital.
 Holes in septum be-
tween the left and right
sides of the heart.
 May occur either in in-

teratrial or interven-
tricular septum.
 Blood passes from left
to right.
MECHANICAL PROPERTIES OF THE HEART

Heart Rate
Stroke volume
Cardiac Output (CO)
Ejection Fraction
Preload
Afterload
Contractility
Frank-Starling Mechanism
Factors on Cardiac Output
Heart Rate
the number of heart
beats in 1 minute. Nor-
mal value: 60-100/min
SV
Stroke volume
the volume of blood
pumped out by each
ventricle per each con-
traction.
Cardiac Output (CO)
the amount of blood pumped out by each ventricle in
1 minute.
Cardiac output = stroke volume x heart rate

Example:
70
ml
70 ml x 75 beat/min = 5,250 ml/min

75 beat/min
Ejection Fraction
= stroke volume end-diastolic ventricular volume
70 ml  130 ml = 54%

SV =
70 ml

60 ml
130 ml

End of diastole End of systole

Ejection Fraction

increases during exercise

120 ml  133 ml = 90%

SV =
120 ml

133 ml

End of diastole End of systole

Preload
the force that stretches the muscle before con-
traction.
Afterload
the force that stretches muscle during contrac-
tion.

afterload
preload
Preload to ventricles = ventricular end diastolic pressure

- the degree of stretch of the ventricular muscle cells

just before they contract.
- determined by ventricular filling.
Afterload to left ventricle: aortic arterial pressure

Afterload to right ventricle: pulmonary arterial pressure

Afterload Aortic arterial pressure

to the left
ventricle
is greater
than that
to the
right ven-
tricle.
Contractility
- the intrinsic strength of cardiac muscles.
Factors on Cardiac Output

1) Preload:

2) Afterload:
3) Contractility:

4) Heart Rate:
 Factors on Cardiac Output

1) Preload:

 Preload   cardiac output

(Starling-Frank Mechanism)
 Factors on Cardiac Output

More out
1) Preload:

 Preload   cardiac output

(Starling-Frank Mechanism) More in

PRELOAD

 Ventricular wall stress at end-diastole

 Force imposed on a resting muscle i.e. prior to the on-
set of muscle contraction which stretches the muscle
to a new length
 Determined by
 ventricular EDV
 Ventricular EDP
 Wall thickness
 Frank-Starling Law

Force of con-
traction of
myocardium

Initial length of my-

ocardial fibers

 Extent of preload (venous return)

 Increased by  Decreased by
1. Increase in total blood volume 1. Decrease in total blood volume
2. Increase venous tone 2. Increase in intra-pericardial pressure
3. Increase pumping of skeletal muscle (e.g. 3. Increase in intrathoracic pressure – during
exercise) expiration
4. Atrial contraction 4. Body position – sitting or standing
5. Decrease in intrathoracic pressure – during
inspiration
 Factors on Cardiac Output

R
1) Preload:

2) Afterload:

 afterload   CO
 Factors on Cardiac Output

1) Preload:

2) Afterload:
3) Contractility:

 contractility   CO
 CARDIAC CONTRACTILITY
 Intrinsic property of the cardiac cell that defines the
amount of work heart can perform at a given load
 Determined primarily by the availability of Ca 2+

 Attributed to interactions between contractile proteins

arranged in parallel rows in the sarcomere
FACTORS AFFECTING MYOCARDIAL CON-
TRACTILITY

Effect of changes in myocardial contractility on the Frank-

Starling curve
 Other chemicals can affect contractility:
- Positive inotropic agents: glucagon, epinephrine,
thyroxine, digitalis.
- Negative inotropic agents: acidoses, rising K+, Ca2+
channel blockers.
Regulation of Heart Rate
 Autonomic nervous system

 Chemical Regulation: Hormones (e.g., epinephrine, thyroxine)

and ions.
 Factors on Cardiac Output

1) Preload:

2) Afterload:
3) Contractility:

4) Heart Rate:
dual effects
CO = Heart Rate x Stroke Volume
DISTRIBUTION OF CARDIAC OUTPUT AT REST
AND DURING EXERCISE

Data from A.J. Vander, J.H. Sherman, and D.S. Luciano, 1985, Human physiology: The mechanisms of body
function, 4th ed. (New York: McGraw-Hill Companies).
 CARDIOVASCULAR RESPONSE TO
EXERCISE
• Heart rate (HR), stroke volume (SV), and cardiac output (CO)
increase.
• Blood flow and blood pressure change.
• All result in allowing the body to efficiently meet the in-
creased demands placed on it.
 RESTING HEART RATE

• Averages 60 to 80 beats per minute (bpm);

• Tends to decrease with age and with increased cardiovascular
fitness
• Is affected by environmental conditions such as altitude and
temperature
 MAXIMUM HEART RATE
• The highest heart rate value one can achieve in an all-out ef-
fort to the point of exhaustion
• Remains constant day to day and changes slightly from year
to year
• Can be estimated: HRmax = 220 – age in years
 STROKE VOLUME
• Determinant of cardiorespiratory endurance capacity at max-
imal rates of work
• May increase with increasing rates of work up to intensities
of 60% of max
• May continue to increase up through maximal exercise inten-
sity
• Depends on position of body during exercise
CHANGES IN STROKE VOLUME (SV) AS A
SUBJECT EXERCISES
 STROKE VOLUME INCREASES
DURING EXERCISE
• Frank Starling mechanism: more blood in the ventricle causes it to
stretch more and contract with more force
• Increased ventricular contractility (without end-diastolic volume
increases)
• Decreased total peripheral resistance due to increased vasodilation
of blood vessels to active muscles
CARDIAC OUTPUT

• Resting value is approximately 5.0 L/min.

• Increases directly with increasing exercise intensity to 20 to 40 L/
min.
• Value of increase varies with body size and endurance condition-
ing.
• When exercise intensity exceeds 60%, further increases in CO are
more a result of increases in HR than SV.
 .
CHANGES IN CARDIAC OUTPUT
CHANGES IN (A) HEART RATE, (B) STROKE
VOLUME, AND (C) CARDIAC OUTPUT WITH
CHANGES IN POSTURE

a
 b
 c
CARDIOVASCULAR DRIFT

• Gradual decrease in stroke volume and systemic and pul-

monary arterial pressures and an increase in heart rate
• Occurs with steady-state prolonged exercise or exercise in
a hot environment
CARDIOVASCULAR DRIFT
 BLOOD PRESSURE

Cardiovascular Endurance Exercise

• Systolic BP increases in direct proportion to increased
exercise intensity.
• Diastolic BP changes little, if at all, during endurance
exercise, regardless of intensity.
 Electrical Activity of the Heart
 SA node:
 Demonstrates automaticity:
 Functions as the pacemaker.
 Spontaneous depolarization
(pacemaker potential):
 Spontaneous diffusion caused
by diffusion of Ca2+ through
slow Ca2+ channels.
 Cells do not maintain a stable
RMP.
 Pacemakers AP
 Depolarization:
 VG fast Ca2+ channels open.
 Ca2+ diffuses inward.
 Opening of VG Na+ channels may also contribute to the
upshoot phase of the AP.
 Repolarization:
 VG K+ channels open.
 K+ diffuses outward.
 Ectopic pacemaker:
 Pacemaker other than SA node:
 If APs from SA node are prevented from reaching these areas,
these cells will generate pacemaker potentials.
 Myocardial APS
 Majorityof myocardial cells have a RMP of –90 mV.
 SA node spreads APs to myocardial cells.
 When myocardial cell reaches threshold, these cells depo-
larize.
 Rapid upshoot occurs:
 VG Na+ channels open.
 Inward diffusion of Na+.
 Plateau phase:
 Rapid reversal in membrane polarity to –15 mV.
 VG slow Ca2+ channels open.
 Slow inward flow of Ca2+ balances outflow of K+.
 Myocardial APS (CONTINUED)

 Rapid repolarization:
 VG K+ channels open.
 Rapid outward diffusion
of K+.
 Conducting Tissues of the Heart
 APs spread through myocardial cells through gap junc-
tions.
 Impulses cannot spread to ventricles directly because
of fibrous tissue.
 Conduction pathway:
 SA node.
 AV node.
 Bundle of His.
 Purkinje fibers.
 Stimulationof Purkinje fibers cause both ventricles to
contract simultaneously.
Conducting Tissues of the Heart (CONTINUED)
CONDUCTION SYSTEM OF HEART
BEATS
Refer to your
textbook to
identify
the structures
of the heart’s
conduction
system in the
correct se-
quence for the
heart to beat.
 Conduction of Impulse
 APs from SA node spread quickly at rate of 0.8 -
1.0 m/sec.
 Time delay occurs as impulses pass through AV
node.
 Slow conduction of 0.03 – 0.05 m/sec.
 Impulse conduction increases as spread to Purk-
inje fibers at a velocity of 5.0 m/sec.
 Ventricular contraction begins 0.1–0.2 sec. after con-
traction of the atria.
Regulation of the Heart function
Regulation of the Cardiac Function

1) Nervous control
• Sympathetic control
• Parasympathetic control
• Higher centers
• Reflexes
2) Hormonal Control
3) Autoregulation
4) Other factors
Regulation of the Cardiac Function

1) Nervous control
• Sympathetic control
• Parasympathetic con-
trol
Sympathetic Nervous System
- controls all components of the heart.
- release Norepinephrine (NE).
- increases heart rate (positive chronotropic) and con-
tractility (positive inotropic).

1

Cell
Parasympathetic Nervous System (PNS)
- controls SA node and AV node.
- releases Acetylcholine (Ach).
- decreases heart rate (negative chronotropic).
- prolongs delay at AV node.
- has little effect on contractility.

Cell
Higher Centers of Auto-
nomic Nervous System

- Medulla Oblon-
gata

- Hypothalamus,
Thalamus, Cerebral
cortex
Centers in Medulla Oblongata
Sympathetic center:
distinct accelerator and augmentor
Parasympathetic center:
Nucleus vagus and nucleus ambiguus
Hypothalamus, Thalamus, Cerebral cortex
Involved in the cardiac response to environmental
temperature changes, exercise, or during excite-
ment, anxiety, and other emotional states
Neural Control via Reflexes
Baroreceptors
1) Baroreceptor Reflex

- stimulated by increase in arterial pressure (stretch)

- Effect: negative chronotropic and inotropic
- regulate the heart when BP increases or drops
- involved in short term regulation of BP
Chemoreceptors

Chemoreceptors

Chemoreceptors
2) Chemoreceptor Reflex

- stimulated by oxygen, pH, or CO2

- overall effect: positive choronotropic and inotropic.
- less important in regulating cardiac function
 3) Proprioceptor Reflex

- Stimulated by muscle and joint movement

- Effects: increase heart rate during exercise
Regulation by Hormones

Epinephrine
- released from adrenal
gland.
- increases heart rate
and contractility.

Thyroxin
- released from thyroid
gland.
- increases heart rate.
Autoregulation of the Heart

Stroke volume is autoregulated by ventricular

filling (Frank-Starling law).

More in SV
More out
4) Other Factors
- Blood level of ionic calcium, sodium, and potas-
sium
Hypercalcemia (high plasma Ca++):
positive inotropic
Hypernatremia (high plasma Na+):
negative chronotropic
Hyperkalemia (high plasma K+):
negative chronotropic
used in lethal injection

- Age, gender, exercise, and body temperature

 Refractory Periods
 Heart contracts as
syncytium.
 Contraction lasts al-
most 300 msec.
 Refractory periods last
almost as long as con-
traction.
 Myocardial muscle
cannot be stimulated
to contract again until
it has relaxed.
 Summation cannot oc-
cur.
 Excitation – Contraction Coupling in
Heart Muscles
 Depolarization
of myocardial cell stimulates
opening of VG Ca2+ channels in sarcolema.
 Ca2+ diffuses down gradient into cell.
 Stimulates opening of Ca2+-release channels in SR.
 Ca2+ binds to troponin and stimulates contraction
(same mechanisms as in skeletal muscle).
 During repolarization Ca2+ actively transported
out of the cell via a Na+-Ca2+- exchanger.
 Electrocardiogram (ECG/EKG)

 The body is a good conductor of electricity.

 Tissue fluids have a high [ions] that move in response to
potential differences.
 Electrocardiogram:
 Measure of the electrical activity of the heart per unit
time.
 Potential differences generated by heart are conducted to body
surface where they can be recorded on electrodes on the skin.
 DoesNOT measure the flow of blood through the
heart.
 ECG LEADS
 Bipolar leads:
 Record voltage between elec-
trodes placed on wrists and legs.
 Right leg is ground.
 Unipolar leads:
 Voltage is recorded between a
single “exploratory electrode”
placed on body and an electrode
built into the electrocardiograph.
 Placed on right arm, left arm, left
leg, and chest.
 Allow to view the changing pat-
tern of electrical activity from dif-
ferent perspectives.
 ECG

 P wave:
 Atrial depolariza-
tion.
 QRS complex:
 Ventricular depo-
larization.
 T wave:
 Ventricular repo-
larization.
ASSIGNMENT
Write on ECG Intervals and Segment
 Correlation of ECG with Heart Sounds

 First heart sound:

 Produced immediately af-
ter QRS wave.
 Rise of intraventricular
pressure causes AV valves
to close.
 Second heart sound:
 Produced after T wave be-
gins.
 Fall in intraventricular
pressure causes semilunar
valves to close.
 SYSTEMIC CIRCULATION

Arteries.
Arterioles.
Role is to direct
the flow of blood
Capillaries.
from the heart to
Venules.
the capillaries, and
Veins. back to the heart.
 BLOOD VESSELS

 Walls composed of 3 “tunics:”

 Tunica externa:
 Outer layer comprised of connective tissue.
 Tunica media:
 Middle layer composed of smooth muscle.
 Tunica interna:
 Innermost simple squamous endothelium.
 Basement membrane.

 Layer of elastin.
 BLOOD VESSELS (CONTINUED)

 Elastic arteries:
 Numerous layers of elastin fibers between smooth mus-
cle.
 Expand when the pressure of the blood rises.
 Act as recoil system when ventricles relax.
 Muscular arteries:
 Are less elastic and have a thicker layer of smooth mus-
cle.
 Diameter changes slightly as BP raises and falls.
 Arterioles:
 Contain highest % smooth muscle.
 Greatest pressure drop.
 Greatest resistance to flow.
 BLOOD VESSELS (CONTINUED)

 Mostof the blood volume is contained in the ve-

nous system.
 Venules:
 Formed when capillaries unite.
 Very porous.
 Veins:
 Contain little smooth muscle or elastin.
 Capacitance vessels (blood reservoirs).
 Contain 1-way valves that ensure blood flow to the heart.
 Skeletal
muscle pump and contraction of di-
aphragm:
 Aid in venous blood return of blood to the heart.
 TYPES OF CAPILLARIES
 Capillaries:
 Smallest blood vessels.
 1 endothelial cell thick.
 Provide direct access to cells.
 Permits exchange of nutrients and wastes.

 Continuous:
 Adjacent endothelial cells tightly joined together.
 Intercellular channels that permit passage of molecules (other than proteins)
between capillary blood and tissue fluid.
 Muscle, lungs, and adipose tissue.

 Fenestrated:
 Wide intercellular pores.
 Provides greater permeability.
 Kidneys, endocrine glands, and intestines.

 Discontinuous (sinusoidal):
 Have large, leaky capillaries.
 Liver, spleen, and bone marrow.
 ATHEROSCLEROSIS

 Most common form of arteriosclerosis (hardening

of the arteries).
 Mechanism of plaque production:
 Begins as a result of damage to endothelial cell wall.
 HTN, smoking, high cholesterol, and diabetes.
 Cytokines are secreted by endothelium; platelets,
macrophages, and lymphocytes.
 Attract more monocytes and lymphocytes.
 ATHEROSCLEROSIS (CONTINUED)

 Monocytes become
macrophages.
 Engulf lipids and trans-
form into foam cells.
 Smooth muscle cells
synthesize connec-
tive tissue proteins.
 Smooth muscle cells
migrate to tunica in-
terna, and proliferate
forming fibrous
plaques.
 CHOLESTEROL AND PLASMA
LIPOPROTEINS
 High blood cholesterol associated with risk of atheroscle-
rosis.
 Lipids are carried in the blood attached to protein carriers.
 Cholesterol is carried to the arteries by LDLs (low-density
lipoproteins).
 LDLs are produced in the liver.
 LDLs are small protein-coated droplets of cholesterol, neutral fat, free
fatty acids, and phospholipids.
 CHOLESTEROL AND PLASMA
LIPOPROTEINS (CONTINUED)

 Cells in various organs contain receptors for pro-

teins in LDL.
 LDL protein attaches to receptors.
 The cell engulfs the LDL and utilizes cholesterol for different
purposes.
 LDL is oxidized and contributes to:
 Endothelial cell injury.
 Migration of monocytes and lymphocytes to tunica interna.

 Conversion of monocytes to macrophages.

 Excessive cholesterol is released from the cells.

 Travel in the blood as HDLs (high-density lipoproteins), and re-
moved by the liver.
 Artery walls do not have receptors for HDL.
 ISCHEMIC HEART DISEASE
 Ischemia:
 Oxygen supply to tissue is
deficient.
 Most common cause is ath-
erosclerosis of coronary ar-
teries.
 Increased [lactic acid] pro-
duced by anaerobic respira-
tion.
 Angina pectoris:
 Substernal pain.
 Myocardial infarction
(MI):
 Changes in T segment of
ECG.
 Increased CPK and LDH.
 ARRHYTHMIAS DETECTED ON
ECG

 Arrhythmias:
 Abnormal heart rhythms.
 Flutter:
 Extremely rapid rates of excita-
tion and contraction of atria or
ventricles.
 Atrial flutter degenerates into
atrial fibrillation.
 Fibrillation:
 Contractions of different groups
of myocardial cells at different
times.
 Coordination of pumping impos-
sible.
 Ventricular fibrillation is life-
threatening.
 ARRHYTHMIAS DETECTED ON
ECG (CONTINUED)

 Bradycardia:
 HR slower < 60 beats/min.
 Tachycardia:
 HR > 100 beats/min.
 First–degree AV nodal block:
 Rate of impulse conduction through AV node exceeds
0.2 sec.
 P-R interval.
 Second-degree AV nodal block:
 AV node is damaged so that only 1 out of 2-4 atrial APs
can pass to the ventricles.
 P wave without QRS.
 ARRHYTHMIAS DETECTED ON
ECG (CONTINUED)

 Third-degree(com-
plete) AV nodal block:
 None of the atrial
waves can pass through
the AV node.
 Ventricles paced by ec-
topic pacemaker.
Take into account
that great love and
great achievements
involve great risk.