Download Overview of the Cardiovascular System

11/28/11
Overview of the Cardiovascular System
The Heart: high-pressure pump
Blood Vessels (vasculature):
distribute blood to all parts of
the body and return blood to
the heart
Blood: transport medium in which
materials to be transported
are dissolved or suspended
2 vascular (blood vessel) loops:
Pulmonary circulation: from heart to
lungs and back)
Systemic circulation: from heart to
other organs and back
Overview of Cardiovascular System Functions
Most basic and important function: to provide adequate blood flow to all the organs
and tissues of the body
Transport
Respiratory gases: oxygen & carbon dioxide
Nutrition: absorbed products of digestion
Excretion: metabolic wastes delivered (to liver and kidneys)
Regulation & Protection: hormones, immune cells, clotting proteins
Regulation
Hormones
Thermoregulation (skin blood flow)
Protection
Blood clotting (protects against haemorrhage)
Pathogens (immune system)
Exchange between blood and tissue takes place in capillaries
Blood gases:
Pulmonary capillaries
Blood entering lungs is deoxygenated
Oxygen diffuses from tissue to blood (CO2 from blood to tissue)
Blood leaving lungs is oxygenated
Systemic capillaries
Blood entering tissues is oxygenated
Oxygen diffuses from blood to tissue (CO2 from tissue to blood)
Blood leaving tissues is deoxygenated
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Blood
On average, 5L of blood (approx 8% body weight)
Arterial Blood
Leaving the heart
Bright Red
High oxygen content
(oxyhaemoglobin)
Venous blood
Returning to the heart
Darker colour
Lower oxygen content
(deoxyhaemoglobin)
Cellular portion of blood (45% blood volume)
a) Erythrocytes (red blood cells): oxygen transport
b) Leukocytes (white blood cells): immune function
c) Platelets: Blood clotting
Plasma (55% blood volume)
a) Water
b) Dissolved solutes eg. ions
c) Plasma proteins
d) Other components eg. metabolites, hormones, enzymes, antibodies.
Anatomy of the heart
Size of fist
Weighs approximately 250 – 350 grams
Location
Located in thoracic
cavity - Diaphragm
separates abdominal
cavity from thoracic
cavity
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The Heart: anatomy
Ventricle walls thicker
Four chambers: 2 Atria & 2 Ventricles
than atrial walls
Dual pump: right & left sides
Left ventricle wall
Septum prevents mixture of blood between the 2 thicker than right
sides
ventricle wall
Atria and ventricles separated by dense connective
tissue: the fibrous skeleton
(allows them to contract separately)
Cardiac Muscle (myocardium)
Gap junctions - Contracts as a unit
Desmosomes - Resist stress
Atria & Ventricles are separate units
separated by fibrous skeleton
99% contractile cells
1% autorhythmic cells
Function:
Rhythmic contraction and relaxation generates heart pumping action
Contraction pushes blood out of heart into vasculature
Relaxation allows heart to fill with blood
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Valves and Unidirectional Blood Flow
Pressure within chambers of heart vary with heartbeat cycle
Pressure difference drives blood flow: High pressure to low pressure
Normal direction of flow: Atria to ventricles, then ventricles to arteries
Valves prevent backward flow of blood
All valves open passively based on pressure gradient
Atrioventricular valves = AV valves
R: tricuspid valve; L: bicuspid (mitral)
Papillary muscles and chordae
tendinae keep AV valves from everting
Semilunar valves
Aortic Valve
Pulmonary Valve
Electrical Activity of the Heart
Autorhythmic cells generate their own rhythm
Conduction System
Pacemaker cells: Coordinate and provide rhythm to heartbeat
The Sinoatrial (SA) node is the pacemaker of the heart
Conduction fibers: Rapidly conduct action potentials initiated by pacemaker
cells to myocardium
Atrioventricular (AV) node
Bundle of His
Purkinje fibers
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Spread of Excitation
Atria contract first, then ventricles (fibrous skeleton)
Coordination due to presence of gap junctions and
conduction pathways
Recording the Electrical Activity of the Heart
with an Electrocardiogram
ECG: non-invasive technique that tests for clinical abnormalities in
electrical activity of the heart
Body is conductor: currents in body spread to surface (ECG, EMG, EEG)
Distance & amplitude of spread depends on size of potentials and
synchronicity of potentials from other cells
Cardiac electrical activity is synchronized
Standard ECG Trace
P wave
atrial depolarization
QRS complex
ventricular depolarization
T wave
ventricular repolarization
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Abnormal Heart Rates
“Sinus rhythm”: generated by SA node
Abnormal Heart Rates:
Tachycardia- fast
Bradycardia- slow
Pathophysiology
If the SA node is damaged, other cardiac cells
can take over its pacemaker role.
AV node and Purkinje fibres: these are latent
pacemakers
Artificial pacemakers can also be used
Fibrillation
Loss of coordination of electrical activity. Can be
corrected by defibrillation
Atrial fibrillation - weakness
Ventricular fibrillation - death within minutes
Damage to heart muscle
Cardiac Cycle
Events associated with the flow of blood through the heart
during a single complete heartbeat
Mechanical Events
Systole - Ventricular contraction and blood ejection
Diastole - Ventricular relaxation and filling
Opening of Valves
Valves open passively due to pressure gradients
AV valves open when P atria > P ventricles
Semilunar valves open when P ventricles > P arteries
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Pressure & volume changes during cardiac cycle
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START
Isovolumic ventricular
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relaxation: as ventricles
relax, pressure in ventricles
falls, blood flows back into
cups of semilunar valves
and snaps them closed. Ventricular ejection:
4
as ventricular pressure
rises and exceeds
pressure in the arteries,
the semilunar valves
open and blood is
ejected. Late diastole: both sets of
chambers are relaxed and
ventricles fill passively.
2
Atrial systole: atrial contraction
forces a small amount of
additional blood into ventricles.
Isovolumic ventricular
3
contraction: first phase of
ventricular contraction pushes
AV valves closed but does not
create enough pressure to open
semilunar valves.
Ventricular Volume and Stroke Volume
EDV = end diastolic volume = volume of blood in ventricle at
end of diastole
ESV = end systolic volume = volume of blood in ventricle at
end of systole
SV = stroke volume = volume of blood ejected from heart each
cycle = SV = EDV - ESV
130 mL – 70 mL = 60 mL
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Cardiac Output
Volume of blood pumped by each ventricle per minute
Cardiac Output = CO = SV x HR
Equal on both sides of the heart
Average CO = 5 litres/min at rest (70ml/beat x 70beat/min)
Can increase 5-fold during exercise
Regulation of Cardiac Output
Regulate heart rate and stroke volume
These can change from moment to moment
Extrinsic and Intrinsic regulation
Extrinsic - outside
»  hormones (adrenaline)
»  nerves (autonomic nervous system)
Intrinsic - local
Autonomic nervous system
Efferent nervous system
Autonomic
(involuntary)
Somatic
(voluntary)
Parasympathetic
Sympathetic
Motor
Parasympathetic and sympathetic have opposing effects
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Factors Affecting Cardiac Output
Heart Rate
Neuronal:
Pacemaker (SA node) initiates
contraction – innervated by autonomic
nerves
Parasympathetic slows heart rate
(dominant at rest)
Sympathetic increases heart rate
Balance between sympathetic and
parasympathetic is key
Stroke Volume
Primary factors affecting stroke
volume
1)  Afterload:
Pressure in aorta during ejection
This is the force that the heart must
pump against
2) End-diastolic volume (preload)
3) Ventricular contractility
Hormonal:
Adrenaline (epinephrine) - same effect
as sympathetic nervous system
Glucagon - increases heart rate
2) EDV
3) ventricular contractility
Length-Tension Curve (Starling Curve)
for cardiac muscle
End-diastolic volume is the preload – the work
the heart must do.
Increased EDV stretches the cardiac muscle
fibres: closer to optimum length
Next contraction is greater: increased SV
Increased EDV= increased SV: this is called
the Starling Effect
An intrinsic mechanism ensures that venous
return matches cardiac output – the heart
pumps out the blood that is returned to it
If ventricles contract with more force they
eject more blood & SV increases
Sympathetic nerves increase SV
Parasympathetic have no effect
Adrenaline increases SV
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Autonomic regulation of Cardiac Output
Remember: CO = HR x SV
Autonomic nerves affect both variables to influence CO
Increases in Cardiac Output: exercise
CO can increase 5 fold during exercise
Exercise affects HR and SV
Influence of autonomic nerves
Increased venous return eg via skeletal muscle pump
One-way valves in peripheral veins
Skeletal muscle contracts and
squeezes veins: increased pressure
Blood moves toward heart
Blood cannot move backwards
(valves)
Skeletal muscle relaxes
Blood flows into veins
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Distribution of Cardiac Output at rest and during exercise
Independent regulation of blood
flow during exercise
Cardiac output increases during
exercise
Distribution of blood does not
increase proportionally
Dilation to eg. skeletal muscle
and heart increases blood flow
Constriction to GI tract and
kidneys decreases blood flow
Overview of the Vasculature (Blood vessels)
Heart →Arteries → Arterioles → Capillaries → Venules → Veins
Arteries: relatively large, branching
vessels that conduct blood away from
the heart. Major artery is aorta
Microcirculation
Arterioles: small branching vessels with
high resistance
Capillaries: site of exchange between
blood and tissues
Venules: small converging vessels that
drain blood to veins
Veins: relatively large converging
vessels that conduct blood to the heart.
Major vein is vena cava (superior and
inferior)
Arteries branch; veins converge
Differences between blood vessel types:
Structure: diameter; composition of walls
Function
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Arteries
Rapid transport pathway: large diameter - little resistance
Under high pressure: walls contain elastic and fibrous tissue
Arteries are pressure reservoirs
Thick elastic arterial walls expand as
blood enters arteries during systole &
recoil during diastole
Arteries & disease
Atherosclerosis - ‘hardening of the arteries’
A plaque composed of cholesterol, calcium
and other substances builds up in an artery
Plaques reduce blood flow; they can rupture &
cause clots – heart attacks or strokes can
result
Risk factors: age; smoking; diabetes; obesity
Treatments: Angioplasty; stent implantation
Arterioles
Resistance vessels in microcirculation
Connect arteries to capillaries
Contain smooth muscle: regulate
radius (& thus resistance; below)
Arterioles provide greatest resistance
to blood flow
Largest pressure drop in vasculature
(90 mmHg to 40 mmHg)
Radius dependent on contraction state of smooth muscle in
arteriole wall
Vasoconstriction: increased contraction (decreased radius)
Vasodilation: decreased contraction (increased radius)
Functional importance
Controlling blood flow to individual capillary beds
Regulating mean arterial pressure
Vasoactivity influenced by:
Autonomic nerves (sympathetic constricts)
Hormones (eg adrenaline constricts)
Metabolism (eg. decreased O2 causes dilation)
These factors therefore influence blood flow
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Capillaries
Site of exchange between blood and tissue
Materials exchanged:
O2, CO2, glucose, fatty acids, hormones etc.
1 mm length; 5-10 µm diameter (small diffusion
distance)
Walls - 1 endothelial cell layer plus basement
membrane (small diffusion barrier)
10-40 billion per body; total SA = 600 m2
Most cells within 2 or 3 cell diameters of a capillary
Capillaries can be continuous
or fenestrated
Fenestrated capllaries are more permeable.
Located in kidneys, liver, intestines, bone marrow
Cerebral vessels
The arborizing network of cerebral arteries
is demonstrated here in this cerebral
angiogram seen laterally after injection of
contrast into the right internal carotid
artery
Blood-brain barrier
Tight junctions between endothelial cells lining
cerebral blood vessels
Prevents easy passage of large
macromolecules and pathogens between the
circulation and the brain
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Venules
Smaller than arterioles
Connect capillaries to veins
Thin walls
Little smooth muscle in walls
Some exchange of material between blood and interstitial
fluid
Veins
Large diameter, but thin walls, which contain muscle and
elastic tissue
Valves allow unidirectional blood flow
Volume reservoirs: at rest, systemic veins contain 60% of
total blood volume
Return of blood to heart from veins is called venous return
Path of blood flow through cardiovascular system
Cardiovascular system is a closed system
Flow through systemic and pulmonary circuits
are in series
Left ventricle  systemic circuit  right atrium
 right ventricle pulmonary circuit  left
atrium  left ventricle
Flow within systemic (and pulmonary) circuit is
in parallel: allows independent regulation of
blood flow to organs
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Blood Flow and Blood Pressure
Physical laws governing blood flow:
Pressure Gradients & Resistance in the Cardiovascular System
Pressure gradients: Flow occurs from high pressure to low pressure
Heart creates the pressure gradient for flow of blood
A gradient must exist throughout circulatory system to maintain blood flow
Resistance: systemic circuit is high pressure (gradient is approx 90mmHg),
high resistance;
pulmonary circuit is low pressure (gradient is approx 15mmHg), low resistance
Pressures
throughout the
vasculature are
variable
Flow = ΔP/R = pressure gradient/resistance
Pressure gradient across systemic circuit
Pressure gradient = pressure in aorta minus pressure in vena
cava just before it empties into right atrium
Pressure in aorta = mean arterial pressure (MAP) = 90 mm Hg
Pressure in vena cava = central venous pressure (CVP) = 0
mm Hg
Pressure gradient = MAP – CVP = 90 – 0 = 90 mm Hg
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Resistance in the Cardiovascular System
The lower the resistance, the greater the flow
Factors affecting resistance to flow
Poiseuille’s Law
R=
8ηL
πr4
8 & π = constants
L=length of vessel (normally doesn’t change)
η=viscosity of fluid (normally doesn’t change)
r=radius of vessel
In arterioles (and small arteries) – radius is regulated
RADIUS IS THE MOST IMPORTANT FACTOR
Flow = ΔP/R =
ΔPπ r4
8ηL
Regulate blood flow by regulating radius: vasoactivity
Vasodilation & vasoconstriction Functional importance
Controlling blood flow to individual capillary beds
Regulating mean arterial pressure
Vasoactivity influenced by:
Autonomic nerves (sympathetic constricts)
Hormones (eg adrenaline constricts)
Metabolism (eg. decreased O2 causes dilation)
These factors therefore influence blood flow
Control of blood flow distribution to organs
Regulation of organ blood flow based on need (eg to skeletal muscles during exercise)
Regulated by varying radius (and therefore resistance)
Organ blood flow = MAP / organ resistance
ie
driving force for blood flow
resistance to flow in that organ
For any given P gradient, blood flow
changes when resistance changes
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Distribution of Cardiac Output at rest and during exercise
Independent regulation of blood
flow during exercise
Cardiac output increases during
exercise
Distribution of blood does not
increase proportionally
Dilation to eg. skeletal muscle
and heart increases blood flow
Constriction to GI tract and
kidneys decreases blood flow
Blood pressure: Mean Arterial Pressure
MAP = driving force for blood flow
F = ΔP/R
Regulating MAP critical to normal function
MAP < normal: Hypotension
Clinical risk: Inadequate blood flow to tissues
MAP > normal: Hypertension
Clinical risk: Stress on heart and walls of blood vessels (heart attack, stroke)
Regulation of MAP
Flow = pressure gradient
resistance
CO = MAP
TPR
Therefore MAP=CO x TPR = HR x SV x TPR
TPR is the total peripheral resistance: this is the combined resistance of all
blood vessels (remember the importance of vasodilation and vasoconstriction)
This means that MAP is completely determined by HR, SV & TPR
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Short- and long-term regulation of MAP
Short-term regulation:
seconds to minutes
Involves heart and blood vessels
Primarily neuronal control
Long-term regulation:
minutes to days
Regulation of blood volume
Involves kidneys
Primarily hormonal control
Short-Term Regulation of MAP
The baroreceptor reflex:
A negative feedback loop that helps maintain
normal blood pressure
Baroreceptors are stretch receptors
(mechanoreceptos)
Arterial baroreceptors
High pressure baroreceptors
Sinoaortic baroreceptors
Location
Carotid sinus
Aortic arch
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Cardiovascular Control Centre
Medulla oblongata
Integration center for blood pressure regulation
Output
• Sympathetic nerves
• Parasympathetic nerves
Sympathetic:
SA node (increase HR)
Ventricles (increase contractility)
Arterioles (increase resistance)
Veins (increase venomotor tone)
Parasympathetic:
SA node (decrease HR)
Major neural pathways in the control
of cardiovascular function
Components of Baroreceptor Reflex
Detectors = baroreceptors
Afferents = nerves
Integration center = cardiovascular control center
Efferents = autonomic nervous system
Effectors = heart, arterioles, veins
Example: a person who had been lying down stands up quickly
•  Gravity causes venous pooling in the legs.
•  This causes a decrease in VR, causing a decrease in CO
•  This causes a decrease in blood pressure.
•  Baroreceptors sense the decrease: reflex occurs
•  The reflex causes increased sympathetic and decreased
parasympathetic activity.
•  CO and TPR are increased.
•  Blood pressure is increased back to normal.
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Baroreceptor Reflex in response to a decrease in MAP
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