Download Cardiac Output Regulation of Cardiac Output Autonomic nervous

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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)
ie at rest you circulate twice your entire blood volume every minute
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
Parasympathetic and sympathetic have opposing effects
Factors Affecting Cardiac Output:
Heart Rate
Pacemaker (SA node) initiates contraction – innervated by autonomic
Parasympathetic slows heart rate (dominant at rest)
Sympathetic increases heart rate
Balance between sympathetic and parasympathetic is key
Adrenaline (epinephrine) - same effect as sympathetic nervous system
Glucagon - increases heart rate
Factors Affecting Cardiac Output:
Stroke Volume
Primary factors affecting stroke volume
1) Ventricular contractility
2) End-diastolic volume (preload)
3) Afterload
Afterload = pressure in aorta during ejection
This is the force that the heart must pump against
1) ventricular contractility
If ventricles contract with more force they eject
more blood – SV increases
Sympathetic nerves increase SV
Parasympathetic have no effect
Adrenaline increases SV
2) EDV
End-diastolic volume: intrinsic
control mechanism
Length-Tension Curve (Starling Curve)
for cardiac muscle
EDV is the preload – the work
the heart must do
Increased EDV stretches the
myocardium (cardiac muscle)
The resulting contraction is
Increased EDV= increased
SV: this is called the Starling
This mechanism ensures that
venous return matches
cardiac output – the heart
pumps out the blood that is
returned to it
Increase EDV stretches muscle
fibres: closer to optimum length
Greater strength of contraction:
increased SV
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
Skeletal muscle relaxes
Blood flows into veins
Distribution of Cardiac Output at rest
and during exercise
Independent regulation of blood
flow during exercise
Cardiac output increases during
Distribution of blood does not
increase proportionally
Dilation to skeletal muscle and
heart increases blood flow
Constriction to GI tract and
kidneys decreases blood flow
Overview of the Vasculature
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 - drain blood to veins
–  Veins – relatively large converging vessels that conduct blood to the
heart. Major vein is vena cava (superior and inferior)
–  Closed system
–  Arteries branch; veins converge
–  Differences between blood vessel types:
•  Structure: diameter; composition of walls
•  Function
Blood Vessel anatomy
Carry blood away from heart
Thick, elastic walls
Large diameter, therefore low resistance to blood flow
Pressure remains relatively constant through arteries.
Pressure reservoirs because
of thick elastic walls that
stretch during systole - elastic
recoil helps maintain blood
pressure during diastole
Physiology research focus: Arteries and disease
Atherosclerosis - ‘hardening of the arteries’: wall thickens and hardens
One of the leading causes of death worldwide.
A plaque composed of cholesterol, calcium and other substances builds up
in an artery
Plaques reduce blood flow
They can rupture and cause clots - heart
attacks or strokes can result
Often occurs with age
Smoking, diabetes and obesity are
other risk factors
Angioplasty or stent implantation
can be used as treatments
Arterioles are resistance vessels
Small diameter
Walls contain smooth muscle: regulation of radius, and thus, resistance
Functions: Regulate blood pressure
•  Control distribution of blood to body organs
Effect of diameter.
•  Wider diameter – vasodilation (vasodilatation)
•  Narrower diameter - vasoconstriction
•  Greater diameter, greater blood flow
Influenced by nerves, hormones and local effects in tissues eg. during
Arterioles: vasoactivity
–  Radius dependent on contraction state
of smooth muscle in arteriole wall
–  Vasoconstriction: increased contraction
(decreased radius)
–  Vasodilation: decreased contraction
(increased radius)
–  Functions of Varying Arteriole Radius
–  Controlling blood flow to individual capillary beds
–  Regulating mean arterial pressure
Factors that influence vasodilation and
Autonomic nerves (sympathetic constricts)
Hormones (eg adrenaline constricts)
Metabolism (eg. decreased O2 causes dilation)
These factors therefore influence blood flow
Site of exchange between blood and tissue
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
1 mm long
Materials exchanged:
Fatty acids
Hormones etc.
Capillaries can be continuous or
Fenestrated capllaries located in kidneys, liver, intestines, bone marrow
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
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
Physiology research focus: cerebral blood flow
and disease
Pathophysiology of the cerebral
vasculature is associated with
many brain diseases/injuries
including stroke, traumatic brain
injury and Alzheimer’s Disease.
However we still do not
understand the underlying
mechanisms – this is a very
active area of research in
Smaller than arterioles
Connect capillaries to veins
Thin walls
Little smooth muscle in walls
Some exchange of material between blood and interstitial
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