Cardiovascular physiology. Cardiac enzymes and their effects in the body system. Cardiac output and effects increasing and decreasing it. Calculations if Ejected fraction and other cardiac parameters.
2. Cardiovascular Physiology
Cardiac Output
• Cardiac Output (CO) is the volume pumped by
the left ventricle each minute
– influenced by
• Stroke Volume (SV)
EDV – ESV = SV
135ml – 65ml = 70ml
• Heart Rate (HR) bpm
80 bmp
– CO = SV x HR
70ml/b x 72bpm = 5040 ml/min
=5.04L/min
– How is this controlled to account for changing
conditions? (exercise, disease, stress…)
• What influences SV?
• What influences HR?
3. Cardiovascular Physiology
Cardiac Output
• Influencing stroke volume
– Pre Load
• The amount of stretch
within the contractile
myocardial fibers
• Represents the “load”
placed on the muscle
fibers before they
contract
• They respond
according to length-
tension patterns
observed in muscle tissue
by Frank, then by Starling
– Became known as the Frank-Starling Law of the Heart
– “The heart will pump all the blood that is returned to it”
Relationship between Stretch and
Force within the left ventricle
4. Cardiovascular Physiology
Cardiac Output
• Influencing stroke volume
– Pre Load
• operates under Frank-Starling Law of the Heart
• What then influences the stretch applied to cardiac
muscle tissue prior to contraction?
– Venous return, driven by
» Skeletal muscle pump
» Respiratory pump
» Atrial Suction
5. Cardiovascular Physiology
Cardiac Output
• Influencing stroke volume
– Contractility
• Stronger contraction = larger stroke volume
• Due to inotropic agents
– Epinephrine, Norepinephrine, Digitalis* are (+) inotropic
agents
– ACh is a (-) inotropic agent
– How do they work?
*digitalis – a cardiac glycoside drug that lowers Na+/K+ ATPase activity and
therefore the NCX transporter activity, resulting in elevated ICF Ca2+ which
creates a stronger graded contraction.
7. Cardiovascular Physiology
Cardiac Output
• Influencing stroke volume
– Afterload
• This is the amount of pressure that is sitting on the semilunar
valves that must be overcome before ventricular ejection can
occur
• The more pressure that must be built up during Isovolumetric
ventricular contraction reduces the time that ejection can occur
– Reduces the ejection fraction (SV/EDV)
» Normal 70ml/135ml = 52%
» Elevated aortic pressure causes the reduction from normal
» 60ml/135ml = 44%
• indirect relationship
– Higher aortic pressure = lower stroke volume
• Causes?
– Elevated blood pressure
– Loss of compliance in aorta (loss of elasticity)
8. Cardiovascular Physiology
Cardiac Output
• Influencing Heart Rate
– Rate is set by pacemaker cells rate of
depolarization
• Chronotropic effects may be excitatory
– Sympathetic activity
• Or inhibitory
– Parasympathetic activity
9. Lecture Outline
• Cardiac Output & Controls
• Blood Flow & Blood Pressure Controls
• Medullary Center for Cardiovascular
Control & the Baroreceptor Reflex
10. Cardiac Physiology
Blood Flow & Blood Pressure Controls
• CO tells us how much blood is ejected per
minute and is influence by both intrinsic &
extrinsic factors
• Extrinsic factors (besides ANS) include
– blood vessels & blood pressure
– blood volume & viscosity
– capillary exchange & the lymphatic return
– cardiovascular disease
11. Cardiac Physiology
Blood Flow & Blood Pressure Controls
• Blood Vessels Function to
– Provide route (arteries – away, veins –
towards)
– Allow for exchange (capillaries)
– Control & regulate blood pressure
13. Cardiac Physiology
Blood Flow & Blood Pressure Controls
• Blood Vessel Structure
enables specific
functions
– Aorta
• absorb pulse pressure
(systolic pressure –
diastolic pressure) and
release energy creating
diastolic pulse
– Large arteries
• conduct and distribute
blood to regional areas
– Arterioles
• Regulate flow to tissues
and regulate MAP (mean
arterial pressure)
14. Cardiac Physiology
Blood Flow & Blood Pressure Controls
– Capillaries
• Allow for exchange
– Venules
• Collect and direct
blood to the veins
– Veins
• Return blood to heart
and act as a blood
reservoir
15. Windkessel Vessel --- Aorta and
big arteries.
Contain a large amount of elastic tissue besides the
smooth muscle.
Transiently store blood during systole, and then shrink
to produce onward blood flow during diastole.
16. Windkessel effect.
Convert the sharp pressure fluctuations in the left
ventricle (0 to 120 mmHg) into much smaller pressure
fluctuations in the arteries (80 to 120 mmHg).
Convert the intermittent ventricular ejection into
continuous blood blood in the vessels
17. Cardiac Physiology
Blood Flow & Blood Pressure Controls
• Blood Vessels & Blood Pressure
– Systolic Pressure
• The pressure that is created when the ventricles
contract
• Usually around 120 mm Hg
18. Cardiac Physiology
Blood Flow & Blood Pressure Controls
• Blood Vessels & Blood Pressure
– Diastolic Pressure
• The pressure that is created by the recoil of the
aorta AND the closure of the aortic semilunar valve
• Usually around 80 mm Hg
19. Cardiac Physiology
Blood Flow & Blood Pressure Controls
• Blood Vessels & Blood Pressure
– Pulse Pressure
• The difference between the systolic and diastolic pressures
– Usually 40 mm Hg (120 mm Hg – 80 mm Hg)
• Only applies to arteries
– Why do we care about systolic, diastolic and pulse
pressures?
• We can determine the average pressure within the arterial
system = Mean Arterial Pressure (MAP)
MAP = diastolic Pressure + 1/3 Pulse Pressure
MAP = 80 mm Hg + 1/3( 120 mm Hg – 80 mm Hg)
MAP = 93 mm Hg
• Then we can determine general health of the cardiovascular
system
20. Cardiac Physiology
Blood Flow & Blood Pressure Controls
• MAP is proportionate to the cardiac output and
the amount of peripheral resistance
– If CO increases but resistance to the outflow does not
change
• Then more blood is flowing into the system than out and
arterial pressure must go up to allow inflows to equal
outflows
21. Cardiac Physiology
Blood Flow & Blood Pressure Controls
• MAP is proportionate to the cardiac output and
the amount of peripheral resistance
– The opposition to blood flow in the arterioles
• Resistance is directly proportional to the length (L) of the
vessel, and the viscosity(η) (thickness) of the blood and
inversely proportional (to the 4th power) of the vessel radius,
so….
R L η/r4
However as the L and η should remain relatively constant, we
can determine that peripheral resistance is mainly a factor of
the vessel diameter
R 1/r4
22. Cardiac Physiology
Blood Flow & Blood Pressure Controls
• So… if resistance is
affected by the radius,
and flow is inversely
proportionate to the
resistance
– What effect will
vasoconstriction /
vasodilation have on
blood pressure and
blood flow? And what
controls it?
– What will obesity do to
blood pressure and
blood flow & why?
23. – Radius the main
determinant of
resistance
– Increased surface area
exposed to blood
increases resistance
– Flow is faster in larger
vessels than smaller
24. Conductance is a measure of the blood flow through
a vessel for a given pressure difference.
Small changes in diameter alter vessels ability to
conduct blood
25. States ‘the rate of blood flow is directly proportional to the
pressure difference and radius (^4) and inversely
proportional to viscosity and length of the vessel’
F is the rate of blood flow,
ΔP is the pressure difference between the ends of the vessel,
r is the radius of the vessel,
l is length of the vessel, and
η is viscosity of the blood.
26. Tension in Arterial Walls
The tension in the walls of arteries and veins in the
human body is a classic example of
• LaPlace's law.
• This geometrical law applied to a tube or
pipe says that for a given internal fluid
pressure, the wall tension will be
proportional to the radius of the vessel.
12/21/16 18
27. The implication of this law for the large arteries, which have
comparable blood pressures, is that the larger arteries must have
stronger walls since an artery of twice the radius must be able to
withstand twice the wall tension.
Arteries are reinforced by fibrous bands to strengthen them against
the risks of an aneurysm. The tiny capillaries rely on their small size.
Law of Laplace- Application
28. The walls of the capillaries of the human circulatory
system are so thin as to appear transparent under a
microscope, yet they withstand a pressure up to about
half of the full blood pressure.
LaPlace's law gives insight into how they are able to
withstand such pressures: their small size implies that
the wall tension for a given internal pressure is much
smaller than that of the larger arteries.
12/21/16 20
Capillary
Walls
29. Arterioles control blood flow
to organs
• The arterioles control vessel diameter through local and
reflex control
– Local controlling mechanisms include;
• Myogenic response by smooth muscle of arterioles
– Increased stretch due to increasing blood pressure causes vessel
constriction due to mechanically gated Ca2+ channel activation
– HYPEREMIA
• Paracrines – local substances which alter smooth muscle activity
– Serotonin
» Secreted by activated platelets
– Endothelin
» secreted by vascular endothelium
– NO secreted by vascular endothelium
– Bradykinin – from various sources
– Histamine – from mast cells in connective tissues
30. Arterioles control blood flow
to organs
• Local control through hyperaemia;
–Active Hyperaemia- increased
metabolic activity and accumulation
of metabolites such as Adenosine
secreted by cells in low O2
(hypoxic) conditions.
–O2, CO2, K+, H+, temp
• -Reactive Hyperaemia – Increased blood
flow after an ischemic event due to
accumulation of metabolites.
31. ARTERIOLES CONTROL OF BLOOD FLOW
• Hyperemia is locally mediated increases in blood
flow, may be
– Active or Reactive
32. Arterioles control blood flow
to organs
• REFLEX CONTROL
• Sympathetic control through;
Norepinephrine produces vasoconstriction in
most if not all organs via α1 receptors
epinephrine dilates the blood vessels in skeletal
muscle and the liver via β2 receptors
33. Epinephrine
Norepinephrine
α1 receptor on vessels
β1 receptor on heart
β2 receptor on vessels
(skeletal muscle and liver)
Vasoconstriction
Positive effect
Vasodilation
Sympathetics- through
adrenergic receptors
34. Parasympathetic nerve fiber to
peripheral vessels
Parasympathetic nerve fibers innervate
vessels of the blood vessels in
Meninges
the salivary glands
the liver
the viscera in pelvis
the external genitals
Importance: Regulate the blood flow of
these organs in some special situations.
36. Cardiac Physiology
Neural Regulation of Blood Pressure
• CNS contains the Medullary Cardiovascular
Control Center
– Receives inputs from carotid and aortic baroreceptors
– Creates outflow to sympathetic and parasympathetic
pathways
• Sympathetic to SA & AV nodes and myocardium as well as to
arterioles and veins
• Parasympathetic to the SA Node
– Baroreceptors initiate the baroreceptor reflex
37. 2 Cardiovascular Center
The control center of cardiovascular
activities is the nucleus groups at different
levels
spinal cord
brain stem
hypothalamus
limbic system
cerebral cortex
cerebellum
38. Cardiovascular centers of the
brainstem
vasoconstrictor-area
vasodilator area
cardioinhibitory area
relay station of afferent nerve
41. Long term Regulation
• This is achieved through hormones and the renal
system.
• Decrease through haemorrhage is one of the major
causes of this mechanism.
42. Angiotensin II
very potent vasoconstrictor
formed in the plasma through a chain reaction.
triggered by a substance, renin, released form kidneys.
Renin is released from kidneys in response to renal
ischemia, which may be due to a fall in blood pressure.
43. Effect of Angiotensin II
powerful constrictor
release aldosterone from the
adrenal cortex
acts on the brain to create the
sensation of thirst.
inhibit the baroreceotor reflex
and
increase the release of
norepinephrine from the
sympathetic postganglionic
fiber.
44. Vasopressin
antidiuretic hormone (ADH),
formed in the hypothalamus (mainly)
secreted through the posterior pituitary gland.
more powerful than angiotensin as a
vasoconstrictor.
during hemorrhage – increased
vasopressin - raise the arterial pressure as
much as 40 to 60 mmHg.
45. Vasopressin
Vasoconstriction has not a physiological
function
does not increase blood pressure when small
doses are injected in vivo
In healthy person, the plasma concentration is
too low to induce vasoconstrion
Acts on the brain to cause a decrease in
cardiac output.
in the area of postrema
Acts on the kidney – physiological (ADH)