Cardiovascular Dynamics During Exercise - e
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Transcript Cardiovascular Dynamics During Exercise - e
Cardiovascular Dynamics
During Exercise
Chapters 15 & 16
Introduction
At rest: O2 supply = O2 demand
Exercise: O2 demand increases
To the muscles
To the heart
To the skin
Maintain flow to the brain
How does the heart increase O2
supply to meet the O2 demand?
Cardiac Output
Q = heart rate times stroke volume
Cardiac Output
Blood flow per minute.
At rest Q = 5-6
liters/min
Q increases linearly
with the demand for
more O2
Indicator of oxygen
supply
How does cardiac output increase?
Increase heart rate
Increase stroke volume
Heart Rate
Resting heart rate
Anxiety
Dehydration
Temperature
Digestion
Over-training
The most important factor for increasing Q
during acute exercise.
Heart Rate
What causes HR to increase during exercise?
Decrease parasympathetic (vagal) stimulation
Increase sympathetic stimulation
Heart Rate
Steady state exercise
Why does heart rate level off during steady
state exercise?
Heart Rate
Increases with intensity and levels off
at maximal effort.
–
HRmax = 220 – age
–
(± 12)
Stroke Volume
Volume pumped per
beat of the heart
Influenced by preload
and afterload
Stroke
Volume
Increases until
about 25-50%
of maximum
After that it may
plateau
(untrained) or
continue to
increase
(trained)
Decrease at
maximum
effort?
Stroke Volume
How does stroke volume increase during
exercise?
Increase preload (EDV)
–
Increase venous return
•
Muscle pump, etc.
Decrease afterload
–
Vasodilation
•
Metabolic control and sympathetic stimulation
Increase contractility (ESV)
–
Increase sympathetic stimulation
Frank-Starling Mechanism
Frank-Starling mechanism: the ability of the heart to
alter the force of contraction is dependent on changes
in preload.
As the myocardial fibers are stretched, the force of
contraction is increased.
Because the length of the fiber is determined primarily
by the volume of blood in the ventricle, EDV is the
primary determinant of preload
This graph depicts the Frank-Starling mechanism of
compensation in CHF.
The black curves represent ventricular function in a
normal subject and the colored curve is with left
ventricular dysfunction.
Line N to A represents the initial reduction in cardiac
output due to CHF.
Line A to B represents the Frank-Starling mechanism of
compensation; an increase in left ventricular end-diastolic
pressure needed to maintain cardiac output.
Stroke Volume
Stroke Volume
Increased
sympathetic
stimulation
Vasodilation from
‘autoregulation’
Cardiovascular drift
Caused by a decrease in venous return
Cardiac output is maintained by…..?
Cardiovascul
ar Drift
Stroke Volume
SV greater in
trained
Most significant
effect of training
Result
•
•
An increase in cardiac output…
•
Increase HR
•
Increase SV
…results in an increase in O2 supply
Hemodynamics
Blood Vessels
Arteries
Arterioles
Capillaries
Venules
Veins
Physical Characteristics of
• Plasma
Blood
Liquid portion of blood
Contains ions, proteins, hormones
•
Cells
Red blood cells
Contain hemoglobin to carry
oxygen
White blood cells
Platelets
The Blood
Arterial blood carries 20 ml of oxygen
per 100 ml of blood
Hematocrit
Percent of blood composed of cells
The Blood
•
Arterial blood:
97-98%
saturated with
O2
•
Venous blood
–
Rest – 75%
–
Exercise – 25%
Blood
Pressure
Expressed as
systolic/diastolic
Normal is 120/80 mmHg
High is 140/90 mmHg
Systolic pressure (top
number)
Pressure generated during
ventricular contraction
(systole)
Diastolic pressure
Pressure in the arteries
during cardiac relaxation
Blood Pressure
•
Pulse pressure
Difference between systolic and
diastolic
Pulse Pressure = Systolic - Diastolic
•
Mean arterial pressure (MAP)
Average pressure in the arteries
MAP = Diastolic + 1/3(pulse pressure)
Mean Arterial
Pressure
• Blood pressure
of 120/80 mm
Hg
•
MAP = 80 mm Hg +
.33(120-80)
•
= 80 mm Hg + 13
•
= 93 mm Hg
Hemodynamics
•
Based on interrelationships
between:
– Pressure
– Resistance
Hemodynamics:
Pressure
Blood flows from high low
pressure
Proportional to the difference
between MAP and right atrial
pressure (P)
Blood Flow Through the
Systemic Circuit
Hemodynamics:
Resistance
Resistance depends upon:
Length of the vessel
Viscosity of the blood
Radius of the vessel
A small change in vessel diameter
can have a dramatic impact on
resistance!
Length x viscosity
Resistance =
Radius4
Hemodynamics:
Blood Flow
Directly proportional to the pressure
difference between the two ends of the
system
Inversely proportional to resistance
Pressure
Flow =
Resistance
Sources of Vascular
Resistance
MAP decreases throughout the
systemic circulation
Largest drop occurs across the
arterioles
Arterioles are called “resistance
vessels”
Pressure Changes Across
the Systemic Circulation
Pressure
Changes
During the
Cardiac
Cycle
Factors That Influence
Arterial Blood Pressure
Cardiovascular Control
How can the blood vessels increase blood
flow?
Vasodilation to increase blood flow to
muscles and skin
Waste products (metabolic or local control)
Sympathetic stimulation (cholinergic)
Vasoconstriction to maintain blood
pressure
Sympathetic stimulation (adrenergic)
Maximum muscle blood flow is limited by
the ability to maintain blood pressure
Vasodilation
Vasoconstriction
Blood Vessels
Oxygen Extraction
Measured as a-v
O2 difference
•
a = O2 in arteries (20 ml/100 ml of blood)
•
v = O2 in veins (15 ml/100 ml of blood)
•
(a-v)O2 = 5 ml/100 ml of blood
a-v O2 difference
No change in O2 content in the
blood
Remains at 20 ml/100 ml of blood
Decrease in O2 inside the
muscle
High pressure to a Low pressure
Greater pressure difference
between the blood and the
muscles
Oxygen moves from a HIGH
pressure area (blood) to a LOW
pressure area (muscle)
Therefore, more O2 is extracted
from the blood
High pressure to a Lower pressure
RESTING
20 ml or P02 98
EXERCISE
20 ml or P02 98
5 ml extracted
PO2 = 40
15 ml extracted
PO2 = 20
Lower PO2 due to an
increase in O2
consumption (VO2)
during exercise
Oxygen Consumption
VO2
liters per minute
milliliters per kilogram per minute
VO2 = oxygen supply x oxygen
extraction
VO2 = Q x a-v O2 difference
VO2 = HR x SV x a-v O2 difference
Oxygen Consumption
An increase in oxygen supply leads to an
increase in oxygen consumption
Increase in cardiac output
With help from HR and SV
Increase in (a-v)O2
More O2 is supplied and extracted
Therefore, more O2 can be used by the
muscle fibers (mito)
Oxygen Consumption
Q and a-v O2 difference each account
for 50% of the increase in VO2 during
exercise
Near maximal exercise, Q accounts for
75% of the increase in VO2
Oxygen Consumption
VO2 increases with intensity
VO2 = rate of blood flow times the O2
extracted from a given amount of blood
VO2 = cardiac output x a-vO2 difference
VO2 can increase by
A greater blood flow
Taking more oxygen out of every 100 ml of
blood
What limits aerobic
exercise?
Lack of oxygen supply?
If so, wouldn’t the muscles be more
anaerobic?
And, wouldn’t the heart also be more
anaerobic?
But an anaerobic heart produces angina
Maybe the central nervous system protects
the heart from ischemia by causing muscle
fatigue before the heart becomes