Cardiovascular Dynamics During Exercise Chapters 15 & 16.
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Transcript of Cardiovascular Dynamics During Exercise Chapters 15 & 16.
Cardiovascular Dynamics During
ExerciseChapters 15 & 16
IntroductionAt 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 OutputQ = heart rate times stroke volume
Cardiac OutputBlood 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 RateResting heart rate
Anxiety
Dehydration
Temperature
Digestion
Over-training
The most important factor for increasing Q during acute exercise.
Heart RateWhat causes HR to increase during exercise?
Decrease parasympathetic (vagal) stimulation
Increase sympathetic stimulation
Heart RateSteady 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 VolumeIncreases until about 25-50% of maximum
After that it may plateau (untrained) or continue to increase (trained)
Decrease at maximum effort?
Stroke VolumeHow 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
Increased sympathetic stimulation
Vasodilation from
‘autoregulation’
Vasodilation from
‘autoregulation’
Cardiovascular driftCaused by a decrease in venous return
Cardiac output is maintained by…..?
Cardiovascular 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 Blood
• Plasma
Liquid portion of blood
Contains ions, proteins, hormones
• Cells
Red blood cells
Contain hemoglobin to carry oxygen
White blood cells
Platelets
Important in blood clotting
The Blood
Arterial blood carries 20 ml of oxygen per 100 ml of blood
HematocritPercent of blood composed of cells
The Blood
• Arterial blood: 97-98% saturated with O2
• Venous blood
– Rest – 75%
– Exercise – 25%
Blood PressureExpressed 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 (diastole)
Blood Pressure
• Pulse pressure
Difference between systolic and diastolic
• Mean arterial pressure (MAP)
Average pressure in the arteries
Pulse Pressure = Systolic - Diastolic
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 (ΔP)
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!
Resistance = Length x viscosity
Radius4
Hemodynamics: Blood Flow
Directly proportional to the pressure difference between the two ends of the system
Inversely proportional to resistance
Flow = Δ PressureResistance
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 differenceNo change in O2 content in the blood
Remains at 20 ml/100 ml of blood
Decrease in O2 inside the muscle
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 Low pressure
High pressure to a Lower pressure
20 ml or P02 98 20 ml or P02 98
PO2 = 40 PO2 = 20
RESTING EXERCISE
15 ml extracted5 ml extracted
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 ConsumptionAn 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 ‘anaerobic’?