Transcript mechanisms

Cardiovascular Homeostasis
2nd Phase Medicine
2007-2008
CVS Module
2nd phase medicine 2007-2008
Objectives
• To describe the effect of exercise on the
following aspects of CVS:
• Heart rate
• Contractility
• Stroke volume
• cardiac output
• Venous return, systemic circulatory flow
• Total peripheral resistance
• Blood pressure
• To describe the effect of training
2nd phase medicine 2007-2008
Central Command
• ↑ sympathetic outflow to the
heart & blood vessels
• ↓ parasympathetic outflow to
the heart.
2nd phase medicine 2007-2008
Effect on the Heart
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Β1 receptor activity-↑
Heart rate- ↑
Contractility-↑
Stroke volume- ↑
Cardiac output volume- ↑ The increase in
cardiac output is essential in the
cardiovascular response to exercise. It
ensures that 02 and nutrients are delivered
to the exercising skeletal muscle.
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Venous return
• ↑ venous return-due to contraction of
skeletal muscles & venoconstriction.
• This also contributes to ↑ in cardiac
output.
2nd phase medicine 2007-2008
Vascular Response
• Arteriolar vasodilation occurs in the
exercising vessels.
• Coronary blood flow increases.
• Vasoconstriction occurs in the
– Splanchinic circulation.
– Kidney
– Inactive muscles
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Skin
• Initial vasoconstriction followed by
vasodilatation.
• Vasoconstriction is in response to ↑
sympathetic activity.
• Vasodilation is due to increase in body
temperature which is dissipated through
the skin.
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Local Responses in Muscles
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Active hyperemia
↑ in metabolic rate
↑ in vasodilator metabolites
Vasodilatation
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Total Peripheral Resistance
• As a consequence of vasodilation in the
exercising muscles the total peripheral
resistance decreases.
• This leads to a
– ↓ in diastolic pressure.
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Effect on blood pressure
• ↑ in systolic pressure.
• ↓ in diastolic pressure.
• ↑ in pulse pressure.
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02 consumption
• 02 consumption by the tissues is
increased
• Atriovenous 02 difference increases.
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Training
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Larger stroke volume
Lower heart rate
Larger hearts
V02max is high (maximum c.o x maximum
02 extraction)
• ↑ in number of mitochondria
• The number of capillaries ↑
• Less increase in lactate production
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Cardiac reserve
Cardiac reserve = Maximal COP (during ms. exercise) – COP (During rest).
mechanisms of cardiac reserve:
Short term mechanisms
Long term mechanisms
-Rapid onset.
-Slow and gradual.
- Increase cop according
to moment to moment
increase in body needs.
-Used in case of prolonged
excess work done by heart
ex. Increased ABP (hypertension).
2nd phase medicine 2007-2008
Cardiac reserve
Cardiac reserve = Maximal COP (during ms. exercise) – COP (During rest).
mechanisms of cardiac reserve:
Short term mechanisms
Long term mechanisms
-Rapid onset.
-Slow and gradual.
- Increase cop according
to moment to moment
increase in body needs.
-Used in case of prolonged
excess work done by heart
ex. Increased ABP (hypertension).
2nd phase medicine 2007-2008
A-Short term (lived) mechanisms: It include:
1-Heart rate (HR) reserve:
The possibility of the increase of heart rate up to 2 – 3 times
(associated with increase venous return as in muscle exercise) causes
increase in cop.
-Heart rate reserve is limited because the increase in heart rate above
180 beats/min causes decrease in the COP.
-As this marked increase in the heart rate will be associated with
marked decrease in diastolic period causing:
Decrease in ventricular filling
Decrease in SV and COP
Decrease in coronary blood flow
Decrease in myocardial contraction
2nd phase medicine 2007-2008Decrease
in COP
2-Stroke volume reserve:
The increase in SV causes increase of COP.
* This mechanism is mediated by either:
*
Increase of the EDV
(EDV reserve)
Decrease of the ESV
(ESV reserve)
EDV reserve:
* Increase of the venous return (as in ms exercise)
increases EDV
according to
Starling law
Increases the force of contraction of cardiac muscle
increase SV and COP.
*This mechanism is limited as the marked increase in EDV causes
overstretch of ventricular muscle fibers
decreases force of contraction of
cardiac muscle. This will decrease the SV and the COP.
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ESV reserve:
-Increased
sympathetic stimulation to the heart increases
the force of cardiac muscle contraction and decreases the
ESV. This will increase SV and COP.
-This mechanism is also limited as the marked decrease in
ESV causes myocardial injury (athletic injury).
2nd phase medicine 2007-2008
B-Long term (lasting) mechanisms:
1- Cardiac muscle hypertrophy:
*It is the increase in the size of the individual cardiac muscle fiber
(increase its protein content). This increases the force of contraction
of cardiac muscle
increase SV and COP.
*It is slow gradual mechanism occurring in cardiac strain as in
hypertension.
*This mechanism is also limited as the marked hypertrophy of the
myocardium is not associated with parallel increase in coronary
blood flow.
*This cause myocardial ischemia with subsequent decrease in the
force of contraction of cardiac muscle. This will decrease the SV and
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COP.
2-Dilatation of cardiac chambers:
-This
mechanism occurs when the blood accumulated
inside the cardiac chambers as in case of heart failure.
-This dilatation of the cardiac chambers causes stretch of
the cardiac muscle fibers
Increases its force of
contraction according to Starling law.
-This mechanism is limited as the marked increase in EDV
causes overstretch of ventricular muscle fibers and
decreases force of contraction of cardiac muscle.
-This will decrease the SV and the COP.
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Effects of change in posture
• 1- The pressure at the hydrostatic indifferent level is
unchanged.
• HIL : It is the level in the intraqvascular level at which
changes in body position does not affect the
intravascular pressure. It is 11 cm below the diaphragm.
• 2- The artterial blood pressure rises as we go down from
HIL. Reaching 180 mmhg in feet arteries. The ABP
decreases as we go up from HIL to reach 65 mmhg in
head arteries.
• 3- The venous blood pressure:
• It increases in the feet veins to reach 105 mmhg. And
decreases when we go up to be -10 mmhg in the sagittal
sinus.
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• 4- Pooling of blood in the lower veins.
• 5- Edema of the lower limbs due to the
rise in the capillary blood pressure causing
the escape of fluid to the interstitial
tissues.
• 6- Decrease in blood volume due to
escape of fluid from limb veins to
interstitial tissue fluid.
• Decrease in VR, SV, and COP by about 25
%. The cerebral blood flow decreases by
about 20 %.
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Cardiovascular adjustments during
change in posture
• The major compensations on assuming the upright position are
triggered by the drop in blood pressure in the carotid sinus and
aortic arch.
• The heart rate increases, helping to maintain cardiac output.
• There is relatively little venoconstriction in the periphery, but there is
a prompt increase in the circulating levels of renin and aldosterone.
• The arterioles constrict, helping to maintain blood pressure.
• The actual blood pressure change at heart level is variable,
depending upon the balance between the degree of arteriolar
constriction and the drop in cardiac output
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• In some individuals, sudden standing causes a fall in blood
pressure, dizziness, dimness of vision, and even fainting.
• The causes of this orthostatic (postural) hypotension are
multiple.
• It is common in patients receiving sympatholytic drugs.
• It also occurs in diseases such as diabetes and syphilis, in which
there is damage to the sympathetic nervous system.
• Another cause of postural hypotension is primary autonomic
failure
• Autonomic failure occurs in a variety of diseases. One form is
caused by a congenital deficiency of dopamine β- hydroxylase (with
little or no production of norepinephrine and epinephrine.
• Baroreceptor reflexes are also abnormal in patients with primary
hyperaldosteronism. However, these patients generally do not have
postural hypotension, because their blood volumes are expanded
sufficiently to maintain cardiac output in spite of changes in position.
• Indeed, mineralocorticoids are used to treat patients with postural
hypotension.
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• The effects of gravity on the circulation in
humans depend in part upon the blood
volume. When the blood volume is low,
these effects are marked; when it is high,
they are minimal.
2nd phase medicine 2007-2008