Cardiovascular Homeostasis

2nd Phase Medicine

2007-2008
CVS Module

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 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

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 Central Command
• ↑ sympathetic outflow to the
heart & blood vessels
• ↓ parasympathetic outflow to
the heart.

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 Effect on the Heart
• 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.

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 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
• 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
• 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
(During rest).
reserve
Cardiac reserve = Maximal COP (during ms. exercise) – COP

mechanisms of cardiac reserve:

Short term Long term

mechanisms mechanisms
-Rapid onset. -Slow and gradual.

-Used in case of prolonged

- Increase cop excess work done by heart
according ex. Increased ABP
to moment to (hypertension).
moment 2nd phase medicine 2007
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 Cardiac
(During rest).
reserve
Cardiac reserve = Maximal COP (during ms. exercise) – COP

mechanisms of cardiac reserve:

Short term Long term

mechanisms mechanisms
-Rapid onset. -Slow and gradual.

-Used in case of prolonged

- Increase cop excess work done by heart
according ex. Increased ABP
to moment to (hypertension).
moment 2nd phase medicine 2007
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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

2nd phase medicine 2007 Decrease in
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 2-Stroke volume
reserve:
* The increase in SV causes increase of COP.
* This mechanism is mediated by either:

Increase of the EDV Decrease of

EDV
the ESV reserve:
(EDV
* Increase of thereserve) (ESV increases
venous return (as in ms exercise)
EDV
reserve)
according to
Increases the force of contraction of
cardiac muscle
Starling law increase SV and COP.

*This mechanism is limited as the marked increase in EDV causes

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overstretch of ventricular muscle fibers decreases force of
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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).

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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.
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2-Dilatation of cardiac
chambers:
-Thismechanism 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
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ventricular muscle
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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.

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