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
1 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.
2nd phase medicine 2007-2008
 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

2nd phase medicine 2007-2008

 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.

2nd phase medicine 2007-2008

 Local Responses in Muscles
Active hyperemia
in metabolic rate
in vasodilator metabolites
Vasodilatation

2nd phase medicine 2007-2008

 Total Peripheral Resistance
As a consequence of vasodilation in the
exercising muscles the total peripheral
resistance decreases.
This leads to a
in diastolic pressure.

2nd phase medicine 2007-2008

 Effect on blood pressure
in systolic pressure.
in diastolic pressure.
in pulse pressure.

2nd phase medicine 2007-2008

 02 consumption
02 consumption by the tissues is
increased
Atriovenous 02 difference increases.

2nd phase medicine 2007-2008

 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

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 -Used in case of prolonged

to moment to moment excess work done by heart
increase in body needs. 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 -Used in case of prolonged

to moment to moment excess work done by heart
increase in body needs. 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 coronary blood flow

Decrease in SV and COP 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 Decrease of the ESV

(EDV reserve) (ESV reserve)

EDV reserve:
* Increase of the venous return (as in ms exercise) increases EDV
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

overstretch of ventricular muscle fibers decreases force of contraction of
cardiac muscle. This will decrease the SV and the COP.
2nd phase medicine 2007-2008
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
COP. 2nd phase medicine 2007-2008
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.

2nd phase medicine 2007-2008
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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.

2nd phase medicine 2007-2008

 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 %.

2nd phase medicine 2007-2008

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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

2nd phase medicine 2007-2008

 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 - 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.

2nd phase medicine 2007-2008

 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