2nd phase medicine 2007-2008 cardiovascular homeostasis 2 nd phase medicine 2007-2008 cvs module

2nd phase medicine 2007-2008

Cardiovascular Homeostasis

2nd Phase Medicine

2007-2008

CVS Module


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


Central Command

• ↑ sympathetic outflow to the heart & blood vessels

• ↓ parasympathetic outflow to the heart.


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.


Venous return

• ↑ venous return-due to contraction of skeletal muscles & venoconstriction.

• This also contributes to ↑ in cardiac output.


Vascular Response

• Arteriolar vasodilation occurs in the exercising vessels.

• Coronary blood flow increases.

• Vasoconstriction occurs in the– Splanchinic circulation.– Kidney– Inactive muscles


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.


Local Responses in Muscles

• Active hyperemia

• ↑ in metabolic rate

• ↑ in vasodilator metabolites

• Vasodilatation


Total Peripheral Resistance

• As a consequence of vasodilation in the exercising muscles the total peripheral resistance decreases.

• This leads to a– ↓ in diastolic pressure.


Effect on blood pressure

• ↑ in systolic pressure.

• ↓ in diastolic pressure.

• ↑ in pulse pressure.


02 consumption

• 02 consumption by the tissues is increased

• Atriovenous 02 difference increases.


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


Cardiac reserveCardiac reserve = Maximal COP (during ms. exercise) – COP

(During rest).

Short term mechanisms

Long term mechanisms

mechanisms of cardiac reservemechanisms of cardiac reserve::

-Rapid onset. - Increase cop according to moment to moment increase in body needs.

-Slow and gradual. -Used in case of prolonged excess work done by heart ex. Increased ABP (hypertension).


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

Decrease 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.


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).


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.


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.


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.


• 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 %.


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

•

mk:@MSITStore:C:%5CDocuments%20and%20Settings%5CAdministrator%5CDesktop%5CGyton%20&%20Ganong%5CGanong%20-%20Review.of.Medical.Physiology.21st.Ed.eBook-EEn.chm::/Page_0787.html


• 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.


• 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 cardiovascular homeostasis 2 nd phase medicine 2007-2008 cvs module

Documents

increase of heart rate

increase cop

cvs module2nd phase

heart rate reserve

heart rate hr reserve

increase venous return

exercise cop

cardiac reservecardiac