Cardiovascular Physiology

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Cardiovascular Physiology

• Dr. Abdulhalim Serafi, MB ChB,MSc,PhD,FESC
• Assistant Professor Consultant Cardiologist
• Faculty of Medicine and Medical Sciences
• Umm Al-Qura University
• Makkah Al-Mukarramah
• Saudi Arabia

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Blood vessels
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(No Transcript)
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Pressure Drop in the Vascular System
ELASTIC TISSUE
MUSCLE
LARGE ARTERIES
SMALL ARTERIES
MEAN PRESSURE
ARTERIOLES
CAPILLARIES
VENULES VEINS
SMALL
LARGE
LARGE
INSIDE DIAMETER
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Part II CARDIOVASCULAR PHYSIOLOGY
LECTURE IV REGULATION OF THE DIAMETER
OF ARTERIOLES

• Outline
• - Function of the arterioles.
• - The vasomotor centre (VMC) and vasomotor
  tone.
• - Nervous regulation of the diameter of
  arterioles.
• - Chemical regulation of the diameter of
  arterioles
• - Reactive nerves.
• - Vasomotor nerves (VC and VD).
• - Local regulation of blood flow.
• Further Reading
• Guyton Textbook of Medical Physiology
• Ganong Review of Medical Physiology

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• REGULATION OF THE DIAMETER OF THE ARTERIOLES
• - The diameter of the arterioles is a very
  important factor in
• regulation of the ABP because the arterioles
  represents the
• main site of peripheral resistance in the
  vascular system.
• - The plain muscles present in the wall of the
  arterioles act
• as sphincters their contraction ? constriction
  and their
• relaxation ? dilatation of the arterioles.
• The vasomotor center (VMC) present in medulla
  oblongata.
• The chemical composition of the blood and
  local factors.

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• The vasomotor center (VMC)
• - The VMC is present in the medulla oblongata and
  is
• composed of 2 centers
• a. Vasoconstrictor center (VCC) present in the
  Pressor area of the medulla oblongata,
• b. Vasodilator center (VDC) present in the
  depressor area of the medulla oblongata.
• - Vasomotor tone This is continuous
  vasoconstrictor
• impulses sent by the vasomotor center (VMC)
  under normal
• level of ABP through sympathetic nerve fibers to
  the
• various arterioles to keep them in a state of
  moderate
• constriction. The vasomotor tone is important to
  maintain
• normal ABP. It is sympathetic vasoconstrictor
  tone.

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? vasomotor tone ? more vasoconstriction ?
vasomotor tone ? less vasoconstriction ??
vasomotor tone ? vasodilatation Function of the
arterioles The arterioles regulate the local
blood flow to the tissues and are also called
the main site of peripheral resistance to the
blood flow (which maintains the arterial B.P
specially the diastolic pressure) such functions
are door-med through variations in the
arteriolar diameter.
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Factors that affect the vasomotor centre
(VMC) The VMC consists of (a) VCC or Pressor
area (because its stimulation tends to elevate
the arterial B.P.) (b) VDC or depressor area. It
is affected by the following factors 1. Nervous
factors The VMC is affected by signals
discharged from a- The arterial and
atrial baroreceptors (depressor). b- The
cerebral cortex (Pressor e.g. in mental strain or
depressor). c- The hypothalamus (Pressor
or depressor e.g. during exposure to cold and
heat respectively). d- The respiratory centre
(Pressor). e- From skeletal muscles and pain
receptors (mostly Pressor).
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2. Chemical factors O2 lack, CO2 excess and
rise of H are Pressor by stimulating the
VCC both directly and through exciting
the chemoreceptors. Factors regulating the
arteriolar diameter a) Local Factors These
include the following 1. O2 supply A local
O2 lack causes V.D. except in the
lungs). 2. Metabolites (e.g. CO2, lactic
acid, K and adenosine) cause V.D. 3.
Temperature (e.g. local heat causes V.D.) 4.
Auto regulation 5. Locally released procaine
V.C. substances (e.g. serotonin,
endothelins and thromboxane A2) and
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V.D. substances e.g. prostacyclin
(prostaglandin I2) and the endothelium-derived
relaxing factor (EDRF). b) Central Factors
These include hormonal (chemical) and
neural factors I. Nervous regulation of the
diameter of arterioles Factors influencing
the VMC 1. Afferent impulses from the
cardiovascular system a. Right atrium
decrease of pressure in the right atrium e.g.
during severe haemorrhage ? stimulation of atrial
volume receptors ? afferent impulses along the
vagus nerve ? stimulation of the VCC ?
generalized vasoconstriction ? ? of ABP.
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b. Vasosensory areas (baroreceptors
chemoreceptors - Baroreceptors in the aortic
arch and carotid sinus send inhibitory impulses
to VCC along the buffer nerves when the ABP is
normal. If the ABP is increased, more
inhibitory impulses will reach the VCC from
the baroreceptors ? vasodilatation and drop of
ABP to normal. If the ABP is decreased, less
inhibitory impulses will reach the VCC from
the baroreceptors ? vasoconstriction
? ? ABP to normal. - Chemoreceptors in aortic
carotid bodies are stimulated by O2 lack or CO2
excess ? excitatory impulses along the buffer
nerves to vasomotor centre arch and carotid
sinus send inhibitory impulses ? along to VCC
along the buffer nerves when the ABP is
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2. Impulses from the higher centers - Cerebr
al cortex Impulses from certain areas of the
cerebral cortex ? stimulation of the VCC in
medulla oblongata (Pressor area) ?
vasoconstriction ? ? ABP as during emotions and
muscular exercise. Also conditioned reflexes
which have their centers in the cerebral cortex
may be accompanied by vasoconstriction or
vasodilatation. - Hypothalamus The
hypothalamus contains sympathetic and
parasympathetic. Centers which modify the
activity of the vasomotor center ?
vasoconstriction or vasodilatation of the
arterioles. The hypothalamus also contains the
center for body temp. regulation and it controls
blood flow in the skin vessels e.g. ?
vasoconstriction in cold weather and
vasodilatation in hot weather.
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2. Afferent impulses from other parts of the
body - Skeletal muscles (Lovens reflex)
Over activity in an organ (e.g. skeletal muscles
during muscular exercise) ? reflex vasodilatation
in the active organ and reflex vasoconstriction
in the other less active or resting tissues (e.g.
intestine) in the body. This reflex helps
redistribution of blood in the body. - Trigger
areas Painful stimuli applied to certain areas
as larynx, ear, epigastrium and testicles
(trigger areas) ? reflex vasodilatation ? ?
ABP However, slight or moderate painful
stimuli ? reflex vasoconstriction ? ?
ABP. - SKIN (Cold pressure reflex) cold shower
? reflex vasoconstriction due to stimulation of
cold receptors in the skin ? ? ABP.
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II. Chemical substances influencing the
diameter of the arterioles directly
Chemical or humoral regulation of the diameter of
the arterioles 1. Vasoconstrictor
substances Adrenaline and noradrenalin ?
constriction of the arterioles all over the body
except in the heart and skeletal muscles where
they produce vasodilatation. Noradrenalin has
a stronger vasoconstrictor effect than
adrenaline. Vasopressin (antidiuretic
hormone) secreted by the posterior pituitary
gland ? constriction of the arterioles.
Angiotensin II Potent vasoconstrictor
substance generalized vasoconstriction.
Serotonin (5 hydroxy tryptamine, 5HT) released
from the blood platelets ? vasodilatation.
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2. Vasodilator substances Metabolites
such as lactic acid, CO2 and histamine have
direct effect on the plain muscles of the
arterioles ? their dilatation. Acetyl
Choline ? vasodilatation by direct effect on
arteriolar wall. Thyroxin ? stimulation of
tissue metabolism ? production of metabolites ?
dilatation of the arterioles. Bradykinine
ATP ? VD. N.B The important circulating
V.C. substances include the catecholamine,
vasopressin and angiotensin II, while the
important circulating V.D. substances include
kinins (specially bradykinine) VIP (vasoactive
intestinal polypeptide) and the atrial
natriuretic peptide (ANP). Other circulating
vasoactive substances include histamine,
serotonin and certain prostaglandins.
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• N.B
• The endothelium-derived relaxing factor
• This is a powerful V.D. substance that is
  secreted by the vascular endothelium, and us
  chemically nitric oxide (NO). Many substances act
  through releasing this EDRF (e.g. acetylcholine,
  bradykinine, substance P and VIP). It is also a
  transmitter in the CNS and is released by the
  parasympathetic nerves in the penis (helping
  erection).
• Substances released by the vascular endothelium
• EDRF
• Endothelins
• Prostacyclin
• Thrombomodulin
• Interleukins
• Platelet derived growth factor (PDGF)
• Endothelial cell growth factor
• Von Willebrand factor

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• Reactive Hyperemia
• Definition Reactive hyperemia means marked
  increase in blood flow to an organ after removal
  of temporary occlusion of its arterial supply.
• Explanation If a sphygmomanometer cuff is
  wrapped around the upper arm and the pressure is
  raised in the cuff to occlude the arterial
  supply of the forearm for 2-3 minutes, there
  will be marked increase of blood flow to the
  forearm after removal of the occlusion.
• Also, if a muscle is tetanised, the blood flow
  during the period of tetanus is markedly reduced
  or completely stopped due to collapse of the
  blood vessels by the contracting muscle. On
  relaxation, the blood flow is much increased.

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• Cause of reactive hyperemia is the
  accumulation of vasodilator metabolites such as
  lactic acid, CO2, histamine ? O2 (hypoxia)
  during occlusion.
• These metabolites ? vasodilatation of the
  arterioles by direct action ? ? blood flow.
• N.B. Hyperemia also occurs with increased
  tissue activity.
• Vasomotor nerves
• Vasomotor nerves include both vasoconstrictor
  and vasodilator nerves.
• 1. Vasoconstrictor nerves
• a. Sympathetic vasoconstrictor fibers to all
  blood vessels of the body, except those
  supplying the coronary vessels and blood
  vessels in skeletal muscles.

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• b. Parasympathetic vasoconstrictor fibers (vagus
  n) to the coronary blood vessels.
• 2. Vasodilator nerves
• a. Parasympathetic vasodilator nerves e.g.
• - Choda tympani to BV of submandibular
  sublingual salivary glands ant. 2/3 of
  tongue.
• - Glassopharyngeal to BV of parotid gland
  post. 1/3 of tongue.
• - Vagus n to lungs, stomach pancreas.
• - Sacral autonomic (pelvic n.) to blood vessels
  of the pelvic viscera.
• b. Sympathetic vasodilator nerves e.g.
• - Sympathetic to coronary vessels to blood
  vessels in skeletal muscles.

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• - Sympathetic to blood vessels of areas not
  supplied by parasympathetic as limbs.
• c. Antidromic vasodilators These are branches of
  afferent fibers but they carry impulses in a
  direction opposite to usual i.e. towards organs
  and not towards CNS.
• LOCAL REGULATION OF BLOOD FLOW
• Blood flow in different organs is generally
  regulated by adjusting the diameter of the
  arterioles. The main mechanisms of regulation of
  regional blood flow include 3 mechanisms
  (short-term mechanisms) of local auto
  regulation
• 1. Metabolic Auto regulation
• - Local auto regulation regulates the blood
  flow according to the local metabolic needs
  of the tissues.

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• - Increased metabolic activity of tissues ?
  increased production of metabolites which
  act on the smooth muscle in the wall of the
  arterioles ? vasodilatation of the
  arterioles ? ? blood flow and vice versa.
• - Increased tissue activity ? ? O2 (hypoxia),
  ? CO2, ? H (lactic acid), ? adenosine and
  K release ? vasodilatation of
  the arterioles ? ? blood flow.
• - Therefore, metabolic auto regulation
  enables tissues to regulate their blood
  flow according to their metabolic activity.
• This is particularly effective in the
  regulation of local blood flow in the
  cardiac muscle and the skeletal muscle.

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• N.B.
• Increase of blood flow to an organ is called
  hyperemia. Hyperemia may be active or reactive.
• Active hyperemia means ? in blood flow to an
  organ when its activity increases.
• Reactive hyperemia means ? in blood flow to an
  organ after removal of temporary occlusion of
  its arterial blood supply.
• 2. Myogenic Auto regulation
• - This is an intrinsic mechanism which
  maintains relatively constant blood
  flow, in some organs, over wide range of ABP
  changes (80-160 mm Hg).
• - This mechanism depends on vasoconstriction
  of the arterioles when the perfusion
  pressure (ABP) increases and vasodilatation
  of the arterioles when the perfusion
  pressure decreases i.e.

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• ? ? ABP ? ? tension on the wall of the
  arterioles and their distension ? intrinsic
  myogenic contraction of the smooth muscle
  in the wall of the arterioles ?
  vasoconstriction. Thus, the blood flow is kept
  constant, in spite of the increased ABP.
• ? If the ABP decreases, the reverse occurs.
• The myogenic auto regulation mechanism is well
  developed in the kidney and the brain.
• This mechanism enables the kidney to maintain
  constant blood flow over wide range of ABP
  changes (80-160 mm Hg)
• 3. Humoral regulation of blood flow
• - This is regulation of blood flow by
  vasoactive substance which are released from
  tissues into the tissue fluids and blood
  under certain conditions e.g.

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• a. Histamine- It is strong vasodilator
  substance which is released in inflamed or
  damaged tissues. It is also released in allergic
  reactions.
• b. Serotonin- This is vasoconstrictor
  substance which is released from blood platelets.
  It helps to stop bleeding from wounds i.e.
  serotonin ? local vasoconstriction of the small
  vessels in the injured area.
• c. Prostaglandins (PGs)- These are hormone
  like substance, some of them (e.g. PGF are
  vasoconstrictors, but most of them (e.g. PGA
  PGE) are vasodilators. They are found in almost
  all cells and they are released in some
  physiological and pathological conditions.
• d. Bradykinine- This is a vasodilator substance
  which is formed in tissues during inflammation or
  increased tissue activity. Bradykinine is a
  mediator of vasodilatation in sweat glands and
  digestive glands when they become activated.

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Part II CARDIOVASCULAR PHYSIOLOGY
LECTURE V WORK OF THE HEART CARDIAC
RESERVE

• Outline
• - Metabolism of the cardiac muscle
• - Work of the heart
• - Cardiac reserve
• Mechanisms of the cardiac reserve
• Limits of the reserve mechanism
• Significance of the cardiac reserve
• Further Reading
• Guyton Textbook of Medical Physiology
• Ganong Review of Medical Physiology

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• METABOLISM OF THE CARDIAC MUSCLE
• The metabolic reactions which occur in the muscle
  include
• the following
• 1- Breakdown of the ATP (adenosine triphosphate)
  
• ATP ATP-ase ADP P E for systole
• This reaction is anaerobic (does not need O2)
  gives
• energy for contraction.
• 2- Breakdown of CP (creatinine phosphate)
• CP ? Creatinine P E for reformation of
  ATP.
• It is also anaerobic reaction.

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3- Oxidation of lactic acid Lactic acid ?
CO2 H2O) E for reformation of CP. This
reaction is aerobic O2 lactic acid is taken
directly from the coronary blood. Fat
glucose may be also oxidized to give
energy. N.B. Lactic acid produced by the
skeletal muscles is used as fuel by the
cardiac muscle. The cardiac muscle can not
continue its activity inn absence of O2 i.e.
there is no O2-debt. O2 consumption of the
cardiac muscle is about 25 mL O2/ minute.
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• Under normal conditions, the calorie needs of
  the heart
• are provided mainly by carbohydrates and fat.
  The
• cardiac muscle does not use its glycogen as a
  source of
• energy except in emergencies as severe
  hypoxia.
• WORK OF THE HEART
• Mechanical efficiency of the heart (ME) is the
  percentage of
• the total energy expenditure which is converted
  into
• mechanical work.
• ME WORK done x 100
• Total energy expenditure
• Under basal conditions, the ME of the heart is
  about 20-25
• (80-75 of the energy is lost as heat). In
  well-trained
• athletes, the ME may be ? to 30-40 or even more.

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CARDIAC RESERVE CARDIAC RESERVE is the
difference between the work performed by the
under resting conditions and that performed
during severe muscular exercise. The AIM OF THE
CARDIAC RESERVE is to increase the cardiac output
(COP) ? increase of blood flow to the active
muscles and tissues. Thus, cardiac reserve can
also be defined as the maximal increase in the
cardiac output that can be attained. It is about
300-400 in normal young adults and about
600- 700 in well-trained athletes.
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The cardiac reserve is the ability of the heart
to increase its work and output when required
(e.g. during muscular exercise). Accordingly, it
can be defined as the difference between the
resting and maximal cardiac work. Mechanisms of
Cardiac Reserve - The heart performs its
extra-work through 3 mechanisms 1. Increase
in heart rate (acceleration of the heart) -
The heart rate may be increased from 70 to a
maximum of about 200 beats/minute thus
increasing the cardiac output 3 folds its
normal level provided that venous return is
adequate.
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- The increase in heart rate in muscular
exercise is due to a. Bainbridge reflex (due
to ? venous return pressure in right
atrium). b. Alam-Smirks reflex (due to
afferent impulses from contracting
muscles). c. ? of sympathetic activity and ?
secretion of adrenaline from ad.
Medulla. d. Stimulation of resp. centre,
stimulation of chemoreceptors in aortic
carotid bodies. e. Rise of blood
temperature. 2. Increase in stroke volume
(dilatation of heart) - The stroke volume
may be increased from 70 ml to 100 ml or
more/beat to a maximum of about 200 ml/heat
i.e., 3 folds the normal volume. SVEDV-ESV
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- The stroke volume is increased due to a.
More efficient emptying of the ventricles ?
decrease of end-systolic volume (ESV). b.
Dilatation of the heart by ? venous return ? ?
end-diastolic volume (EDV) ? better systole
(Starlings Law). 3. Hypertrophy of the cardiac
muscle - The size of each cardiac muscle fiber
may be increased ? ? bulk of the heart muscle
? ? power of cardiac contraction ? ? cardiac
output. - This hypertrophy occurs very gradually
due to prolonged strain on the heart e.g.
continuous severe exercise for a long
period.
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• Limits of Cardiac Reserve Mechanisms
• Excessive acceleration about 200 beat/min
  shortens the period of cardiac filling during
  diastole and thus decrease the cardiac output.
• Excessive dilatation of the heart (over stretch)
  ?? in the force of cardiac contraction ?? cardiac
  output.
• Hypertrophy is of limited value because there is
  no corresponding increase in blood supply to the
  hypertrophied muscle fibers.
• N.B. The mechanisms of cardiac reserve occur only
  during
• muscular exercise in normal hearts. However, in a
  diseased
• heart some of these mechanisms may be used during
  rest.

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Part II CARDIOVASCULAR PHYSIOLOGY
LECTURE VI CARDIOVASCULAR CHANGES
DURING MUSCULAR EXERCISE

• Outline
• - General (systemic) changes
• heart rate and stroke volume
• Cardiac output and arterial blood pressure
• Redistribution of blood.
• - Local changes
• Blood flow and oxygen uptake.
• Capillary changes and lymph flow
• Further Reading
• Guyton Textbook of Medical Physiology
• Ganong Review of Medical Physiology

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• CARDIOVASCULAR CHANGES
• DURING MUSCULAR EXERCISE
• Cardiovascular changes during muscular exercise
  include
• general changes and local changes (in skeletal
  muscles)
• General Changes
• ? Heart Rate up to 140 heat/ minute due to
• ? Emotional effect by impulses from cerebral
  cortex and hypothalamus ? inhibition of CIC and
  stimulation of CAC.
• ? Stimulation of the respiratory centre by
  excess CO2 and other metabolites such as lactic
  acid ? irradiation of inhibitory impulses to CIC
  and stimulatory impulses to CAC.

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• ? Stimulation of chemoreceptors in aortic and
  carotid bodies by O2 lack, CO2 excess and ? H.
• ? Bainbridge reflex due to ? venous return and
  pressure in right atrium.
• ? Rise of blood temperature ? stimulation of CAC
  and SA node.
• ? Afferent impulses from the proprioceptors of
  skeletal muscles ? stimulation of CAC.
  Alam-Smirk reflex
• ? Secretion of adrenaline from adrenal medulla
  (due to sympathetic overactivity) ? direct
  stimulation of SA node.

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• ? Venous Return due to active contraction of
  skeletal muscles (muscular pump) and respiratory
  muscles (respiratory pump).
• ? Cardiac Output up to 25 liters/ min due to ?
  heart rate, ? stroke volume. Stroke volume is ?
  due to ? venous return (Starlings Law) and ? of
  force of ventricular contraction ? ? of end
  systolic volume.
• ? arterial blood pressure ? systolic BP due to ?
  cardiac output. Diastolic BP remains unchanged or
  slightly decreased due to vasodilatation of the
  arterioles of the active skeletal muscles.
• Redistribution of blood (Lovens reflex) i.e.
  blood is shifted from gastrointestinal tract,
  kidney (vasoconstriction) to the active skeletal
  muscles (vasodilatation).

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• ? Venous Return due to active contraction of
  skeletal muscles (muscular pump) and respiratory
  muscles (respiratory pump).
• ? Cardiac Output up to 25 liters/ min due to ?
  heart rate, ? stroke volume. Stroke volume is ?
  due to ? venous return (Starlings Law) and ? of
  force of ventricular contraction ? ? of end
  systolic volume.
• ? arterial blood pressure ? systolic BP due to ?
  cardiac output. Diastolic BP remains unchanged or
  slightly decreased due to vasodilatation of the
  arterioles of the active skeletal muscles.
• Redistribution of blood (Lovens reflex) i.e.
  blood is shifted from gastrointestinal tract,
  kidney (vasoconstriction) to the active skeletal
  muscles (vasodilatation).

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• Local Changes
• ? Blood Flow to the active skeletal muscles due
  to
• ? Dilatation of the muscle arterioles and
  capillaries in active muscles by ? CO2 and other
  metabolites.
• ? ? of cardiac output and systolic BP.
• ? Lovens Reflex i.e. shift of blood (COP) to
  the arterioles of active skeletal muscles since
  there is vasoconstriction of the arterioles of
  gastrointestinal tract and kidneys.
• ? O2 uptake by the active muscles because the
  affinity of ? PCO2, ? H, ? temperature ? ?
  release of O2 from oxyhaemoglobin.

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• Capillary changes
• ? Number of the open capillaries due to
  relaxation of the precapillary sphincters.
• Capillary dilatation ? ? capillary blood flow, ?
  capillary blood pressure ? ? capillary
  permeability ? ? filtration ? ? interstitial
  fluid in active skeletal muscles.
• ? Lymph flow from active muscles due to increased
  pumping power of the muscles.