CARDIOVASCULAR PHYSIOLOGY

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(No Transcript)
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The control of the heart rate
Cerebral cortex
Inspiratory center
The hypothalamus and limbic system
Cardiovascular centers
Chemical factors Physical factors Mechanical
factors
S-A node
Reflexes
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The peripheral resistance

• As the blood flows from the arterial to the
  venous side of the circulation, it meets
  resistance because of the smaller caliber of the
  vessels and the viscous nature of the blood. This
  is called the peripheral resistance. It is an
  important factor in generating and maintaining
  the arterial blood pressure. Vasoconstriction of
  the small vessels increases the peripheral
  resistance, which in turn elevates the arterial
  blood pressure. Whilst vasodilatation decreases
  the resistance and lowers the pressure.
• The main factor is a gradient of blood pressure.

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RESISTANCES IN SERIES
RT RA RC RV
RESISTANCES IN PARALLEL
R1
PA
PV
1 RT
1 R1
1 R2
1 R3
R2



R3
1
RT

1 R1
1 R2
1 R3


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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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Nervous factors

• The most important factor in the regulation of
  the heart rate is the activity of the
  cardiovascular centers in the medulla oblongata.
• This activity is transmitted to the heart via its
  sympathetic and parasympathetic nerve supply.

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Sympathetic nerve supply

• There is a resting sympathetic tone that tends to
  increase the heart rate up to 120 beats/min.
• This tone is weak and is masked by the strong
  inhibitory vagal tone that decreases the heart
  rate down to 75 beats/min during rest.
• However, stimulation of the sympathetic cardiac
  nerves has a ve chronotropic effect. The heart
  rate may go up to 200 beats/min.
• The sympathetic chemical transmitter
  noradrenaline decreases the permeability of the
  pacemaker membrane to K. This accelerates the
  depolarization of the membrane ? shortens the
  duration of the pacemaker potential ? increases
  the frequency of discharge of impulses from the
  S-A node ? increases the heart rate.

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Parasympathetic nerve supply

• There is a resting inhibitory vagal tone that
  keeps the heart rate at its resting level of 75
  beats/min.
• During deep quite sleep, the vagal tone increase
  and the heart rate decreases down to 60
  beats/min.
• Vagal stimulation has a ve chronotropic effect.
• The parasympathetic chemical transmitter acetyl
  choline increases the permeability of the
  pacemaker membrane to K. This slows down the
  depolarization of the membrane ? prolongs the
  duration of the pacemaker potential ? deccreases
  the frequency of discharge of impulses from the
  S-A node ? decreases the heart rate.

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Heart rate

• A change in the heart rate produces a stepwise
  change in the force of myocardial contraction
  until a final steady level of contractility is
  reached.
• has a negative inotropic The steady level of
  myocardial contractility is directly proportional
  to the heart rate, within limits. In other words,
  cardiac acceleration has a ve inotropic effect
  and cardiac slowing effect.

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INCREASING HEART RATE INCREASES CONTRACTILITY
Ca
Ca
Normal Heart Rate
Fast Heart Rate
Ca
Ca
Ca
Ca
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CARDIAC FUNCTION CURVE
Cardiac Output Stroke Volume x Heart Rate
Constant
If
STROKE VOLUME
Then
? CO reflects ?SV
DIASTOLIC FILLING
Right Atrial Pressure (RAP) reflects Diastolic
Filling
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CARDIAC FUNCTION CURVE
THE FRANK- STARLING LAW OF THE HEART
15-
10-
CARDIAC OUTPUT (L/min)
Pressure
5-
Volume
-4
0
4
8
RAP mmHg
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CARDIAC FUNCTION CURVE
THE FRANK- STARLING LAW OF THE HEART
15-
Increased Contractility
10-
CARDIAC OUTPUT (L/min)
5-
-4
0
4
8
RAP mmHg
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CARDIAC FUNCTION CURVE
THE FRANK- STARLING LAW OF THE HEART
15-
10-
Decreased Contractility
CARDIAC OUTPUT (L/min)
5-
-4
0
4
8
RAP mmHg
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CARDIAC FUNCTION CURVE
THE FRANK- STARLING LAW OF THE HEART
15-
Increased Heart Rate
10-
CARDIAC OUTPUT (L/min)
5-
-4
0
4
8
RAP mmHg
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CARDIAC FUNCTION CURVE
THE FRANK- STARLING LAW OF THE HEART
15-
10-
Decreased Heart Rate
CARDIAC OUTPUT (L/min)
5-
-4
0
4
8
RAP mmHg
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CARDIAC CENTRES CARDIAC INNERVATION

• Outline
• Cardiac Centers
• - Pressor Area vasomotor area or vasomotor
  centre
• (VMC)
• - Depressor Area cardiac inhibitory centre
  (CIC)
• Cardiac Innervations
• - Sympathetic nerve supply
• - Parasympathetic nerve supply
• Arterial baroreceptors and peripheral
  chemoreceptors
• Further Reading
• Guyton Textbook of Medical Physiology
• Ganong Review of Medical Physiology

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• HEART RATE ITS REGULATION
• CARDIAC CENTRES AND CARDIAC INNERVATION
• The activity of the heart (CVS) is under the
  control of 2 bilateral areas in the medulla
  oblongata Pressor area and depressor area.
• THE PRESSOR AREA
• - It is also called the vasomotor area or
  vasomotor centre (VMC).
• - It is present in the ventrolateral parts of
  the medulla oblongata and it is connected with
  preyganglionic sympathetic neurons in the spinal
  cord.
• - The Pressor area contains 2 centers
• a) Cardiac acceleratory centre (CAC) also
  called cardiac stimulatory centre (CSC).
• b) Vasoconstrictor centre (VCC)

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• Stimulation of the Pressor area produces
  sympathetic effects i.e.
• a) Increase of heart rate and increase of
  myocardial
• contractility
• b) Vasoconstriction of the arterioles
• Normally and under resting condition, the VCC
  discharges impulse continuously at a certain
  rate. This is called vasomotor tome (
  vasoconstrictor sympathetic tome) which leads to
  partial VC of the arterioles and venules all over
  the body.
• ? of the VM tone ? more vasoconstriction
• ? of the VM tone ? less vasoconstriction
  (vasodilatation)
• THE DEPRESSOR AREA
• - It is inhibitory area in the medulla
  oblongata and it
• contains a cardio-inhibitory centre (CIC)
  dorsal
• motor nucleus of the vagus nerve.

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• - Stimulation of this area produces
  parasympathetic (vagal) effects on the heart
  i.e. decrease of heart rate and decrease of
  atrial contractility.
• - Normally and under resting condition the CIC
  discharges continuous inhibitory impulses along
  the vagus nerve to the heart. This is called
  vagal tone which checks the high inherent rhythm
  of the SA node.
• ? of vagal tone to the heart ? ? of heart rate
• ? of vagal tone to the heart ? ? of heart rate
• INNERVATION OF THE HEART
• - The heart receives its nerve supply from both
  divisions
• of the ANS i.e.
• Sympathetic nervous system and
• Parasympathetic nervous system

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CARDIOVASCULAR CENTRES (CVCs) - CARDIOVASCULAR
CENTRES are present in the medulla oblongata in 2
areas 1) Pressor area which contains CAC (CSC)
and VCC 2) Depressor area which contains CIC
VOC THE PRESSOR AREA - It contains 2
centers 1) CAC cardiac accelerator
centre CSC cardiac stimulatory
centre 2) VCC vasoconstrictor
centre - Stimulation of Pressor area ?
sympathetic effects 1) ? heart rate 2) VC of
the arterioles and venules
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• Normally, during rest the VCC discharges
  continuously at a certain rate i.e it exerts a
  tone known as vasoconstrictor tone (sympathetic
  tone) ? partial VC of the arterioles.
• DEPRESSOR AREA
• - It contains
• ? CIC Cardiac Inhibitory Centre
• - Stimulation of the depressor area
  parasympathetic effects
• ? ? heart rate.
• - Normally, during rest the CIC discharges
  continuously at a certain rate through the vagus
  nerves i.e. it exerts a tone known as vagal tone
  (parasympathetic tone) ? ? HR.

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• SYMPATHETIC NERVE SUPPLY
• - The preyganglionic sympathetic fibers arise
  from the lateral horn cells of the upper 4
  thoracic segments of the spinal cord (T1-T4).
• - The preyganglionic fibers relay in the
  cervical ganglia (superior, middle inferior)
  and the upper 4 thoracic ganglia of the
  sympathetic chain.
• - Postganglionic fibers arise from these ganglia
  to supply
• ? The atria and the ventricles of the heart
  including the specialized tissues (SA node,
  AV node, AV bundle,
• bundle branches and the purkinje fibers)
• ? The coronary vessels
• - FUNCTIONS OF SYMPATHETIC CARDIAC NERVES
• 1) Stimulation of all properties of the cardiac
  muscle
• 2) Vasodilatation of the coronary arteries
• 3) Increase of O2 consumption of the cardiac
  muscle

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• PARASYMPATHETIC NERVE SUPPLY
• - The parasympathetic supply is through the two
  vagi
• - The preyganglionic vagal fibers arise from the
  dorsal vagal nucleus (CIC) in the medulla
  oblongata.
• - The preyganglionic fibers relay in terminal
  ganglia located in the atria
• - The postganglionic fibers are short they
  arise from the terminal ganglia to supply the
  atrial muscle, SA node, AV node, main stem of the
  AV bundle and the coronary vessels.
• - FUNCTIONS OF THE PARASYMPATHETIC SUPPLY
• 1) Inhibition of all properties of the cardiac
  muscle
• Stimulation of all properties of the cardiac
  muscle
• 2) Vasoconstriction of the coronary arteries
• 3) Decrease of O2 consumption of the heart

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• VAGAL TONE
• Vagal Tone is the continuous inhibitory impulses
  carried by the vagus nerve from the CIC to the
  heart to inhibit the high inherent rhythm of the
  SA node. This occurs under resting condition and
  produces a basal heart rate (about 70/ min).
• Vagal tone is a baroreceptors reflex i.e. it is
  produced by impulses from the baroreceptors
  present in the aortic arch and carotid sinus.
  These impulses stimulate the CIC.
• Evidences of Vagal tone
• 1) Injection of atropine (parasympathetic drug)
  causes increase of heart rate.
• 2) Cutting of both vagi in experimental animals
  causes increase of heart rate.
• At rest, the vagal tone to the heart is dominant
  over the weak sympathetic tone. During muscular
  exercise, heart rate is increased due to decrease
  of vagal tone and increase of sympathetic
  activity.

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• THE CARDIOVASCULAR RECEPTORS
• The walls of the heart and some blood vessels
  contain specific types of sensory receptors for
  several reflexes which control and circulation
  and respiration.
• Examples
• ? Arterial baroreceptors and peripheral
  chemoreceptors
• ? Atrial receptors
• ? Ventricular receptors
• ? Pulmonary receptors
• The most important of these receptors are
• 1) The arterial baroreceptors located in the
  aortic arch and carotid sinus
• 2) The peripheral chemoreceptors located in the
  aortic and carotid bodies
• 3) The atrial (volume or stretch) receptors
  located in the
• right atrium

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• THE ARTERIAL BARORECEPTORS OF THE AORTIC ARCH
  AND CAROTID SINUS
• These receptors are stretch receptors located in
  the wall (adventia) of
• ? the aortic arch (curve between the ascending
  and descending parts of the aorta).
• ? the carotid sinus ( dilation at the beginning
  of the internal carotid artery.
• These receptors send their afferent impulses
  through 2 nerves
• ? the aortic nerve which is a branch of the
  vagus nerve (10th cranial nerve)
• ? the sinus nerve which is a branch of the
• glassopharyngeal nerve (9th cranial nerve)

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• THE TWO NERVES ARE CALLED THE BUFFER NERVES
• The arterial baroreceptors are not stimulated at
  all by arterial pressures between 0 and 60 mm Hg
  but above 60 mm Hg they start to discharge
  impulses to the cardiovascular centers in the
  medulla oblongata along the buffer nerves.
• The rate of discharge from the baroreceptors is
  directly proportional to the systemic ABP i.e.
  the higher the blood pressure, the higher the
  frequency of impulses generated in the
  baroreceptors.
• The maximal discharge from the baroreceptors
  occurs at arterial blood pressure of about 180 mm
  Hg (180-200 mm Hg).

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• Functional of the baroreceptors the
  baroreceptors reflexes
• ? The arterial baroreceptors are sensitive to
  any change in the ABP, so they are important to
  keep the ABP normal (through baroreceptors
  reflexes)
• ? At normal level of ABP, the baroreceptors
  discharge excitatory impulses to the depressor
  area (CIC) and inhibitory impulses to the
  Pressor area (VMC or CAC VCC) at a certain rate
  ?
• - Stimulation of CIC which produces normal
  vagal tone ? (resting heart rate)
• - Inhibition of CAC
• - Inhibition of the inherent high activity of
  the VCC ?
• partial VC.

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• Therefore, at normal ABP, the baroreceptors
  discharge ?
• normal degree of vagal tone (basal heart rate)
  and
• sympathetic vasoconstrictor tone (partial VC of
  the
• arterioles).
• When the ABP is increased, the rate of discharge
  from the baroreceptors to the medullar CV centers
  is also increased ?
• More stimulation of the depressor area (CIC) ?
  increase of vagal tone and decrease of heart
  rate.
• More inhibition of the Pressor area (VMC VCC)
  ? vasodilatation of the arterioles.
• These effects (?HR VD) may decrease the high BP
  towards
• normal.

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• When the ABP is decreased, the rate of discharge
  from the baroreceptors to the medullar CV centers
  is also decreased ?
• Inhibition of the depressor area (CIC) ?
  decrease of vagal tone and increase of heart
  rate.
• Stimulation of the vasomotor centre (Pressor
  area) ? marked vasoconstriction dilatation of the
  arterioles.
• These effects (?HR VD) may decrease the high
  BP
• towards normal.
• The arterial baroreceptors of the aortic arch
  and carotid sinus their afferent connections to
  the medullar CV centers and the efferent pathways
  from these centers to the heart and the
  arterioles constitute a reflex feedback control
  mechanism that operates to stabilize the ABP i.e

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• The arterial baroreceptors reflex mechanism
• Feedback control system for regulation of ABP
• Arterial pressure buffer system (i.e. buffers
  acute changes in ABP).
• Moderator mechanism (i.e. it moderates acute
  changes in ABP).
• THE PERIPHERAL CHEMORECEPTORS
• OF THE AORTIC CAROTID BODIES
• The peripheral chemoreceptors are located in
• The aortic body which lies very close to the
  aortic arch
• The carotid body which lies very close to the
  carotid sinus.
• These receptors have rich blood supply i.e. they
  have high rate of blood flow in relation to their
  size.

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• FUNCTION OF THE PERIPHERAL CHEMORECEPTORS the
  chemoreceptor reflexes
• The peripheral chemoreceptors are sensitive to
  changes in H concentration (pH).
• If PO2, PCO2 pH are normal in the arterial
  blood, these receptors send impulses (at a
  certain rate) along the buffer nerves to CV
  centers in the medulla oblongata ?
• - Inhibition of the depressor area (CIC).
• - Stimulation of the Pressor area (VMC) ?
  partial VC of
• the arterioles
• If PO2 is decreased (hypoxia), PCO2 is increased
  (hypercapnia) , or H conc. is increased ( ?pH
  or acidosis), the peripheral chemoreceptors are
  stimulated and they discharge more impulses to
  the medullar CV centers ?
• - More inhibition of the depressor area (CIC).

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• - More stimulation of the Pressor area (VMC) ?
  increase of the Pressor area (VMC) ?
  increase of heart rate and vasoconstriction of
  the arterioles ? increase of ABP.
• This chemoreceptor reflex occurs in case of
  acute
• drop of the ABP to 40-60 mm Hg as during severe
  haemorrhage.
• This is because of the rich blood supply of the
  peripheral
• chemoreceptors which makes them sensitive to
  changes in
• ABP. Thus, ? ABP ? ischemia of these receptors ?
  local
• hypoxia (O2 lack) ? their stimulation which in
  turn,
• excites the vasomotor area ? ? HR VC ? ? ABP
  towards
• normal.
• N.B
• Central chemoreceptors are present in the medulla
  oblongata and they are sensitive to H changes in
  the cerebrospinal fluid (CSF).
• The baroreceptors are more concerned with
  regulation of circulation and the chemoreceptors
  are more concerned with regulation of
  respiration.

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REGULATION OF HEART RATE

• Outline
• Normal value and methods of counting of heart
  rate (HR)
• Physiological variations of heart rate
• Nervous regulation of heart rate (HR)
• - Bainbridge reflex, Mary's reflex (law)
  respiratory
• sinus arrhythmia
• - Alam-Smirk reflex and trigger Jones reflexes.
• Chemical regulation of HR (effect of hypoxia,
  hypercapnia, hormones drugs).
• Physical regulation of HR (effect of hyperthermia
  hypothermia).
• Tachycardia and bradycardia causes of exercise
  tachycardia
• Further Reading
• Guyton Textbook of Medical Physiology
• Ganong Review of Medical Physiology

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• REGULATION OF HEART RATE
• The normal heart rate (number of heart beats/
  min) is about 70 minute.
• The heart rate can be counted by
• a) Palpitation of the arterial pulse (e.g.
  radial pulse) or
• palpitation of the apex.
• b) Auscultation of the heart sounds
• c) ECG (electrocardiogram)
• The resting heart rate is determined by the
  degree of the vagal tone i.e. increase if vagal
  tone ? decrease of heart rate decrease of vagal
  tone ? increase of heart rate.

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• The resting heart rate is determined by the
  degree of the vagal tone i.e. increase if vagal
  tone ? decrease of heart rate decrease of vagal
  tone ? increase of heart rate.
• Vagal tone is greater in males than females, in
  adults than in children and athletes than
  non-trained persons. Therefore, physiological
  variations in heart rate are related to age, sex,
  physical training and metabolic rate.
• Regulation of heart rate includes 3 mechanisms
• a) Nervous regulation Changes in heart rate by
  afferent impulses that modify the activity of
  the cardiac centers in the medulla oblongata.
• b) Chemical regulation Changes in heart rate
  due to changes in the chemical composition of
  blood.
• c) Physical regulation Changes in heart rate
  due to changes in body (blood) temperature.

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• (a) NERVOUS REGULATION
• Nervous regulation of heart rate depends on
  afferent impulses that reach the cardiac centers
  in the medulla oblongata to change their activity
  ? changes on the heart rate.
• 1) Impulses from the right atrial receptors
  Bainbridge reflex
• - Bainbridge reflex is the reflex increase of
  heart rate due to increase of the right atrial
  pressure.
• Therefore, increase of venous return and venous
  pressure in the right atrium (e.g. during
  muscular exercise) causes reflex heart
  acceleration.
• - The increased right atrial pressure ?
  stimulation of stretch receptors (volume
  receptors) in the atrial wall ? discharge of
  impulses along afferent vagal fibers to the
  medulla oblongata ? stimulation of the vasomotor
  centre ?

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• efferent impulses along the sympathetic nerves
  to the heart ? increase of the heart rate.
• - Cardiac acceleration helps pumping of excess
  venous return into the arterial side of the
  circulation, so it prevents stay nation of blood
  in veins.
• Impulses from the arterial baroreceptors of the
  aortic arch carotid sinus Mary's reflex.
• - Mary's reflex (Mary's Law) states that the
  heart rate is inversely proportional to the
  arterial blood pressure provided that other
  factors affecting heart rate remain constant.
• Thus, increase of ABP ? decrease of heart rate
  
• decrease of ABP ? increase of heart rate.

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• - Mareys reflex is a baroreceptors reflex i.e.
• ? ABP ? stimulation of the arterial baroreceptors
  in the aortic arch and carotid sinus ? afferent
  impulses along the buffer nerves ? stimulation of
  cardio inhibitory centre (CIC) ? ? vagal tone
  and in turn decrease of heart rate.
• ? ABP (as in haemorrhage) ? decrease of number of
  impulses from the arterial baroreceptors to the
  CV centers in the medulla oblongata ? inhibition
  of the CIC and stimulation of the vasomotor
  centre (VMC) ? increase of heart rate.
• Impulses from the respiratory centre and the
  lungs Respiratory sinus arrhythmia
• Normally, there is regular increase of heart rate
  during inspiration and decrease of heart rate
  during expiration. This phenomenon is called
  respiratory sinus arrhythmia. It occur during
  deep respiration.

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• The increase of heart rate during inspiration may
  be due to inhibition of the depressor area (CIC)
  and decrease of the vagal tone by the following
  mechanisms
• a) During inspiration, the activity of the
  inspiratory centre irradiates inhibitory
  impulses to CIC.
• b) During inspiration, expansion of the lungs ?
  stimulation of stretch receptors in the wall of
  the alveoli ? discharge of impulses along
  afferent pulmonary vagal fibers ? inhibition of
  CIC.
• c) During inspiration, the venous return to the
  heart is increased ? stimulation of the stretch
  receptors in the right atrium ? discharge of
  impulses along afferent vagal fibers ?
  inhibition of CIC.

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• Impulses from the higher centers (cerebral cortex
  hypothalamus)
• Certain areas in the cerebral cortex can
  influence heart rate through their effects on the
  hypothalamus and the cardiac centers in the
  medulla oblongata e.g.
• During emotions muscular exercise, impulses
  from the cerebral cortex ? stimulation of the
  vasomotor centre ? increase of heart rate.
• The conditioned reflexes which mediated via the
  cerebral cortex ? increase or decrease of heart
  rate in response to visual or auditory stimuli.
• The hypothalamus also contain nuclei which can
  modify heart rate e.g. during sleep or emotions.

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• Impulses from other parts of the body
• a) Skeletal muscles (Alam Smirk reflex)
• - During muscular activity, the proprioceptors
  of the active muscles discharges impulses along
  afferent nerve fibers to the medulla oblongata ?
  stimulation of the vasomotor centre (VMC) ?
  increase of heart rate to supply the active
  muscles with more blood.
• b) Trigger areas (eyeball, ear, larynx,
  epigastrium, testicles etc)
• - If painful stimuli (e.g. heavy blows) are
  applied to one of the trigger areas, this leads
  to reflex decrease of heart rate (bradycardia).
• Slight or moderate (sematic or visceral) pain
  usually causes increase of heart rate. However,
  severe pain (specially visceral pain) is usually
  associated with decrease of heart rate.

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• (b) CHEMICAL REGULATION
• This includes the effect of changes in blood
  gases (O2 and CO2), the effect of some hormones
  (thyroxin, adrenaline noradrenalin) and the
  effect of some autonomic drugs (e.g. adrenaline
  atropine).
• Effect of changes in PO2 and PCO2
• This includes the effect of changes in blood
  gases (O2 and CO2), the effect of some hormones
  (thyroxin, adrenaline noradrenalin) and the
  effect of some autonomic drugs (e.g. adrenaline
  atropine).
• Hypoxia (O2 Lack)
• - Slight or moderate hypoxia ? ? PO2 in blood ?
  increase of heart rate due to stimulation of the
  peripheral chemoreceptors in the aortic and
  carotid bodies ? stimulation of the vasomotor
  centre in the medulla oblongata chemoreceptor
  reflex.

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• - hypoxia occurs in anemia, heart failure,
  haemorrhage and at high attitudes.
• - Severe hypoxia ? decrease of heart rate
  (brady cardia) due to direct depression of the
  SA node.
• Hypercapnia (increased CO2)
• - Slight or moderate hypercapnia ? ?PCO2 in
  blood ? increase of heart rate due to
• - Direct stimulation of the vasomotor centre in
  the medulla oblongata.
• - Stimulation of the peripheral chemoreceptors
  in the aortic and carotid bodies ? stimulation
  of the vasomotor centre (chemoreceptor
  reflex.
• Severe Hypercapnia (marked Co2 excess in blood)
  ? decrease of heart rate due to direct depression
  of the SA node.

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• Effect of hormones (thyroxin, adrenaline
  noradrenalin)
• Thyroxin
• - Thyroxin increases heart rate due to
• a) Direct stimulation of the SA node and
  increase of its sensitivity to catecholamine.
• b) Increase of metabolic rate.
• Adrenaline
• - Adrenaline (like sympathetic) causes increase
  of heart rate due to direct stimulation of the SA
  node.
• Noradrenalin
• - Noradrenalin is a strong vasoconstrictor agent
  ? generalized vasomotor constriction ? ?ABP.
  Increase of ABP ? decrease of heart rate (Mareys
  Reflex).
• Effect of autonomic drugs
• Parasympatholytic drugs (e.g. atropine) ?
  increase of heart rate.
• Sympathomimetic drugs (e.g. adrenaline) ?
  increase of heart rate.

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• (c) PHYSICAL REGULATION
• Effect of changes in the blood (body)
  temperature
• Increase of blood temperature (hyperthermia or
  fever)
• - Increase of the blood temperature above normal
  ? increase of heart rate due to
• a) Direct stimulation of the SA node.
• b) Stimulation of the vasomotor centre in the
  medulla oblongata by impulses discharged by
  the hypothalamus (thermo-regulatory centre).
• - Arise of 1C in the blood (body) temperature ?
  increase of heart rate by about 10 beats.
• However, in diphtheria, the heart rate is
  decreased though the body temperature is
  increased.
• This is due to the effect of diphtheria toxins
  on the heart ? depression of the cardiac muscle.

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• Decrease of blood temperature (hypothermia)
• - Decrease of the blood (body) temperature below
  normal ? brady cardia
• TACHYCARDIA BRADYCARDIA
• Tachycardia means increase of heart rate. It may
  be physiological or pathological
• Physiological e.g. as during emotions and
  muscular exercise.
• Pathological e.g. as in fevers, hyperthyroidism
  haemorrhage.
• Bradycardia means decrease of heart rate. It may
  be physiological or pathological
• Physiological as during quiet sleep and well
  trained athletes (due to high vagal tone).
• Pathological as in hyperthermia, hypothyroidism
  heart block

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• Causes of heart acceleration during muscular
  exercise
• Heart rate is markedly increases (140/min or
  more) during muscular exercise. This is due to
• 1) Emotional Effect by impulses from the
  cerebral cortex and hypothalamus ? stimulation
  of the vasomotor centre.
• 2) Chemoreceptor reflex i.e. stimulation of the
  peripheral chemoreceptors in the aortic and
  carotid bodies by ?PO2 PCO2 ? ? H
• 3) Bainbridge Reflex i.e. due to increase of
  venous pressure in the right atrium which
  results from increase of venous return.
• 4) Reflex activation of the vasomotor centre by
  afferent impulses from the proprioceptors of the
  active muscles.
• 5) Secretion of adrenaline from the
  adrenal medulla
• ? direct stimulation of the SA node.
• 6) Sympathetic over activity ? stimulation of
• sympathetic nerves of the heart.
• 7) Increase of the blood temperature during
  exercise ? stimulation of the SA node.