Just checking CVS-2nd-year-Medicine9,10.ppt

Just checking

2. The control of the heart rateThe control of the heart rate
Cardiovascular centers
Inspiratory
center
The hypothalamus
and limbic system
Cerebral cortexCerebral cortex
Reflexes
S-A S-A
nodenode
Chemical factors
Physical factors
Mechanical factors

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

4. RESISTANCES IN SERIESRESISTANCES IN SERIES
R
T
= R
A
+ R
C
+ R
V
RESISTANCES IN PARALLEL
R
1
R
2
R
3
P
A
P
V
1
R
T
1
R
1
1
R
2
1
R
3
=+ +
1
R
1
1
R
2
1
R
3
R
T
1
++
=

5. Pressure Drop in the Vascular SystemPressure Drop in the Vascular System
LARGE ARTERIES
SMALL ARTERIES
ARTERIOLES
CAPILLARIES
VENULES &VEINS
M
E
A
N
P
R
E
S
S
U
R
E
INSIDE DIAMETER
SMALL LARGELARGE
ELASTIC TISSUE
MUSCLE

6. Nervous factorsNervous factors
The most important factor in the The most important factor in the
regulation of the heart rate is the activity regulation of the heart rate is the activity
of the cardiovascular centers in the of the cardiovascular centers in the
medulla oblongatamedulla oblongata . .
This activity is transmitted to the heart via This activity is transmitted to the heart via
its sympathetic and parasympathetic its sympathetic and parasympathetic
nerve supplynerve supply..

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

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

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

10. INCREASING HEART RATE INCREASING HEART RATE
INCREASES CONTRACTILITYINCREASES CONTRACTILITY
Normal
Heart Rate
Ca
++ Ca
++
Fast
Heart RateCa
++
Ca
++ Ca
++
Ca
++

11. CARDIAC FUNCTION CURVECARDIAC FUNCTION CURVE
S
T
R
O
K
E

V
O
L
U
M
E
DIASTOLIC FILLING
Cardiac Output = Stroke Volume x Heart Rate
ConstantIf:
Then: CO reflects SV
Right Atrial Pressure (RAP) reflects Diastolic Filling

12. CARDIAC FUNCTION CURVECARDIAC FUNCTION CURVE
C
A
R
D
I
A
C


O
U
T
P
U
T


(
L
/
m
i
n
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
Volume
P
r
e
s
s
u
r
e
THE FRANK- STARLING “LAW OF THE HEART”

13. CARDIAC FUNCTION CURVECARDIAC FUNCTION CURVE
C
A
R
D
I
A
C


O
U
T
P
U
T


(
L
/
m
i
n
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
I
n
c
r
e
a
s
e
d
C
o
n
t
r
a
c
t
i
l
i
t
y

14. CARDIAC FUNCTION CURVECARDIAC FUNCTION CURVE
C
A
R
D
I
A
C


O
U
T
P
U
T


(
L
/
m
i
n
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
D
e
c
r
e
a
s
e
d
C
o
n
t
r
a
c
t
i
l
i
t
y

15. CARDIAC FUNCTION CURVECARDIAC FUNCTION CURVE
C
A
R
D
I
A
C


O
U
T
P
U
T


(
L
/
m
i
n
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
I
n
c
r
e
a
s
e
d
H
e
a
r
t

R
a
t
e

16. CARDIAC FUNCTION CURVECARDIAC FUNCTION CURVE
C
A
R
D
I
A
C


O
U
T
P
U
T


(
L
/
m
i
n
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
D
e
c
r
e
a
s
e
d
H
e
a
r
t

R
a
t
e

17. 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

18. HEART RATE & ITS REGULATIONHEART 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)

19. -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].

20. - 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.
oSympathetic nervous system and
oParasympathetic nervous system

21. CARDIOVASCULAR CENTRES CARDIOVASCULAR CENTRES (CVCs)(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

22. -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.

23. A)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

24. B)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

25. 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.

26. 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

27. 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 (10
th

cranial nerve)
 the sinus nerve which is a branch of the
glassopharyngeal nerve (=9
th
cranial nerve)

28. 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).

29. -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.

30. 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 
a)More stimulation of the depressor area (CIC)  increase of
vagal tone and decrease of heart rate.
b)More inhibition of the Pressor area (=VMC = VCC) 
vasodilatation of the arterioles.
These effects (HR + VD) may decrease the high BP towards
normal.

31. When the ABP is decreased , the rate of discharge from the
baroreceptors to the medullar CV centers is also decreased 
a)Inhibition of the depressor area (CIC)  decrease of vagal tone
and increase of heart rate.
b)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:

32. 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.

33. 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).

34. - 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.BN.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.

35. 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

36. REGULATION OF HEART RATEREGULATION 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.

37. 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.

38. (a) (a) NERVOUS REGULATIONNERVOUS 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 

39. 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.
2)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.

40. - Marey’s 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.
3)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.

41. -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.

42. 4)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.

43. 5)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.

44. (b) CHEMICAL REGULATION(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).
1)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”.

45. - 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.

46. 2)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 (Marey’s Reflex).
3)Effect of autonomic drugs:
Parasympatholytic drugs (e.g. atropine)  increase of heart
rate.
Sympathomimetic drugs (e.g. adrenaline)  increase of heart
rate.

47. (c) PHYSICAL REGULATION(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 1°C 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.

48. Decrease of blood temperature (hypothermia):
- Decrease of the blood (body) temperature below
normal  brady cardia
TACHYCARDIA & BRADYCARDIATACHYCARDIA & BRADYCARDIA
-TachycardiaTachycardia 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.
-BradycardiaBradycardia 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

49. 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.