The document discusses the mechanisms that regulate blood pressure in the short term, including the nervous system and chemicals. It explains that the nervous system, including the baroreceptor reflex and chemoreceptors, controls blood pressure by changing peripheral resistance within seconds or minutes in response to changes in blood pressure. The document also outlines the roles of the vasomotor center, sympathetic and parasympathetic activity, and adrenal glands in short term blood pressure regulation.

1. BLOOD PRESSURE
CONTROL
MECHANISM

2. Introduction
• There are two basic mechanisms for regulating blood
pressure:
(1) short-term mechanisms.
regulate blood vessel diameter, heart rate and
contractility
(2) long-term mechanisms.
regulate blood volume
• Blood Pressure = cardiac output x peripheral resistance
• Any change in cardiac output, blood volume or peripheral
resistance will lead to a change in blood pressure.

3. • Short term control of Blood pressure is mediated by the :
I. Nervous system
II. Chemicals
• It controls blood pressure by changing peripheral
resistance. ( in sec or minutes)
• Rapidity of response (beginning within seconds and often
increasing the pressure to 2X normal (5 to 10 seconds).
• Sudden inhibition of nervous cardiovascular stimulation
can decrease the arterial pressure (one half normal)(10-
40 seconds).

4. I. Nervous System
• Control BP by changing blood distribution in the body and by
changing blood vessel diameter.
• Sympathetic & Parasympathetic activity will affects veins,
arteries & heart to control HR and force of contraction
The vasomotor center
• cluster of sympathetic neurons found in the medulla.
• It sends efferent motor fibers that innervate smooth muscle of
blood vessels.
Sympathetic activity Sympathetic activity
VASOCONSTRICTION VASODILATATION

5. Innervation of blood vessels
 Sympathetic
vasoconstrictor fiber
 Distribution: Almost all
segments of the circulation.
 The innervation is powerful
in the kidneys, gut, spleen
and skin
 is less potent in both skeletal
and cardiac muscle and in the
brain.

6.  Parasympathetic nerve fiber to
peripheral vessels
 Parasympathetic nerve fibers innervate vessels
of the blood vessels in
 Meninges
 the salivary glands
 the liver
 the viscera in pelvis
 the external genitals
 Importance: Regulate the blood flow of these
organs in some special situations.

7. Innervation of blood vessels
 Almost all vessels, such as arteries, arterioles, venules
and veins are innervated.
except the capillaries, precapillary
sphincters and most of the metarterioles.
 Tone: Usually the sympathetic vasoconstrictor fibers
keep tonic.

8. Short-term Regulation of Rising Blood Pressure
Rising blood pressure
Stretching of arterial walls
Stimulation of baroreceptors in carotid
sinus, aortic arch, and other large
arteries of the neck and thorax
Increased impulses to the brain

9. Increased
Parasympathetic Activity
Effect of increased parasympathetic and
decreased sympathetic activity on heart and
blood pressure:
• Increased activity of vagus (parasympathetic) nerve
• Decreased activity of sympathetic cardiac Nerves
• Reduction of heart rate
• Lower cardiac output
• Lower blood pressure

10. Decreased
Sympathetic Activity
Effect of decreased sympathetic activity on
arteries and blood pressure:
• Decreased activity of vasomotor fibers (sympathetic
nerve fibers)
• Relaxation of vascular smooth muscle
• Increased arterial diameter
• Lower blood pressure

11. Short-term Regulation of Falling BloodPressure
Baroreceptors inhibited
Decreased impulses to the brain
Decreased parasympatheticactivity,
increased sympathetic activity
Effects
Heart
increased heart rateand
increasedcontractility
Vessels
increasedvasoconstriction
Adrenal gland
release of epinephrine and
norepinephrine which enhance heart rate
Contractility and vasoconstriction
Increased blood pressure

12. • Sympathetic Activity on Heart and Blood Pressure
Effect of Increased Sympathetic Activity on Heart and
Blood Pressure:
• Increased activity of sympathetic cardiac nerves
• Decreased activity of vagus (parasympathetic) nerve
• Increased heart rate and contractility
• Higher cardiac output
• Increased blood pressure

14. I. Baroreceptors
• The best known of nervous mechanisms for arterial
pressure control (baroreceptor reflex)
• Baroreceptors are stretch receptors found in the
carotid body, aortic body and the wall of all large
arteries of the neck and thorax.
• Respond progressively at 60-180 mm Hg.
• Respond more to a rapidly changing pressure than
stationary pressure.

15. Baroreceptors

16. • Rapidly Acting Pressure Control Mechanisms, Acting Within
Seconds or Minutes.
A. Baroreceptor reflexes (60 – 100 mmHg)
Change peripheral resistance, heart rate, and stroke volume in
response to changes in blood pressure
B. Chemoreceptor reflexes (40 – 60 mmHg)
Sensory receptors sensitive to oxygen lack, carbon dioxide
excess, and low pH levels of blood
C. Central Nervous System ischemic response (< 40 mmHg)
Results from severe decrease blood flow to the brain

17. Baroreceptor reflexes
Baroreceptors are found in :
• Carotid Sinuses (blood going to brain) by glossopharyngealnerve
• Aortic Arch (systemic blood going to body) by vagusnerve
As MAP increases this stretches the receptors and they send a fast trainof
impulses to the Vasomotor Centre. After the signals enter the tractus
solitarius, secondary signals inhibit vasoconstrictor centres and excite the
vagal parasympathetic center. This results in a decrease in the frequency
of impulses from the Vasomotor Centre and arterioles dilate. Final result
is vasodilation and decreases MAP.
*CIC activity increases (stimulating the Vagus nerve) - decreases HR and
SV.
* CAC activity decreases (inhibiting Sympathetic nerves) - decreases CO.

18. Effect of Baroreceptors
Baroreceptors entered the medulla (tractus solitarius)
Secondary signals inhibit the vasoconstrictor center of medulla
and excite the vagal parasympathetic center
VASODILATATION OF THE
VEINS AND ARTERIOLES
Therefore, excitation of baroreceptors by high pressure in the arteries
reflexly causes arterial pressure to decrease (as decrease in PR and CO)
DECREASED HEART RATE AND
STRENGTH OF HEART
CONTRACTION
EFFECT
NOTE : Conversely, low pressure has opposite effects,reflexly causing the pressure rise
back to normal.

19. II. Chemoreceptor

20. Chemoreceptor
• Chemosensitive cells that respond to changes in pCO2 and
pO2 and pH levels (Hydrogen ion).
pO2 andpH
 2pCO 
Stimulation of
vasomotor center
CO  HR vasoconstriction
BP (speeding return of blood
to the heart and lungs)

21. Chemoreceptor

22. CNS Ischemic Response
Severe decrease blood flow to brain
Cerebral hypoxia
Vasomotor center stimulated – causes powerful
vasoconstriction
( INCREASE SYMPATHETIC DISCHARGE – Norepinephrine)
Increase blood pressure & blood flow

23. Cushing Reaction
- Special type of CNS Ischemic Response
Increased pressure of cerebrospinal fluid (cranial vault)
Increase intracranial tension
Compress whole brain & arteries in the brain
Cuts off blood supply to brain
CNS Ischemic Response initiated & arterial pressure rises
Relieve brain ischemia

24. Cardiac Centres (Higher Centres)
-IN MEDULLA-
1. Cardio Acceleratory Centre sends sympathetic neurones down the spineto
between T1 and T5, where they exit to the periphery.
2.Cardio Inhibitory Centre originates with the Vagus Nucleus in themedulla
and this parasympathetic nerve leaves the cranium as the Vagus (X)Nerve.
3. Vasomotor Centre - is a cluster of sympathetic fibres in theMedulla.
- transmits impulses via sympathetic vasomotorfibres
from T1 to L2 to blood vessels (arterioles)
Vasoconstriction is caused by increased frequency of impulses (Noradrenaline)
Vasodilation is caused by decreased frequency of impulses.

25. Brainstem contains:
Pons
Medulla
In the Medulla are the:
Cardiac AcceleratoryCentre
Cardiac Inhibitory Centre
Vasomotor Centre

30. ELECTROCARDIOGR
AM Normal ECG and Leads

31. What is ECG?
• Transthoracic interpretation of
the electrical activity of
the heart over time captured and externally
recorded by skin electrodes.
• The sum of the electrical activity generated by
the heart.

32. How do ECG works?
• It works by detecting and amplifying the tiny
electrical changes on the skin that are caused
when the heart muscle "depolarises" during
each heart beat.
• ECG is measured by placing skin electrodes on
the body surface at different locations.
• This electrodes are connected in different
configuration to a amplifier and a recorder.

33. Normal ECG Character?
The ECG comprise of several waves:
• P wave
• QRS complex
• T wave

35. What is P wave?
• Caused by the electrical potentials generated
when the atria depolarise before the
contractions begins.
• This is depolarization wave.

37. What is QRS complex?
• It is caused by potentials generated when the
ventricles depolarized before contraction.
• This is depolarization wave.

39. What is T wave?
• It is caused by potential generated as the
ventricles recover from the state of
depolarization.
• It is known as repolarization wave.

42. What is ECG Leads?
• They are electrical cable attaching
the electrodes to the ECG recorder.
• They also may refer to the tracing of
the voltage difference between two of the
electrodes and is what is actually produced by
the ECG recorder.

43. How many leads are there?
There are 12 leads:
• 3 limbs lead (I, II, III)
• 3 Augmented leads (aVR, aVL, aVF)
• 6 Precordial Leads (V1 – V6)

44. Limbs lead

45. Precordial Leads

46. Augmented Leads

47. THANK YOU

48. Action Potential And Impulse Conduction

49. What is action potential
• Action potential: electrical stimulation created by a
sequence of ion fluxes through specialized channels in the
membrane (sarcolemma) of cardiomyocytes that leads to
cardiac contraction.
• Action potential in cardiomyocytes
• The action potential in typical cardiomyocytes is
composed of 5 phases (0-4), beginning and ending with
phase 4.

50. Phase 4: The resting phase
The resting potential in a
cardiomyocyte is −90 mV
due to a constant outward
leak of K+ through inward
rectifier channels.
Na+ and Ca2+ channels are
closed at resting TMP.

51. Phase 0: Depolarization
Fast Na+ channels start to open
one by one and Na+ leaks into
the cell, further raising the
TMP.
TMP approaches −70mV,
the threshold potential in
cardiomyocytes, i.e. the point
at which enough fast
Na+ channels have opened to
generate a self-sustaining
inward Na+ current.

52. Phase 1: Early repolarization
TMP is now slightly
positive.
Some K+ channels open
briefly and an outward
flow of K+ returns the
TMP to approximately 0
mV.

53. Phase 2: The plateau phase
Ca2+ channels are still open
and there is a small,
constant inward current of
Ca2+.
K+ leaks out down its
concentration gradient
through the delayed
rectifier K+ channels.
These two counter currents
are electrically balanced,
and the TMP is maintained
at a plateau just below 0
mV throughout phase 2

54. Phase 3: Repolarization
Persistent outflow of K+, now
exceeding Ca2+ inflow, brings
TMP back towards resting
potential of −90 mV to prepare
the cell for a new cycle of
depolarization.
Normal transmembrane ionic
concentration gradients are
restored by returning Na+ and
Ca2+ ions to the extracellular
environment, and K+ ions to the
cell interior.

55. Action potential in
Cardiac pacemaker cells
SA/av Node, Purkinjee fibres

56. • Automaticity: unlike other cardiomyocytes, pacemaker cells do not
require external stimulation to initiate their action potential; they are
capable of self-initiated depolarization in a rhythmic fashion. This
property is known as automaticity.
• Unstable membrane potential: Pacemaker cells have an unstable
membrane potential and their action potential is not usually divided
into defined phases.
• No rapid depolarization phase: Pacemaker cells have fewer
inward rectifier K+ channels than do other cardiomyocytes, so their
TMP is never lower than −60 mV.