- Baroreceptors: - Chemoreceptors: - Depressor area:  ABP via para - Baroreceptors: - Chemoreceptors: - Baroreceptors: - Chemoreceptors: - Baroreceptors: - Chemoreceptors: - Baroreceptors: - Chemoreceptors: - Baroreceptors: - Chemoreceptors: - Baroreceptors: - Chemoreceptors: - Baroreceptors: - Chemoreceptors: - Baroreceptors: - Chemoreceptors:

1. Cardiovascular system (CVS)
Nermeen Bastawy
Physiology , MD
Faculty of Medicine
Cairo University

2. Cardiovascular system (CVS)
4 valves:
2 atrioventricular valves: tricuspid & mitral
2 semilunar valves: pulmonary & aortic
Systole = contraction
Diastole = relaxation

3. CVS
CVS is formed of:
 Central pump (Rt and Lt)
 Closed system of blood vessels
The function are:
Supply the different organs with
adequate blood flow.
Secrete hormones regulate BLOOD
PRESSURE

4. CVS is divided into:
1.The left ventricle:
 Acts as a pressure pump.
 Pumps oxygenated blood at a high
pressure into systemic circulation
2.The arteries (e.g.the aorta):
(elastic vessels)
 Stretch during systole and recoil
during diastole
3.The arterioles (muscular vessels)
 The main sites of resistance to
regulate blood flow and pressure.

5. CVS is divided into:
4.The capillaries
 They are the exchange sites for
nutrients and waste products.
 Thin walls with pores
 Large cross-sectional area.
5.The venules and veins
(distensible vessels)
• Returning blood from capillaries to heart.
• Have a large capacity.

6. 6.The right ventricle
A volume pump as it pumps the
same volume of blood as the left
ventricle, but at a lower pressure, to
the pulmonary circulation.
7.The pulmonary vessels
They have the important function of
gas exchange and also they act as a
volume reservoir.

7. 8.The lymphatic vessels
 They are permeable to fluids and large compounds.
 Functions: drainage system that returns tissue fluids to blood stream
N.B
 All arteries carry
oxygenated blood
except pulmonary
artery
 All veins carry venous
blood except pulmonary
veins

8. Pulmonary and Systemic Circuits
 Systemic Circuit
◦ Left ventricle to
◦ arteries & arterioles
& capillaries to
◦ body systems
◦ Returns through
venules & veins
deoxygenated blood
to right atrium
 Pulmonary Circuit
◦ Right ventricle
◦ to via pulmonary
arteries
◦ To the lungs
◦ Returns oxygenated
blood to left heart
via 4 pulmonary
veins

9. Functional histology
Gap junction
Intercalated discs:
o Areas of contact between cardiomyocytes
o Provide a strong union
Gap junctions:
oAreas of low resistance between cells for rapid spread of excitation
& ions
oAllow cardiac muscle to function as one syncytium (one unit)

10. Contractility

11. 1- Rhythmicity = Automaticity
 Def.Ability of heart to initiate its own regular
impulses independent to nerve supply
 Site: SAN,AVN, Purkinje fibers
 Characters: Unstable membrane potential
Auto-generation of impulses

12. 1- Rhythmicity = Automaticity
SAN: Sino-atrial node
• Located in the right atrium
• It is the normal pacemaker Why?
SA node has the fastest rate 90 / min
AVN: Atrio-ventricular node
• Located in the right atrium
• Its rate is 60 / min.
Purkinje fibers
• Located in the wall of both ventricles
• rate is 30 / min.

13. Vagal tone Vs Sympathetic tone
60
Vagal Tone: predominance inhibitory effect of Parasympathetic
nervous system on SAN during rest
This keep normal heart rate 60-100 bpm during rest
Sympathetic Tone predominant on SAN during exercise

14. +ve chronotropic
Tachycardia
-ve chronotropic
Bradycardia
Sympathetic nervous system, Exercise
Fever
RapidArrhythmia
Drugs as troxin
Hyperthyroidism
Heart failure
Parasympathetic nervous system
Hypothermia
SomeArrhythmia
Drugs as beta blockers, anesthesia
Hypothyroidism
Myocardial infarction

15. 2- Conductivity
It is the property by which the
excitation wave is conducted through
the cardiac tissue.
The atrial and ventricular functional
syncytia are completely separated by
fibrous rings and the only connection
between them is through the
specialized system.

16. Spread of cardiac excitation
Depolarization is initiated in the SAN which spread to both atria and AVN
Internodal tracts
AVN receives impulses from SAN, delays the conduction before transmit
them to ventricles
From AVN, impulses pass in the AV bundle (bundle of His), that divides into right and left
branches, and give off Purkinje fibres (fastest conduction rate) branches that terminate
on the ventricular muscle fibres
AV node can generate
impulses at slower rate
than SAN

17. Spread of cardiac excitation
Depolarization initiated in the SAN
Internodal tracts
AVN receives impulses, transmits them
to ventricles & delays the conduction
AV node can generate impulses at slower rate than SAN
From AVN, impulses pass in the AV bundle (bundle
of His), that divides into right and left branches,
and give off Purkinje fibres (fastest conduction
rate) branches that terminate on the ventricular
muscle fibres
2- Conductivity

19. Slow at AVN Rapid at Purkinje
This delay is important as it
allows sufficient time for atria to
empty their blood into the
ventricles to complete filling
before systole begins.
This ensure contraction of
both ventricle at same
time → efficient pump

20. 3- Excitability (Ventricular AP)
RMP - 90 mv
Depolarization
+20 mv
0 mv
Repolarization
Plateau
3

21. 3- Excitability (Ventricular AP)
RMP - 90 mv
Depolarization
+20 mv
0 mv
Repolarization
Plateau
3
▪ Depolarization (Phase 0):
Cause: opening of fast Na+ & Slow Ca- Na channels
▪ Repolarization: Triphasic:
Phase 1: due to:
✓ Closure of fast Na+ channels
✓ Opening of Cl- channels → Cl- influx
✓ Opening of K+ channels →K+ efflux
Phase 2: plateau: due to balance between Ca++ inflow & K+ outflow
Phase 3: late repolarization: due to closure of Ca++ channels → K+ outflow is not
antagonized by Ca inflow till return to RMP (Phase 4).

22. Contraction Relaxation
Mechanical
response
(Contraction)
Long refractory period prevents tetanic contraction
Excitability
Changes during
AP

23. Absolute refractory period
(ARP)
Relative refractory period
(RRP)
▪ Excitability is zero → no
response to any stimuli
▪ Coincide with systole &
beginning of diastole
(phases 0-2 & half of 3)
▪ Importance: prevent
tetanus
▪ Excitability is below normal →
respond to stronger stimulus
▪ From end of ARP till phase 4
Excitability Changes during AP

24. 4- Contractility (Inotropic State)
Cardiac contraction lasts 1.5 times the
duration of action potential.
Excitation–Contraction Coupling: Cardiac
contraction depends on Extracellular Ca
influx during the plateau phase
++ Ca++ influx→ +ve inotropics
--- Ca++ influx → -ve inotropics

25. 4- Contractility (Inotropic State)
Cardiac muscle obeys 2 laws:
1. Starling law (length -tension relationship):
“The more the initial length (end diastolic volume) the more the force of
contraction (tension) “
2. All or non law: whole cardiac muscle (both atria or both ventricles) acts
as one functional syncytium: contract to threshold stimulus or don’t
respond to subthreshold stimulus
N.B Excitation-Contraction Coupling of cardiac muscle is similar to that of skeletal
muscle

26. Factors affecting the Contractility
Positive Inotropics
(↑ contractility & COP)
1/ Sympathetic nervous system
Mechanism: catecholamines (norepinephrine) act on B1 receptors → more open time of Ca
channels
2/Xanthine: caffeine & theophylline
3/Glucagon
4/Digitalis (but it is a negative chronotropic): used in heart faiure
5/ ↑ ECF Ca++
→stop heart in systole (Ca rigor)

27. Factors affecting the Contractility
Negative Inotropics
(↓ contractility & COP)
1/Parasympathetic nervous system
Mechanism: acetyl choline: has negative effect on atrial muscle
2/Ca antagonists: (calcium blockers)
Anesthetics,Anti arrhythmic agents, antihypertention
3/ Ischemia, hypoxia, acidosis
4/↓ ECF Ca→ stop heart in diastole

28. CARDIAC
OUTPUT
VR
CO
CO = MinuteVolume:
It is the volume of the blood pumped by
each ventricle per minute.
Normally:
• Venous return = CO
• CO of left ventricle = CO of
right ventricle
• CO = 5L/min

29. Stroke volume (SV ) : volume of blood pumped by each ventricle per beat = 70ml.
End diastolic volume (EDV): vol. of blood in the ventricle at the end of diastole.
End systolic volume (ESV): vol. of blood in the ventricle at the end of Systole.
SV = End diastolic vol. - End systolic vol. = EDV - E SV
= 135 - 65 = 70ml

30. 70
SV
70 70
70
70
SV X HR=
COP

32. Variations of CO
1- sympathetic stimulation (Exercise,
Anxiety, Excitement, adrenaline and
noradrenaline secretion)
2- Shifting from standing to recumbent
position
3- After meals
4- High environmental temperature
5- Pregnancy
1- Standing from supine position
2- Heart diseases: Rapid arrhythmias,
Heart failure, cardiomyopathy,
concentric hypertrophy
Unchanged in Sleep & Moderate change in
external temperature

33. Preloa
d /
Afterl
oad
Contract
ility(Inot
ropy)
Contr
ol

34. Factors control CO
Inotropy

35. Factors control CO
1- Preload : ↑ Venous return → ↑ EDV → ↑contraction force →↑SV → ↑CO
2- Afterload : ↑ Aortic pressure (hypertension) or aortic valve diseases →↑ ESV → ↓SV →↓ CO
3- Inotropic state
✓ +Ve inotropics →↑contraction force→ ↓ ESV → ↑SV →↑ CO
✓ -Ve inotropics →↓contraction force →↑ ESV → ↓SV →↓ CO
4- ↑ HR if during:
✓ Exercise → ↑ CO
✓ Arrhythmia → ↓ CO
5- Heart size
✓ Eccentric Hypertrophy in athletes→↑ EDV → ↑SV → ↑ CO
✓ Concentric Hypertrophy → ↓EDV → ↓ SV → ↓ CO

36. Cardiac
Hypertrophy

37. Regulation of
COP
EXTRINSIC
1. Nervous (ANS)
2. Hormonal
HR SV
INTRINSIC
Independent of nerves
or hormones
↑venous return → ↑ EDV → ↑
muscle length → the force of
contraction (Starling’s law ) →↑ SV

38. Nervous regulation of CO
1- Parasympathetic (Vagus) 2- Sympathetic
Supplies Only atria Atria and ventricles
Action on
• Cardiac
Properties
Inhibits atrial only Stimulate atrial + vent.
• Inotropic -ve (atrial) + ve
• Chronotropic(HR) - ve + ve
• Cardiac work &
O2 consumption
 
• Coronary vessels vasoconstriction vasodilatation
• CO  by decreasing the H.R.
only (not supply vent.)
 by increasing both HR &
SV.

39. CARDIAC CYCLE
Events occurs during one beat
(during Relaxation & contraction of heart)
Systole
Diastole

40. CARDIAC CYCLE
It starts by systole of both atria followed by
systole of both ventricles, and then diastole of
the whole heart. -If heart rate is 75/minute,
the duration of each cycle is 0.8 sec. -When
the heart accelerates, the cycle shortens,
especially the diastole.
If HR is 75/min (60 second/75) →
Diastole = 0.5 s
Diastole is important bcz it is time of:
a. Coronary blood flow
b. Ventricles rest
c. Ventricular filling mainly (70 %) in EARLY
diastole →ensures that ventricular filling is
not much decreased with↑ HR
70 %
30 %
RESERVOIR OF
BLOOD

41. 30 %
70 %
1. Atrial Systole (LATE DIASTOLE)
2. Isometric contraction
3. Maximum ejection
4. Reduced ejection
5. Isometric relaxation
6. Maximum filling
7. Reduced filling (MID DIASTOLE)
CARDIAC CYCLE : 8 PHASES
S
D
1

42. Volume of blood retuning to heart/min.
COP =VR = 5 L/min

44. Factors help venous return against
gravity
Muscle pump
• During musDuring muscle contractions: veins are compressed and
squeezed, so blood is directed upward
• cle relaxation: healthy valves allow movement in one direction and
prevent return of blood backward
• In paralysed person, the leg is edematous and cold
• Destruction of valves → backwards of blood flow
→ varicose veins

46. Factors help venous return against gravity
Cardiac pump
- Atrial suction: During ventricular systole
- Ventricular suction: During ventricular diastole
Thoracic pump
During inspiration: negative intrathoracic pressure → ↑VR

47. Blood flow
1- Laminar
• Normal flow
• Silent
• Blood flows in one direction
2- Turbulent flow
• Abnormal flow
• Has sound
• Blood flows in different
directions
• Causes: obstruction,  velocity,
↓ blood viscosity as in anemia
Def. Volume of blood crosses a point per/min
Types:

48. Nervous control of diameter of
arterioles
Vasoconstrictors
(VC)
Vasodilators (VD)
Sympathetic system Sympathetic to blood vessels of
skeletal muscle or coronaries
Parasympathetic system
Pain VD fibers

49. Hormonal control of diameter of arterioles
VC VD
Catecholamines kinins
Angiotensin II Atrial natriuretic peptide
(ANP)
Antidiuretic peptide (ADH) Nitric oxide (NO)
Endothelin (ET1) Prostacyclin

50. Arterial blood pressure (ABP)

51. ABP
Systolic pressure (SP): Maximum Pressure during systole 120 mmHg (90
– <140).
Diastolic pressure (DP): Minimum Pressure during diastole 80 mmHg
(60 – <90).
Pulse pressure (PP): difference between systolic & diastolic pressure
SP – DP = 50 mmHg
Mean arterial pressure (MAP):
DP + 1/3 PP

52. Physiological Variations in ABP
Age & Sex
Race
Emotions
Exercise
Gravity
 Circadian rhythm
(↑ABP at morning)
Respiration

53. 1. Age: ↑ABP with age due to loss of elasticity of blood vessels
2. Sex: < 45 years females have less ABP than males.
> 45 years the pressures  in females due to hormonal changes.
3. Emotions  ++ sympathetic → ↑ABP especially systolic.
4. Exercise  static exercise ↑ABP
5. Gravity: blood pressure in the lower limbs in higher than upper limb
• New born = 80/40 mmHg
• 20 years = 120/ 70 mmHg
Physiological Variations in ABP

54. Factors determine ABP
 ABP = COP xTPR
 ABP = SV x HR xTPR
 Elasticity of arteries
# atherosclerosis → ++TPR
(total peripheral resistance)

55. Regulation of ABP
▪ Rapid: Nervous (within
minutes)
▪ Intermediate: Capillary shift
(within hours)
▪ Slow: Hormonal (renal, within
days)

56. Nervous regulation of ABP

-

57. Nervous regulation of ABP
 2 Centers in CNS:
- Pressor area:
 ABP via
sympathetic nerves
- Depressor area:
↓ ABP via vagus

58. Intermediate regulation of ABP
- ABP
→  capillary hydrostatic pressure
→  fluid filtration
→ edema
& vice versa
Capillary shift mechanism:

59. Slow regulation of ABP through the kidney
1. Renin angiotensin system (RAS)
Hypotension
stimulates
kidney to
secrete renin

61. 2. Atrial mechanoceptors
 ↑ABP → stretch of atria that stimulate atrial mechanoceptors → ↑ atrial
natriuretic peptide (ANP)
Action ofANP: decrease ABP by:
✓ ↓ aldosterone & ADH
✓  Na+ & H2O excretion
Slow regulation of ABP through the kidney

62. Causes of edema
  Capillary hydrostatic pressure:
Rt Heart failure, Pregnancy,
hypertension & venous obstruction
  Capillary permeability e.g. allergy
  plasma proteins:
Nutritional / Hepatic / renal
 Lymphatic obstruction
 Drugs : oral contraceptive
 Endocrine: myxedema
Edema : increase interstitial fluid

63. SHOCK
Def. Inadequate tissue perfusion i.e inadequate COP
4Types:
Hypovolemic shock: hemorrhage, dehydration, burn
Distributive Shock (Vasogenic = low resistance): anaphylactic
shock, nervous shock, septicemia
Cardiogenic shock: myocardial infarction, arrhythmia
Obstructive shock: pulmonary embolism

64. Hemorrhage shock
Manifestation:
ABP & skinTemperature
 HR & respiratory rate
Pallor, thirst
Oliguria and acidosis

65. Rapid compensatory reactions
Aim: Protective i.e. maintains adequate perfusion of heart + brain
Mechanisms:
Nervous Hormonal
Sympathetic NS
Peripheral chemoreceptors
Catecholamines
Angiotensin II
Vasopressin (ADH)
Slow compensatory
reactions
Aim: Correction
plasma is replaced within hours
plasma proteins are replaced
within days
RBC are replaced within weeks