CARDIOVASCULAR PHYSIOLOGY

1
CARDIOVASCULAR PHYSIOLOGY Dr J. du Toit Room
511 Fisan building
Text books Human Physiology An Integrated
Approach. Silverthorn. Human Physiology. Rhodes
and Pflanzer.
2

• Functions of the CVS
• Transport of 1) nutrients and water and,
  2) gases

DS Lungs

• Cells
  Liver Cells
• 
  Kidneys
• Cell ? cell communication - hormones
• Transport fatty acids from adipose tissue
  glucose from the liver
• Transport WBC antibodies
• NB in temperature regulation

3

• Anatomy of the Heart
• Size of fist
• Between lungs - base under sternum and apex on
  diaphram

Epi- en pericardium fibrous and serous tissue
Wall Myocardium - contractile cells
Endocardium endothelium continuous with blood
vessel endothelium

• 2 Atria
• 4 Chambers

2 Ventricles
4
Right Tricuspid valve (3-leaflets)

• Atria ventricles separated by AV valves
  Cordae tendinae en papillary muscles
• Left Bicuspid Mitral valve (2
  leaflets)
• Ventricles of pulmonary artery and aorta
  separated by semilunar valves Aortic valve and
  
• Pulmonary valve
• Arteries ? oxygenated blood - red

VASCULAR SYSTEM Veins ? deoxygenated
blood - blue
5
B. Anatomy and direction of blood flow through
the heart
6
(No Transcript)
7
(No Transcript)
8
(No Transcript)
9
(No Transcript)
10
(No Transcript)
11
(No Transcript)
12
The Heart wall a) Epicardium/Pericardium 2
layers nl. i) Outside fibrous pericardium
ii) Inside serous pericardium Functions 1)
Prevents excess stretching of heart 2) Provides
smooth, lubricated outside surface b)
Myocardium Contractile part of the heart
wall. c) Endocardium Connective tissue attaches
the myocardium to the endothelium. The latter
provides smooth surface and prevents clotting.
13

• Properties of the cardiomyocyte
• Is striated
• Contains one or more nuclei
• Cells are branched
• More mitochondria than skeletal muscle
• Contains tight junctions and gap junctions.
• 2 Types of cardiomiocytes
• 1) normal cardiomyocytes
• 2) pacemaker and conducting cardiomyocytes

ELECTRICAL ACTIVITY OF THE HEART Structure of the
cardiomyocyte

14
(No Transcript)
15
(No Transcript)
16
(No Transcript)
17

• AP of Skeletal and Heart
  muscle
• Depolarisation due to Na influx
• Repolarisation due to K efflux
• Heart muscle AP has plato due to Ca2 influx
  ?longer AP

18
(No Transcript)
19
(No Transcript)
20
(No Transcript)
21
(No Transcript)
22

• Importance of the Refractory Period
• Prevents tetanus

Ensures diastolic relaxation
23
(No Transcript)
24
(No Transcript)
25
(No Transcript)
26
(No Transcript)
27
(No Transcript)
28
(No Transcript)
29

• SA node
• wall of the RA near superior vena cava.
• primary pacemaker at rest ? 70bpm.
• Parasympathetic ACh - ? heart rate
• Sympathetic adren. nor-adren. - ? heart rate
  and contractile force
• Sensitive to temp., stretch, touch and chem.
  stimulation
• AV node
• Bottom wall of the RA - interatrial septum
• Firing frequency 40-60bpm
• 1) Delays heart impulse 0.1 sec ?complete
  ventricular filling
• 2) Delays frequency of impuls propagation

30

• AV bundle
• From the AV-node to interventricular septum.
• Right bundle branch right of the septum to the
  apex of the heart
• Left bundle branch posterior/inferior branch
• anterior/superior branch
• functional link between atria and ventricles
• Purkinje fibres
• branches of the left and right bundle branch
• impulse propagation to contractile cells in
  ventricle

31
(No Transcript)
32
AP Origin and Propagation SA-node propagation
speed fast (1 m/sec) ? AV-node propagati
on speed slow (0.05-0.1 m/sec)
?
no direct conduction from atria to
?
ventricle muscle Fibrous
plate/sheath Bundle of His
propagation speed fast ? Purkinje system
propagation speed fast (2
m/sec) ? Ventricular contractile cells
33

• Wave of depolarization over heart creates a
  potential difference - dipole
• Dipole (hart) surrounded by conductor
  (elektroliete water)
• Elektrodes on surface attached to galvanometer
  measures potential differences

ECG measures electrical changes in heart
34

• ECG
• The sum of all the potentials that are created
  by the cells of the heart at any given moment
• Each component of the ECG reflects a de- or
  repolarisation of a part of the heart ?can
  associate parts of the ECG with parts of the
  cardiac cycle.
• Clinical application of the ECG
• Determination of
• HR, heart rhythm
• Presence of hypertrophy or atrophy
• Abnormal conduction paterns
• The cardiac axis (electrical axis)
• Normal heart rhythm
• Sinus rhythm bradycardia or tagycardia

35

• ECG Leads
• Position of the electrodes leads
• 6 peripheral leads and 6 precordial leads
• a) 3 bipolar limb leads (standard leads)
  measure the potential differences between 2
  points (Einthoven triangle)
• b) 9 unipolar leads measure the potential at a
  point on the body
• 3 unipolar limb leads aVR, aVL en aVF
• 6 unipolar chest leads V1-V6

36
(No Transcript)
37
(No Transcript)
38
(No Transcript)
39
(No Transcript)
40

• 
  Normal heart rhythm
• Sinus rhythm
• Sinus tachycardia gt 100 bpm
• Causes exercise, emotional excitement,
  heart failure, fever, anemia.
• Sinus bradycardia lt 60 bpm
• Causes long term exercise, hypothyroidism.
• Sinus arrhythmias irregular firing of the
  SA-node (fast and slow beats)
• Ectopic heart beats the impulse that causes
  heart contraction originates outside
• the SA-node and causes extrasystoles.

41

• The QRS complex may be abnormally large
  (ventricular hypertrophy) or
• abnormally small (ventricular atrophy).
• The QRS complex does not follow the P-wave.
  Sometimes several P-waves
• followed by the QRS-complex. Causes, heart
  block. The impulse is not always conducted
  through the AV-node.
• The Q-wave is enlarged, abnormal QRS-complex,
  ST-segment is elevated above baseline and
  inverted T-waves are indicative of necrotic heart
  muscle. Therefore MI.

42
(No Transcript)
43
(No Transcript)
44
(No Transcript)
45
(No Transcript)
46
(No Transcript)
47
(No Transcript)
48
Abnormal ECG Heart defect ECG
Defect Ventricular hypertrophy QRS complex
with high amplitude Ventricular atrophy QRS
complex with low amplitude Ischaemia and
infarction Abnormal QRS complex, ST
segment elevated, T-wave inverted. Bun
dle branch block wide QRS complex due to
delayed conduction Heart block P wave not
followed by QRS complex 1st degree
delayed QRS complex 2nddegree absent QRS
complex 3rd degree total AV
dissosiasion VT Abnormal QRS complex, no P
wave VF No QRS complex distinguishable
49
Heart sounds and Heart murmurs
50
Heart sounds 1st heart sound
during ventricular systole low tone closing
of AV valves 2nd heart sound end of
ventricular systole sharp with high tone
closing of the semilunar valves. 3rd heart
sounds end of systole - AV valves open
blood flows through 4th heart sounds artial
systole vibrasion of the ventricular wall
51
Heart murmurs
Due to abnormalities of the heart

• Narrowed valves (stenosis) and/or leaking
  valves (incompetence)
• Whistle Swish
• Aortic valve stenosis Rheumatic fever
• Type of murmur loud coarse systolic murmur
  max. intensity middle systole
• Ventricular systolic pressure very high
• ECG Hypertrophy Large QRS komplex
• Aortic pressure stays relatively low during
  systole

52

• Mitral valve stenosis
• Type of murmur long rumbeling diastolic
  murmur, intensity high - end diastole
• Pressure in LV and aorta low or normal
• Right venticle hypertrophic
• Aortic valve incompetence
• Type of murmur Soft, high pitched diastolic
  murmur
• Pressure in aorta systolic pressure high
• Left ventricle end-diastolic pressure high
• Mitral valve incompetence
• Type of murmur systolic murmur
• Pressure in left atrium elevated
• Left ventricle elevated end-diastolic pressure

53
(No Transcript)
54
(No Transcript)
55
(No Transcript)
56
(No Transcript)
57
(No Transcript)
58

• Pulmonary Circulation
• Pressure changes qualitatively similar
  pressures however far lower
• Pulmonary artery diastolic and systolic pressure
  8-24mmHg
• Pulmonary circulation low pressure system

59
(No Transcript)
60

• CARDIAC OUTPUT (CO)
• Vol blood that leaves LV per min into systemic
  circulation - 5-6 L/min - adult
• strenuous exercise - 35-50 L/min
• by exercise, fever, stress, anemia, gender, and
  thyroid defects.
• CO determined by two variables nl. 1) Heart
  rate (HR) and,
• 2) Stroke volume (SV)
• SV and HR - regulated by two mechanisms
• Intrinsic (auto-regulation), eg. Stretch of
  muscle fibers, frequency of
• contraction, tension and temperature.
• 2) Extrinsic, eg. by nerves, hormones and
  electrolytes.

61

• Stroke volume (SV) volume of blood leaving
  ventricle per heartbeat.
• End-diastolic volume (EDV) End systolic volume
  (ESV) SV
• 120 ml 50 ml 70 ml
• The Ejection fraction is SV/EDV 70/120 0.58
  of 58
• Factors that determine SV
• Preload (intrinsic mech.)
• Afterload (intrinsicmech.)
• Contractility of the myocardium (exstrinsic
  mech.)

62
Preload degree of stretch of muscle fiber which
is determined by the EDV volume blood entering
ventricle during diastole. EDV is influenced by
1) filling pressure ?venous return
06h00-08h00 24h00-05h00
2.5 bar 3.5 bar
63
1.5 L/min
0.75 L/min
64
2) Filling time ? HR Pressure in A
Pressure in B
Time in A- 1sec Time in B 0.6 sec
65

• Filling pressure function of central venous
  pressure (CVP) pressure in RA
• During diastole CVP 0mm Hg
• During systole CVP 8 mm Hg
• CVP determined by
• the ability of the heart to pump blood away
  heart failure - ? CVP
• Volume of the system.
• The pressure around the heart also influences the
  CVP

66

• Significance of the CVP
• Determines RV filling ? EDV ? SV ?CO
• Controls venous return - ? CVP ? ? venous return
  ? edema
• Clinically present with heart abnormalities and
  lung diseases
• Asthma en emphysema ? ? CVP
• Accumulation of fluid in vascular system ? ? CVP
• Preload also influenced by compliance of the
  heart chambers.
• ? venous return ? ? EDV ? ? preload
• ? compliance ? ? EDV ? ? preload

67
INTRINSIC CONTROL OF SV ? blood volume in
ventricles ? ? stretch of the ventricular
fibers ? Stronger contraction during systole ? ?
Stroke volume ? ? cardiac output ? better
tissue perfusion
68
(No Transcript)
69

• Afterload on the Heart
• Pressure against which the ventricle must eject
  blood.
• Influenced by
• Arterial BP
• Elasticity of the arterial bloodvessel wall
• Arterial resistance

20 mmHg
20 mmHg
40 mmHg
5 liter/min 2.5 liter/min 5
liter/min
70
(No Transcript)
71
CONTRACTILITY Extrinsic factors Adrenalin
en Noradrenalin ? influenced by intracellular
Ca2 levels
Chemical substances influence contractility
positive en negative inotropic agents
Catecholamines digitalis
Anaesthetics ACh
72
(No Transcript)
73
(No Transcript)
74

• Regulation of heart rate (HR)
• Heart rate is regulated not controlled.
• Factors that determine HR
• a) Inside the heart
• ? temperature
• anemia, hipoxia, blood loss
• b) Outside the heart
• Nerves
• parasimpathetic stimulation - vagal-nerve - ACh
• sympathetic stimulation (T1-T6) - noradrenalin
• Hormones
• particularly adrenalin en noradrenalin

75
(No Transcript)
76
(No Transcript)
77
BLOOD FLOW F ? ?P Pressure declines due to
resistance (R) in blood vessels R 8 ? L
? r 4 - Poiseuille Law
r very NB in determining the resistance to
flow.
vasoconstriction vasodilatation
78
BLOOD FLOW AND THE CIRCULATORY SYSTEM Blood flow
influenced by BP resistance to flow. F ? ?P,
where ?P P1 - P2 . (1)
F 1/R(2)
79

• Resistance to blood flow influenced by
• The length of the blood vessel (L)
• The radius of the blood vessel (r)
• The viscosity of the blood (?)
• Factors in Poiseuilles law
• R 8 ? L
• ? r4
• With 8 a constant
• ? blood viscosity constant
• L Length of the tube constant
• ? constant
• r radius of the tube
• Change in the radius of the tube makes the
  biggest difference
• to resistance to flow.
• ? in radius vasodilatation
• ? in radius vasoconstriction

80
(No Transcript)
81
Flow velocity of blood Flow velocity is the
distance a given volume of blood will move in a
given time (mm/sec).
The cross-sectional area of all the capillaries
together is very large - flow velocity is the
slowest in the capillaries.
82
(No Transcript)
83
Flow of flow rate F ?P -
liters/min R
Flow velocity distance that a given volume
of blood moves in a given time mm/sec
H2O in
H2O uit
Cross-sectional area NB for flow velocity see
capillaries
84
(No Transcript)
85

• TYPE OF BLOOD VESSELS
• Arteries ? arterioles ? capillaries ? venules ?
  veins
• Arteries (distribution vessels large diameter,
  little resistance)
• Large arteries
• Aorta en pulmonary arteries
• Elastic vessels lots of elastin and collagen
  little smooth muscle
• Functions
• Temporary reservoir
• Pump of blood
• Monitor system for BP

86

• Medium arteries
• Cerebral and brachial arteries
• Muscle type arteries (little elastin and more
  smooth muscle)
• Functions link between large and small arteries

• Arterioles (NB for regulation of blood flow to
  capillaries)
• Distribution arteries and resistance vessels
• Thick layer of smooth muscle supplied with
  sympathetic nerves also
• sensitive to some hormones and chemical changes
  in blood
• Always partially constricted
• Functions control vascular resistance and
  determines distribution of blood to
• different organs.
• Assists with regulation of BP

87

• Veins
• Walls are thinner and their diameter larger than
  arteries
• Veins are more compliant than arteries
• Does not have much smooth muscle and connective
  tissue
• Valves prevents backflow of blood
• Functions i) transport blood from distal
  vascular bed to the heart.
• ii) Serves as reservoir (66 of blood)

88
(No Transcript)
89
(No Transcript)
90

• Capillaries
• Capillaries branch out of arterioles or
  metarterioles (serve as throughway/canal
• between arterioles and venules).
• Has largest cross-sectional area flow velocity
  is very slow
• Walls very permeable
• Diameter 3-8 ?m thichness 1-2 ?m
• 3 layers
• Endothelial cells
• basal membrane of proteoglycans
• thin collagen and reticular fibers. NB no smooth
  muscle layer
• Functions link between blood and tissue for
  exchange of water, gasses,
• electrolytes, nutrients etc.
• Tissue that is metabolically more active has
  larger capillary bed.

91
(No Transcript)
92
(No Transcript)
93

• ARTERIAL SYSTEM
• Conduction vessels
• Pressure buffer/reservoir
• Regulates blood distribution
• Pressure in arteries serves as driving force for
  blood through the
• vascular system back to the heart.
• F ?P
• R
• F P (aorta) P (vena cava)
• R
• F MAP 0 mmHg
• R

94

• MAP Diastolic pressure systolic pressure
  diastolic pressure
• 
  3
• F MAP or MAP ? F X R (F CO)
• R
• MAP is influenced by
• F and R in arteriole
• Blood volume
• Blood volume distribution veins contain 60 of
  total blood volume

95
(No Transcript)
96

• Pulse pressure - n function of SV and compliance
  of the aorta.
• an increase in SV - ?? stretch of the aorta - ?
  systolic BP and consequent high
• pulse pressure.
• The less compliant the aorta, the larger the ?
  systolic BP - ? pulse pressure.
• Heart rate ? - diastolic filling ? - MAP ? and
  pulse pressure ?
• Tachycardia reduction in pulse pressure (small
  SV)
• Bradycardia increase in pulse pressure (larger
  SV).

97
TOTAL PERIPHERAL RESISTANCE
Mean pressure in arteries F MAP R
Resistance in blood vessels from aorta to
the heart TPR Due to changes in R
1. Changes in MAP 2. Changes in blood
distribution MAP F X R ? R Achieved by
arterioles (60 van TPR)
98
NEURAL CONTROL OF BLOOD
DISTRIBUTION ? Vasodilatation of all vascular
beds heat exhaustion

• Inadequate perfusion of vital organs?communicatio
  n NB nerve and hormone control
• Arterioles are well supplied with nerves
  nor-epinephrine ? ? receptor ? contraction
• At rest all arterioles stimulated by sympathetic
  nervous system.
• Parasympathetic nerves dont play a role in the
  control of blood flow
• How is vasodilatation achieved ?

99
Short term processes that control BP Receptor
baroreceptor ? Nerve ? Integrator ? Nerve
(ONS) ? Heart of arteriole
100
Long term processes that control BP Receptor
baroreceptor ? Nerve ? Integrator ? Nerve
(ANS) ? Endocrine gland or kidney ?
?
Hormone ? fluid retention or excretion
101

• Baroreceptors
• In aortic arch and carotid sinus
• Reacts to stretch of the elastic walls of the
  arteries
• Reseptors always tonically active

102
(No Transcript)
103
(No Transcript)
104
Systemic BP determination
105

• TOTAL
  RERIPHERAL RESISTANCE
• Resistance that blood vessels present against
  blood flow - TPR arterioles
• contribute 60 to TPR
• R 8 ? L ? 1
• ? r 4 r4
• Radius controlled by A Local control
  mechanisms (intrinsic).
• B.
  Reflex control (exstrinsic).
• Myogenic autoregulation, due to ? in pressure or
  ? in pressure
• ?
• RESTING TONE depolarises spontaneously
• MAP ? ? Blood flow and blood vessel diameter ?
  vasoconstriction ?
• ? blood vessel diameter and blood flow or,
• MAP ? ? Blood flow and blood vessel diameter?
  vasodilatation ? ? blood

106
(No Transcript)
107

• B. Reflex (exstrinsic) control mechanisms.
• Hormones
• Bradykinin, histamin vasodilators
• Noradrenalin, Angiotensin II en ADH
  vasoconstrictors

108
(No Transcript)
109

• Venous System
• Thin walls and very compliant
• Degree to which blood is stored in the veins
  dependent on smooth
• muscle tone sympathetic nerve activity.
• Venous return dependent on
• Pressure in RA
• Total blood volume
• Sympathetic activity on veins
• Skeletal muscle and respiratory pump

110

• SYSTEMIC BLOOD PRESSURE
• MAP diast BP pulse pressure
• 3
• Normal BP 120/80 mmHg
• Method of measuring
• Indirect
• Direct
• Low in children, women and when lying down
• High in elderly, obese, with stress and severe
  exercise

111

• Factors that determine BP
• BP CO X TPR
• CO SV X HR
• TPR
• Elasticity of blood vessels
• Volume of blood
• Viscosity of blood

112

• Question
• Why would MAP rise as HR rises even if diastolic
  filling of the ventricle
• decreases (at an increased CO)?
• NB MAP CO X TPR
• CO ?
• TPR
• ?
• ? CO ? ? MAP

113

• CO SV and HR
• SV and HR can only change BP if CO changes
• If CO ? then BP decreases if TPR remains constant
• If CO ? then BP will be maintained by increasing
  TPR
• If CO ? as with exercise, then BP rises unless
  TPR decreases (this is the
• normal situation)
• Peripheral resistance dependent on diameter of
  the arteriole (and therefore
• resistance in arterioles)
• The BP will increase with a decrease in
  compliance of the elastic
• blood vessels.
• Pulse pressure will rise as a result of a
  decrease in compliance of the
• blood vessels ? MAP

114

• Hipertensie
• BD van ?140/90 mmHg skeidingslyn tussen normaal
  en hipertensief
• Gewoonlik agv verlaagde radius van die arteriole
• Gewoonlik is die oorsaak onbekend essensiële
  hipertensie
• Moontlike oorsake
• Baie wetenskaplike bewyse dat oormaat natrium
  retension kan
• hipertensie veroorsaak
• Behandeling met n lae natrium dieet of die
  gebruik van diuretikums
• (diuretics) verlaag BD
• Vetsug risiko faktor vir hipertensie oefening
  en gewig verlies kan
• die hoë BD laat afneem
• Gevolge
• Hipertrofie van hart en beroerte (stroke)

115

• Behandeling van hipertensie
• Diuretika - ? water en natrium uitskeiding
  (niere) ? ? KO
• ?-blockers ? KO ( ? effek op oefeningsvermoeë)
• Kalsium antagoniste ? baie spesifiek vir
  gladdespier kalsium kanale ? ? TPW
• ACE inhibeerders
• Angiotensienogeen ? Angiotensien I ?
  Angiotensien II ? vasokontriksie
• ?
• ACE
• ?
• ACE - inhibeerder

116
(No Transcript)
117
(No Transcript)
118
(No Transcript)
119
Control of BP

120
Sensor Baroreseptor
(carotid sinus, aortic arch,
RA, LA LV en pulmonary
art.)
Volume en chemoreceptors
Brain cortex en
Hypothalamus
Cardiovascular control centre in medulla
Sensory area
Vasomotor center
Pressor area Depressor
area
- Chronotropic
Chronotropic and dromotropic
vasoconstrictor
SA en AV node A en V muscle fibers
Blood vessel and smooth muscle
121
(No Transcript)
122
(No Transcript)
123
(No Transcript)
124
(No Transcript)
125
Afferent impulses from other centers
Cerebral cortex (limbic region) Excitement
and rage anxiety, fear, sadness ? ?
CMC CMC
(? vagal act.) (? vagal act.)
? ? ?
BP ? HR ? BP ? HR
126
(No Transcript)
127

• MICROCIRCULATION AND LYMPH
• Molecular exchange at the capillaries
• Transcytosis en endocytosis
• Diffusion
• Bulk flow

128
Filtration and Absorption
129
(No Transcript)
130
(No Transcript)
131
(No Transcript)
132
(No Transcript)
133
(No Transcript)
134
(No Transcript)
135
(No Transcript)
136
(No Transcript)
137
(No Transcript)
138
(No Transcript)
139
(No Transcript)
140
(No Transcript)
141
(No Transcript)
142
(No Transcript)