PHYSIOLOGY OF

CARDIOVASCULAR SYSTEM

CHAPTER 6
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 FUNCTIONS OF THE CVS

• Transport and distribute essential substances to

the tissues (O2, nutrients, water, and drugs).
• Remove metabolic byproducts.
• Adjustment of oxygen and nutrient supply in
different physiologic states.
• Regulation of body temperature.
• Humoral communication.
• Vital role in reproduction- hydraulic mechanism for
penile erection
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 Components of the CVS

CVS composed of
 Heart: Pumping center
 Blood vessels
 Arteries: Distributing
system
 Capillaries: Exchange system
 Veins: Collecting
system
 Blood: circulating connective tissue

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 Distribution of Blood

1. Veins, venules,
venous sinuses=
64%
2. Pulmonary
Circulation=9%
3. Heart=7%
4. Capillaries =7%
5. Arteries = 13%
 The Heart
• Heart is the hollow, muscular
organ that plays a central
pumping role
• Composed of 4-chambers; 2
atria and 2 ventricles
• Size: Approximately
equivalent to clenched fist
• Weight: 280 to 320 grams in
average adults
• Located in the midiastenum

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Blood vessel functions: overview
Strong and elastic arteries
Arterioles control blood flow
and pressure

Capillaries: thin and

with large area for
diffusional exchange

Veins: compliant, large, low R veins with

valves assures blood return 6
 General Plan of CVS
1. Main propulsive organ (e.g. heart) forces blood
through body
2. An arterial system that distributes blood & acts
as a pressure reservoir
3. Capillaries – transfer material between blood
and other tissues
4. A venous system that acts as blood storage
reservoir & as a system for returning blood to
heart

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 Mechanisms of Movement of Blood
1. Forces imparted by rhythmic contractions of the heart
2. Elastic recoil of arteries following filling by the action of the
heart
3. Squeezing of blood vessels during body movements
4. Peristaltic contractions of smooth muscle surrounding blood
vessels

 Valves or septa determine direction of blood flow

 Smooth muscle surrounding blood vessels alters vessel
diameter
 = regulating amount of blood that flows through a particular
pathway & controlling the distribution of blood within the
body
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9
 Division of the circulatory system
• In the CVS, blood passes through two (double)
circulations:
 Systemic circulation
 Pulmonary circulation
• Systemic circulation:
Starsts in the LV→ Aorta → Systemic arteries
→Systemic capillaries →Veins →SVC & IVC →ends
in RA
• Pulmonary circulation:
Starts in the RV →Pulmonary trunk →Pulm. arteries
→ Pulm capillaries →Pulm veins →ends in the LA.
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Pathway of Blood Through the Heart and Lungs

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 Properties of cardiac muscles
Cardiac muscles have 4 physiological properties,
which are essential for the function of the heart
as the central pumping organ.
These are
Autorythmicity
Excitability
Conductivity
Contractility

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 Autorhythmicity
• Autorhythmicity is the ability of the heart
to generate cardiac impulse and to beat
regularly independent of any external
stimulus.
• The heart is provided with specialized
excitatory and conductive muscle systems
having two functions:
1. They generate rhythmic cardiac impulse
2. They conduct cardiac impulse
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 Specialized excitatory and conductive system of the heart
1. Sino-atrial node (SA-node):
in which the normal (80-120
x/min) rhythmical self-
excitatory impulse is generated
2. Internodal pathways: conduct
impulse from the SA-node to
the AV-node
3. Atrioventricular node (AV-
node): in which impulse from
the atria delayed to be
conducted to the ventricle. Site
of nodal delay. 40-60 x/min
4. Atrioventricular bundle
(bundle of His) : Rt. And Lt.
which conducts impulse from
the atria to the ventricle.
5. Purkinje fibers: conduct
•Bundle branches & Purkinje
cardiac impulse to the fibers : 20 - 40 per minute.
ventricles 14
 Conduction of pacemaker potential from nodal tissue to adjacent
contractile cells and beyond, through gap junctions in intercalated
disks.
 Electrophysiology of the heart
Phases and ionic bases of
myocardial action potential ↑PCl
It has 5-phases
Phase-0: Rapid depolarization
Caused by rapid Na-influx
Phase-1: Early partial repolarization
Caused by Cl- influx
Phase-2: The plateau (prolonged
depolarization) RMP = -90 mv

Caused by Ca2+influx via L-

channels
Phase-3: Repolarization
Action potential of the ventricular muscle
Caused by K+ efflux
Phase-4: Complete repolarization
RMP reestablished
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Caused by Na-K-ATPase
Excitation-contraction coupling in cardiac muscle

• It is a mechanism by which an action potential causes

contraction of myocardium.
• It has the following sequences
Auto-rhythmicity Membrane depolarization T-
tubule depolarization Release of Ca2+ from SR +
from T-tubule (ECF) Ca2+ activates contractile
molecules Sliding of filaments Contraction
• The action potential of cardiac muscle has a prolonged
refractory period.
Advantage: prevents tetanic contraction of the heart
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 Cardiac valves
Cardiac valves are made up
of fibrous connective tissues
There are 4 valves
1. Tricuspid valve (RAV-valve,
T-valve)
2. Bicuspid valve (LAV-valve,
M-valve)
3. Pulmonary semi lunar valve
(P-valve)
4. Aortic semi lunar valve
(A-valve)
Function: prevent back flow
of blood
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 Cardiac valves
All valves consist of connective tissue (not cardiac
muscle tissue) and, therefore, open & close passively.
Valves open & close in response to changes in
pressure:
AV valves - open when pressure in the atria is greater
than pressure in the ventricles (i.e., during ventricular
diastole) & closed when pressure in the ventricles is
greater than pressure in the atria (i.e., during ventricular
systole)
Semi lunar valves - open when pressure in the
ventricles is greater than pressure in the arteries (i.e.,
during ventricular systole) and closed when pressure in
the pulmonary trunk & aorta is greater than pressure 20in
the ventricles (i.e., during ventricular diastole)
 Important terms
• Ventricular volumes: The volume of blood in the ventricles
• Ventricular end diastolic volume (VEDV): The volume of blood
in the ventricle at the end of ventricular diastole
VEDV = 120-140ml
• Ventricular end systolic volume (VESV): The volume of blood
that remains in the ventricle at the end of ventricular systole.
VESV = 50-60 ml
• Stroke volume (SV): the volume of blood ejected from the
ventricle during ventricular systole.
SV = VEDV – VESV, 70 – 80 ml
• Cardiac output: the volume of blood ejected from the heart per
minute. CO = SV x HR, 6 L/min
• Ejection fraction: proportion of blood that enters the ventricles
during diastole to the amount ejected.
EF = SV/VEDV, 60% - 70% 21
 Cardiac Output (CO) and Reserve
• CO is the amount of blood pumped by each ventricle
in one minute
• CO is the product of heart rate (HR) and stroke
volume (SV)
• HR is the number of heart beats per minute
• SV is the amount of blood pumped out by ventricle
with each beat
• Cardiac reserve is the difference between resting and
maximal exercise CO
– CO = 5-6 liters per minute at rest
– CO = 20-40 liters per minute at maximum exercise
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 Cardiac output
CO is determined by SV & HR
SV is determined by 3 factors
1. Preload/VR/EDV
2. Myocardial contractility
3. Afterload
• VR is affected by the following factors
1. Mean systemic filling pressure
2. Central venous pressure
3. Systemic vascular resistance
4. Other factors
 Sympathetic stimulation
 Blood volume
 Respiratory movements
 Sk/muscle contraction
 Factors affecting stroke volume
• Preload – the degree of
tension on the muscle
when it begins to contract
(EDV)
• Afterload –the load
against which the muscle
exerts its contractile force
(MAP)
• Contractility – cardiac cell
contractile force due to
factors other than EDV
 Cardiac output

•CO (ml/min) = HR (72 beats/min) x SV (75ml/beat)

Autoregulation
(Frank-Starling “Law of the Heart”)

CARDIAC OUTPUT = STROKE VOLUME x HEART RATE

Contractility

Sympathetic
Nervous System
Parasympathetic
Nervous System
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 Heart Rate
• HR is the number of cardiac cycles per minute
• Normal HR: 60 to 100 beats/minute
• < 60 beats/minute, bradycardia but normal in athletes
• > 100 beats/minute, tachycardia
HR varies with the following factors
1. Age: higher in newborn infants (120 b/min)
2. Sex: higher in females (85 b/min)
3. Time of the day: ↓morning, ↑evening
4. Resting and sleep: decreased
5. Physical training: low in athletes (45-60 b/min)
6. Body position: ↑standing, ↓supine positions
How to count HR
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Counting arterial pulsation, heart sound and ECG cycles
 FACTORS AFFECTING VR
Resistance to venous return (RVR)
• Resistance blood meets(1mmHg/L/min) during its flow from
arterial side to RA
• Occurs at arterioles and veins
Sympathetic stimulation  VR by inducing vasoconstriction,
improved cardiac pumping power and arteriolar dilatation 
resistance to VR.
Blood volume: Blood volume  VR by MSFP and vice versa
Arteriolar dilatation RVR and VR
Capillary dilatation vascular capacity, MSFP and VR
Skeletal muscle contraction Squeezes veins b/n muscles  MSFP
 VR
Gravity: Standing motionless for some time pooling of blood in
lower extremities  MSFP  VR  C.O hypotension brain
ischaemia syncope.
 Cardiac cycle
Activities in the heart in a single beat
Contraction and relaxation of cardiac chambers
A single cardiac cycle comprised of
-Atrial diastole + atrial systole and
-Ventricular diastole + ventricular systole
75 cycles completed per minute
Duration of each cycle = 0.8 second
-Ventricular diastole = 0.5 second
-Ventricular systole = 0.3 second
Means of exploring activities accomplished in a cardiac cycle
1. Auscultation of heart sounds, recording phonograph
2. ECG tracing
3. Palpitation
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 Heart Sounds
Heart sounds (lubb-dubb) are associated with closing of heart
valves
4-separate audible heart sounds (S1, S2, S3 and S4)
Means of identification
1. Auscultation: direct/immediate auscultation
Stethoscope mediated auscultation
2. Phonocardiographic based recording

S3
S4 S1 S2
S1: is always audible, has a LUBB-sound
S2: is always audible, has DUBB-sound
Continuous heart sound: Lubb-Dubb, Lubb-Dubb
Duration of Lubb-Dubb is shorter than that of Dubb-Lubb
S3: is audible in children and in adults during exercise 30
S: is audible very rarely
 Heart Sounds (cont’d)
S1: First heart sound
Causes: sudden closure of AV-valves.
Timing: Occurs at the beginning of ventricular systole
S2: Second heart sound
Cause: Sudden closure of semilunar valves
Timing: Occurs at the beginning of ventricular diastole
S3: Third heart sound
Cause: rapid filling of the ventricles with blood during
ventricular diastole
• It is audible in children and in adults during exercise
S4: Fourth heart sound
Cause: rapid ventricular filling during atrial systole
Timing: during atrial systole
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 Phases of the Cardiac Cycle
Cardiac cycle has 3 major phases
I. Atrial systole
II. Ventricular systole
III. Deiastole of the whole heart
I. Atrial systole
Duration: 0.15 second
Valvular events: SL-valves closed, AV-valves opened
Phonocardiogram: S4
ECG: P-wave
Ventricular volume : increased
Ventricular pressure: increased
Atrial pressure: pumps blood to the relaxed ventricles.
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 Phases of the Cardiac Cycle (cont’d)
II. Ventricular systolic phase (contraction)
 Duration: 0.3 sec., has 3 phasses
A. Isovolumic phase
 Ventricles contract with no change in volume (EDV=130 ml)
 Ventricular pressure rises from 4-80 mm Hg
 All valves are closed
 S1 is produced, QRS- complex is recorded
B. Rapid ejection phase
 Maximum contraction of the ventricle
 Ventricular pressure rises from 80-120 mm Hg
 SL-valves opened
 Blood will be ejected (70% of SV), ↓Ventr. Volume
 Aortic pressure increases
 Atrial pressure decreases
C. Slow ejection phase
 The remaining 30% of the SV is ejected
 Ventricles start to relax 33
 Phases of the cardiac cycle (cont’d)
III. Diastole of the whole heart: duration 0.5 sec, 4-phase
A. Protodiastolic phase
 A transition phase
 Ventricular pressure drops rapidly
 SL-valves are closed and S2 is produced
 Aortic pressure declines
B. Isovolumic relaxation phase
 Ventricular pressure drops from 80 to 4 mm Hg
 4-valves are closed, no change in volume
 T-wave completes, ventricles relax
C Rapid ventricular filling phase
 Atrial pressure is higher than ventricular pressure
 AV-valves opened, S3 is produced
 Ventricular pressure falls near 0 mm Hg
 Ventricular volume rises sharply
 80% of the filling blood run to the relaxed ventricle
D. Slow filling pressure
 20% of EDV fills the ventricle, pumped by atrial contraction 34
 Ventricular volume still increasing, S4 produced
35
Cardiac cycle, summary

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 Arterial blood pressue
• It is a pressure caused by the blood on the wall of the
blood vessels
• Normal Ps: 90 – 140 mm Hg (120 mm Hg)
Pd: 60 – 90 mm Hg (80 mm Hg)

• Hypotension vs Hypertension
• Three factors determine ABP: ABP = CO x TPR
1. Cardiac output
2. Peripheral vascular resistance
3. Blood volume
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Blood Pressure Measurement

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 Variations in ABP
1. Age: ABP rises as age increases
Newborne: 70/50, infants: 90/60, children: 100/70
Adults: 120/80 and old age (>60 yrs): 150/90
2. Sex: After the age of 50, F > M by 5 mm Hg
3. Time of the day: ↓morning, ↑evening
4. Body wt: ABP higher by 10-15 mm Hg in obese
5. Gravity: every 1 cm distance below the level of the heart
increases pressure by 0.77 mm Hg
6. Exercise: increases ABP by 40 – 50 mm Hg
7. Emotion: increases ABP by 10 – 30 mm Hg
8. Deep sleep: decreases ABP by 20 mm Hg
9. Thermal stress; decreases ABP
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 Regulation of ABP
A. Short-term controlling mechanisms
CNS ischemic response
Baroreceptor reflex
Chemoreceptor reflex
Atrial stretch reflex
Stress relaxation and reverse stress relaxation
Hormonal mechanisms: AD, ND, VP
B. Long-term controlling mechanisms
The renal mechanism
The RAAS
BP Regulation:
Baroreceptors
↑BP stimulates
baroreceptors

Impulse goes
to MO

Stimulation of PNS ↓BP

Regulation of Blood Pressure
Blood Pressure
Regulation

Figure 15-22: The baroreceptor reflex: the response to increased blood pressure
RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM

Angiotensinogen (renin substrate)

 BP (Kidney)
Renin
Angeotensin-I
ACE
Angiotensin-II

Vasoconstriction Aldosterone

↑BP Venoconstriction Kidney

 ADH secretion
 sodium & water retention
↑H2O reabsorption
↑ECF volume ↑BP
 Reading assignment
• Microcirculation

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 CVS abnormalities
• Hypertension
• Hypotension
• Arrhythmia and heart block
• Myocardial ischemia and infarction
• Heart failure
• Circulatory shock
• Edema

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