Cardiovascular system

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Cardiovascular System: Heart
Dr. Mrs. Deepa K. Ingawale (Mandlik)
Department of Pharmacology
Poona College of Pharmacy, Pune

Heart
 Cardiology: It is the branch of science that deals with study of
heart & disease of heart.
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Heart Anatomy
 Shape: Cone shaped
 Weight: 250 gm in adult females
300 gm in adult males
 Size: Approximately the size of closed
fist
 Location:
 Above the diaphragm
 Near the middle of thoracic cavity
 Between the lungs
 Dimensions: 12 cm long, 9 cm wide
& 6 cm thick
Parts:
Four chambers
2 Atria
2 Ventricles
Parts:
Four chambers
2 Atria
2 Ventricles

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Coverings of Heart: Paricardium
 Pericardium – Double walled membrane that surrounds &
protects the heart
 It confines the heart to its position & allows sufficient freedom
of movement for contraction.
 It is composed of:
1. A superficial fibrous pericardium
2. A deep serous pericardium:
 Parietal layer
 Visceral layer

Pericardium
 Fibrous pericardium:
 It is made of tough inelastic, dense irregular connective tissue.
 It prevents over stretching of heart, provides protection & holds the
heart at particular position.
 Serous pericardium:
 Is a thinner, more delicate membrane that forms double layer around
the heart.
 Outer parietal layer fused with fibrous pericardium.
 Inner visceral layer called as epicardium (external layer of heart
wall)
 Space between parietal & visceral layer is called as pericardial
cavity and filled with pericardial fluid. 7

Function of Pericardium
 The Function of the Pericardium:
 Protects & anchors the heart
 Prevents overfilling of the heart with blood
 Allows the heart to work in a relatively friction-free
environment

Heart Wall
 Wall of heart consists of 3 layers;
o Epicardium (External layer)
o Myocardium (Middle layer)
o Endocardium (Inner layer)
 Epicardium:
 Outermost, thin, transparent layer of heart wall.
 Also called as visceral layer of serous pericardium.
 Composed of delicate connective tissue that imparts smooth,
slippery texture to outer surface of heart.

Heart wall
 Myocardium:
 Middle layer, made up of cardiac muscle tissue, make up the bulk
of heart.
 Responsible for pumping action
 Endocardium:
 Inner layer of heart wall made up of endothelial cells
 Provides smooth lining for the chambers of heart & covers the
valve of heart.

 Vessels returning blood to the heart include:
1. Superior and inferior vena cava
2. Right and left pulmonary veins
 Vessels conveying blood away from the heart include:
1. Pulmonary trunk, which splits into right & left pulmonary
arteries
2. Ascending aorta (3 branches) –
a. Brachiocephalic artery
b. Left common carotid artery
c. Subclavian arteries
External Heart: Major Vessels of the Heart

Blood Vessels
• 5 types of blood vessels
• Taking blood to the tissues & back
Arteries
Arterioles
Capillaries
Venules
Veins

Blood Vessels
 Arteries Arterioles carry blood away from the heart
Elastic Fibers
Smooth Muscle
 Capillaries – where gas exchange takes place.
One cell thick
Serves the Respiratory System
 Veins Venules moves blood towards the heart
One way valves
When they break - varicose veins form

The ARTERY
thick muscle and
elastic fibres
Arteries carry blood away from the heart.
the elastic fibres allow the
artery to stretch under
pressure

The VEIN
Veins carry blood towards the heart
thin muscle and
elastic fibres
veins have valves which
stop the blood from going
in wrong direction.

The CAPILLARY
Capillaries link Arteries with Veins
Wall of capillary
is only one cell thick
They exchange materials
between the blood and other
body cells.

artery vein
capillaries
body cell
The CAPILLARY
A collection of capillaries is known as a capillary bedcapillary bed.

Blood Vessels: Anatomy
• Three layers (tunics)
• Tunic intima
• Endothelium
• Tunic media
• Smooth muscle
• Tunic externa
• Fibrous connective tissue

Artery/Vein differences
Arteries Veins
Direction of
flow
Blood Away from
Heart
Blood to Heart
Pressure Higher Lower
Walls THICKER: Tunica
media is thicker
THINNER: Tunica externa is
thinner
Lumen Smaller Larger
Valves No valves Valves

Gross Anatomy of Heart: Frontal Section

Chambers of the Heart
 4 chambers of heart
 2 ventricles & 2 atria
 Right atrium (RA): collects blood from systemic circuit
 Right ventricle (RV): pumps blood to pulmonary circuit
 Left atrium (LA): collects blood from pulmonary circuit
 Left ventricle (LV): pumps blood to systemic circuit

Right Atrium (RA)
 Atria are the receiving chambers of the heart
 RA is roughly quadrangular in shape.
 Divided into 2 parts;
 Upper part
 Lower part
 Superior vena cava present at the upper part
 Inferior vena cava present at lower part

Right Ventricle (RV)
 Ventricles are the pumping chambers of the heart
 It is convex & forms large part of heart.
 The wall of RV is much thinner than LV.

Left Atrium (LA)
 Smaller in shape than RA.
 Roughly cuboidal in shape
 Four pulmonary veins open at the upper part of LA.

Left Ventricle (LV)
 It functions as a powerful pump operating at high pressure.
 The walls are three times more thicker as that of RV.
 Cone shaped, longer and narrower than RV

Myocardial Thickness &Function
Thickness of myocardium varies according to the function of chamber
Atria are thin walled, deliver blood to adjacent ventricles
Ventricle walls are much thicker and stronger

Pathway of Blood Through Heart & Lungs

 Right atrium  tricuspid valve  right ventricle
 Right ventricle  pulmonary semilunar valve  pulmonary
arteries  lungs
 Lungs  pulmonary veins  left atrium
 Left atrium  bicuspid valve  left ventricle
 Left ventricle  aortic semilunar valve  aorta
 Aorta  systemic circulation

 The right side of heart pumps blood into the pulmonary
circuit:
 Blood returning from the body is relatively oxygen-poor and
carbon dioxide-rich
 Blood enters the right atrium and passes into the right
ventricle, which pumps it to the lungs via the pulmonary
arteries (conduct blood away from the heart)
 In the lungs, the blood unloads carbon dioxide and picks up
oxygen (oxygenated)
 The left side of the heart pumps blood into the systemic
circuit

Coronary Circulation
 Coronary circulation is blood supply to the heart
muscle itself
Arterial Supply Venous Supply

Heart Valves
 As each chamber of heart contracts, it pushes a portion of blood
into a ventricle or out of heart through an artery.
 To prevent back flow of blood, the heart has valve.
 Made up of dense connective tissue covered by endocardium
 2 types of valve
 Atrioventricular valve (AV valve)
 Tricuspid valve
 Bicuspid valve
 Semilunar valve (SL valve)

Atrioventricular (AV)
 Atrioventricular (AV) valves lie between the atria and ventricles
 AV valves prevent backflow of blood into the atria when
ventricles contract
 2 types
 Tricuspid valve
 Bicuspid valve

Atrioventricular (AV)
 Tricuspid valve:
 It is present between RA and RV is called as tricuspid valve
 Consist of 3 cusp (flaps)
 Septal cusp
 Anterior cusp
 Posterior cusp
 Bicuspid valve:
 It is present between LA and LV is called as bicuspid valve.
 Consist of 2 cusps.
 Also called as mitral valve.

Semilunar valves
 Semilunar valves prevent backflow of blood into the ventricles
 Aortic semilunar valve lies in the aorta
 Pulmonary semilunar valve lies in the pulmonary trunk
 Both the valves consist of 3 half moon shaped cusps.
 Permits blood flow in only one direction.

Conducting system of heart
 A special system is available in the heart responsible for the
rhythmic contraction and conduction of impulses in the heart.
 Divided into 5 parts;
 SA Node or Sinoatrial Node
 AV Node or Atrioventricular Node
 AV Bundle (Bundle of His)
 Right & Left Bundle Branches
 Conduction Myofibers (Purkinje Fibers)

 Sinoatrial (SA) node:
 It is located in the right atrial wall just below the opening of
superior vena cava.
 Cardiac excitation begins in the SA node,
 Each SA node impulse travels throughout the heart via the
conduction system
 Atrioventricular (AV) node:
 It is located in the septum between the two atria.
 The cardiac impulses spreads from SA node to AV node.

 Atrioventricular bundle (bundle of His):
 From AV node, the impulse enters the Bundle of His, only
electrical connection between atria and ventricle.
 AV bundle splits into two pathways
1. Bundle branches carry the impulse toward the apex of the
heart
2. Purkinje fibers carry the impulse to the heart apex and
ventricular walls

 Right & left bundle branches:
 From the bundle branches the impulses then enters the right &
left bundle branches that runs towards the apex of the heart.
 Perkinje Fibers:
 The impulse from right and left bundle branches enters into
Perkinje fibers.
 These conduct impulses to all parts of ventricles.
 Then the ventricles contracts pushing the blood upwards towards
the SA node.

Electrocardiogram
 Conduction of action potential through heart generates electrical
currents that can be detected at the surface of the body.
 A recording of electrical changes during each cardiac cycle is
called as electrocardiogram (ECG).
 The instrument used to record the change is called as an
electrocardiograph.
 It consist of 3 waves;
 P wave
 QRS wave
 T wave

Electrocardiogram
 P wave:
 It is small upward wave.
 It represents atrial depolarization which spreads from SA node
throughout both atria.
 QRS wave:
 The complex represents 3 separate waves.
 Q wave, R wave and S wave
 The complex begins with downward deflection of Q wave,
continues as a large, upright, triangular defection of R wave &
ends as a downward deflection of S wave.
 The QRS complex represents ventricular depolarization.

Electrocardiogram
 T wave:
 It represents ventricular repolarisation.
 Third dome shaped upward deflection
 The T wave is small & more spread out than QRS complex
because repolarisation occurs more slow than the depolarisation.
 PQ or PR interval:
 The duration between beginning of P wave & beginning of QRS
wave is called as PQ interval.
 It is also called as PR interval because the Q wave is frequently
absent.
 It is interval between beginning of contarction of atria &
beginning of contraction of ventricles.

Electrocardiogram
 ST Segment:
 It begins at the end of S wave & starting of T wave.
 QT interval:
 The QT interval extends from the start of QRS complex to
the end of T wave.
 It is the time from beginning of ventricular depolarization
to the end of ventricular repolarization.

Electrocardiogram
 Following conclusions can be made with the altered ECG notes.
 Larger P wave: It indicates enlargement of atrium.
 Enlarged Q wave: It indicates myocardial infarction.
 Enlarged R wave: It indicated enlargement of ventricles.
 Flatter T wave: It indicates insufficient oxygen supply to
myocardium.
 Larger PQ interval: It indicates formation of scar tissue in heart
due to coronary artery disease.
 Larger ST segment: It indicates acute myocardial infarction
when elevated above the baseline & insufficient oxygen supply
to heart muscle when depressed below the baseline.

 Renin:
 It is secreted by the juxtaglomerular cells in Kidney
 Angiotensinogen:
 It is a glycoprotein synthesized by liver & secreted into the
bloodstream
 Aldosterone:
 It is a mineralocorticoid produced in the adrenal cortex
 It plays a central role in the regulation of blood pressure mainly
by acting on the distal tubules & collecting ducts of nephron
Renin-Angiotensin-Aldosterone System

 Angiotensin
 It is a peptide hormone that causes vasoconstriction
and a subsequent increase in blood pressure.
 Angiotensin-I
 Angiotensin-II
 Angiotensin converting enzyme (ACE):
 It converts angiotensin I to II (vasoconstrictor)
Renin-Angiotensin-Aldosterone System

Renin Angiotensin aldosterone System (RAA)

 Stimuli that initiate the renin–angiotensin–aldosterone
pathway include dehydration, Na+
deficiency, or hemorrhage.
 These conditions cause a decrease in blood volume.
 Decreased blood volume leads to decreased blood pressure.
 Lowered blood pressure stimulates certain cells of the
kidneys, called juxtaglomerular cells, to secrete the enzyme
renin.
 The level of renin in the blood increases.
 Renin converts angiotensinogen, a plasma protein produced
by the liver, into angiotensin I.

 Blood containing increased levels of angiotensin I circulates
in the body.
 As blood flows through capillaries, particularly those of the
lungs, the enzyme angiotensin-converting enzyme (ACE)
converts angiotensin I into the hormone angiotensin II.
 Blood level of angiotensin II increases.
 Angiotensin II stimulates the adrenal cortex to secrete
aldosterone.
 Blood containing increased levels of aldosterone circulates
to the kidneys.

 In the kidneys, aldosterone increases reabsorption of Na+
and
water so that less is lost in the urine. Aldosterone also stimulates
the kidneys to increase secretion of K+
and H+
into the urine.
 With increased water reabsorption by the kidneys, blood volume
increases.
 As blood volume increases, blood pressure increases to normal.
 Angiotensin II also stimulates contraction of smooth muscle in
the walls of arterioles. The resulting vasoconstriction of the
arterioles increases blood pressure and thus helps raise blood
pressure to normal.
 Besides angiotensin II, a second stimulator of aldosterone
secretion is an increase in the K+
concentration of blood (or
interstitial fluid). A decrease in the blood K+
level has the opposite
effect.

Pulse ratePulse rate
• Pulse: Means expansion and elongation of arterial walls by
the pressure changes during systole (contraction) and
diastole (relaxation)
Pulse rate is recorded for 1
minute
Normal ranges:
New born: 140 beats/minutes
Children: 100 beats/minutes
Adult human: 60-80 beats/minutes
Tachycardia: Increase in HR than normal
Bradycardia: Decrease in HR than normal

Blood PressureBlood Pressure
• Blood pressure: It is the pressure excreted by blood
on the wall of arteries.
• Systolic BP–Ventricular contraction
• Diastolic BP–Ventricles relaxation
• Normal BP = 120/80 mm Hg
• Pressure in blood vessels decreases as the distance
from the heart increases
• It is essential to record both BP’s as it gives
information regarding the status of working heart.
• BP varies from different physiological parameters like
age, sex, exercise, posture, sleep during
emotions, etc.

Methods of BP determination
 Oscillatory method
 Palpatory method
 Auscultatory method
Stethoscope
Sphygmomanometer

Blood pressure
It depends on the speed of blood coming into a vessel and width of
vessel itself.
Arteries
Speed: high
Width: medium
Pressure: high
Capillaries
Speed: medium
Width: narrow
Pressure: medium
Veins
Speed: low
Width: wide
Pressure: low

Blood pressure
An individual’s blood pressure is affected by a number of factors.
Age – It increases as you get older.
Gender – Men tend to have higher blood pressure than
women.
Stress - Can cause increase blood pressure.
Diet – Salt and saturated fats can increase blood pressure.
Exercise – Exercise lowers the blood pressure
Having high blood pressure puts stress on heart. It can lead to
angina, heart attacks and strokes.

Auscultatory method
 Initially the cuff is inflated to a level higher than the systolic pressure.
 Thus the artery is completely compressed, there is no blood flow, and
no sounds are heard.
 The cuff pressure is slowly decreased. At the point where the systolic
pressure exceeds the cuff pressure, the Korotkoff sounds are first
heard and blood passes in turbulent flow through the partially
constricted artery.
 Korotkoff sounds will continue to be heard as the cuff pressure is
further lowered.
 However, when the cuff pressure reaches diastolic pressure, the sounds
disappear.
 Now at all points in time during the cardiac cycle, the blood pressure is
greater than the cuff pressure, and the artery remains open.

 Auscultation – listening to heart sound via stethoscope
 Four heart sounds
 S1– “lubb” caused by the closing of the AV valves
 S2 – “dupp” caused by the closing of the semilunar valves
 S3 – a faint sound associated with blood flowing into the
ventricles
 S4 – another faint sound associated with atrial contraction
Heart sounds

Variations in Blood PressureVariations in Blood Pressure
• Human normal range is variable
• Normal
• 140–110 mm Hg systolic
• 80–75 mm Hg diastolic
• Hypotension
• Low systolic (below 110 mm HG)
• Often associated with illness
• Hypertension
• High systolic (above 140 mm HG)
• Can be dangerous if it is chronic

Control of BP
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 Blood pressure is controlled in 2 ways:
 Short term control: Mainly involves the baroreceptor reflex,
chemoreceptor & circulating hormones
 Long term control: Involves regulation of blood volume by the kidneys
and RAA system
 The cardiovascular centre (CVC) is a collection of
interconnected neurons in the brain
 The CVC receives, integrates & coordinates inputs
from:
 Baroreceptors (pressure receptors)
 Chemoreceptor
 Higher centers in the brain

Baroreceptors
 These are nerve endings sensitive to pressure changes (stretch)
within the vessel, situated in the arch of the aorta
 Rise in B.P. in these arteries
 Stimulation of Baroreceptors
 Increasing their input to the CVC
 Increases parasympathetic nerve activity to heart
 Decreases HR & decreases FC
 Vasodilation
 Fall in systemic blood pressure
71

Conversely
 Fall in B.P. aortic arch and carotid sinuses
 Deactivation of Baroreceptors
 Decreasing their input to the CVC
 Increases sympathetic nerve activity to heart
 Increases HR & FC
 Vasoconstriction
 Rise in systemic blood pressure

Chemoreceptor
 These are nerve endings situated in the carotid and aortic
bodies.
 Involved in control of respiration.
 Sensitive to changes in the levels of carbon dioxide, oxygen &
the acidity of the blood (pH).

Hormonal regulation of BP
 Renin-angiotensin-Aldosterone System: Discussed above
 Epinephrine & Nor-epinephrine: Adrenal medulla releases
epinephrine and nor-epinephrine. These changes increases CO by
increase in the HR & FC.
 Antidiuretic hormone (ADH): It is produced by hypothalamus
causes vasoconstriction that increases BP.
 Hence, it is also called as vasopressin.
 Atrial natriuretic peptide (ANP): It is released by the cells in
the atria of heart. ANP lowers BP by causing vasodilation and by
promoting the loss of salt & water in urine which reduces blood
volume.

Auto regulation of blood pressure
 The ability of a tissue to automatically adjust its blood flow to
match its metabolic demands called as auto regulation.
 Two general types of stimuli cause auto regulatory
changes in blood flow.
 Physical change:
 Warming promotes vasodilation & cooling causes
vasoconstriction.
 Vasodialating & vasoconstricting chemicals:

Auto regulation of blood pressure
 Several types of cells such as WBC, Platelets, smooth muscle
fibers, macrophages, endothelial cells-release a wide variety of
chemicals that alters blood vessels diameter.
 Vasodialating chemicals released by metabolically active tissue
cells include K+
, H+
, lactic acid & adenosine (From ATP).
 Important vasodilator released by endothelial cell is NO named as
endothelium derived relaxation factor (EDRF).

Filling of Heart Chambers – Cardiac CycleFilling of Heart Chambers – Cardiac Cycle

Cardiac Cycle
 The event occurring in the heart from the beginning of one
heart beat to the beginning of other is called as cardiac cycle.
 In normal cardiac cycle the two atria contracts while the two
ventricles relax. Then, while the two ventricles contract, the two
atria relax.
 Cardiac cycle consists of systole and diastole of both the atria &
ventricles.
 Cardiac cycle refers to all events associated with blood flow
through the heart
 Systole – contraction of heart muscle
 Diastole – relaxation of heart muscle

Phases of the Cardiac Cycle
 Cardiac cycle is divided into 3 phases
 Ventricular filling
 Ventricular contraction
 Ventricular relaxation

Ventricular Filling
 During ventricular relaxation, large amount of blood collects in
the atria, as the AV valve are closed.
 This increases the pressure in the atria and AV valves get opens
and semilunar valve are closed.
 So, the blood flow rapidly into the ventricles.
 First 1/3th
time of ventricular filling is called as period of rapid
ventricular filling.
 Later on only small amount of blood flows into the ventricles.
 P wave on ECG indicates atrial depolarization

Ventricular contraction
 Period of isovolumetric contraction:
 Immediately after ventricular filling the pressure inside the
ventricles rises suddenly.
 This rise in pressure tries to push blood back to the atria and
due to this AV valves get closed.
 At this particular junction, the AV valves and SL valves are
closed and the volume inside the ventricles does not change
called as period of isovolumetric contraction.

Ventricular contraction
 Period of ventricular ejection:
 As further ventricles starts contracting the pressure inside rises
sharply.
 When the pressure rises above the aortic pressure and
pulmonary trunk pressure SL valve get opens.
 As the SL get opens the blood get ejected out of the ventricles.
This period is called as ventricular ejection.
 After this ventricular pressure falls, the period of ventricular
relaxation is repeated.

Ventricular relaxation
 Ventricles starts to relax at the end of heart beat.
 At this particular point all the chambers of heart are
relaxing.
 This represent T wave on ECG.
 As the ventricles starts relaxing pressure inside the
ventricles drops suddenly.
 This drop in pressure leads to back flow of blood from the
pulmonary trunk and aorta.
 This forceful back flow of blood closes the SL valves
suddenly.

Ventricular relaxation
 This pressure produces a bump called as dicrotic wave.
 At this particular point both the SL valve and AV valves are
closed.
 Due to this the ventricular volume does not change and
this period is called as isovolumetric relaxation.
 With the further relaxation of ventricles there is further fall
in pressure inside the ventricles.
 When this ventricular pressure drops below the atrial
pressure AV valves opens and ventricular filling begins.

Cardiac Output (CO) and Reserve
 Cardiac Output 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 a ventricle
with each beat
 Cardiac reserve is the difference between resting and
maximal CO
 CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
 CO = 5250 ml/min (5.25 L/min)

Stroke Volume
 SV = End diastolic V(EDV) - End systolic V (ESV)
 EDV = amount of blood collected in a ventricle
during diastole
 ESV = amount of blood remaining in a ventricle after
contraction

Factors Affecting Stroke Volume
 Afterload is the tension developed in the wall of the left ventricle
during ejection
 Preload is pressure that stretches the right or left ventricle of the
heart to its greatest geometric dimensions under variable
physiologic demand

89
Congestive Heart Failure (CHF)
 Congestive heart failure (CHF) is caused by:
 Coronary atherosclerosis
 Persistent high blood pressure
 Multiple myocardial infarcts
 Dilated cardiomyopathy (DCM) – main pumping
chambers of the heart are dilated and contract poorly

Chapter 18, Cardiovascular System 90
Congestive Heart Failure
 Causes of CHF
 coronary artery disease, hypertension, MI, valve disorders,
congenital defects
 Left side heart failure
 less effective pump so more blood remains in ventricle
 heart is overstretched & even more blood remains
 blood backs up into lungs as pulmonary edema
 suffocation & lack of oxygen to the tissues
 Right side failure
 fluid builds up in tissues as peripheral edema

Coronary Artery Disease
 Heart muscle receiving
insufficient blood supply
 narrowing of vessels---
atherosclerosis, artery
spasm or clot
 atherosclerosis--smooth
muscle & fatty deposits in
walls of arteries
 Treatment
 drugs, bypass graft,
angioplasty, stent

Chapter 18, Cardiovascular System 93
Artificial Heart

Cardiovascular system

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