Review on Anatomy and Physiology of cardiovascular system.

SHIMLA NURSING COLLEGE ANNANDALE
SHIMLA
ASSIGNMENT
ON
REVIEW OF ANATOMY AND PHYSIOLOGY OF CARDIO VASCULAR AND
RESPIRATORY SYSTEM
SUBMITTED TO: SUBMITTED BY:
Dr. Pallavi Pathania Priyanka Thakur
Associate Professor M.Sc. Nursing 2nd year
H.O.D. of Medical- Surgical Nursing Shimla Nursing College Annandale
SUBMITTED ON:30, March, 2021

INDEX
SR.NO TOPIC PAGE NO.
Review of anatomy and physiology of cardio
vascularand respiratory system
1 Embryology of heart and Lung
 Embryology of lung
 Embryology of heart
1-14
2-7
8-14
2 Anatomy and physiology of heart 15-24
3 Anatomy and physiology of lung 25-33
4 Anatomy and physiology of thoracic cavity 34-36
5 Anatomy and physiology of blood vessel 37-45
6 Coronary circulation 46-50
7 Hemodynamics and electrophysiology of heart
 Hemodynamics of heart
 Electrophysiology of heart
51-76
51-65
66-76
8 Bio-chemistry of blood in relation to cardio pulmonary
function
77-91
9 Bibliography 92

REVIEW OF ANATOMY AND PHYSIOLOGY OF CARDIO VASCULAR AND
RESPIRATORY SYSTEM

EMBRYOLOGY OF LUNG
Development of the lower respiratory tract begin on day 22 and continue to form the trachea, lungs, bronchi and
alveoli.
LUNG DEVELOPMENT STAGES:
Babies breathe in the womb: Before the baby born, the lungs are filled with fluid. Baby gets oxygen from the
mother’s blood through the placenta. The fluid in the womb help baby’s lungs develop and mature, ready for
birth. Baby will not take their first breath of air until they are born. Things always happen in the order we have
outlined below, but the exact timings can be slightly different.
Children’s lungs develop in 5 stages. These stages happen in the womb, but the final stage does not complete
until later in childhood or early adolescence.
Stage 1: After Conception (Embryonic Stage)
(Happens At 3-5 Weeks)
 At 5 weeks baby is just 2mm long.
 A lung bud develops from a tube of cells called the foregut (which will itself later go
on to form the gut). This bud separates into two.
 These two buds will eventually become baby’s right and left lungs.
 Baby makes lung movements in the womb as if they are practicing breathing. These
movements start at the end of this stage.
Stage 2: Airways Begin to Form (Pseudoglandular stage)
(Happens From 5-16 Weeks)
 Baby is growing rapidly. The major internal organs are in place by 12 weeks. At 14
weeks the baby measures 85mm from head to toe.
 Baby’s lungs start to develop the tree-like structure that see in adult lungs.
 Each lung bud starts to divide again and again, like the branches of a tree.
 At first, they form 3 buds on the right side – these will become the upper, middle and

lower lobes of the right lung. They only form 2 buds on the left side - the upper and
lower lobes of the left lung.
 Baby’s right lung will be bigger because the left lung has to share space with the
baby’s heart.
 These buds continue to divide throughout this stage. They may divide up to 20 times.
 By 16 weeks baby’s lungs have all of their main airways (bronchi) and smaller
airways (bronchioles). Cells that will eventually become the tiny air sacs (alveoli)
have started to appear at the end of these smaller airways, like buds on trees.
Stage 3: Getting Ready to Make Air Sacs and Small Blood Vessels (Canalicular Stage)
(Happens From 16-26 Weeks)
 Baby starts to develop the areas where air sacs and blood vessels will eventually
form, at the end of the smallest airways. These air sacs will be needed to get oxygen
into their blood when they breathe outside the womb.
 The cells that will become the air sacs carry on developing even after baby is born.
 Small blood vessels called capillaries grow close to these cells.
Stage 4: Preparing the Lungs for Breathing (Saccular Stage)
(Begins At 26 Weeks and Carries on Until Birth)
 In this stage, the end of the smallest airways (called saccules) grow in size. They will
develop into early air sacs but they still don’t look like adult air sacs yet.
 The walls of these growths get thinner to make more room for air in baby’s lungs.
 A substance called surfactant is produced during this stage.
 Surfactant is a mixture of fats and proteins that help make sure the air sacs don’t
collapse at the end of each breath out.
Stage 5: Air Sac (Alveoli) Development (Alveolar Stage)
(Starts At 32 Weeks and Continues Into Childhood, After Baby Is Born)
 In the last few weeks of pregnancy the first true air sacs (alveoli) develop.
 More surfactant is produced as the lungs carry on developing.
 The lungs develop and grow to enable oxygen to get into the blood. This prepares
baby’s lungs to breathe outside the womb.
 Things always happen in this order but the exact timings can be slightly different.
 In the womb the lungs are filled with fluid. Baby gets oxygen from the mother’s
blood.

FetalRespiratoryMovements
 Fetal respiratory movements (FRM) or Fetal breathing movements (FBM) are regular muscular contractions occurring
in the third trimester.
 preparing the respiratory muscular system for neonatal function.
 may also have a role in late lung development.
The first Breath:
ALVEOLAR SAC STRUCTURE
The mother's placenta helps the baby "breathe" while it is growing in the womb. Oxygen and carbon dioxide
flow through the blood in the placenta. Most of it goes to the heart and flows through the baby's body.
Once the baby takes the first breath, a number of changes occur in the infant's lungs The respiratory system does
not carry out its physiological function (gas exchange) prenatally and remain entirely fluid-filled until birth. The
baby takes the first breath within about 10 seconds after delivery.

 At birth, fluid in the upper respiratory tract is expired and fluid in the lung aveoli is rapidly absorbed this
event has also been called "dewatering of the lung".
 The lung epithelia has to now rapidly change from its prenatal secretory function to that of fluid
absorbtion.
The exchange of lung fluid for air leads to:
 fall in pulmonary vascular resistance
 increase in pulmonary blood flow
 thinning of pulmonary arteries (stretching as lungs increase in size)
 blood fills the alveolar capillaries
In the heart - pressure in the right side of the heart decreases and pressure in the left side of the heart increases
(more blood returning from pulmonary).
Postnatal:
Alveoli
 At birth about 15% of adult alveoli number have formed
 20 - 50 million to in the adult about 300 million.
 remaining subdivisions develop in the first few postnatal years

Respiratory Rate
 neonatal rate is higher (30-60 breaths/minute) than adult (12-20 breaths/minute).
 tachypnea - (Greek, rapid breathing) an increased respiratory rate of greater than 60 breaths/minute in a quiet
resting baby
Age Rate (breaths/minute)
Infant (birth - 1 year) 30 – 60
Toddler (1 - 3 years) 24 – 40
Preschool (3 - 6 years) 22 – 34
School age (6 - 12 years) 18 – 30
Adolescent (12 - 18 years) 12 – 16
Rib Orientation
 Infant rib - is virtually horizontal, allowing diaphragmatic breathing only.
 Adult rib - is oblique (both anterior and lateral views), allows for pump-handle and bucket handle types of inspiration.

EMBRYOLOGY OF HEART
 The heart is a muscular organ located in the middle mediastinum that pumps blood through the circulatory
system.
 It is one of the earliest differentiating and functioning organs in the human body.
 In human embryos, the heart begins to beat at about 22-23 days, with blood flow beginning in the 4th
week.
 It begins very early in mesoderm within the trilaminar embryonic disc.
 The heart forms initially in the embryonic disc as a simple paired tube inside the forming pericardial
cavity, which when the disc folds, get carried into the correct anatomical position in the chest cavity.
 Heart development is also known as cardiogenesis refers to the prenatal development of the human heart.
Developmentof the Heart (Heart Embryology)
 Cardiogenesis begins with the formation of two endocardial tubes which merge to form the tubular heart,
also called the primitive heart tube that loops and separates into the four chambers and paired arterial
trunks that form the adult heart.
 The tubular heart quickly differentiates into the truncus arteriosus, bulbus cordis, primitive
ventricle, primitive atrium, and the sinus venosus.
 The truncus arteriosus splits into the ascending aorta and pulmonary artery.
 The bulbus cordis forms part of the ventricles.
 The sinus venosus connects to the fetal circulation.
 The heart tube elongates on the right side, looping and becoming the first visual sign of the left-right
asymmetry of the body.
 Septa form within the atria and ventricles to separate the left and right sides of the heart.
The development of the heart can be studied under the following headings:
1. Generation and fusion of the developing heart tubes
 The heart fields are of mesodermal origin and established in the cranial-most end of the embryo.
 The heart fields are patterned into primary and secondary heart fields:
 Primary heart field will develop into left and right atria and the left ventricle
 Secondary heart field will become the right ventricle and outflow tract

2. Repositioning the cardiogenic fields
 Lateralfolding brings the forming heart tubes to the midline to fuse into a single tube
 Cranio-caudal folding swings the heart tube into a position just ventral to the foregut pocket in the neck of the
embryo with the inflow oriented toward the tail of the embryo and outflow oriented toward the head.
 The heart tube is suspended from the body wall by a sling of connective tissue called the dorsal mesocardium.
 Differential growth of the embryo causes the heart to be displaced toward the tail of the embryo such that the heart
ends up in the chest.
3. Folding of the developing heart
 Degeneration of the central portion of the dorsal mesocardium leaves the primitive heart attached at the outflow and
inflow ends (this is how the transverse pericardial sinus forms).
 The heart grows rapidly, but it is still fixed at both ends so it loops.
4. Partitioning the Atrio-Ventricular Canal
 The atrioventricular canalis divided by the fusion of the dorsal and ventral AV cushions.
 The AV cushions are formed by the conversion of endogenous heart tissue in the endocardium of the AV canal into
mesenchyme that proliferates to form the two “cushions” or swellings that grow toward each other.
 The cushions fuse in the middle of the AV canal to form a left and right AV canal.
 However, the two canals initially empty into the future left ventricle –with additional growth and remodeling, the
canals shift toward the middle such that the left AV canallines up with the left ventricle and the right AV canal lines
up with the right ventricle.

5. Partitioning the Atria
 A septum, the septum primum (“first” septum) grows down from the roof of the primitive atrium toward the AV
cushions that have fused into a block of tissue dividing the left and right AV canals.
 The foramen primum is the space between the free edge of the septum primum and AV cushions –it becomes
progressively smaller as the septum primum grows toward the AV cushions and eventually closes off completely
when the septum primum fuses with the AV cushions.
 As the foramen primum is closed off, programmed cell death in the wall of the septum primum near the roof of the
atrium opens up a second foramen, the foramen secundum.
 A second, more rigid, septum called the septum secundum grows down on the right side of the septum primum from
the roof of the atrium toward the AV cushions.
 However, the septum secundum does not grow all the way down to the cushions but leaves an oval opening, the
foramen ovale, located toward the lower back wall of the right atrium (near the opening of the inferior vena cava).
 Over time, the tissues of the two septa grow together with such that they typically become anatomically
fused. However, in about 25% of the population, this fusion is not complete and said to be “probe patent” (meaning
a probe pushed into the foramen ovale would push open the septum secundum and pass into the left atrium).
Aortic Arches: The early arterial system begins as a bilaterally symmetrical system of arched vessels, which
then undergo extensive remodelling to create the major arteries that exit the heart.
The derivatives of the aortic arches in the adult are as follows:
1st arch Contributes to the maxillary, hyoid and stapedial arteries.
2nd arch Contributes to the maxillary, hyoid and stapedial arteries.
3rd arch Forms the common carotid artery and part of the proximal internal carotid artery.
4th arch
Right arch forms the right subclavian artery
Left arch forms part of the arch of the aorta
5th arch Either never forms, or forms incompletely and regresses
6th arch
Right arch forms the right pulmonary artery
Left arch forms the left pulmonary artery and the ductus arteriosus.
Each of the arches has a corresponding nerve during development. The most important of these is the recurrent
laryngeal nerve (a branch from CN X) – which is associated with the 6th arch:
 Right recurrent laryngeal nerve – initially hooks around the right 6th aortic arch. However, when the
distal part of the right 6th arch disappears, it moves up to hook around the right subclavian artery
(4th arch).
 Left recurrent laryngeal nerve – hooks around the left 6th aortic arch. The distal part of the left
6th aortic arch persists as the ductus arteriosum, and so the nerve remains in this position.
The long course of the left recurrent laryngeal nerve is clinically relevant, as it is susceptible to pathology in the
chest (e.g. compression by an aortic aneurysm).

6. Partitioning the ventricles
 A ridge of muscular tissue from the wall of ventricles proliferates at the transition from the future left ventricle and
future right ventricle to form the “muscular interventricular septum” that almost completely separates the right and
left ventricles.
 The upper portions of the left and right ventricles (near the AV valves and semilunar valves) are divided by a much
thinner septum known as the “membranous interventricular septum.”
7. Partitioning the Outflow Tract
 Neural crest cells associated with pharyngeal arches 4 and 6 migrate into the truncus arterosus (undivided outflow
tract) and conus cordis (aka bulbus cordis, which is the conical-shaped outflow portion of the primitive right
ventricle) and transform into mesenchymal tissue that proliferates to form two so-called truncoconal or truncobulbar
cushions (or ridges).
 The two truncoconal ridges grow toward each other and fuse first at the truncoconal transition and then “zip” distally
(toward the outflow tract) and proximally (toward the ventricles.
 As the ridges zip together, they spiral in a right-handed twist such that the pulmonary trunk ends up anterior to the
aorta.
 As the truncoconal ridges grow toward the ventricles, they also contribute a portion of the membranous
interventricular septum.
8. Formation of valves in the heart
 Semilunar (pulmonary and aortic) valves are formed via cavitation of truncoconal ridge tissue to form three
triangular valve leaflets in each of the outflow vessels in a highly stereotypical pattern:
 the pulmonary semilunar valve develops three cusps: left, right, and anterior
 the aortic semilunar valve also develops three cusps: left, right and posterior
 Atrioventricular (tricuspid and mitral, or bicuspid) valves are formed via cavitation of atrioventricular cushion tissue
and ventricular walls to form valve leaflets attached via chordae tendinae to the myocardium (i.e. papillary muscles).

Outflow Tract: Endocardial cushions also appear within the truncus arteriosus which grow towards each other.
As they grow towards each other they twist around each other and form a spiral septum, dividing the outflow
tract into left and right sides.
Circulatory Shunts: In the fetal circulation, vascular shunts are required to bypass the liver and non-
functioning lungs. The lungs are bypassed by two separate shunts, firstly the foramen ovale between the
two atria, which is responsible for bypassing the majority of the circulation. Any blood that does not pass
through the foramen ovale enters the pulmonary trunk, which is linked to the distal arch of aorta by the ductus
arteriosus. These two separate shunts allow the circulation to bypass the lungs.
The oxygenated blood entering the fetus also needs to bypass the primitive liver, this ensures that enough
oxygen reaches the developing brain. This is achieved by passage through the ductus venosus, which is
estimated to shunt around 30% of umbilical blood directly to the inferior vena cava.
PHYSIOLOGY OF HEART AT BIRTH:

At birth, these shunts need to close to allow the normal adult circulation to be established:
 Foramen ovale – intake of air leads causes pulmonary resistance to fall. The pressure within the left
atrium is now higher than the right. As blood cannot flow through the foramen ovale left to right, this
effectively closes the shunt. It fuses shut in most individuals by the age of 1 year.
 Ductus arteriosus – muscular wall contracts to close after birth (a process mediated by bradykinin).
The circulatory shunts are summarised in the table below:
Fetal shunt Adult remnant Closure at
Foramen ovale Fossa ovalis 1 year
Ductus arteriosus Ligamentum arteriosum 2- 3 week
Ductus venosus Ligamentum venosum 1 week
Umbilical vein Ligamentum teres (hepatis) 2-3 month

ANATOMY AND PHYSIOLOGY OF HEART

ANATOMY AND PHYSIOLOGY OF HEART
INTRODUCTION
The circulatory system, also called the cardiovascular system or the vascular system, is an organ system that
permits blood to circulate and transport nutrients (such as amino acid and electrolytes), Oxygen, carbon
dioxide, hormones and blood cells to from cells in the body to provide nourishment and help in fighting disease,
stablishing temperature and PH and maintain homeostasis.
CIRCULATORY SYSTEM
ORGAN/COMPONENTS PRIMARY FUNCTION
HEART Propels blood, maintains blood pressure
BLOOD VESSELS Distribute blood around the body
ARTERIES Carry blood heart to capillaries
CAPILLARIES Permit diffusion between blood and interstitial fluids
VEINS Return blood from capillaries to the heart
BLOOD Transport oxygen, carbon dioxide and blood cells, delivers nutrients
and hormones, remove waste products, assists in temperature regulation
and defence against disease

PROCESS OF BLOOD FLOW
HEART: The heart is a muscular organ in most animals, which pumps blood through the blood vessels of the
circulatory system. The pumped blood carries oxygen and nutrients to the body, while carrying metabolic waste
such as carbon dioxide to the lungs.
LOCATION AND SURFACE PROJECTION
• Apex- lower, cone shaped, Base- border, superior portion
• The heart is the hollow, cone shaped about the size of closed fist
• It lies in the mediastinum between the lungs and rests upon the diaphragm
• Two- third of its mass lies to left of the midline
POSTION OF HEART
• Normally located in the middle and slightly to the left side of the thoracic
• The apex is about 9 cm to the left of the midline at the level of the 5th intercostal space and the base
extends to the levels of the 2nd rib .
• Weighs about 325 gm is males and about 275 gm in females.
Heart
Arteries
Arterioles
Capillaries
Venules
Veins

LAYERS OF HEART WALLS
PERICARDUIM/ EPICARDUIM:
It is the layer immediately outside of the heart muscle proper (the myocardium). The epicardium is largely made
of connective tissue and functions as a protective layer.
Pericardium is the membrane (sac) that surrounds and protects the heart by the help of two layers.
a. Fibrous pericardium- superficial layer, tough, inelastic, prevents overstretching, provide protection and
anchors the heart in place.
b. Serous pericardium-
1. Parietal layer- fused to the fibrous pericardium
2. Visceral layer or epicardium- adheres to the heart itself
c. Pericardial cavity – Present between two layers is filled with pericardial fluids which reduce friction
MYOCARDUIM
The myocardium of the left ventricle is the thickest, as this ventricle is responsible for generating the power
needed to pump oxygenated blood from the heart to the rest of the body
ENDOCARDUIM
• Endocardium (endo-cardium) is the thin inner layer of the heart wall. This layer lines the inner heart
chambers, covers heart valves, and is continuous with the endothelium of large blood vessels.
• The endocardium of heart atria consists of smooth muscle, as well as elastic fibers.
CHAMBERS OF HEART
Four chambers
• Right Atrium

• Right Ventricle
• Left atrium
• Left ventricle
RIGHT ATRIUM
• Receives venous blood from whole of the body via the superior vena cava (SVC) at its upper end and
inferior vena cava (IVC) at its lower end.
• It pumps into Right ventricle (RV)through the tricuspid valve during the ventricular diastole
RIGHT VENRTICLE
• Triangular shaped or crescent shaped
• Opens into pulmonary artery through pulmonary valve
• Most anterior chamber
LEFT ATRIUM
• Posterior most chamber
• Receives oxygenated blood from pulmonary veins
• Pulmonary veins open into LA from the posterior wall
RIGHT VENRTICLE
• Chambers and is responsible for pumping oxygenated blood to tissues all over the body.

VALVES OF HEART
• There are also 4 one-way valves that direct flow of blood through the heart in one direction
 2 Atrioventricular (AV) valves
• Bicuspid (Mitral) valve - separates left atrium and ventricle, consists of two flaps of tissues
• Tricuspid valve – separates right atrium and ventricle - consists of three flaps of tissue prevent backflow
(eversion) keeps valves pointed in direction of flow)
 2 Semilunar valves
• at beginning of arteries leaving the ventricles
Aortic SL valve- at beginning of aorta
Pulmonary SL valve-at beginning of pulmonary trunk.
Normal Heart Sounds:
 The first heart sounds (S1) Lubb:
The first heart sounds (S1) occur with the closure of the atrioventricular valves (mitral and tricuspid valves)
and thus it signals the beginning of systole. The mitral component of the first heart sound (M1) Slightly
precedes the tricuspid component (T1), but you usually hear the two components fused as one heart sound.
You can hear S1 over all the precordium but its usually loudest at the apex. Its intensity is increased in
mitral stenosis due to an increased left atrial pressure and decreases in low cardiac output conditions.
 The second heart sound (S2) Dubb:
The second heart sound (S2) occurs with the closure of the semilunar valves (aortic and pulmonary valves)
and signals the end of systole. The aortic component of the second sound (A2) Slightly precedes the
pulmonic component (P2). Although it is heard over the precordium, S2 is loudest at the base (left sternal
edge). Decreased intensity heard in low cardiac output, calcified aortic stenosis, and aortic incompetence.
When compared with the first heart sound, S2 is shorter, softer and is slightly higher pitched.

SYSMATIC CIRCULATION/PULMONARY CIRCULATION
PULMONARY CIRCULATION: Transports oxygen-poor blood from the right ventricle to the lungs
where blood picks up a new oxygen supply.
SYSTEMATIC CIRCULATION: It returns oxygen rich blood and nutrients to the left atrium and is
pumped out all over the body. It also picks up carbon dioxide and other waste products.
CORONARY CIRCUALTION: Coronary arteries supply blood to the heart muscle. Like all other tissues
in the body, the heart muscle needs oxygen-rich blood to function. Also, oxygen-depleted blood must be
carried away. The coronary arteries wrap around the outside of the heart. Small branches divide into the
heart muscle to bring it blood.
CARDIC CONDUCTION SYSTEM

• To pump blood throughout the body, the muscles of the heart must be coordinated perfectly —
squeezing the blood in the right direction, at the right time, at the right pressure. The heart’s activity is
coordinated by electrical impulses.
• Electrical signals arising in the SA node (located in the right atrium) stimulate the atria to contract. Then
the signals travel to the atrioventricular node (AV node), which is located in the interatrial septum.
• After a delay, the electrical signal diverges and is conducted through the left and right bundle of His to
the respective Purkinje fibers for each side of the heart, as well as to the endocardium at the apex of the
heart, then finally to the ventricular epicardium; causing its contraction.
• These signals are generated rhythmically, which in turn results in the coordinated rhythmic contraction
and relaxation of the heart.

CARDIC CYCLE
• The cardiac cycle is the performance of the human heart from the ending of one heartbeat to the
beginning of the next. It consists of two periods: one during which the heart muscle relaxes and refills
with blood, called diastole following a period of robust contraction and pumping of blood,
dubbed systole.
CARDIC OUTPUT
• The cardiac output is the amount of the blood ejected from each ventricle every minutes.

• The amount of expelled by each contraction of each ventricles is the stroke volume
cardiac output = stroke volume x heart rate
• For a resting adult
CO = 70mL/beat x75beats/min
= 5250 mL/min
= 5.25 L/min
Function of Heart
The heart plays a key role in the circulation of blood and maintaining the mechanism of the whole body. It is the
most vital organ of the human body.
The heart performs the following important functions:
 The primary function of the heart is to pump blood throughout the body.
 It supplies oxygen and nutrients to the tissues and removes carbon dioxide and wastes from the blood.
 It also helps to maintain adequate blood pressure throughout the body.
The heart functions in the following ways:
1. The arteries receive oxygenated blood from the heart and supply it throughout the body. Whereas, the
veins carry the deoxygenated blood from all the body parts to the heart for oxygenation.
2. The right atrium receives blood from the veins and pumps it to the right ventricle.
3. The right ventricle pumps the blood received from the right atrium to the lungs.
4. The left atrium receives oxygenated blood from the lungs and pumps it to the left ventricle.
5. The left ventricle pumps the oxygenated blood throughout the body.

ANATOMY AND PHYSIOLOGY OF LUNGS

ANATOMY AND PHYSIOLOGY OF LUNGS
 POSITION AND GROSS STRUCTURE:
 There are two lungs, one lying on each side of the midline in the thoracic cavity. The left and the
right lung are separated by the mediastinum.
 They are cone-shaped, weight 600-700gms and have:
1) Apex,
2) Base,
3) Tip,
4) Costal surface and
5) Medial surface.
1) Apex:
 Rounded and rises into the root of the neck.
 About 25 mm above the level of the middle third of the clavicle.
 It lies close to the first rib and the blood vessels and nerves in the root of the neck.
2) Base:
 Concave and semilunar in shape.
 Lies on the upper (thoracic) surface of the diaphragm.
3) Costal surface:
 The broad outer surface of the lung that lies directly against the costal cartilages, the ribs and
the intercostal muscles.
4) Medial surface:
 The surface of each lung faces the other directly across the space between the lungs, the
mediastinum.
 Concave and has roughly triangular-shaped area, called hilum (at the level of 5th to 7th thoracic
vertebrae).

 The primary bronchus, the pulmonary artery supplies the lung and the 2 pulmonary veins
draining it, the bronchial artery and veins, and the lymphatic and nerve supply enter and leave the
lung at the hilum.
 The mediastinum contains the heart, great vessels, trachea, right and left bronchi, esophagus,
lymph nodes, lymph vessels and nerves.
TWO LUNGS:
1. Right lung: Has more lobes and segments than the left. It is divided into three lobes:
(i) Upper or superior lobe
(ii) Middle lobe
(iii) Lower or inferior lobe
 They separate by two fissures
(i) One oblique fissure which separates middle & lower lobe.
(ii) One horizontal fissure which separates middle & upper lobe
2. Left lung: It is small because the heart occupies space left of the midline. It is divided into only two lobes:
(i) upper/superior lobe
(ii) lower/inferior lobe
 They separate by the oblique fissure & does not have a middle lobe.
MECHANICS OF VENTILATION
Ventilation, or breathing, is the movement of air through the conducting passages between the atmosphere and
the lungs. The air moves through the passages because of pressure gradients that are produced by contraction of
the diaphragm and thoracic muscles.
Pulmonary ventilation
Pulmonary ventilation is commonly referred to as breathing. It is the process of air flowing into the lungs during
inspiration (inhalation) and out of the lungs during expiration (exhalation). Air flows because of pressure
differences between the atmosphere and the gases inside the lungs.
Muscular breathing movements and recoil of elastic tissues create the changes in pressure that result in
ventilation. Pulmonary ventilation involves three different pressures:
 Atmospheric pressure
 Intra-alveolar (intrapulmonary) pressure
 Intrapleural pressure

VENTILATION PROCESS:
 INTERIOR OF THE LUNGS
 The lungs are composed of the bronchi and smaller air passages, alveoli, connective tissue, blood
vessels, lymph vessels and nerves, all embedded in an elastic connective tissue matrix.
 Each lobe is made up of a large number of lobules.
 PULMONARY BLOOD SUPPLY
 Pulmonary Arteries:
 The pulmonary trunk divides into the right and left pulmonary arteries, carrying deoxygenated
blood to each lung.
 Within the lungs each pulmonary artery divides into many branches, which eventually end in a
dense capillary network around the alveoli.
 Pulmonary veins:
 Merge into a network of pulmonary venules, which in turn form two pulmonary veins carrying
oxygenated blood from each lung back to the left atrium of the heart.

BRONCHI & BRONCHIOLES
 The two primary bronchi are formed when the trachea divides, at about the level of the 5th
thoracic vertebra.
 There are two bronchus:
1. Right Bronchus
2. Left Bronchus
1. THE RIGHT BRONCHUS:
 This is wider, shorter and more vertical than the left bronchus.
 Length-2.5cm long.
 After entering the right lung, it divides into 3 branches, one to each lobe.
2. THE LEFT BRONCHUS:
 This is narrower than the right
 Length-5cm long.
 After entering the left lung, it divides into 2 branches, one to each lobe.
STRUCTURE OF BRONCHI
 The bronchi are composed of the same tissues as the trachea. Are lined with ciliated columnar
epithelium changes gradually to non-ciliated cuboidal-shaped cells in the distal bronchioles.
 The bronchi progressively subdivide into bronchioles, terminal bronchioles, respiratory
bronchioles, alveolar ducts and finally, alveoli. The wider passages are called conducting airways.

 STRUCTURAL CHANGES IN THE BRONCHIAL PASSAGES
 As the bronchi divide and become progressively smaller, their structure changes to match their
function i.e.
 Cartilage
 Smooth Muscle
 Epithelial lining
1. Cartilage:
 Rigid cartilage would interfere with expansion of lung tissue and the exchange of gases
(present for support in the larger airways only).
 The bronchi contain cartilage rings like the trachea, but as the airways divide, these rings
become much smaller plates, and at the bronchiolar level there is no cartilage present in the
airway walls at all.
2. Smooth muscle.
 As the cartilage disappears from airway walls, it is replaced by smooth muscle.
 This allows the diameter of the airways to be increased or decreased through the influence
of the autonomic nervous system, regulating airflow within each lung.
3. Epithelial lining:
 The ciliated epithelium is gradually replaced with non-ciliated epithelium, and goblet cells
disappear.
 BLOOD & NERVE SUPPLY
 Arterial Supply: Bronchial Arteries
 Venous Supply: Bronchial Veins
 Nerve Supply: Vagus Nerves
 Lymph Supply: The Thoracic Duct
FUNCTIONS OF BRONCHI
1. Control of air entry
2. Warming and humidifying
3. Support and patency
4. Removal of particular matter
5. Cough reflex
 RESPIRATORY BRONCHIOLES AND ALVEOLI
STRUCTURE:
 Within each lobe, the lung tissue is further divided by fine sheets of connective tissue into lobules.

 Each lobule is supplied with air by a terminal bronchiole, which subdivides into respiratory
bronchioles, alveolar ducts and large numbers of alveoli (air sacs), 150 million alveoli in the adult
lungs.
 In these structures that the process of gas exchange occurs.
 As airways progressively divide and become smaller and smaller, their walls gradually become
thinner (muscle and connective tissue disappear), leaving a single layer of simple squamous
epithelial cells in the alveolar ducts and alveoli.
 These distal respiratory passages are supported by a loose network of elastic connective tissue &
alveoli are surrounded by a dense network of capillaries.
 Exchange of gases in the lung (external respiration) takes place across a membrane made up of the
alveolar wall and the capillary wall fused firmly together. This is called the respiratory membrane.
 Lying between the squamous cells are septal cells that secrete surfactant, a phospholipid fluid which
prevents the alveoli from drying out and reduces surface tension preventing alveolar collapse during
expiration.
 NERVE SUPPLY TO BRONCHIOLES
 Parasympathetic stimulation (bronchoconstriction), from the vagus nerve.
 Sympathetic stimulation relaxes bronchiolar smooth muscle (bronchodilation).
 FUNCTION OF BRONCHIOLES
1. External respiration: This is exchange of gases by diffusion between the alveoli and the blood.
2. Defence against microbes: Protective cells present within the lung tissue, include lymphocytes &
plasma cells, which produce antibodies.

3. Warming and humidifying: These continue as in the upper airways. Inhalation of dry or
inadequately humidified air over a period of time irritates the mucosa and encourages infection.
 PLEURA AND PLEURAL CAVITY
 The pleura consists of a closed sac of serous membrane (one for each lung) which contains a small
amount of serous fluid.
 The lung is pushed into this sac so that it forms two layers:
 Visceral Pleura and
 Parietal Pleura.
1) Visceral Pleura: Adherent to the lung, covering each lobe and passing into the fissures that
separate them.
2) Parietal Pleura: Adherent to the inside of the chest wall and the thoracic surface of the
diaphragm. It is not attached to other structures in the mediastinum and is continuous with the
visceral pleura round the edges of the hilum.
 PLEURAL CAVITY
 This is a potential space and contains no air, so the pressure within is negative relative to
atmospheric pressure.

 In this, the two layers of pleura are separated by a thin film of serous fluid (pleural fluid), which
allows them to glide over each other, preventing friction between them during breathing.
 The pleural fluid is secreted by the epithelial cells of the membrane.
 The two layers of pleura, with pleural fluid between them, behave as two pieces of glass separated
by a thin film of water.
 They glide over each other easily but can be pulled apart only with difficulty, because of the surface
tension between the membranes and the fluid.
 This is essential for keeping the lung inflated against the inside of the chest wall.
 The airways and the alveoli of the lungs are embedded in elastic tissue, which constantly pull the
lung tissues towards the hilum, but because pleural fluid holds the two pleura together, the lung
remains expanded.
FUNCTION:
The main functions of the lungs are to transfer oxygen from the air to the blood and to release carbon dioxide
from the blood to the air.
Air enters the mouth or nose and travels through the windpipe, bronchi and bronchioles to the alveoli. The
exchange of oxygen and carbon dioxide happens in the alveoli.
 The alveoli absorb oxygen from the air and pass it into the blood, which circulates the oxygen around the
body.
 Carbon dioxide, which is a waste product of the body’s cells, passes from the blood into the alveoli and
is breathed out.
 The lungs produce a mixture of fats and proteins called lung or pulmonary surfactant. The surfactant
coats the surfaces of the alveoli, making it easier for them to expand and deflate with each breath.
The lungs also help protect the body from harmful substances in the air, such as smoke, pollution, bacteria and
viruses. These substances can pass through the nose and become trapped in the lungs. The lungs produce a
thick, slippery fluid (mucus), which can trap and partly destroy these substances from the air. The cilia move
rapidly to push the mucus up through the bronchi, where it is removed by coughing or swallowing.

ANATOMY AND PHYSIOLOGY OF THORACIC
CAVITY

ANATOMY AND PHYSIOLOGY OF THORACIC CAVITY
Thoracic cavity, also called chest cavity, the second largest hollow space of the body. It is enclosed by the 12
pairs of ribs, the vertebral column, and the sternum, or breastbone, and is separated from the abdominal
cavity (the body’s largest hollow space) by a muscular and membranous partition, the diaphragm.
It contains 3 compartments:
1. Pleural cavity: There are 2 pleural cavities, right and left. Each of 2 pleural cavities surrounds a
lung. Each pleural cavity is a small fluid filled space between the parts of the serous membrane
that cover the lungs is called visceral pleura and the part that lines the wall of the thoracic cavity
is called parietal pleura.
2. Pericardial cavity: It is a fluid filled space between the part of the serous membrane that cover
the heart called visceral pericardium and the part that lines the thoracic cavity is called parietal
pericardium.
3. Mediastinum: It is the region between the lungs extending from the sternum to the vertebra
column or backbone. It contains all the content of the thoracic cavity except the lung themselves
i.e. heart and its attach blood vessels, esophagus, trachea, thymus gland, lymph node, thoracic
duct, phrenic and vagus nerves and pericardial cavity.
Pleural Blood Supply:
 Visceral pleura: Artery supplied by bronchial and pulmonary arterial systems.
 The parietal pleura: Artery supply is from various systemic arterial supply the chest wall, diaphragm
and mediastinum.
Pleural Venous Drainage:
 Visceral pleura: Vein drain is pulmonary vein.
 The parietal pleura: Vein is to the superior vena cava.
Pleural Nerve Supply:

 Visceral pleura: it receives an autonomic nerve supply from the pulmonary plexus.
 The parietal pleura: It is supplied by intercostal nerve and is pain sensitive.
Function:
 The thoracic cavity contains organs and tissues that function in the respiratory (lungs, bronchi, trachea,
pleura), cardiovascular (heart, pericardium, great vessels, lymphatics), nervous (vagus nerve,
sympathetic chain, phrenic nerve, recurrent laryngeal nerve), immune (thymus) and digestive
(esophagus) systems.
 The thoracic cavity protects delicate internal organs.

INTRODUCTION
The blood vessels are the components of the circulatory system that transport blood throughout the human
body. These vessels transport blood cells, nutrients, and oxygen to the tissues of the body. They also take waste
and carbon dioxide away from the tissues. Blood vessels are needed to sustain life, because all of the body's
tissues rely on their functionality
DEFINITION
Blood vessel, a vessel in the human or animal body in which blood circulates. The vessels that carry blood away
from the heart are called arteries, and their very small branches are arterioles. Very small branches that collect
the blood from the various organs and parts are called venules, and they unite to form veins, which return the
blood to the heart.
TYPES OF BLOOD VESSELS
1. Arteries & Arterioles
2. Veins & Venules
3. Capillaries
1.Arteries & Arterioles
• built to withstand the greatest pressure of the system
a. strong resilient walls,
b. thick layers of connective tissues
c. more muscular than veins
• Arteries and arterioles typically contain ~25% of all blood in circulation (15% in arteries; 10% in
arterioles)
• Pressure is variable MAP ~ 93 varies from 100 – 40 mmHg
• Most organs receive blood from >1 arterial branch provides alternate pathway
2. Veins & Venules
• Generally, have a greater diameter than arteries but thinner walls, flaccid
• Three layers are all thinner than in arteries tunica adventitia is thickest of three
• But not as elastic as arteries
• Little smooth muscle

• 70% of all blood is in veins & venules (~60% in veins, ~10% in venules)
• low pressure:
• 12 – 8 mmHg venules
• 6 – 1 mmHg veins larger veins near
3. Capillaries:
• Actual site of exchange of materials the rest is just pumps and plumbing
• Consist of only a single layer of squamous epithelium= endothelial layer (=tunica intima)
• Arranged into capillary beds = functional units of circulatory system
• Capillaries are extremely abundant in almost every tissue of the body
• Only 5% of blood at any one time is in capillaries
MEMBRANE OF VESSELS
Walls of arteries and veins consist of three layers:
a. Tunica Externa
b. Tunica Media
c. Tunica Interna
a. Tunica Externa (= T. adventitia)
• outer loose connective tissue
• anchors the vessel and provides passage for small nerves, lymphatic vessels and smaller blood vessels
b. Tunica Media
• middle, made mainly of smooth muscle with some elastic tissue and collagen fibers strengthens vessel
walls
• prevent high pressure from rupturing them allows vasodilation and vasoconstriction
• usually the thickest layer, especially in arteries
c. Tunica Interna (=T. Intima)

• inner endothelium
• exposed to blood when damaged or inflamed induce platelets or
• WBC’s to adhere
• may lead to plaque build up and atherosclerosis
AORTA
• The aorta is the main and largest artery in the human body originating from the left ventricle of
the heart and extending down to the abdomen, where it splits into two smaller arteries (the common iliac
arteries). The aorta distributes oxygenated blood to all parts of the body through the systemic circulation
• part of the aorta is by anatomical compartment, where the
1. Thoracic aorta (or thoracic portion of the aorta) runs from the heart to the diaphragm.
2. Abdominal aorta (or abdominal portion of the aorta) from the diaphragm to the aortic bifurcation
THORACIC AORTA
• This part of the aorta lies above the diaphragm and is described into 3 parts:
• Ascending aorta
• Arch of the aorta
• Descending aorta in the thorax
ASCENDING AORTA
• It is a portion of the aorta commencing at the upper part of the base of the left ventricle, on a level with
the lower border of the third costal cartilage behind the left half of the sternum
• Right and left coronary arteries are branches of ascending aorta.
ARCH OF AORTA
• The aortic arch is the connection between the ascending and descending aorta, and its central part is
formed by the left 4th aortic arch during early development

• Three branches arise from upper aspect:
• Brachiocephalic artery or trunk
• Left common carotid artery
• Left subclavian artery
DESENDING AORTA
• The descending aorta is the part of the aorta, the largest artery in the body, that runs down through the
chest and the abdomen. The descending aorta starts after the arch of the aorta and ends by splitting into
two great arteries (the common iliac arteries) that go to the legs.
ABDOMINAL AORTA
• The abdominal aorta, is the final section of the aorta. It begins at the diaphragm as a continuation of the
thoracic aorta and runs down to where the aorta ends (by splitting into the two leg arteries) or right/left
common iliac artery. The abdominal aorta supplies oxygenated blood to all of the abdominal and pelvic
organs and the legs.
VENAE CAVAE
• The venae cavae cava the Latin for "hollow veins", singular "vena cava" are two large veins (venous
trunks) that return deoxygenated blood from the body into the heart. In humans there are the superior
vena cava and the inferior vena cava and both empty into the right atrium. They are located slightly off-
center, toward the right side of the body.
• The superior vena cava (SVC) is the superior of the two venae cave, the great venous trunks that return
deoxygenated blood from the systemic circulation to the right atrium of the heart.
• It is a large-diameter (24 mm) short length vein that receives venous return from the upper half of the
body, above the diaphragm
• The inferior vena cava (or IVC) is a large vein that carries the deoxygenated blood from the lower and
middle body into the right atrium of the heart.
• Its walls are rigid and it has valves so the blood does not flow down via gravity. It is formed by the
joining of the right and the left common iliac veins, usually at the level of the fifth lumbar vertebra.
PULMONARY ARTERIES AND VEINS
Pulmonary arteries:
• Right ventricle -> pulmonary trunk -> right and left pulmonary arteries
Purpose: deliver deoxygenated blood to the respective lung
Pulmonary veins:
• Lung capillaries -> 4 pulmonary veins (2 from each lung) -> left atrium
Purpose: deliver oxygenated blood to the left ventricle which will distribute it to the body
VASCULAR SYSTEM
• Provide conduits for blood to travel from the heart to nourish the body.

• Carry cellular wastes to the excretory organs.
• Return blood to the heart for recirculation.
ARTIAL SYSTEM
• Delivers blood to various tissues for nourishment
• Transport of cellular wastes
• Contribute to thermal regulation
Arteries
of the
Thoracic
Region
Vessel Description
Visceral
branches
A group of arterial branches of the thoracic aorta; supplies blood to the
viscera (i.e., organs) of the thorax
Bronchial
artery
Systemic branch from the aorta that provides oxygenated blood to the
lungs; this blood supply is in addition to the pulmonary circuit that brings
blood for oxygenation
Pericardial
artery
Branch of the thoracic aorta; supplies blood to the pericardium
Esophageal
artery
Branch of the thoracic aorta; supplies blood to the esophagus
Mediastinal
artery
Branch of the thoracic aorta; supplies blood to the mediastinum
Parietal
branches
Also called somatic branches, a group of arterial branches of the thoracic
aorta; include those that supply blood to the thoracic wall, vertebral
column, and the superior surface of the diaphragm
Intercostal
artery
Branch of the thoracic aorta; supplies blood to the muscles of the thoracic
cavity and vertebral column
Superior
phrenic
artery
Branch of the thoracic aorta; supplies blood to the superior surface of the
diaphragm

Aortic Arch
Branches
and Brain
Circulation
Vessel Description
Brachiocephalic
artery
Single vessel located on the right side of the body; the first vessel
branching from the aortic arch; gives rise to the right subclavian
artery and the right common carotid artery; supplies blood to the
head, neck, upper limb, and wall of the thoracic region
Subclavian
artery
The right subclavian artery arises from the brachiocephalic artery
while the left subclavian artery arises from the aortic arch; gives rise
to the internal thoracic, vertebral, and thyrocervical arteries; supplies
blood to the arms, chest, shoulders, back, and central nervous system
Internal
thoracic artery
Also called the mammary artery; arises from the subclavian artery;
supplies blood to the thymus, pericardium of the heart, and anterior
chest wall
Vertebral artery
Arises from the subclavian artery and passes through the vertebral
foramen through the foramen magnum to the brain; joins with the
internal carotid artery to form the arterial circle; supplies blood to the
brain and spinal cord
Thyrocervical
artery
Arises from the subclavian artery; supplies blood to the thyroid, the
cervical region, the upper back, and shoulder
Common
carotid artery
The right common carotid artery arises from the brachiocephalic
artery and the left common carotid artery arises from the aortic arch;
each gives rise to the external and internal carotid arteries; supplies
the respective sides of the head and neck
External carotid
artery
Arises from the common carotid artery; supplies blood to numerous
structures within the face, lower jaw, neck, esophagus, and larynx
Internal carotid
artery
Arises from the common carotid artery and begins with the carotid
sinus; goes through the carotid canal of the temporal bone to the base
of the brain; combines with the branches of the vertebral artery,
forming the arterial circle; supplies blood to the brain
VENOUS SYSTEM
• Series of veins located adjacent to arterial system

• Veins collect blood from the capillaries & terminal arterioles
• Acts as reservoir for blood
Major Veins of the Head and Neck
Vessel Description
Internal
jugular
vein
Parallel to the common carotid artery, which is more or less its counterpart, and
passes through the jugular foramen and canal; primarily drains blood from the
brain, receives the superficial facial vein, and empties into the subclavian vein
Temporal
vein
Drains blood from the temporal region and flows into the external jugular vein
Maxillary
vein
Drains blood from the maxillary region and flows into the external jugular vein
External
jugular
vein
Drains blood from the more superficial portions of the head, scalp, and cranial
regions, and leads to the subclavian vein
Veins of the
Thoracic Region
Vessel Description
Superior vena cava
Large systemic vein; drains blood from most areas superior to the diaphragm;
empties into the right atrium
Subclavian vein
Located deep in the thoracic cavity; formed by the axillary vein as it enters
the thoracic cavity from the axillary region; drains the axillary and smaller
local veins near the scapular region and leads to the brachiocephalic vein
Brachiocephalic
veins
Pair of veins that form from a fusion of the external and internal jugular veins
and the subclavian vein; subclavian, external and internal jugulars, vertebral,
and internal thoracic veins flow into it; drain the upper thoracic region and
lead to the superior vena cava

Vertebral vein
Arises from the base of the brain and the cervical region of the spinal cord;
passes through the intervertebral foramina in the cervical vertebrae; drains
smaller veins from the cranium, spinal cord, and vertebrae, and leads to the
brachiocephalic vein; counterpart of the vertebral artery
Internal thoracic
veins
Also called internal mammary veins; drain the anterior surface of the chest
wall and lead to the brachiocephalic vein
Intercostal vein Drains the muscles of the thoracic wall and leads to the azygos vein
Esophageal vein Drains the inferior portions of the esophagus and leads to the azygos vein
Bronchial vein Drains the systemic circulation from the lungs and leads to the azygos vein

CORONARY CIRCULATION
Coronary circulation is the circulation of blood in the blood vessels that supply the heart
muscle (myocardium). Coronary arteries supply oxygenated blood to the heart muscle, and cardiac veins drain
away the blood once it has been deoxygenated. Because the rest of the body, and most especially the brain,
needs a steady supply of oxygenated blood that is free of all but the slightest interruptions, the heart is required
to function continuously.
Therefore its circulation is of major importance not only to its own tissues but to the entire body and even
the level of consciousness of the brain from moment to moment. Interruptions of coronary circulation quickly
cause heart attacks (myocardial infarctions), in which the heart muscle is damaged by oxygen starvation. Such
interruptions are usually caused by ischemic heart disease (coronary artery disease) and sometimes
by embolism from other causes like obstruction in blood flow through vessels.

BRANCHES:
The following are the named branches of the coronary circulation in a right-dominant heart:
 Aorta
o Left coronary artery / Left main coronary artery (LMCA)
 Left circumflex artery (LCX)
 Obtuse marginal artery (OM1)
 Obtuse marginal artery (OM2)
 Left anterior descending artery (LAD)

 Diagonal artery
 Diagonal artery
o Right coronary artery (RCA)
 Atrioventricular nodal branch
 Right marginal artery
 Posterior descending artery (PDA)
 Posteriolateral artery

FUNCTIONS:
 Supply to papillary muscles
 Changes in diastole
 Changes in oxygen demand

HEMODYNAMICS AND
ELECTROPHYSIOLOGY OF HEART

HEMODYNAMICS OF HEART
Hemodynamic is composed of two-word hemo and Dynamics. Hemo mean blood and dynamics is flow rate
mechanism and physiology of blood. Hemodynamic is the study of blood flow. It focuses on how
the heart distributes or pumps blood throughout the body.
Hemodynamic monitoring refers to measurement of pressure, flow and oxygenation of blood within the
cardiovascular system. Hemodynamic monitoring measures the blood pressure inside the veins, heart, and
arteries. It also measures blood flow and how much oxygen is in the blood. It is a way to see how well the heart
is working. Hemodynamic monitoring plays an important role in the management of today's acutely ill patient.
Current hemodynamic monitoring therefore includes measurement of heart rate, arterial pressure, cardiac filling
pressures or volumes, cardiac output, and mixed venous oxygen saturation (SvO2) etc.
Heart rate: It is the number of times a heart beats in a minute. The normal resting heart rate for adults over the
age of 10 years, including older adults, is between 60 and 100 beats per minute (bpm). Highly trained athletes
may have a resting heart rate below 60 bpm, sometimes reaching 40 bpm.
Stroke volume: it is the amount of blood pumped by a ventricle when it contracts. The stroke volumes for each
ventricle are generally equal, both being approximately 70 mL in a healthy 70-kg man.
Its value is obtained by subtracting end-systolic volume (ESV) from end-diastolic volume (EDV) for a given
ventricle.
SV= EDV- ESV
=120-50 = 70 mL
In a healthy 70-kg man, ESV is approximately 50 mL and EDV is approximately 120mL, giving a
difference of 70 mL for the stroke volume

Cardiac output: It is the volume of blood the heart pumps per minute. Cardiac output is calculated by
multiplying the stroke volume by the heart rate. It is calculated using the following formula:
Cardiac Output = Heart Rate x Stroke Volume
Systemic vascular resistance: It is the resistance the heart must overcome to successfully pump blood through
the body. Systemic vascular resistance is the quantitative value for left ventricular afterload.
Systemic Vascular Resistance = 80x(Mean Arterial Pressure - Mean Venous Pressure or CVP) / Cardiac Output
Blood pressure: The force of circulating blood on the walls of the arteries. Blood pressure is taken using two
measurements: systolic (measured when the heart beats, when blood pressure is at its highest) and diastolic
(measured between heart beats, when blood pressure is at its lowest). Blood pressure is written with the systolic
blood pressure first, followed by the diastolic blood pressure (for example 120/80).
Central venous pressure (CVP): It is the blood pressure in the venae cavae, near the right atrium of the heart.
CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into
the arterial system. CVP is often a good approximation of right atrial pressure (RAP), although the two terms
are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium.
CVP and RAP can differ when arterial tone is altered. This can be graphically depicted as changes in the slope
of the venous return plotted against right atrial pressure (where central venous pressure increases, but right atrial
pressure stays the same; VR = CVP − RAP).
CVP has been, and often still is, used as a surrogate for preload, and changes in CVP in response to infusions
of intravenous fluid have been used to predict volume-responsiveness (i.e. whether more fluid will
improve cardiac output). However, there is increasing evidence that CVP, whether as an absolute value or in
terms of changes in response to fluid, does not correlate with ventricular volume (i.e. preload) or volume-

responsiveness, and so should not be used to guide intravenous fluid therapy. Nevertheless, CVP monitoring is a
useful tool to guide hemodynamic therapy.
Normal CVP in patients can be measured from two points of reference:
 Sternum: 0–14 cm H2O
 Midaxillary line: 8–15 cm H2O
CVP can be measured by connecting the patient's central venous catheter to a special infusion set which is
connected to a small diameter water column. If the water column is calibrated properly the height of the column
indicates the CVP.
In most intensive care units, facilities are available to measure CVP continuously.
Normal values vary between 4 and 12 cmH2O.
Site
Normal
pressure range
(in mmHg)
Central venous pressure 3–8
Right ventricular pressure
Systolic 15–30
Diastolic 3–8
Pulmonary artery pressure
Systolic 15–30
Diastolic 4–12
Pulmonary vein/
Pulmonary capillary wedge pressure
2–15
Left ventricular pressure
Systolic 100–140
Diastolic 3–12

PARAMETERS:
PARAMETER EQUATION NORMAL RANGE
Arterial Blood Pressure
(BP)
Systolic (SBP) 90 – 140 mmHg
Diastolic (DBP) 60 – 90 mmHg
Mean Arterial Pressure
(MAP)
(SBP + 2 x DBP)/3 70 – 105 mmHg
Systolic Pressure
Variation (SPV)
(SPmax-SPmin)
<5 mmHg unlikely to be preload
responsive
>5mmHg likely to be preload responsive
Pulse Pressure Variation
(PPV)
(PPmax-PPmin)/[(PPmax +
PPmin)/2] x100
<10% unlikely to be preload responsive
>13-15% likely to be preload responsive
Stroke Volume Variation
(SVV)
(SVmax-SVmin)/[(SVmax
+ SVmin)/2] x100
<10% unlikely to be preload responsive
>13-15% likely to be preload responsive
= averaged over 10 sec. of BP data updated every 4 beats
Right Atrial Pressure
(RAP)
2 – 6 mmHg
Right Ventricular
Pressure (RVP)
Systolic (RVSP) 15 – 25 mmHg
Diastolic (RVDP) 0 – 8 mmHg

Pulmonary Artery
Pressure (PAP)
Systolic (PASP) 15 – 25 mmHg
Diastolic (PADP) 8 – 15 mmHg
Mean Pulmonary Artery
Pressure (MPAP)
[PASP + (2 x PADP)]/3 10 – 20 mmHg
Pulmonary Artery Wedge
Pressure (PAWP)
6 – 12 mmHg
Left Atrial Pressure
(LAP)
6 – 12 mmHg
Cardiac Output (CO) HR x SV/1000 4.0 – 8.0 l/min
Cardiac Index (CI) CO/BSA 2.5 – 4.0 l/min/m2
Stroke Volume (SV) CO/HR x 1000 60 – 100 ml/beat
Stroke Volume Index
(SVI)
CI/HR x 1000 33 – 47 ml/m2/beat
Systemic Vascular
Resistance (SVR)
80 x (MAP – RAP)/CO 800 – 1200 dynes · sec/cm5
Systemic Vascular
Resistance Index (SVRI)
80 x (MAP – RAP)/CI 1970 – 2390 dynes · sec/cm5/m2
Pulmonary Vascular
Resistance (PVR)
80 x (MPAP – PAWP)/CO <250 dynes · sec/cm5

Pulmonary Vascular
Resistance Index (PVRI)
80 x (MPAP – PAWP)/CI 255 – 285 dynes · sec/cm5/m2
HEMODYNAMIC PARAMETERS – ADULT
Left Ventricular Stroke Work
(LVSW)
SV x (MAP – PAWP) x
0.0136
58 – 104 gm-m/beat
Left Ventricular Stroke Work Index
(LVSWI)
SVI x (MAP – PAWP)
x 0.0136
50 – 62 gm-m/m2/beat
Right Ventricular Stroke Work
(RVSW)
SV x (MPAP – RAP) x
0.0136
8 – 16 gm-m/beat
Right Ventricular Stroke Work
Index (RVSWI)
SVI x (MPAP – RAP) x
0.0136
5 – 10 gm-m/m2/beat
Coronary Artery Perfusion Pressure
(CPP)
Diastolic BP – PAWP 60 – 80 mmHg
Right Ventricular End-Diastolic
Volume (RVEDV)
SV/EF 100 – 160 ml
Right Ventricular End-Systolic
Volume (RVESV)
EDV – SV 50 – 100 ml
Right Ventricular Ejection Fraction
(RVEF)
SV/EDV 40 – 60%

Oxygenation Parameters – Adult
Partial Pressure of Arterial Oxygen
(PaO2)
80 – 100 mmHg
Partial Pressure of Arterial
CO2(PaCO2)
35 – 45 mmHg
Bicarbonate (HCO3) 22 – 28 mEg/1
Ph 7.38 – 7.42
Arterial Oxygen Saturation (SaO2) 95 – 100%
Mixed Venous Saturation (SvO2) 60 – 80%
Arterial Oxygen Content (CaO2)
(0.0138 x Hgb x SaO2) +
(0.0031 x PaO2)
17 – 20 ml/dl
Venous Oxygen Content (CvO2)
(0.0138 x Hgb x SvO2) +
(0.0031 x PvO2)
12 – 15 ml/dl
A-V Oxygen Content Difference
(C(a-v)O2)
CaO2 – CvO2 4 – 6 ml/dl
Oxygen Delivery (DO2) CaO2 x CO x 10 950-1150 ml/min
Oxygen Delivery Index (DO2I) CaO2 x CI x 10 500 – 600 ml/min/m2

Oxygen Consumption (VO2) (C(a – v)O2) x CO x 10 200 -250 ml/min
Oxygen Consumption Index (VO2I) (C(a – v)O2 x CI x 10 120 – 160 ml/min/m2
Oxygen Extraction Ratio (O2ER)
[(CaO2-CvO2)/CaO2] x
100
22 – 30%
Oxygen Extraction Index (O2EI)
[SaO2 – SvO2)/SaO2 x
100
20 – 25%
Hemodynamic monitoring:
General Principles of the Hemodynamic monitoring:
1. Hemodynamic monitoring involves assessment of several physiological parameters pertaining to the
circulatory system. With these parameters, the nurse (or doctor) attempts to interpret what physiological
characteristic of the circulatory system needs intervention: preload (blood volume), contractility
(myocardial contraction), or afterload (vascular resistance).
2. Hemodynamic monitoring involves more than tracking numbers and waveforms. The nurse must
also consider physical assessments of the patient and concurrent interventions while interpreting monitor
data.
3. Neverforget that a person is connected to all the monitoring equipment. It is easy for the nurse to
become absorbed in the technical data, the monitoring systems, and the problem-solving required for
hemodynamic management of the patient; but a real person exists in front of the nurse's face. That real
person needs the nurse's attention and presence as much as the monitors.
4. Single readings of data are not as significant as trends of data. Healthy patients do not have
pulmonary artery catheters. When this type of monitoring equipment is utilized, there are usually
significant pathophysiologies present. Therefore, readings are seldom within normal limits. The question
for the nurse is what is the expected range for this particular patient? Use the patient's own values for a
norm of reference for one's expected range.
5. The context of the readings are important. What were the previous readings? How has the patient
changed? What interventions occurred prior to this set of readings? How do the readings compare to the
physical assessment of the patient?

6. Know your equipment. It is the nurse's professional responsibility to know when equipment is
malfunctioning, to recognize critical situations with the equipment, and to respond appropriately to crises
associated with the equipment.
7. The phlebostatic axis on the patient is the anatomical landmarks which show placement of a transducer
level to the right atrium of the heart. (It is important for everyone to use the same location for leveling
than to change the location with every set of measurements. Remember that trends are more important
than single readings.) [Some procedure manuals specify half the distance of the anterior-posterior depth
instead of the midaxillary line.]
INVASIVE MONITORING SET-UP:
Monitoring hemodynamic pressures require the set up of invasive pressure monitoring tubing.
Equipment:
 Sterile sheets
 Personal Protective Equipment
 Pressure tubing with transducer(s)
 Swan ganz catheter
 Pressure bag
 Normal Saline (NS)–500 cc bag
 Heparin 1,000 units
 Invasive catheter
 Carpenter's level
 IV pole with transducer holder
 Monitoring system with matching cable for transducer
Pre- Procedure:
1. Explain the procedure to patient and their family member.

2. Informed consent should be taken by physician.
3. Preparation of environment and patient: Trolley setup, patient site, Cardiac monitor, privacy, clean the
site.
4. Mix 1,000 units of heparin into 500 cc bag of normal saline.
5. Label bag with date and added medication.
6. Tighten all connections on pressure tubing.
7. Spike NS bag and remove air from bag.
8. Insert pressure tubing spike into NS bag securely.
9. Fill drip chamber of tubing halfway.
10. Place pressure bag around NS bag.
11. Flush pressure tubing and all ports completely prior to inflating pressure bag.
12. Inflate pressure bag to 300 mm Hg.
13. Mount bag and transducer onto IV pole
Leveling the Transducer:
 Position the patient supine.
 Identify the phlebostatic axis (4th intercostal space, midaxillary line).
 Mark phlebostatic axis with indelible marker.
 Level the membrane of the transducer directly to the marked phlebostatic axis on the side of the
patient's chest.
Zeroing the Transducer:
 First level the transducer with the patient's phlebostatic axis.
 There's a stopcock immediately below the transducer on the patient's end of the pressure tubing.
 Turn the stopcock off to the patient and remove the yellow cap.
 Flush a little solution out of the stopcock (open to air if solution comes out).

 Press the button which will "zero" the transducer to air. When the transducer is zeroed, the pressure
reading on the monitor will drop to zero and the pressure waveform will flatten along the zero
baseline.
 Turn stopcock off to external port, which should leave the transducer directly open to the patient. If
you have done this correctly, the patient's waveform should show up on the monitor with the
patient's current pressure readings.
Intra Procedure:
1. Check all the equipment working properly.
2. Give proper positioning to patient.
3. Thorough hand washing.
4. Wear personal protective equipment.
5. Clean the procedure site with betadine solution.
6. Cover site and transducer with the sterile sheet.
7. Anasthise the procedure site with injection Lidocain 10% .
8. Check jugular vein through transducer.
9. Insert the CVP line.
10. Continue monitoring the vital sign.
11. Suture the CVP line.
12. Clean the area and apply tegaderm.
Post Procedure:
1. Termination of articles.
2. All-Inclusive Catheter Cart or Kits: Having a cart or kit that has all necessary equipment for
procedures reduces the risk of contamination of equipment when additional items are added to a sterile
field.
3. Hand Hygiene: For all nursing procedures involving a central venous catheter (changing tubing, adding
second infusion line, changing TPN solutions, IV administration of medication) the nursing care should
begin with thorough hand washing with soap and running water to reduce the risk of nosocomial
infections from other sources.
4. Site Care: Maintain a well adhesive transparent dressing over central venous catheters. Cath cares
should involve scrubs of site with chlorhexidine during dressing changes. Transparent dressings only
need to be changed every 7 days. Gauze dressings should be changed every 48 hours. Anytime a
dressing is damp, soiled, or coming loose, then it should be changed with a full skin prep prior to
application of a new dressing.
5. Line Access: The less frequently a central line is accessed from one of its ports (hubs), the higher the risk
of a bloodstream infection. Therefore, do not access a central venous catheter except for essential
procedures requiring the central line.
6. Scrub the Hub: When a hub on a central venous catheter infusion line is accessed, evidence does not
support chlorhexidine over 70% isopropyl alcohol. However, the duration of scrubbing the access hub
influences the risk. Performing a twisting scrubbing motion for 30 seconds with a
disinfectant significantly reduces bloodstream infections.

7. Replacement of IV Administration Sets (Tubing): Replacement of central line tubing every 72 hours is
not associated with lower infection rates compared to 96 hours. Replacement of tubing should be done
with strict asepsis. Special infusions like lipids or TPN may require more frequent tubing changes
because the fluid medium is a greater risk for infection.
8. Appropriate Staffing and Nursing Workloads: Evidence has indicated that the higher the nursing
workloads or the more inadequate the staffing, the less time that is available for safe management of
central venous catheters.
Guidelines for the Prevention of Intravascular Catheter-Related Infections
1. Hand Hygiene: Thorough handwashing prior to insertion or handling of central venous catheters will
reduce risk of nosocomial infections.
2. Maximal Barrier Protection: The insertion of a central venous catheter should be done under sterile
(surgical asepsis) conditions. The clinician inserting the catheter should wear mask, cap, sterile gloves,
and sterile gown. The patient should be draped in a sterile field around the insertion site. Assistants (e.g.,
nurses) should wear masks, protective gowns, and gloves while in the area–if the nurse will be working
with the sterile equipment or supplies, the nurse should wear sterile gown, mask, cap, and sterile gloves
too.
3. Chlorhexidine Skin Antisepsis: Chlorhexidine has been shown to reduce more skin normal flora than
povidone-iodine or alcohol as a skin disinfectant prep prior to insertion of a central venous line.
4. Optimal Catheter-Site Selection: Rates of catheter-related bloodstream infections are lowest among
catheters inserted into subclavian vein compared to internal jugular vein. Femoral vein insertions should
be avoided if possible due to the high rates of bloodstream infections associated with the inguinal area.
5. Daily Medical Reviewof Necessity of Catheter: The medical physician should review daily the need
for a central venous catheter with the goal of early removal as soon as the patient no longer needs the
catheter. The longer a catheter is retained, the higher the probability of bloodstream infection. The nurse
can bring this to the physician's attention during rounds as to whether any critical interventions like TPN
or hemodynamic monitoring is occurring that needs a central venous catheter.
6. Replacement of Catheter: Recent evidence suggests that the rate of infections are not significantly
different when catheters are replaced every 72 hours or less.
Complication of Central venous pressure:
 Bleeding and infection.
 Complications, such as pneumothorax,
 hemothorax,
 arterial puncture
 intrapleural infusion
 infection
 hematoma
 Collapse of a lung is a rare complication of central venous catheters.

ELECTROPHYSIOLOGY OF HEART
The contraction and relaxation of the cardiac muscle follows a specific synchronized pattern
between the atria and ventricles. It includes cardiac cell, depolarization and repolarization, action potential,
refractory and supernormal period, conduction system, Ectopic beats and arrhythmias and automaticity.
1. Cardiac cells:– two types, electrical and myocardial (“working")
A) Electrical cells
a) Make up the conduction system of the heart
b) Are distributed in an orderly fashion through the heart
c) It possess specific properties:
 Automaticity – the ability to spontaneously generate and discharge an electrical impulse
 Excitability – the ability of the cell to respond to an electrical impulse
 Conductivity – the ability to transmit an electrical impulse from one cell to the next
B) Myocardial cells
a) Make up the muscular walls of the atrium and ventricles of the heart
b) It possess specific properties:
 contractility – the ability of the cell to shorten and lengthen its fibers
 extensibility – the ability of the cell to stretch

2. Depolarization and Repolarization
o Cardiac cells at rest are considered polarized, meaning no electrical activity takes place
o The cell membrane of the cardiac muscle cell separates different concentrations of ions, such as
sodium, potassium, and calcium. This is called the resting potential
o Electrical impulses are generated by automaticity of specialized cardiac cells
o Once an electrical cell generates an electrical impulse, this electrical impulse causes the ions to
cross the cell membrane and causes the action potential, also called depolarization
o The movement of ions across the cell membrane through sodium, potassium and calcium
channels, is the drive that causes contraction of the cardiac cells/muscle
o Depolarization with corresponding contraction of myocardial muscle moves as a wave through
the heart
o Repolarization is the return of the ions to their previous resting state, which corresponds with
relaxation of the myocardial muscle
o Depolarization and repolarization are electrical activities which cause muscular activity
o The action potential curve shows the electrical changes in the myocardial cell during the
depolarization – repolarization cycle
o This electrical activity is what is detected on ECG, not the muscular activity

3. Action Potential
 The action potential curve consists of 5 phases (0 to 4)
 The 5 phases:
a) Phase 4 – rest
o This is the cells resting phase
o The cell is ready to receive an electrical stimulus
b) Phase 0 – upstroke
o It is characterized by a sharp, tall upstroke of the action potential
o The cell receives an impulse from a neighboring cell and depolarizes
o During this phase the cell depolarizes and begins to contract
c) Phase 1 – spike
o Contraction is in process
o The cell begins an early, rapid, partial repolarization
d) Phase 2 – plateau

o Contraction completes, and the cell begins relaxing
o This is a prolonged phase of slow repolarization
e) Phase 3 – downslope
o This is the final phase of rapid repolarization
o Repolarization is complete by the end of phase 3
f) Phase 4 – rest
o Return to the rest period
o The period between action potentials
4. Refractory and supernormal periods
a) Absolute refractory period
o a period in which no stimulus, no matter how strong, can cause another depolarization
o onset of phase 0 begin the absolute refractory period, and extends midway through phase 3
o begins with the onset of the Q wave and ends at about the peak of the T wave
b) Relative refractory period
o the cell has partially repolarized, so a very strong stimulus could cause a depolarization
o also called the vulnerable period of repolarization (a strong stimulus occurring during the
vulnerable period may push aside the primary pacemaker and take over pacemaker control)
o occurs in the 2nd half of phase 3
o corresponds with the downslope of the T wave

c) Supernormal period
o near the end of the T wave, just before the cell returns to its resting potential
o is NOT a normal period in a healthy heart
o a period in which a stimulus weaker than normally required can cause a depolarization
o this is a short period at the very end of phase 3 into early phase 4
o extends the relative refractory period
5. Conduction system
A. Inherent firing rate is the rate at which the SA node or another pacemaker site normally generates
electrical impulses
B. SA Node - Sinoatrial node
o Dominant or primary pacemaker of the heart
o Inherent rate 60 – 100 beats per minute
o Located in the wall of the right atrium, near the inlet of the superior vena cava
o Once an impulse is initiated, it usually follows a specific path through the heart, and usually does
not flow backward
C. Intra-atrial tracts - Bachmann's bundle
As the electrical impulse leaves the SA node, it is conducted through the left atria by way of the
Bachmann's bundles, through the right atria, via the atrial tracts
D. AV Junction - Made up of the AV node and the bundle of His
a). AV node

 Is responsible for delaying the impulses that reach it
 Located in the lower right atrium near the interatrial septum
 Waits for the completion of atrial emptying and ventricular filling, to allow the cardiac
muscle to stretch to it's fullest for peak cardiac output
 The nodal tissue itself has no pacemaker cells, the tissue surrounding it (called the
junctional tissue) contains pacemaker cells that can fire at an inherent rate of 40 – 60
beats per minute.
b) Bundle of His
 Resumes rapid conduction of the impulses through the ventricles
 Makes up the distal part of the AV junction then extends into the ventricles next to the
interventricular septum
 Divides into the Right and Left bundle branches.
c) Purkinje Fibers
 Conduct impulses rapidly through the muscle to assist in depolarization and contraction
 Can also serve as a pacemaker, discharges at an inherent rate of 20 – 40 beats per minute
or even more slowly
 Are not usually activated as a pacemaker unless conduction through the bundle of His
becomes blocked or a higher pacemaker such as the SA node or AV junction do not
generate an impulse
 Extends form the bundle branches into the endocardium and deep into the myocardial
tissue

6. Ectopic beats & arrhythmias
A. Any cardiac impulse originating outside the SA node is considered abnormal and is referred
to as an ectopic beat
B. Ectopic beats can originate in the atria, the AV junction, or the ventricles, and are named
according to their point of origin
C. Rate suppression can occur following an ectopic beat, but after several cycles return to basic
rate
D. A series of 3 or more consecutive ectopic beats is considered a rhythm
E. The two causes for ectopic beats include:
a) Failure or excessive slowing of the SA node
 ectopic beats resulting from sinus node failure serve as a protective function by
initiating a cardiac impulse before prolonged cardiac standstill can occur; these
beats are called escape beats
 if the sinus node fails to resume normal function, the ectopic site will assume the
role of pacemaker and sustain a cardiac rhythm; this is referred to as an escape
rhythm
 after the sinus node resumes normal function, the escape focus is suppressed
b) Premature activation of another cardiac site
 impulses occur prematurely before the sinus node recovers enough to initiate
another beat; these beats are called premature beats
 premature beats are produced by either increased automaticity, or by reentry
c) Abnormal conduction system
7. Automaticity
A. Special characteristic of cardiac cells to generate impulses automatically
B. If the cell automaticity is increased or decreased an arrhythmia can occur

a) Reentry events – Reexcitation of a region of cardiac tissue by a single impulse,
continuing for one or more cycles and sometimes resulting in ectopic beats or
tachyarrhythmias.
b) Retrograde conduction
 When an impulse begins below the AV node
 Can be transmitted backward toward the AV node
 Conduction usually takes longer than normal and can cause the atria and ventricles
to be “out of synch”.
Normal adult 12-lead ECG
Electrocardiography is the process of producing an electrocardiogram. It is a graph of voltage versus time of the
electrical activity of the heart using electrodes placed on the skin. These electrodes detect the small electrical
changes that are a consequence of cardiac muscle depolarization followed by repolarization during each cardiac
cycle (heartbeat).

 normal sinus rhythm
 each P wave is followed by a QRS
 P waves normal for the subject
 P wave rate 60 - 100 bpm with <10% variation
 rate <60 = sinus bradycardia
 rate >100 = sinus tachycardia
 variation >10% = sinus arrhythmia
 normal QRS axis
 normal P waves
 height < 2.5 mm in lead II
 width < 0.11 s in lead II
 for abnormal P waves see right atrial hypertrophy, left atrial hypertrophy, atrial premature
beat, hyperkalaemia
 normal PR interval
 0.12 to 0.20 s (3 - 5 small squares)
 for short PR segment consider Wolff-Parkinson-White syndrome or Lown-
Ganong-Levine syndrome (other causes - Duchenne muscular dystrophy, type II
glycogen storage disease (Pompe's), HOCM)

 for long PR interval see first degree heart block and 'trifasicular' block
 normal QRS complex
 < 0.12 s duration (3 small squares)
 for abnormally wide QRS consider right or left bundle branch block, ventricular
rhythm, hyperkalaemia, etc.
 no pathological Q waves
 no evidence of left or right ventricular hypertrophy
 normal QT interval
 Calculate the corrected QT interval (QTc) by dividing the QT interval by the square root
of the preceeding R - R interval. Normal = 0.42 s.
 Causes of long QT interval
 myocardial infarction, myocarditis, diffuse myocardial disease
 hypocalcaemia, hypothyrodism
 subarachnoid haemorrhage, intracerebral haemorrhage
 drugs (e.g. sotalol, amiodarone)
 hereditary
 Romano Ward syndrome (autosomal dominant)
 Jervill + Lange Nielson syndrome (autosomal recessive) associated with
sensorineural deafness
 normal ST segment
o no elevation or depression
 causes of elevation include acute MI (e.g. anterior, inferior), left bundle branch block,
normal variants (e.g. athletic heart, Edeiken pattern, high-take off), acute pericarditis
 causes of depression include myocardial ischaemia, digoxin effect, ventricular
hypertrophy, acute posterior MI, pulmonary embolus, left bundle branch block
 normal T wave
 causes of tall T waves include hyperkalaemia, hyperacute myocardial infarction and left
bundle branch block
 causes of small, flattened or inverted T waves are numerous and include ischaemia, age,
race, hyperventilation, anxiety, drinking iced water, LVH, drugs (e.g. digoxin),
pericarditis, PE, intraventricular conduction delay (e.g. RBBB)and electrolyte
disturbance.
 normal U wave

BIO-CHEMISTRY OF BLOOD IN RELATION TO
CARDIO PULMONARY FUNCTION

BIO-CHEMISTRY OF BLOOD IN RELATION TO CARDIO PULMONARY FUNCTION
Biochemistry of the blood gives us an indication of what is happening with in the body. When different
tissues are damaged the damaged cells release specific enzymes which our equipment detects as abnormal
levels. This then helps localise the problem.
Cardiac Hormone:
ANP and BNP are secreted by the heart and act as cardiac hormones. Human ANP has three molecular forms:
α-ANP, β-ANP, and proANP (or γ-ANP). ProANP and β-ANP are minor forms but are increased in patients
with heart failure. ProBNP is secreted by the heart and is increased in patients with heart failure. C-type
natriuretic peptide (CNP) is the most conserved member of the mammalian natriuretic peptide family, and is
implicated in the endocrine regulation of growth, metabolism and reproduction. CNP is expressed throughout
the body, but is particularly abundant in the central nervous system and anterior pituitary gland. ANP, BNP and
CNP are involved in the maintainance of the electrolyte fluid balance and vascular tone, they promote
natriuresis and diuresis resulting in loss of sodium and water thereby lowering blood volume and blood
pressure.

Important assays that are carried out in cardiac disease are:
1 Creatine Phosphokinase/ Creatine Kinase (CK)
2 Aspartate Transaminase
3 Lactate Dehydrogenase
4 Gamma- Glutamyl Transpeptidase
5 Troponins
6 Myoglobin
1.) CREATINE PHOSPHOKINASE/ CREATINE KINASE (CK)
This test measures the amount of creatine kinase (CK) in the blood. CK is a type of protein, known as an
enzyme. It is mostly found in skeletal muscles and heart, with lesser amounts in the brain. Skeletal
muscles are the muscles attached to the skeleton. They work with bones to help move and give body
power and strength. Heart muscles pump blood in and out of the heart.
There are three types of CK enzymes:
 CK-MM, found mostly in skeletal muscles
 CK-MB, found mostly in the heart muscle
 CK-BB, found mostly in brain tissue
NORMAL VALUE:

 The CPK normal range for a male is between 39 – 308 U/L,
 Females the CPK normal range is between 26 – 192 U/L.
RESULT:
A small amount of CK in the blood is normal. Higher amounts can mean a health problem. It can mean person
have damage or disease of the skeletal muscles, heart, or brain. If results show have a higher-than-normal level
of CK, it may mean person have an injury or disease of the muscles, heart, or brain.
 If higher than normal CK-MM enzymes, it may mean person have a muscle injury or disease, such as
muscular dystrophy or rhabdomyolysis.
 If higher than normal CK-MB enzymes, it may mean person have an inflammation of the heart muscle
or are having or recently had a heart attack. It is more sensitive for finding heart damage from a heart
attack. CK-MB rises 4 to 6 hours after a heart attack. But it is generally back to normal in a day or two.
 If higher than normal CK-BB enzymes, it may mean person have had a stroke or brain injury.
2) ASPARTATE AMINOTRANSFERASE (AST)
This enzyme is found in the cell cytoplasm and mitochondria where it catalyses amino acid activity. AST is
found in all tissues. Raised levels of this enzyme are found in approximately 70 per cent of MI patients.
Although it is less specific than the CK-MB assay, it is quick and inexpensive. AST is also elevated in liver
disease, pulmonary embolism, skeletal muscle injury, shock or intramuscular injections.
Normal findings
Adults: 0-35 units/L or 0-0. 58 μKat/L (SI units) (Values tend to be slightly lower in females than males
3) LACTATE DEHYDROGENASE:
LDH catalyses the conversion of lactate to pyruvate, providing adenosine triphosphate (ATP) for energy during
periods of anaerobic metabolism within cells. LDH is often used to confirm the diagnosis of acute MI,
established by CK-MB. LDH may also be elevated in haemolysis, leukaemia, megablastic anaemia and renal
disease.
Normal LDH levels range from 140 units per liter (U/L) to 280 U/L or 2.34 mkat/L to 4.68 mkat/L.
4) GAMMA- GLUTAMYL TRANSPEPTIDASE
Gamma-glutamyl transferase (GGT) is an enzyme located on the external surface of cellular membranes.
Increased GGT activity is a marker of antioxidant inadequacy and increased oxidative stress. Elevated GGT
activity is associated with increased risk of cardiovascular disease (CVD) such as coronary heart disease (CHD),
stroke, arterial hypertension, heart failure, cardiac arrhythmias and all-cause and CVD-related mortality. The
evidence is weaker for an association between elevated GGT activity and acute ischemic events and myocardial
infarction.
Normal value:
Male and female age 45 years and older: 8-38 units/L or 8-38 international units (IU)/L (SI units

5) TROPONIN:
Troponins are a group of protein found in skeletal and heart (cardiac) muscle fibers that regulate muscular
contraction. Troponin tests measure the level of cardiac-specific troponin in the blood to help detect heart
injury.
There are three types of troponin proteins:
 Troponin C
 Troponin T
 Troponin I.
Troponin C initiates contraction by binding calcium and moves troponin I so that the two proteins that pull the
muscle fiber shorter can interact. Troponin T anchors the troponin complex to the muscle fiber structure. There
is little or no difference in troponin C between skeletal and cardiac muscle, but the forms of troponin I and
troponin T are different. Measuring the amount of cardiac-specific troponin T or troponin I in the blood can help
identify individuals who have experienced damage to their heart.
The test is most often used to diagnose a heart attack. It is sometimes used to monitor angina, a condition that
limits blood flow to the heart and causes chest pain, Angina sometimes leads to a heart attack.
NORMAL VALUE:
 Normal range: below 0.04 ng/ml
 Probable heart attack: above 0.40 ng/ml
Having a result between 0.04 and 0.39 ng/ml often indicates a problem with the heart. However, a very small
number of healthy people have higher than average levels of troponin. So, the doctor may check for other
symptoms and order further tests before making a diagnosis
6) MYOGLOBIN
Myoglobin is a protein in heart and skeletal muscles. Myoglobin has oxygen attached to it, which provides
extra oxygen for the muscles to keep at a high level of activity for a longer period. When muscle is damaged,
myoglobin in muscle cells is released into the bloodstream. The kidneys help remove myoglobin from the
blood into the urine. When the level of myoglobin is too high, it can damage the kidneys. Myoglobin is
sometimes measured in addition to troponin to help diagnose a heart attack. It is also not very specific for
finding a heart attack.
Normal Results
The normal range is 25 to 72 ng/mL (1.28 to 3.67 nmol/L).
An increased level of myoglobin may be due to:
 Heart attack
 Malignant hyperthermia (very rare)
 Disorder that causes muscle weakness and loss of muscle tissue (muscular dystrophy)

 Breakdown of muscle tissue that leads to the release of muscle fiber contents into the blood
(rhabdomyolysis)
 Skeletal muscle inflammation (myositis)
 Skeletal muscle ischemia (oxygen deficiency)
 Skeletal muscle trauma
ELECTROLYTES IN CARDIAC SYSTEM
Electrolyte balance in the event of heart failure Electrolytes or ions are charged particles in body fluids that help
transmit electrical impulses for proper nerve, heart and muscle function. The number of positive ions called
cations and negative ions called anions is supposed to be equal. Anything that upsets this balance can have life
threatening consequences.
1) Sodium: Sodium is the most abundant cation in the extracellular fluids, play a key role in transmitting
nerve impulses. It also helps maintaining serum concentration or osmolality. Hypernatremia, occurs
when either too much water is lost or too much salt is taken in. The elderly is particularly at risk for
hypernatremia following surgery or a fever because of volume depletion and because of diminished
thirst mechanism.
2) Potassium: This electrolyte is the major intracellular cation. The 2% that is found in extracellular fluid
is crucial to neuromuscular and cardiac function. Severe Hyperkalemia will slow cardiac impulse
conduction, producing changes in ECG. Left untreated, the excess potassium will continue to supress
conduction until cardiac arrest occurs.
3) Magnesium: This cation is found primarily in the cells and is responsible for reactions that involve
muscle function, energy production and carbohydrate and protein metabolism. Renal failure is the major
cause of hypermagnesemia.
4) Calcium and Phosphorus: These electrolytes are inversely related in the blood. When calcium levels
are high, phosphorus levels are low and vice-versa. Calcium is a cation with multiple functions,
including transmitting nerve impulses, maintaining cell wall permeability and activating the body’s
clotting mechanism. It is also involved in contracting cardiac and smooth muscle, generating cardiac
impulses, mediating cardiac pacemaker function and forming bones and teeth. Phosphorus, the major
intracellular anion, is necessary for energy production in the cells and for carbohydrate, protein and fat
metabolism, as well. They also helps maintain acid-base balance by buffering hydrogen ions.
5) Chlorides and bicarbonates: These are the major extracellular anions. While both play an important
role in maintaining acid-base balance, bicarbonate is by far the start of the show. Bicarbonate is the
body’s major buffer system. It helps keep the ratio between acids and bases in a tight range that’s
numerically expressed as the pH.

Electrolyte imbalance is one possible cause of abnormal heart rhythms or arrhythmias. The electrical
system of the heart depends on the right amount of electrolytes to function in rhythm, force and rate to
provide adequate blood supply throughout the body. Congestive heart failure treatment may include
medicines to increase the heart functions such as vasodilators, inotropics, beta-blockers and angiotensin II
receptor blockers.
 Pulmonary Artery Pressure
Pulmonary Artery Pressure (PAP) is one of the most commonly measured parameters during a cardiac
catheterization. Mean PAP, systolic PAP and diastolic PAP are often derived by visually marking the waveform
output by a fluid-filled transducer. Normal pulmonary artery pressure is 8-20 mm Hg at rest. If the pressure in
the pulmonary artery is greater than 25 mm Hg at rest or 30 mmHg during physical activity, it is abnormally
high and is called pulmonary hypertension
Pulmonary capillary wedge pressure (PCWP) provides an indirect estimate of left atrial pressure (LAP).
Although left ventricular pressure can be directly measured by placing a catheter within the left ventricle, it is
not feasible to advance this catheter back into the left atrium.
PCWP is measured by inserting balloon-tipped, multi-lumen catheter (Swan-Ganz catheter) into a peripheral
vein (e.g., jugular or femoral vein), then advancing the catheter into the right atrium, right ventricle, pulmonary
artery, and then into a branch of the pulmonary artery.
The catheter has a lumen (port) that opens at the tip of the catheter distal to the balloon.

This port is connected to a pressure transducer. As illustrated below, the location of the catheter can be
determined by viewing the pressure measured from the tip of the catheter.
In the right atrium, the pressure usually averages <5 mmHg and fluctuates a few mmHg.
When the catheter is advanced into the right ventricle, the systolic pressure increases to ~25 mmHg and the
diastolic pressure remains similar to right atrial diastolic pressure.
When the catheter enters the pulmonary artery, the systolic pressure normally is similar to the right ventricular
systolic pressure, but the diastolic pressure increases to about 10 mmHg because of pulmonic valve closure at
the beginning of diastole.
Just behind the tip of the catheter is a small balloon that can be inflated with air (~1 cc). When properly
positioned in a branch of the pulmonary artery, the distal port measures pulmonary artery pressure (~ 25/10
mmHg; systolic/diastolic pressure).
The balloon is then inflated, which occludes the branch of the pulmonary artery. When this occurs, the pressure
in the distal port rapidly falls, and after several seconds, reaches a stable lower value that is very similar to left
atrial pressure (mean pressure normally 8-10 mmHg).
The pressure flucuates during the cardiac cycle and normally shows a, c and v waves similar to the right atrial
pressure tracing. The balloon is then deflated. The same catheter can be used to measure cardiac output by the
thermodilution technique.e
Respiratory (lung) volumes and capacities:
1. Tidal volume (TV): It is the amount of air that can be inhaled and exhaled during one normal (quiet)
breathing cycle (about 500 ml for men & women).

Tidal volume
2. Inspiratory reserve volume (IRV): It is the amount of air that can be forcibly inhaled beyond a tidal
inhalation (about 3,000 ml for men & 2,000 ml for women).
Inspiratory Reserve Volume
3. Expiratory reserve volume (ERV): It is the amount of air that can be forcibly exhaled beyond a tidal
exhalation (about 1200 ml for men & 700 ml for women).

Expiratory Reserve Volume
4. Residual Volume (RV): The amount of air remaining in the lungs after an ERV (= about 1,200 ml in
men & women).
5. Minute volume of respiration: Total air taken in during one minute.
Tidal volume× respiratory rate
500× 𝟏𝟐 = 𝟔000ml/min
In 1 minute about 6 liters of air is moved into and out of lungs white at rest.
CAPACITIES:
Sum of two or more pulmonary volume is capacities.
1. Inspiratory capacity = TV + IRV.
500+3100=3600ml
2. Functional reserve capacity = ERV + RV.
1200+1200=2400ml
3. Vital capacity = TV + IRV + ERV.
3100+500 +1200=4800ml
4. Total lung capacity = RV + VC.
1200+4800=6000ml

BLOOD COMPONENT VALUES
S.NO. BLOOD COMPONENT NORMAL VALUE
1. Complete Blood Count:
White Blood Cells 4500-11,000/mm3
Red Blood Cells Male: 4.3-5.9 million/mm3
Female : 3.5-5.5 million/mm3
Hemoglobin Male: 13.5-17.5 g/dl
Female : 12.0-16.0 g/dl
Hematocrit Male: 41%-53 %
Female : 36%-46%
Mean corpuscular volume 80-100μm3
Mean corpuscular hemoglobin 25.4-34.6 pg/cell
Mean corpuscular hemoglobin concentration 31%- Hb/cell
Platelets 150,000-400,000/ mm3
Differential Count:
Neutrophil 50%-70%
Eosinophils 1%-3%
Basophils 0%- 1%

Lymphocytes 25%-35%
Monocytes 4%-6%
2. Renal Function Test:
Serum Creatinine Male: 0.7-1.3 mg/dl
Female: 0.6-1.1 mg/dl
Creatinine Clearance Male: 97-137 ml/min
Female: 88-128 ml/min
Glomerular Filtration Rate 90-140ml/min/1.73m2
Urine Albumin 0-8 mg/dl
Urine Microalbumin <30 mg
Albumin to Creatinine ratio <30 mg/gm
Sodium 136-145mmol/L
Potassium 3.5-5.1mmol/L
Blood Urea Nitrogen 7-20 mg/dl
Chloride 98-107 mmol/L
Urea 3.0-9.2 mmol/L
3. Liver Function Test
Total bilirubin 03- 1 mg/dl
Bilirubin Conjugated <0.2mg
Total Protein 6.0-8.3g/dl
Albumin 3.5-5.5 g/dl
AST/ SGOT(Aspartate transaminase) <35units/L
ALT/ SGPT(Alanine transaminase) <35units/L
GGTP(γ- glutamyl transpeptidase) 1-94 units/L
AG ratio >1
Prothrombin time(PT) 12-16 sec
Alkaline phosphatase 25-112Iu/L
Globulin 2-3.5gm/dl

4.
Lipid Profile
Serum Cholesterol <200 mg/dl
Serum Triglyceride <150 mg/dl
Serum HDL >60 mg/dl
Serum LDL <130 mg/dl
Serum VLDL <30 mg/dl
5. Cardiac Enzymes
Creatinine Phosphokinase (CPK) 29-90 U/L
Myoglobin 25-72ng/mL
CKMB 5-25IU/L
Troponin I 0-0.4ng/mL
6. Thyroid test
TSH 0.4-4.0 mIU/L
Total T4 5.4-11.5mcg/dL
Free T4 0.7-1.8 ng/dL
Total T3 80-220 ng/dL
Free T3 260-480 pg/dL
7. Blood Sugar Level
Fasting 80-100mg/dL
Random <200 mg/dL
Post Prandial <140 mg/dL
Glycosylated Hemoglobin (HbA1c) 6.5%-8%
8. Immunoglobulins
IgG 640-1430 mg/dL (6.4-14.3 g/L)
IgA 70-300 mg/dL (0.7-3.0 g/L)
IgM 20-140 mg/dL (0.2-1.4 g/L)

IgD Less than 8 mg/dL (80 mg/L)
IgE 0.01-0.04 mg/dL (0.1-0.4 mg/L)
9. Iron studies
Ferritin, serum 15-200 ng/mL (15-200 mg/L)
Iron, serum 60-160 µg/dL (11-29 µmol/L)
Iron-binding capacity, total, serum 250-460 µg/dL (45-82 µmol/L)
Lipase, serum Less than 95 U/L
Transferrin saturation 20%-50%
Lactate dehydrogenase,serum 60-100 U/L
Lactic acid, venous blood 6-16 mg/dL (0.67-1.8 mmol/L)
10. Hematology
Activated partial thromboplastin time 25-35 sec.
Bleeding time Less than 10 min
Erythrocyte count 4.2-5.9 ×106/µL (4.2-5.9 x
1012cells/L)
Erythrocyte sedimentation rate Male: 0-15 mm/h
Female: 0-20 mm/h
Erythropoietin less than 30 mU/mL (30 U/L)
D-Dimer less than 0.5 µg/mL (500 mg/L)
Prothrombin Time 11-13.5 sec.
INR 0.8-1.1 sec.

Review on Anatomy and Physiology of cardiovascular system.

Review on Anatomy and Physiology of cardiovascular system.

Recomendados

Recomendados

Más contenido relacionado

La actualidad más candente

La actualidad más candente (20)

Similar a Review on Anatomy and Physiology of cardiovascular system.

Similar a Review on Anatomy and Physiology of cardiovascular system. (20)

Más de DR .PALLAVI PATHANIA

Más de DR .PALLAVI PATHANIA (20)

Último

Último (20)

Review on Anatomy and Physiology of cardiovascular system.