 The heart is located in the
Week 1
DISTURBANCES IN OXYGENATION
COMPONENTS INVOLVED IN
OXYGENATION
 Heart
 Pumps blood throughout the body
 Supply O2 to the body
 primary purpose: PUMPING
BLOOD
 Found left slightly of the sternum
 5th intercostal space
 Mediastinum
The Following Are The Functions Of The
Heart:
 Generating blood pressure.
Contractions of the heart generate blood
pressure, which is responsible for moving
blood through the blood vessels.
 Routing blood.
The heart separates the pulmonary and
systemic circulations and ensures better
oxygenation of the blood flowing to the
tissues.
 Ensuring one-way blood flow.
The valves of the heart ensure a one-way
flow of blood through the heart and blood
vessels.
 Regulating blood supply.
The rate and force of heart contractions
change to meet the metabolic needs of the
tissues, which vary depending on such
conditions as rest, exercise, and changes in
body position.
 Lungs
 Bring O2 to our bodies and send
CO2 out of the body.
 Red Blood Cells
 A RBC picks up and carry oxygen
from the lungs to the tissues in the
body.
 Blood Vessels
 Deliver blood rich in oxygen to the
organs and tissues in body.
ANATOMY OF THE HEART
 The heart is a cone shaped, hollow,
muscular organ located in the center
of the thorax, where it occupies the
space between the lungs
(mediastinum) and rests on the
diaphragm.
mediastinum , a midline partition of
the thoracic cavity that also contains
the trachea, the esophagus, the
thymus, and associated structures.
 It weighs approximately 300 g (10.6 oz);
the weight and size of the heart are
influenced by age, gender, body
weight, extent of physical exercise
and conditioning, and heart disease.
 The heart pumps blood to the tissues,
supplying them with oxygen and other
nutrients.
 Pumps about 60ml/beat or 5L/min
 Pericardium – protective covering of the
heart
 The heart is encased in a thin, fibrous
sac called the pericardium, which is
composed of two layers.
 Adhering to the epicardium is the
visceral pericardium.
 Enveloping the visceral pericardium is
the parietal pericardium, a tough fibrous
tissue that attaches to the great vessels,
diaphragm, sternum, and vertebral
column and supports the heart in the
mediastinum.
 The space between these two layers
(pericardial space) is normally filled with
about 20 mL of fluid, which lubricates
the surface of the heart and reduces
friction during systole.
 ADDITIONAL NOTES ABOUT
PERICARDIUM:
 The pericardium, or pericardial sac,
is a double-layered, closed sac that
surrounds the heart
 It consists of two layers: the outer
fibrous pericardium and inner
serous pericardium.
 The fibrous pericardium is a tough,
fibrous connective tissue layer that
 prevents overdistension of the pericardial sac and during
heart and anchors it within the systole
mediastinum. Superiorly, the  20 ml
fibrous pericardium is  Pericardial Effusion -
continuous with the connective madaming fluid
tissue coverings of the great  Cardiac Tamponade -
vessels, and inferiorly it is sumobra sa dami ng fluid
attached to the surface of the  Pericardial Friction Rub
diaphragm.  Muffled heart sounds
 The serous pericardium is a layer  Distant Lub Dub
of simple squamous epithelium. The  Lub = Closure of
serous pericardium is further divided Tricuspid and
into two parts. Mitral
 The part of the serous  S1
pericardium lining the fibrous  Ventricle
pericardium and attached to Pump /
the great vessels, diaphragm, Ejection
sternum and vertebral  Systole
column and the one that  Dub = Closure of
supports the heart in the Aortic and
mediastinum is the parietal Pulmonic
pericardium  Ventricle
 The part covering the heart Relax / Filling
surface is the visceral  S2
pericardium, or epicardium  Cardiac tamponade is a
 The parietal and visceral portions of potentially fatal condition in
the serous pericardium are which a large volume of
continuous with each other where fluid or blood
the great vessels enter or leave the accumulates in the
heart. pericardial cavity and
compresses the heart
from the outside.
 Although the heart is a
powerful muscle, it relaxes
passively.
 When it is compressed by
fluid within the pericardial
cavity, it cannot expand
when the cardiac muscle
relaxes.
 Consequently, it cannot fill
with blood during
relaxation; therefore, it
cannot pump blood.
 Cardiac tamponade can
cause a person to die
quickly unless the fluid is
 The space between the visceral and removed.
parietal pericardia is the pericardial  Causes of cardiac
cavity and it is filled with a thin layer tamponade include
of serous pericardial fluid. rupture of the heart wall
 This fluid helps reduce friction following a myocardial
as the heart moves within the infarction, rupture of
blood vessels in the
 pericardium after a
malignant tumor has
invaded the area,
damage to the
pericardium due to
radiation therapy, and
trauma, such as that
resulting from a traffic
accident.
 Pericarditis is an inflammation
of the serous pericardium.
 The cause is frequently
unknown, but it can result from
infection, diseases of
connective tissue, or damage
due to radiation treatment for
cancer.
 The condition can cause
extremely painful sensations
that are referred to the back
and chest and can be confused
with a myocardial infarction
(heart attack).
 Pericarditis can lead to fluid
accumulation within the
pericardial sac.
ADDITIONAL NOTES:
 The adult heart is shaped like a blunt
cone and is approximately the size of a
closed fist, with an average mass of
250 g in females and 300 g in males.
 It is larger in physically active adults
than in other healthy adults.
 The heart generally decreases in size
after approximately age 65, especially
in people who are not physically active.
 The blunt, rounded point of the heart
is the APEX; the larger, flat part at the
opposite end of the heart is the BASE.
3 LAYERS OF CARDIAC MUSCLE
TISSUE:
1. EPICARDIUM
 Outermost layer
 The epicardium or visceral
pericardium, is the superficial layer
of the heart wall.
 It is a thin serous membrane that
constitutes the smooth, outer
surface of the heart.
 The serous pericardium is called the
epicardium when considered a part
of the heart and the visceral
pericardium when considered a part
of the pericardium.
2. MYOCARDIUM
 Middle layer
 It is the thick, middle layer of the
heart.
 It is composed of cardiac muscle
cells and is responsible for the
heart’s ability to contract.
 Responsible for pumping action of
the heart.
 It is composed of specialized cells
called myocytes, which form an
interconnected network of muscle
fibers. These fibers encircle the
heart in a figure-of-eight pattern,
forming a spiral from the base (top)
of the heart to the apex (bottom).
 During contraction, this muscular
configuration facilitates a
twisting and compressive
movement of the heart that
begins in the atria and moves to
the ventricles.
 The sequential and rhythmic pattern
of contraction, followed by
relaxation of the muscle fibers,
maximizes the volume of blood
ejected with each contraction.
 This cyclical pattern of myocardial
contraction is controlled by the
conduction system
3. ENDOCARDIUM
 Innermost layer
 The endocardium is deep to the
myocardium.
 It consists of simple squamous
epithelium over a layer of
connective tissue.
  The endocardium forms the smooth,
inner surface of the heart chambers,
which allows blood to move easily
through the heart.
 The endocardium also covers the
surfaces of the heart valves.
MEMORY TRICK!!
HEART CHAMBERS
 Chambers
 The pumping action of the heart is
accomplished by the rhythmic
relaxation and contraction of the
muscular walls of its four
chambers.
 DIASTOLE
 During the relaxation phase,
called diastole, all four
chambers relax simultaneously,
which allows the ventricles to fill
in preparation for contraction.
 Diastole is commonly referred
to as the period of ventricular
filling.
 SYSTOLE
 Systole refers to the events in
the heart during contraction of
the two top chambers (atria)
and two bottom chambers
(ventricles).
 The heart lies in a rotated position
within the chest cavity.
 The right ventricle lies anteriorly
(just beneath the sternum) and the
left ventricle is situated posteriorly.
 As a result of this close proximity to
the chest wall, the pulsation created
during normal ventricular
contraction, called the apical
impulse (also called the point of
maximal impulse [PMI]), is easily
detected.
 In the normal heart, the PMI is
located at the intersection of the
midclavicular line of the left chest
wall and the fifth intercostal
space.
 SYSTOLE: Ventricle pump /
ejection = LUB (S1)
 DIASTOLE: Ventricle relax /
filling = DUB (S2)
“COZY RED”
CO (contract) ZY (systole)
RE (relax) D (diastole)
 The heart has four hollow cavities,
or chambers— two atria and two
ventricles.
 Each of these chambers is lined
with endocardium, which helps
blood flow smoothly through the
heart.
 The superior atria are primarily
receiving chambers.
 They assist with filling the
ventricles.
 Blood flows into the atria under
low pressure from the veins of
the body and then continues on
to fill the ventricles.
 The inferior, thick-walled
ventricles are the discharging
chambers, or actual pumps of the
heart.
 When they contract, blood is
propelled out of the heart and
into circulation.
 Right atrium (0-5 mmHg)
 SVC, IVC, Coronary sinus
 Superior Vena Cava and
Inferior Vena Cava
 Receive Blood from the
body
 Coronary Sinus
 Receives blood from the
heart itself

 Right Ventricle (25 mmHg)
 About 4–5 mm (0.16–0.2 in.) in
average thickness.
 Forms most of the anterior
surface of the heart.
 Left atrium
 Forms most of the base of the
heart
 Receives blood from the lungs
through four pulmonary veins
 Has four relatively uniform
openings from the four
pulmonary veins that receive
blood from the lungs
 Left ventricle
 The thickest chamber of the
heart.
 Left ventricle pumps the
blood further the body
 Average 10–15 mm (0.4–0.6 in.)
 Forms the apex of the heart.
 Valves
 The four valves in the heart
permit blood to flow in only one
direction.
 The valves, which are composed of
thin leaflets of fibrous tissue, open
and close in response to the
movement of blood and pressure
changes within the chambers.
 There are two types of valves:
atrioventricular and semilunar.
 AV valves
 The atrioventricular valves
separate the atria from the
ventricles.
 An atrioventricular valve is in
each atrioventricular canal and
is composed of cusps, or flaps.
 Atrioventricular valves ensure
Prevents
backflow blood flows from the atria
of blood into the ventricles,
preventing blood from
flowing back into the atria.
 The atrioventricular valve
between the right atrium and
the right ventricle is called the
tricuspid valve because it
consists of three cusps
 The atrioventricular valve
between the left atrium and
the left ventricle is called the
bicuspid valve because it has
two cusps. Another common
term for the bicuspid valve is
the mitral valve.
 During diastole, the tricuspid
and mitral valves are open,
allowing the blood in the atria to
flow freely into the relaxed
ventricles.
 As ventricular systole begins,
the ventricles contract and
blood flows upward into the
cusps of the tricuspid and mitral
valves, causing them to close.
 As the pressure against these
valves increases, two additional
structures, the papillary
muscles and the chordae
tendineae, maintain valve
closure.
 The papillary muscles, located
on the sides of the ventricular
walls, are connected to the
valve leaflets by the chordae
tendineae, which are thin
fibrous bands.
 During ventricular systole,
contraction of the papillary
muscles causes the chordae
 tendineae to become taut,
keeping the valve leaflets
approximated and closed.
 This action prevents backflow
of blood into the atria
(regurgitation) as blood is
ejected out into the pulmonary
artery and aorta.

 Semilunar valves
 A semilunar (half-moon-shaped) valve
is positioned between each ventricle and
its associated great artery.
 The semilunar valves are identified by
the great artery in which each is
located and include the aortic
semilunar valve and pulmonary
semilunar valve.
 Each valve consists of three pocketlike,
semilunar cusps, the free inner borders
of which meet in the center of the artery
to block blood flow.
 Contraction of the ventricles pushes
blood against the semilunar valves,
forcing them to open.
 Blood can then enter the great arteries.
However, when blood flows back from
the aorta or pulmonary trunk toward the
ventricles, it enters the pockets of the
cusps, causing the cusps to meet in
the center of the aorta or pulmonary
trunk.
 This effectively closes the semilunar
valves and prevents blood from
flowing back into the ventricles ADDITIONAL NOTE:
 The two semilunar valves are composed FLOW OF BLOOD THROUGH THE
of three leaflets, which are shaped like HEART
half-moons.
 The valve between the right ventricle
and the pulmonary artery is called the
pulmonic valve.
 The valve between the left ventricle
and the aorta is called the aortic valve.
 The semilunar valves are closed during
diastole.
 At this point, the pressure in the
pulmonary artery and aorta decreases,
causing blood to flow back toward
the semilunar valves.

RIGHT SIDE
 Deoxygenated Blood
 Carries oxygen poor blood from the body  The right side of the heart is
back to the right side of the heart supplied by the right coronary
artery, which leads to the inferior
LEFT SIDE wall of the heart.
 Oxygenated Blood  The posterior wall of the heart
 Oxgentated blood from the lungs receives its blood supply by an
additional branch from the right
1. Superior / Inferior Vena Cava coronary artery called the posterior
2. Right Atrium descending artery.
3. Tricuspid Valve  Superficial to the coronary arteries
4. Right Ventricle are the coronary veins.
5. Pulmonic Valve  Venous blood from these veins
6. Pulmonary Artery returns to the heart primarily
7. Lungs - the deoxygenated blood will through the coronary sinus, which is
enter the lungs for reoxygenation located posteriorly in the right atrium.
8. Pulmonary Vein
9. Left Atrium
10. Bicupsid / Mitral Valve
11. Left Ventricle
12. Aortic Valve
13. Aorta
14. Systemic Circulation - the oxygenated
blood will now flow throughout the body
tissues

 CORONARY ARTERIES Coronary arteries

 The left and right coronary arteries  Left Coronary Artery
and their branches supply arterial  Left anterior descending – LV,
blood to the heart. Ventricular septum, chordae
 These arteries originate from the tendinae, papillary muscle, RV
aorta just above the aortic valve (lesser extent)
leaflets.  Circumflex coronary artery – LA,
 The heart has high metabolic lateral & posterior surfaces of LV,
requirements, extracting portion of interventricular septum,
approximately 70% to 80% of the SA node, AV node
oxygen delivered (other organs  Right Coronary Artery
extract, arteries are perfused  RA, RV, inferior portion of LV
during diastole.
 With a normal heart rate of 60 to 80 Branching pattern of the coronary arteries
bpm there is ample time during varies considerably among individuals
diastole for myocardial perfusion.
 The left coronary artery has three
branches. The artery rom the point
of origin to the first major branch is
called the left main coronary
artery.
 Two branches arise from the left
main coronary artery: the left
anterior descending artery, which
courses down the anterior wall of
the heart, and the circumflex
artery, which circles around to the
lateral left wall of the heart.
  Excitability: ability to respond to an
electrical impulse
 Conductivity: ability to transmit an
electrical impulse from one cell to
another
 Both the sinoatrial (SA) node and the
atrioventricular (AV) node are
composed of nodal cells.
 The SA node, the primary pacemaker
of the heart, is located at the junction of
the superior vena cava and the right
atrium.
 The SA node in a normal resting adult
heart has an inherent firing rate of 60 to
100 impulses per minute, but the rate
changes in response to the metabolic
demands of the body.
FUNCTIONS OF THE HEART
CONDUCTION SYSTEM OF THE HEART
ELECTROPHYSIOLOGIC PROPERTIES  SA node (60-100 times/min)
OF THE HEART  Primary pacemaker of the heart
 Automaticity  AV node (40-60 beats/min)
 initiate an impulse spontaneously &  Bundle of His R & L bundle branches
repetitively  Purkinje fibers (20-40 beats/min)
 Excitability (depolarization)
 respond to a stimulus SEQUENCE OF EVENTS DURING
 Conductivity CARDIAC CYCLE
 Transmit electrical impulses from  Systole(contraction) – emptying
one cell to another  Diastole (relaxation) – filling
 Contractility
 Contract
 Refractoriness MEMORY TRICK!!
 Inability to respond until “COZY RED”
repolarization CO (contract) ZY (systole)
RE (relax) D (diastole)
 The cardiac conduction system
generates and transmits electrical MECHANICAL PROPERTIES OF THE
impulses that stimulate contraction of the HEART
myocardium.  Cardiac Output
 Under normal circumstances, the  HR
conduction system first stimulates  ANS, endogenous
contraction of the atria and then the cathecolamines
ventricles.  Parasympathetic NS (vagus
 The synchronization of the atrial and nerve), beta blockers,Ca++-
ventricular events allows the channel blockers
ventricles to fill completely before  SV
ventricular ejection, thereby  Preload
maximizing cardiac output.  volume of blood distending
 Three physiologic characteristics of two the ventricles at the end of
types of specialized electrical cells, the diastole just before
nodal cells and the Purkinje cells, contraction
provide this synchronization:  Amount of blood retuned to
 Automaticity: ability to initiate an the right side of the heart
electrical impulse at the end of diastole
  Afterload
 resistance that the ventricles
must overcome to eject blood
 Pressure that the left ventricle
has to pump against (the
resistance it must overcome to
circulate blood)
 Clinically measured by systolic
blood pressure!
 Contractility
 Force / strength of contraction
of the heart muscle
 Vascular System
 Provide conduits for blood to travel from
the heart to nourish the various tissues
of the body
 Carries cellular waste to the excretory
organs
 Allows lymphatic flow to drain tissue fluid
back into the circulation
 Returns blood to the heart for
recirculation
CARDIAC CYCLE
 A cardiac cycle is composed of both
systole and diastole.
 It refers to the events that occur in the
heart from one heartbeat to the next.
 These events cause blood to flow
through the heart due to changes in
chamber pressures and valvular
function during atrial and ventricular
diastole and systole.
 During atrial and ventricular diastole,
the heart chambers are relaxed. As a
result, the atrioventricular valves are
open, whereas the semilunar valves
are closed.
 Pressures in all of the chambers are the
lowest during diastole, which facilitates
ventricular filling.
 Venous blood returns to the right atrium
from the superior and inferior vena cava,
then into the right ventricle.
 On the left side, oxygenated blood
returns from the lungs via the four
pulmonary veins into the left atrium and
ventricle.
CARDIAC OUTPUT
 Cardiac output refers to the amount of
blood pumped by each ventricle
during a given period.
 The cardiac output in a resting adult is
about 5 L/min but varies greatly
depending on the metabolic needs of the
body.
 Cardiac output is computed by
multiplying the stroke volume by the
heart rate.
 Stroke volume is the amount of blood
ejected per heartbeat. The average
resting stroke volume is about 70 mL,
and the heart rate is 60 to 80 bpm.
 Cardiac output can be affected by
changes in either stroke volume or heart
rate.
 CONTROL OF HEART RATE
 Cardiac output must be responsive to
changes in the metabolic demands of
the tissues.
 For example, during exercise the
total cardiac output may increase
fourfold, to 20 L/min. This increase
is normally accomplished by
approximately doubling both the
heart rate and the stroke volume.
 Changes in heart rate are
accomplished by reflex controls
mediated by the autonomic nervous
system, including its sympathetic and
parasympathetic divisions.
 The parasympathetic impulses, which
travel to the heart through the vagus
nerve, can slow the cardiac rate,
whereas sympathetic impulses increase
it. These effects on heart rate result from
action on the SA node, to either  In addition, the heart rate is affected by
decrease or increase its inherent rate. central nervous system and
The balance between these two reflex baroreceptor activity.
control systems normally determines the  Baroreceptors are specialized nerve
heart rate. cells located in the aortic arch and in
both right and left internal carotid
arteries (at the point of bifurcation from
the common carotid arteries). The
baroreceptors are sensitive to
changes in blood pressure (BP).
 During significant elevations in BP
(hypertension), these cells increase
their rate of discharge, transmitting
impulses to the cerebral medulla.
 This initiates parasympathetic activity
and inhibits sympathetic response,
lowering the heart rate and the BP.
 The opposite is true during hypotension
(low BP). Hypotension results in less
baroreceptor stimulation, which prompts
a decrease in parasympathetic inhibitory
activity in the SA node, allowing for
enhanced sympathetic activity. The
resultant vasoconstriction and increased
heart rate elevate the BP.
 resistance of the pulmonary BP to right
CONTROL OF STROKE VOLUME ventricular ejection is called
 Stroke volume is primarily determined pulmonary vascular resistance.
by three factors: preload, afterload,  There is an inverse relationship between
and contractility. afterload and stroke volume.
 Preload refers to the degree of stretch  For example, afterload is
of the ventricular cardiac muscle increased by arterial
fibers at the end of diastole. The end vasoconstriction, which leads to
of diastole is the period when filling decreased stroke volume.
volume in the ventricles is the highest  The opposite is true with arterial
and the degree of stretch on the vasodilation: Afterload is reduced
muscle fibers is the greatest. because there is less resistance to
 The volume of blood within the ejection, and stroke volume
ventricle at the end of diastole increases.
determines preload, which directly
affects stroke volume.  Contractility refers to the force
 Therefore, preload is commonly generated by the contracting
referred to as left ventricular end- myocardium.
diastolic pressure (LVEDP).  The percentage of the end-diastolic
 As the volume of blood returning to the blood volume that is ejected with each
heart increases, muscle fiber stretch heartbeat is called the ejection fraction.
also increases (increased preload),  The ejection fraction of the normal left
resulting in stronger contraction and a ventricle is 55% to 65%.
greater stroke volume. This relationship,  The right ventricular ejection fraction is
called the Frank-Starling (or Starling) rarely measured.
law of the heart, is maintained until the  The ejection fraction is used as a
physiologic limit of the muscle is measure of myocardial contractility.
 reached.  An ejection fraction of less than 40%
 The Frank-Starling law is based on the indicates that the patient has
fact that, within limits, the greater the decreased left ventricular function
initial length or stretch of the cardiac and likely requires treatment for heart
muscle cells (sarcomeres), the failure (HF).
greater the degree of shortening that
occurs. ASSESSMENT TECHNIQUES
 Diuretics, venodilating agents (eg,  History (focus: obtaining information
nitrates), excessive loss of blood, or about client’s risk factors &
dehydration (excessive loss of body symptoms of cardiovascular disease)
fluids from vomiting, diarrhea, or  Demographic data – age, gender,
diaphoresis) reduce preload. ethnic origin
 Preload is increased by increasing the  Family history & genetic risk
return of circulating blood volume to  Personal history
the ventricles.  Diet history
 Controlling the loss of blood or body  Socioeconomic status
fluids and replacing fluids (ie, blood Modifiable
transfusions and intravenous [IV] fluid  cigarette smoking
administration) are examples of ways to  physical inactivity
increase preload.  Obesity
 psychological variables
 Afterload, or resistance to ejection of  chronic diseases
blood from the ventricle, is the second Non-modifiable risk factors
determinant of stroke volume.  age, gender, ethnic background,
 The resistance of the systemic BP to family history
left ventricular ejection is called  cigarette smoking – major risk factor
systemic vascular resistance. The for the devp’t of CAD & PVD
 Obesity – strong indicator of CVD  Abnormal Heart Sounds
especially when abdominal obesity is  Murmurs
present  Reflection of turbulence of
blood flow through the normal
 Physical assessment or abnormal valves
 Major symptoms cardiovascular  left ventricular outflow tract
disease (CVD) obstruction.
 Pain or discomfort  Pericardial friction rub
 Dyspnea (DOE, Orthopnea,  Sign of inflammation, infection
Paroxysmal Nocturnal or infiltration
 Dyspnea)  Pericarditis
 Fatigue  Cardiac Tamponade
 Palpitations
 Weight gain– best indicator of fluid  Laboratory Tests
retention (edema)  Serum markers of myocardial
 Syncope – transient loss of damage (cardiac markers)
consciousness ( cerebral  Troponin (T=<0.2ng/ml,
perfusion) I=<0.03ng/ml)
 Extremity pain– due to ischemia &  Creatine Kinase (CK-MB)
venous  Myoglobin (<90mcg/L)
 Skin color – pallor (anemia),  Serum lipids
cyanosis (late sign of decreased  Cholesterol (122-200mg/dl), TGL
perfusion) ( 40-160 35- 135mg/dl)
 skin temperature – due to blood  HDL ( 45-50 55-60mg/dl), LDL
flow ( 60-180mg/dl) HDL:LDL ratio
 Clubbing of fingers – chronic tissue (3:1)
hypoxia  C-Reactive Protein (<1.0mg/dl)
 Edema  Blood coagulation tests (evaluate
 BP changes the ability of the blood to clot-
 Hypertension thrombi)
 Postural Hypotension  ABG
 Pulse pressure (30-40mmHg)  Serum electrolytes (K+, Ca++, Na+,
Magnesium)
 Precordium (area over the heart)  CBC
 Assessment involves:
 Inspection  Radiographic examinations
 Apical impulse  Chest radiography
 Palpation  Determine the size, silhouette &
 Percussion position of the heart
 Auscultation  Angiography (arteriography)
 Normal heart sounds  Invasive procedure involving
 Abnormal heart sounds fluoroscopy & the use of
contrast media
 Normal Heart Sounds
 S1 – closure of AV valves
 Low pitch, long; best heard at
the apex of the heart
 Palpate the carotid pulse while
listening
 Marks the beginning of
ventricular systole
 S2 – closure of semilunar valves
 High pitch, short; best heard at
the base of the heart
  Then contrast material may
be injected and films taken
of the dilution and
circulation of the material.
 As the contrast medium is
administered, the child
may experience warmth,
nausea, vomiting,
restlessness, or headache.
 patent ductus arteriosus,
some atrial septal defects,
and some types of
ventricular septal defects.

 Cardiac catheterization
 Most definitive, most invasive
test used in the diagnosis of
heart disease
 Right-sided heart
catheterization
 Left-sided heart catheterization
 Cardiac catheterization
 Most definitive, most
invasive test used in the
diagnosis of heart disease
 The two main types of  Angiography in action:
diagnostic cardiac  The beating heart and its
catheterization are right- surrounding blood vessels can be
sided, or venous, watched and recorded in
catheterization, in which extraordinary detail as a catheter
the catheter is introduced injects a contrast dye into a patient's
from a vein into the RA, coronary arteries
and left-sided, or arterial,
catheterization, in which  Coronary arteriography
the catheter is threaded by  Technique is the same for left-sided
way of a systemic artery heart catheterization
retrograde into the aorta  Complications: MI, Stroke, Arterial
and LV, from a right-sided bleeding, Thromboembolism, Lethal
approach across the LA by dysrhythmias, Death
means of a septal puncture,
or through an existing  Intravascular ultrasonography (IVUS)
abnormal septal opening.  Catheter with miniature transducer
 As the tubing is advanced, (soundwaves) at the distal tip to
the child may feel pressure visualize the coronary arteries
at the insertion site and
vasospasm (fluttering) of
the small vessels.
 Once the catheter is within
the heart, blood samples
and pressure readings are
taken for analysis.
 Electrocardiography (ECG)  5 large blocks = 1 sec
 Graphically measures & records the  15 large blocks = 3 sec
electrical current traveling through  30 large blocks = 6 sec
the conduction system generated by
the heart
 Measured by electrodes placed on
the skin & connected to an amplifier
& strip chart recorder
 In a standard 12-lead ECG:
 five electrodes attached to the
arms, legs, & chest
 measures electrical current
from 12 different views or leads
 Bipolar limb leads
 Lead I
 Lead II
 Lead III
 Unipolar augmented leads
 aVR
 aVL
 aVF
 Unipolar precordial leads
 V1
 V2
 V3
 V4
 V5
 V6
 Unipolar precordial leads
 V1
 V2
 V3  P wave
 V4  represents atrial depolarization
 V5  PR segment
 V6  represents the time required for the
impulse to travel through the AV
node, where it is delayed, and
through the Bundle of His, Bundle
branches, & Purkinje fiber network,
just before ventricular depolarization
 PR interval
 represents the time required for
atrial depolarization as well as
impulse travel through the
conduction system and Purkinje
fiber network, inclusive of the P
 Electrocardiographic Paper wave and PR segment. It is
 electrocardiogram (ECG) strip: each measured from the beginning of the
small block P wave to the end of the PR
 measures 1 mm in height & width segment (0.12- 0.20 sec)
 standard speed:25mm/sec  QRS complex
 1 small block = 0.04 sec  represents ventricular depolarization
 1 large block = 5 small blocks and is measured from the beginning
 1 large block = 0.20 sec
 of the Q (or R) wave to the end of  Echocardiography
the S wave (0.04 - 0.10 sec)  uses ultrasound waves to assess
 ST segment cardiac structure & mobility,
 represents early ventricular particularly at the valves
repolarization
 T wave
 represents ventricular repolarization
 U wave
 represents late ventricular
repolarization
 QT interval
 represents the total time required for
 Hemodynamic Monitoring
ventricular depolarization and
 Use to assess the volume &
repolarization and is measured from
pressure of blood in the heart &
the beginning of the QRS complex
vascular system by means of a
to the end of the T wave
surgically inserted catheter
 Methods:
 Direct BP monitoring
 Artery used: radial, brachial,
femoral
 Catheter tip contains sensor
that measures & transmits the
fluid pressure to a transducer
 CVP monitoring
 Pulmonary artery pressure
monitoring

 CVP monitoring
 Characteristics of the Normal rhythm:  Pressure produced by venous blood
 HR is 60-100 bpm in the RA
 P waves are found BEFORE the  NV: 2-7 mmHg or 4-10cm H2O
QRS complex
 PR interval is 0.12 to 0.20 seconds
duration
 QRS complex is 0.04 to 0.10
seconds duration
 conduction is forward and cyclical
 The rhythm is regular with no delay
 Pulmonary artery pressure
 Various forms of ECG monitoring
 Resting ECG
 Ambulatory ECG (Holter monitoring)
– 24 hrs.
 Exercise ECG (Stress test)
DISTURBANCES IN O2 TRANSPORT  Echocardiography, CT scan –
MECHANISM reveals thickening of pericardium
 Infectious Disorders  WBC count
 Pericarditis, Myocarditis,  Atrial fibrillation is also common
Endocarditis, RHD  Interventions:
 Coronary Artery Disease  NSAIDs for PAIN
 Atherosclerosis  Corticosteroids
 Angina pectoris  Antibiotics
 Myocardial infarction  Pericardial drainage
 Congestive Heart Failure  Radiation or chemotherapy if
 Pulmonary edema caused by malignancy
 Arrythmias  Hemodialysis (uremic pericarditis)
 Assist to assume position of comfort
 Pericardiectomy (chronic
constrictive pericarditis)
 Monitor for complications:
pericardial effusion
 Monitor for complications:
 Pericardial effusion >>>> cardiac
tamponade
 Findings:
PERICARDITIS  Jugular distention
 Inflammation of the pericardium  Paradoxical pulse (systolic
 Associated w/ the following: BP 10mmHg or more on
 Malignant neoplasms expiration than on
 Idiopathic cause inspiration)
 Infective organisms (bacteria,  Decrease cardiac output
viruses, fungi)  Muffled heart sounds
 Post-MI syndrome (Dressler’s  Circulatory collapse
syndrome)  emergency care: pericardiocentesis
 pericarditis, fever, pericardial &
pleural effusion 1-12 weeks
after MI)
 Postpericardiotomy syndrome
 Systemic connective tissue disease
 Renal failure
 Chronic pericardial inflammation causes
fibrous thickening of the pericardium
 “Chronic Constrictive Pericarditis
 rigid pericardium
 inadequate ventricular filling
 Heart Failure
 Assessment:
 PAIN radiating to the neck, shoulder
& back
 aggravated by inspiration,
coughing & swallowing
 worst in supine position
(relieved by sitting up & leaning
forward)
 Pericardial friction rub (scratchy
high pitch sound)
 If w/ chronic constrictive pericarditis:
Signs of RSHF
 MYOCARDITIS RHEUMATIC FEVER
 Causes:  A systemic inflammatory disease that
 Viral, bacterial, fungal & parasitic usually develops after an URTI
infection  group A ß-hemolytic streptococci
 Chronic alcohol & cocaine abuse  Rheumatic carditis (Rheumatic
 Radiation therapy endocarditis)
 Autoimmune disorders  RHEUMATIC ENDOCARDITIS
 Bulimic patients taking ipecac syrup  Antibodies are formed to destroy the
to facilitate purging (myocardial group A ß- hemolytic strep
damage) microorganism
 Antibodies “mistakenly” cross-react
against the proteins in the
connective tissue of the heart, joints,
skin & nervous system
 PanCARDITIS (all layers)
 due to inflammation, WBC migrate to
endocardium causing accumulation
of inflammatory debris “vegetations”
 Due to inflammation >>>> abnormal around the valve leaflets
function
 Decrease cardiac output, impaired
blood circulation, predispose client
to CHF
 Due to ischemia: tachycardia,
dysrhythmias
 Cardiomyopathy
 Assessment:
 PAIN, Fever, Tachycardia,
Dysrhythmias, Dyspnea, Malaise,
Fatigue, Anorexia, Pale or cyanotic
skin, signs of RSHF
 WBC count, elevated CRP, elevated
cardiac isoenzymes, abnormal ECG
 Abnormal chest radiography,
echocardiography
 Intervention:
 Treatment of underlying cause
(antibiotic)  Assessment:
 Promote bed rest, Na+-restricted diet,  Major/ Classic symptoms
cardiotonic drugs (digitalis) are  Carditis
prescribed  Polyarthritis
 Monitor cardiopulmonary status and  Chorea (Sydenham’s chorea,
complications (CHF, dysrhythmias) St. Vitu’s dance)
 VS  sudden, aimless, irregular
 Daily weight movements of the
 I&O extremities, involuntary
 Heart & lung sounds facial grimaces, speech
 Pulse oximetry measurements disturbances, emotional
 Cardiac monitoring lability and muscle
 Dependent edema weakness
 Definition: Chorea refers to
sudden, aimless
movements of extremities,
 involuntary facial grimaces,
speech disturbances,
emotional lability and
muscle weakness
 Worse with anxiety and
relieved by rest
 Subcutaneous nodules
 small (0.5-1 cm), nontender  Erythema marginatum
swellings found on bony  Red, spotty rashes on the
prominences trunk that disappears
rapidly leaving irregular
circles on the skin

 Erythema marginatum
 erythematous macule with a
clear center and wavy,
well-demarcated border
trunk and proximal portion  Minor symptoms
of extremities , non pruritic  Reliable history of RF or evidence of
pre-existing rheumatic heart disease
 Arthralgia- pain in one or more joints
without evidence of inflammation,
tenderness, or limited movement
 Fever (38.9 - 40°C or 101 - 104°F)
 Diagnostic tests: Increase in ESR
and ASO titer, (+) C- reactive
protein
 Major/ Classic symptoms  ECG changes: prolonged P-R
 Carditis interval
 Characterized by formation
of Aschoff’s bodies
 Murmur (valve damage)
 pericardial friction rub
(pericarditis)
 CHF
 Polyarthritis
 Swelling of several joints
(knees, ankle, hips,
shoulders) that is warm,
red and painful
 Chorea (Sydenham’s chorea,
St. Vitu’s dance)
 Involuntary grimacing &
inability to use skeletal
muscles in a coordinated
manner  Diagnosed clinically through the use of
 Involvement of CNS the JONES criteria
 Subcutaneous nodules  presence of 2 major manifestation or
 Sometimes marble-sized 1 major + 2 minors
nodules appear around the  with supporting evidence of a recent
joints streptococcal infection
 Management/ Intervention:
 PREVENTION- ideal management
 RHD is prevented through early
identification &
 adequate treatment of streptococcal
infection
 A nurse should be familiar with the
signs & symptoms of streptococcal
pharyngitis
 GABHS Infection
 Signs & symptoms of
streptococcal pharyngitis:
 Fever (38.9 - 40°C or 101 -
104°F)
 Chills
 Sore throat (sudden onset)
 diffuse redness of throat with
exudates on oropharynx
 Enlarge & tender lymph
nodes
 Abdominal pain ( common in
children)
 Acute sinusitis & acute otitis
media
 Congestive Heart Failure
 Pulmonary edema
 Arrythmias
HEART FAILURE
 “Pump failure”, inadequacy of the heart
to pump blood throughout the body
 Congestive Heart Failure
 accumulation of blood & fluid in
organs & tissues due to impaired
circulation
 Types:
 Left-sided heart failure
 Right-sided heart failure
 Causes:
 Damage to muscular wall (M.I.),
Cardiomyopathy,
 Hypertension, CAD, Valvular defects,
Infections

 Management/ Intervention:
 Antibiotic: DOC – penicillin
 Aspirin (control blood clot
formation around the valves)
 Steroids (suppresses
inflammation)
 Fever (antipyretics, hydration)
 Antibiotic prophylaxis to prevent
recurrence
 Provide bed rest; provide
diversional activities that
require minimal activity (reading,
putting puzzles together)
 Assess for progression or
improvement of heart
involvement

 Infectious Disorders
 Pericarditis, Myocarditis,
Endocarditis, RHD
 Coronary Artery Disease
 Atherosclerosis
 Angina pectoris
 Myocardial infarction
  Dopamine (Intropin), Dobutamine
(Dobutrex)
 Diuretics: Furosemide (Lasix),
Chlorothiazide (Diuril)
 Vasodilators (Nitroglycerin), ACE
inhibitors (pril)

 Diagnostic Findings:
 Chest x-rays: reveals cardiomegaly
(hypertrophy)
 Pleural effusions develops
 ECG: abnormal findings (ventricular
hypertrophy, dysrhythmias)
 Echocardiography – reveals cardiac
valvular changes, pericardial
effusions, chamber enlargement,
ventricular hypertrophy
 Multigraded angiographic (MUGA)
scans – information about ejection
fraction
 Medical Management:
 Low-sodium diet, fluid restriction
 Inotropic agents:
 Digitalis: Digoxin (Lanoxin)
 INCREASE contractility, HR,
conduction (AV node)
 (-) sympa. activity, (+) parasympa.
Activity
 (+) Inotrophic, (-) chonotrophic, (-)
Dromotropic
 Watch out for DIGITALIS toxicity:
 (0.5 -2 MG/ML)
 loss of apetite, N&V, rapid, slow,
irregular heart rate, disturbance
in color vision
 Yellow halos around lights
 Child apical pulse in 1 minuter
 90 - 110bpm - infants and
children)
 70 bpm (older children)
 60 bpm (adults)
 Antidote: Digibind (Digitalis Immune
Fab)
 Monitor Electrolytes
 Hypokalemia
 Hypomagnesemia