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Disturbances in Oxygenation
Disturbances in Oxygenation
MEMORY TRICK!!
“COZY RED”
CO (contract) ZY (systole)
RE (relax) D (diastole)
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
Right Ventricle (25 mmHg) Prevents
backflow blood flows from the atria
About 4–5 mm (0.16–0.2 in.) in of blood into the ventricles,
average thickness.
preventing blood from
Forms most of the anterior
flowing back into the atria.
surface of the heart.
The atrioventricular valve
Left atrium
between the right atrium and
Forms most of the base of the
the right ventricle is called the
heart
tricuspid valve because it
Receives blood from the lungs
consists of three cusps
through four pulmonary veins
The atrioventricular valve
Has four relatively uniform
between the left atrium and
openings from the four
the left ventricle is called the
pulmonary veins that receive
bicuspid valve because it has
blood from the lungs
two cusps. Another common
Left ventricle
term for the bicuspid valve is
The thickest chamber of the
the mitral valve.
heart.
During diastole, the tricuspid
Left ventricle pumps the
and mitral valves are open,
blood further the body
allowing the blood in the atria to
Average 10–15 mm (0.4–0.6 in.)
flow freely into the relaxed
Forms the apex of the heart.
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
Valves walls, are connected to the
The four valves in the heart valve leaflets by the chordae
permit blood to flow in only one tendineae, which are thin
direction. fibrous bands.
The valves, which are composed of During ventricular systole,
thin leaflets of fibrous tissue, open contraction of the papillary
and close in response to the 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
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: Congestive Heart Failure
PREVENTION- ideal management Pulmonary edema
RHD is prevented through early Arrythmias
identification &
adequate treatment of streptococcal HEART FAILURE
infection “Pump failure”, inadequacy of the heart
A nurse should be familiar with the to pump blood throughout the body
signs & symptoms of streptococcal Congestive Heart Failure
pharyngitis accumulation of blood & fluid in
GABHS Infection organs & tissues due to impaired
Signs & symptoms of circulation
streptococcal pharyngitis: Types:
Fever (38.9 - 40°C or 101 - Left-sided heart failure
104°F) Right-sided heart failure
Chills Causes:
Sore throat (sudden onset) Damage to muscular wall (M.I.),
diffuse redness of throat with Cardiomyopathy,
exudates on oropharynx Hypertension, CAD, Valvular defects,
Enlarge & tender lymph Infections
nodes
Abdominal pain ( common in
children)
Acute sinusitis & acute otitis
media
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