-a muscular, four-

chambered organ

-primary purpose:
PUMPING BLOOD

-located slightly
to the left of the
sternum
THREE LAYERS:

-Endocardium

-Myocardium

-Pericardium
FOUR CHAMBERS:
-2 atria
-2 ventricles

FOUR VALVES:
(AV Valves)
-Tricuspid
-Bicuspid (Mitral)

(Semi-lunar Valves)
-Pulmonic
-Aortic
3 IMPORTANT
STRUCTURES:

Ductus Venosus

Ductus arteriosus

Foramen ovale
DUCTUS VENOSUS

-receives highly
oxygenated blood
from the large
umbilical vein and
delivers the blood to
the inferior vena
cava
FORAMEN OVALE

-an opening
between the right
and left atrium
 DUCTUS
ARTERIOSUS

-Shunts major
portion of the
blood from the
pulmonary artery
directly to the
descending aorta
and some parts
into the lungs
 CLOSURE OF THE FETAL SHUNTS:
FORAMEN OVALE
-Increased oxygen concentration in the blood
-Compression of the two portions of the atrial
septum

DUCTUS VENOSUS
-at 2 months of age

DUCTUS ARTERIOSUS
-Closure on the first breath, and obliteration
until 3 months of age
-inability of the heart to
pump adequate amount
of blood to the
systemic circulation at
normal filling pressure
to meet the body’s
metabolic demands
ETIOLOGIES:
1. Volume overload
(left-to-right shunts → RV hypertrophy)

2. Pressure overload
(obstructive lesions)

3. Decreased contractility
(cardiomyopathy, ischemia)

4. High Cardiac Output

Demands
(sepsis, hyperthyroidism, severe anemia)
 Decreased Cardiac output
Compensatory Mechanism

Cardiac Muscle Cardiac Muscle Dilation

Hypertrophy

Increased ventricular Increased stretch of

pumping pressure muscle fibers

Increased cardiac Increased force of

contraction
output

Prolonged hypertrophy
and dilation

Decreased myocardial Impaired myocardial Prolonged dilation

compliance oxygenation

HEART FAILURE
 Decreased Cardiac output

Compensatory Mechanism

Stimulation of SNS by stretch receptors

and baroreceptors

Release of catecholamines

Peripheral vasoconstriction Increased force and rate of

myocardial contraction

Increased
Increased venous return,
Cardiac output tachycardia, sweating

Decreased
kidney perfusion CONGESTIVE
HEART FAILURE
RAAS activation
Systemic and
Na and Water Increased Blood Pulmonary venous
retention Volume engorgement
Impaired Myocardial
Function
-tachycardia (earliest
sign)
-Diaphoresis (esp. on
the forehead)
-Fatigue
-Irritability
-Cold extremities
-Weak pulse
-Slow capillary refill
-Low BP
-Mottled skin
-Pallor
Pulmonary Congestion
-Tachypnea
-Cyanosis
-Dyspnea at rest
(prominent sign in
infants)
-Orthopnea
-Wheezing
-Dry, hacking cough
-Horseness
-Developmental delays
(gross motor)
Systemic Venous
Congestion
-Weight gain (earliest
sign)
-Hepatomegaly
-Edema
-Ascites
-Distended Neck and
peripheral veins
-Physical Examination
-Chest X-ray
-ECG
-Echocardiography
Improve Cardiac
Function:
-Digitalis glycosides
(+) inotropic
(-)chronotropic
(-) dromotropic

-ACE inhibitors
(SE: hypotension, renal
dysfunction, COUGH)
❑Check the child’s apical pulse in 1 full
minute
❑Withhold:
❑below 90-110 bpm (infants and young
children)
❑Below 70 bpm (older children)
❑Below 60 bpm (adult)
❑WOF signs of toxicity:
❑Bradycardia (most common sign in
infants and children)
❑Anorexia
❑Nausea and Vomiting (unrelated to
feeding)
❑*Neurologic and Visual disturbances
❑Home Instructions:

❑Administer slowly directing it to the

side and back of the mouth
❑Do not mix the drug with food or fluids
❑Give water/brush the teeth if possible
when the child has teeth
❑If the child vomits, do not give second
dose
❑If a dose is missed do not give an extra
dose or increase the dose. Stay on the
medication schedule
Remove Accumulated
Fluid and Sodium:
-Diuretics
(furosemide and
thiazides)
*WOF signs of
hypokalemia (enhances
the effect of digoxin)
*given early in the day
*Potassium-rich food
(banana, orange, whole
grains, legumes, leafy
vegetables)
Decrease cardiac
demand:
-Outline a plan of daily
care
-Temperature
monitoring
-Non-infectious room-
mate
-refers to an arterial
oxygen tension that is
lower than the normal
and can be identified by
measuring arterial
oxygen saturation to
detect low levels
-Pallor
-cyanosis
-cool to touch
-diminished pulses
-lethargy
-HYPERCYANOTIC
SPELLS (blue spells/tet
spells)
Hyperoxia Test
-infant is placed in
100% oxygen
environment

Results:
-Pa02 of 100 mmHg or
higher (Lung disease)

-Pa02 lower than 100

mmHg (Cardiac disease,
due to inadequate
perfusion of pulmonary
bed)
-Prostaglandin E1
administration
(vasodilation and
smooth muscle
relaxation)

-Morphine
-Hydration
TREATING
HYPERCYANOTIC
SPELLS:
-place in knee-chest
position
-calm, comforting
approach
-100% oxygen by mask
-Give morphine
-Begin IVF replacement
and volume expansion
(if needed)
-Repeat morphine
administration
-Prevent dehydration
-Prevent respiratory
infection
 Acyanotic Cyanotic
Increased Obstructive Decreased Mixed blood
Pulmonary blood defects pulmonary blood flow
flow flow

Ventricular Coarctation of Tetralogy Transposition

Septal Defect the Aorta of Fallot of great
Aortic arteries
Atrial Septal Tricuspid
Stenosis atresia Total
Defect
anomalous
Pulmonic
Patent Ductus pulmonary
Stenosis venous return
Arteriosus

Truncus
Atrioventricular arteriosus
Canal
Hypoplastic
left heart
syndrome
Defects with Increased
Pulmonary Blood Flow
 Atrial Septal Defect
(ASD)
▪ Abnormal opening between the atria
▪ S/Sx:
 Harsh systolic murmur
 Dyspnea on mild exertion
 Echocardiography – enlarged right side of
the heart and  pulmonary circulation
-Abnormal opening
between the atria
(left-to-right shunting)
TYPES:
Ostium primum (ASD 1)
-opening at the lower end of
septum
Ostium secundum (ASD 2)
-opening near center of
septum
Sinus Venosus Defect
-opening near junction of
superior vena cava and right
atrium
Atrial Septal defect
Atrial Septal Defect

▪ Therapeutic Management
 Non-surgical
 ASD 2 closure with a device (Amplatzer
septal occluder) during cardiac
catheterization
 Surgical (between 1 & 3 years of age)
 Pericardial patch or Dacron patch
 Cardiopulmonary bypass
 Ventricular
Septal Defect (VSD)
▪ Abnormal opening
between the right and
left ventricles
▪ S/Sx
 easy fatigue
 Slowing of growth
pattern
 ECG – right ventricular
and pulmonary artery
hypertrophy
Normal Heart
vs. VSD
 What to look for:

Loud, harsh, widely transmitted systolic murmur

heard best along the left sternal border at the third or
fourth intercostal space
PMI displacement to the left
Liver, heart and spleen enlargement
Feeding difficulties
Diaphoresis, tachycardia, rapid, grunting respirations
 Ventricular
Septal Defect (VSD)
▪ Surgical treatment
 Cardiac catheterization
 Cardiopulmonary bypass
 Suture or placement of Dacron
patch
Atrioventricular Canal Defect
(AVC)
▪ aka Endocardial cushion defect
▪ Incomplete fusion of endocardial cushion or
in the septum of the heart at the junction of
the atria and the ventricles
▪ S/Sx:
 Moderate to severe CHF
 Characteristic murmur
 Cyanosis that increases with crying
Atrioventricular Canal defect
Atrioventricular Canal Defect
(AVC)
▪ Surgical Treatment
 Patch closure and
reconstruction of AV valve
tissue
▪ Post operative care
 Observe for jaundice
Patent Ductus Arteriosus

▪ Failure of the ductus arteriosus to close within

the first weeks of life.
▪ An opening between the pulmonary artery and
aorta
▪ S/Sx a
 Machinery-like murmur
 Widened pulse pressure
 Bounding pulses
 Low diastolic pressure
 ECG – normal; ventricle enlargement (large shunt)
Patent Ductus Arteriosus

▪ Medical Management
 INDOMETHACIN administration
 WOF: bleeding, reduced glomerular filtration,
diminished GI and cerebral blood flow
▪ Surgical Management
 Insertion of Dacron-coated stainless steel coils
thru cardiac catheterization (6 months-1 year)
 Ductal ligation thru left thoracotomy or video-
assisted thoracoscopic surgery
Defects with Obstruction to Blood Flow
Pulmonic Stenosis

▪ Narrowing at the entrance to the pulmonary

artery
▪ Pulmonary atresia – extreme form of PS
▪ S/Sx
 Cyanosis
 Chest X-Ray – Cardiomegaly
 ECG – right ventricular hypertrophy
Pulmonic Stenosis

▪ Nonsurgical Management
 Balloon angioplasty
(treatment of choice)
▪ Surgical Management
 Pulmonary valvotomy
a balloon is
advanced into
the heart and
placed across
the pulmonary
valve and
inflated
Aortic Stenosis
▪ Narrowing or stricture of the aortic
valve
▪ S/Sx
 Faint pulse, hypotension, tachycardia
and inability to suck for long periods –
severe
 Pain similar to angina when child is
active
 Dizziness when standing for long periods
 ECG – left ventricular hypertrophy
 Aortic Stenosis

▪ Nonsurgical treatment
 Stabilization with beta blocker or
calcium channel blocker before
procedure
 Balloon valvuloplasty – treatment of
choice
▪ Surgical treatment
 Aortic valvotomy
Coarctation
of the aorta
▪ Localized narrowing near the insertion of the
ductus arteriosus
▪ S/Sx:
 Absence of palpable femoral pulses
 High blood pressure and bounding pulses in the
arms
 Weak or absent femoral pulses
 Cool lower extremities with lower blood pressure
Coarctation
of the Aorta
▪ Surgical Management
 Scheduled at 2 years of age
 End-to-end anastomosis -
treatment of choice for children
younger than 6 months
 Digoxin and diuretics before
surgery
Defects with decreased Pulmonary Blood Flow
Tetralogy of Fallot

▪ The classic form includes four defects:

 Ventricular septal defect (VSD)
 Pulmonic stenosis
 Overriding of the aorta
 Right ventricular hypertrophy
▪ S/Sx:
 Skin acquires a bluish tint
 Blue spells or tet spells
 Anoxic spells – crying or feeding
 Polycythemia
 Squatting or a knee-chest position when resting
Tetralogy of Fallot

▪ Therapeutic Management
 Surgery done at 1 to 2 years of age
 Blalock-Taussig procedure – temporary
 creates ductus arteriosus – allows blood to leave the
aorta and enter the pulmonary artery, oxygenate in
the lungs and return to the left side of the heart
 (-) palpable pulse in the right arm
 Brock procedure - full repair
 Hypoxic episodes – Oxygen administration, knee-
chest position, morphine sulfate
Tricuspid Atresia

▪ Tricuspid valve fails to develop (completely

closed)
▪ S/Sx
 Cyanosis
 Tachycardia
 Dyspnea
 Chronic hypoxemia with clubbing
Tricuspid Atresia

▪ Therapeutic Management
 Continuous infusion of
prostaglandin
 Fontan procedure (Glenn shunt
baffle)
 restructures the right side of the
heart
Defects with mixed Blood flow
Transposition of the Great
arteries
▪ Aorta rises from the right ventricle instead of
the left, and the pulmonary artery arises from
the left ventricle instead of the right
▪ S/Sx
 Cyanotic at birth
 Cardiomegaly a few weeks after birth
 Therapeutic Management

❑ PGE1 administration
❑Temporarily increase blood mixing and provide an oxygen
saturation
❑ Rashkind procedure (balloon atrial septostomy)
❑to create artificial ASD
❑ Surgical correction – done at 1-3 months of age
❑ Arterial switch procedure
❑Transecting the great arteries and anastomosing the main
pulmonary artery to the proximal aorta and anastomosing
the ascending aorta to the proximal pulmonary artery
 Therapeutic Management

❑Intraatrial baffle repairs

❑Divert venous blood to mitral valve and
pulmonary venous blood to the tricuspid
valve using the patient’s atrial septum
SENNING PROCEDURE or prostethic
material MUSTARD PROCEDURE
Total Anomalous Pulmonary Venous
return
▪ Pulmonary veins return to the right atrium of
the superior vena cava instead of to the left
atrium
▪ Absent spleen – associated with this disorder
▪ S/Sx
 Cyanosis
 More pulmonary blood flow, less cyanotic
 Tire easily
Total Anomalous Pulmonary Venous
return

▪ Therapeutic Management
 Continuous PGE Iv infusion
 Surgical management –
reimplanting the pulmonary
veins into the left atrium
Truncus Arteriosus

▪ One major artery or “trunk” arises from the

left and right ventricles in place of a separate
aorta and pulmonary artery
▪ S/Sx
 Variable cyanosis
 Poor growth
 Activity intolerance
Truncus Arteriosus

▪ Therapeutic Management
 Restructuring the common trunk to
create separate vessels
 Homografts - cadaver aorta and
pulmonary artery that are treated with
antibiotics and cryopreserved
 One or more conduit replacement will
be needed in childhood
Hypoplastic Left Heart syndrome

▪ Underdevelopment of the left side of the

heart, resulting in a hypoplastic left ventricle
and aortic atresia
▪ Usually fatal in the first months of life without
intervention
▪ S/Sx
 Mild to moderate cyanosis
 Signs of congestive heart failure
Hypoplastic left heart syndrome

▪ Therapeutic Management
 PGE infusion – ensure
adequate systemic blood
flow
 Surgical treatment
 Heart transplantation
Norwood procedure

anastomosis of the main

pulmonary artery to the aorta
to create a new aorta shunting
to provide pulmonary blood
flow
Glenn shunt

involve anastomosing the superior

vena cava to the right pulmonary
artery so svc flow bypasses the
right atrium and flows directly to
the lungs – reduce volume load in
the right ventricle
Acquired Cardiovascular Disorders
Bacterial Endocarditis

▪ Also called Infective Endocarditis or

Subacute bacterial endocarditis
▪ Inflammation and infection of the
endocardium or valves of the heart
▪ Causative agents:
 Streptococcus viridans – most common
 Staphylococcus aureaus
 Fungi – Candida albicans
Signs and Symptoms of Bacterial
Endocarditis

▪ Low-grade, intermittent fever

▪ Pale
▪ Malaise
▪ Myalgia, arthralgia
▪ Headache, diaphoresis
▪ Weight loss
▪ Significant murmurs
▪ Splenomegaly
Signs and Symptoms of Bacterial
Endocarditis
▪ Other signs that result from embolus
formation
 Splinter hemorrhages under the nails
▪ Osler – red, painful intradermal nodes with
white centers found on the pads of the
fingers
▪ Janeway – painless, hemorrhagic areas on the
palms and soles
 Petechiae on the oral mucous membrane
Diagnostic Evaluation of “BE”

▪ Duke criteria – guideline for the Diagnosis of

Infective Endocarditis
▪ ECG changes
▪ Echocardiography
▪ Laboratory studies
 Anemia
 Leukocytosis
 Hematuria or proteinuria
Therapeutic Management of “BE”

▪ High-dose antibiotic administration

▪ Antifungal agents administration
▪ Surgical intervention
▪ PREVENTION
 Administration of prophylactic antibiotic therapy
- 1 hour before procedures
Nursing Care for Bacterial
ENdocarditis
▪ Advise the family’s regular dentist of existing
cardiac problems in the child
▪ Maintain highest level of oral health
▪ Stress to parents that any unexplained fever,
weight loss, or change in behavior must be
brought to practitioner’s attention
▪ Observation during antibiotic administration
Rheumatic Fever

▪ Occurs after pharyngitis caused by a beta-

hemolytic streptococci
▪ A self-limited illness that involve the joints,
skin, brain, serous surfaces and heart
▪ Cardiac valve damage - complication of RF
Signs and Symptoms of “RF”

▪ Aschoff bodies
▪ Carditis involving muscles of the heart
 May lead to permanent damage
▪ Polyarthritis
▪ Erythema marginatum
▪ Subcutaneous nodules
▪ Chorea (St. Vitus dance or Sydenham chorea)
▪ Arthralgia
▪ Fever
inflammatory hemorrhagic
bullous lesions found in the
heart, blood vessels, brain and
serous surfaces of joints and
pleura
erythematous macule with a clear
center and wavy, well-demarcated
border trunk and proximal portion
of extremities , non pruritic
small (0.5-1 cm), nontender swellings found
on bony prominences
sudden, aimless, irregular
movements of the extremities,
involuntary facial grimaces, speech
disturbances, emotional lability and
muscle weakness
Diagnostic Evaluation for “RF”

▪ Antistreptolysin O (ASLO) titer – measure

concentration of antibodies formed in the
blood against streptolysin O
 Normal – 0 to 120 Todd units
 Over 333 Todd units – recent strep infection
Therapeutic Management for “RF”

▪ Reduce cardiac workload

▪ Antibiotic administration
 Penicillin or other macrolides and cephalosporins
▪ Salicylates – inflammation
▪ Digitalis
▪ Diuretics
 Kawasaki Disease

▪ Also called
Mucocutaneous
Lymph Node
Syndrome
▪ Vasculitis – principal
finding → formation
of aneurysm and
myocardial
infarction
Signs and Symptoms of “KD”

▪ Acute phase
 Abrupt onset of high fever
 Reddened conjunctivae of the eyes without
discharge
 Red, cracked lips
 “strawberry tongue”
 Cervical lymph nodes are enlarged
 Rash – perineal area
 Edema on hands and feet
 Erythema on palms and soles with peeling
Signs and symptoms of “KD”

▪ Subacute phase
 Resolution of fever
 Damage vessels continue to enlarge
 Periungual desquamation of hands and feet
 Arthritis
 Irritability
▪ Convalescent phase
 all s/sx have resolved
 Elevated C-reactive protein level
 Thrombocytosis
 Arthritis
Therapeutic Management for “KD”

▪ High-dose IVIG (2g/kg over 10-12 hrs)

▪ Salicylate therapy
▪ Anticoagulatory therapy (warfarin
administration) – aneurysms
Nursing Care for “KD”

▪ Monitor cardiac status

▪ Monitor temperature
▪ Record I and O and daily weight
▪ Extra fluid; Monitor IV fluid
▪ Application of cool cloths and unscented
lotions
▪ Mouth care, lubricating ointment on lips
▪ Clear liquids and soft foods
▪ Place on quiet environment