Pediatric Week 5 Notes

Cardiovascular Assessment
Precordium, Apex, and Base

Tips; 4th and 5th intercostal cage.

Heart Sounds

 First heart sound (S1) Lub

o Occurs with closure of AV valves—signals beginning of systole
o Mitral component of first sound (M1) slightly precedes tricuspid
component (T1).
o Systole: heart’s contraction, blood pumped from ventricles fills
pulmonary and systemic arteries; 1/3 of cardiac cycle
 Second heart sound (S2) Dub
o Occurs with closure of semilunar valves—signals end of systole
o The aortic component of the second sound (A2) slightly precedes
the pulmonic component (P2).
o S2 loudest at base
o Diastole: ventricles relax and fill with blood; 2/3 of cardiac cycle

Auscultatory Areas
Heart Murmurs

 Gentle, blowing, swooshing sound that can be heard on chest wall –

audible when blood volume in the heart increased or its flow is
impeded or altered.
 Conditions that create turbulent blood flow and collision currents
 Conditions that can result in murmurs:
o Velocity of blood increases.
o Viscosity of blood decreases.
o Structural defects in valves

Cardiovascular Dysfunction
Anatomy

 4 Chambers:
o RL Atrium: thin-holding blood
o RL Ventricle: thick pumping
 Valves – prevent back flow of blood:
o 2 Atrioventricular Valves: Tricuspid/ Mitral
o 2 Semilunar Valves: Pulmonic/Aortic
 Semilunar – pulmonic Right side and aortic Right side
 Diastole- AV valves open to fill the blood
 Systole- Pumping, AV valves are closed, prevent back flow
  Heart Wall

o Pericardium: tough, fibrous, double-walled sac protects heart

o Myocardium: muscular wall of heart
o Endocardium: thin inner surface lines chambers and valves
 No valves between vena cava and right atrium, between pulmonary veins and left atrium:
 ápressure in L heart = pulmonary congestion.
 ápressure in R heart =neck veins and abdomen.

Normal Cardiac Blood Flow

Fetal Circulation
  Fetal blood does not need to go to lungs for oxygen – that comes from the placenta via
large umbilical vein → liver → liver gets some oxygen while goes to the inferior vena
cave via ductus venosus → Right atrium → Left atrium (instead of to the Right ventricle
and then the lungs) → Left ventricle → Aorta → head and upper extremities.
 Blood from the head and upper extremities → Right atrium from the supervisor vena
cava → Right ventricle (via through tricuspid valve) → pulmonary artery → descending
aorta via ductus arteriosus.

Fetal Circulation: Three Shunts

 Ductus Venosus
o Fetal blood vessel connecting the umbilical vein to the IVC
 Inferior vena cava
o Blood flow regulated via sphincter
o Carries mostly high oxygenated blood
 Foramen Ovale
o Shunt highly oxygenated blood from right atrium to left atrium
 Ductus Arteriosus
o Protects the lungs against circulatory overload
o Allows the right ventricle to strengthen
o High pulmonary vascular resistance, low pulmonary blood flow
o Carries mostly medium oxygen saturated blood into the bodies
 Defects that increase Pulmonary Blood Flow
Acyanotic Congenital Defects

 The 3’Ds of acyanotic defects- ASD, VSD, PDA

 Untreated left-to-right shunts (acyanotic heart defects) may progress
to right-to-left shunts (cyanotic defects) if right ventricular pressure
exceeds left ventricular pressure due to pulmonary arterial
hypertension
 Left for lungs
 Right for systemic
Patent Ductus Arteriosus (PDA)

 PDA important to fetal circulation: the fetus’ blood does not need to go
to the lungs to pick up O2
o Should close within 72 hours
 Failure of the ductus arteriosus to close
 Linked with:
o Prematurity: occurs more often in females
o Maternal viral infections (CMV, Rubella)
o Family history of congenital heart defects
o Maternal meds (amphetamines, antiepileptics)
 Murmur is very loud
 PDA does not close
 Clinical presentation:
o Signs of heart failure
o Wide pulse pressure
o Bounding pulses
o ** machine like murmur (systolic and diastolic)
 Non-surgical:
o Indomethacin: choice of drug for non-surgical
o Ibuprofen
o Coils to occlude the PDA (placed during cardiac catheterization)
 Surgical
o Ligation of the vessel via a thoracotomy

Atrial Septal Defect (ASD)

 Abnormal opening between the left and right atria

 ASD: systolic murmur
 May not cause any problems until later in life
 May have atrial dysrhythmias
 Aspirin helps prevent strokes and PE
 Clinical presentation:
o May be asymptomatic
o Can develop heart failure
o *** systolic murmur with fixed split-second heart sound
 Nonsurgical
 o Closure during cardiac catheterization
o Most successful with smaller defect
o Low dose aspirin from 6 months
 Surgical
o Pericardial or Dacron patch closure
 Requires open repair with bypass

Ventricular Septal Defect (VSD)

 Abnormal opening between the right and left ventricles

 VSD: loud, harsh murmur a left sternal border
o Loudest at the apex
 Many close spontaneously
 Clinical presentation:
o Heart failure:
 Crackles
 Diaphoresis
o ** loud harsh murmur at left sternal border
 Nonsurgical:
o May be able to close during cardiac catheterization if small
 Surgical:
o Palliative
 Pulmonary artery banding
o Complete repair
 Sutures for small defects
 Dacron patch closure for large defects

Defects That Decrease Pulmonary Flow

Tetralogy of Fallot
 Decreased pulmonary flow- cluster to decrease cardiac workload
 The mnemonic for the four abnormalities associated with tetralogy of
Fallot (TOF) is PROVe:
o P: Pulmonary infundibular stenosis
o R: Right ventricular hypertrophy
o O: Overriding aorta
o V: Ventricular septal defect
 Clinical presentation:

o Cyanosis at birth
 May initially be mild and progress over the first year of life
o Systolic murmur
o “Tet” spells
 Episodes of acute cyanosis and hypoxia
 Occurs when oxygen requirements exceed blood supply
 Position with knees to chest
 Kinks femoral artery -> increases vascular resistance
and systemic pressure -> reverses shunt
 Surgical Treatment:
o Modified Blalock-Taussig shunt placement
 Provides blood flow to the pulmonary arteries
o Complete repair performed within first year of life
 Septal defect closed and right ventricular outflow tract is
enlarged -> resolving other 2 defects
 Right Ventricle returns to normal thickness
 Oxygen-rich blood gets through the aorta
 Nursing Care
o Decreased oxygen demand
  Preemie nipple
 Time-limited meals
 Cluster care
o Manage Tet spells

Cyanotic Congenital Heart Defects

 Assessment:
o Cyanosis
o Tachycardia
o Tachypnea
o Cool extremities
o Polycythemia
 Increased HCT; a lot of red blood cells; the body tries to
compensate for the deoxygenation but it is not a blood
thing.
o Irritability
o Difficulty feeding
o Clubbing
o Squatting
 Nursing considerations
o Oxygen needed
 Oxygen needs are decreased
 Will expect sats to be lower and will maintain them there
o Preemie nipples
 Decrease suck effort required
o Knee to chest
o Increase calories, decrease volume
o Endocarditis prophylaxis
o Monitor temperature
 Too hot/cold can increase cardiac workload
o Medications: Penicillin/ Ampicillin

Mixed Defects
Transposition of the Great Vessels
  Septal defects and/or PDA are necessary to allow the mixing of blood
within the systemic and pulmonary circulation
 Great arteries (the aorta and the pulmonary artery) are switched, also
called transposed
 Keep the PDA open so you can get oxygenated blood
 Clinical presentations:
o Degree of cyanosis depends on size of the defect
o Presence of large septal defects or PDA- less cyanosis
o Cardiomegaly
o Heart failure
 Treatment:
o Prostaglandin E to keep PDA open
o Ballon atrial septostomy
 Increases mixing by opening the atrial septum
o Surgery to switch the arteries within first 2 weeks of life
 Photo: Complete transposition of the great arteries, also called
dextro-transposition of the great arteries (D-TGA). This type reduces
the amount of oxygen-rich blood to the body.

Hypoplastic Left Heart Syndrome (HLHS)

 Mitral stenosis or atresia; aortic stenosis or atresia
 Fontan: separates oxygenated and unoxygenated blood inside the
heart and eliminates excess volume load on the ventricle
 Oxygenated blood ventricle is very small
 Prostaglandin E to keep the PDA open
 Clinical presentation:
o Mild cyanosis
o Heart failure
o Lethargy
o Fatigue
o Poor eating
o May be asymptomatic until PDA closes
 If PDA closes, there will be increased cyanosis and cardiac
collapse
 Treatment:
o Prostaglandin E to keep PDA open
o Multi-stage surgical approach to reconfigure the cardiovascular
system
 Norwood: anastomosis of pulmonary artery to the aorta
creating a new aorta
 Bi-directional Glenn: anastomosis of SVC to right
pulmonary artery; reduces volume load on the right
ventricle
 Fontan: separates oxygenated and unoxygenated blood
inside the heart and eliminates excess volume load on the
ventricle
 Obstructive Defects: Defects That Decrease
Systemic Blood Flow
Coarctation of the Aorta

 Narrowing at or near the insertion of the ductus arteriosus, which

results in increased pressure proximal to the defect and decreased
pressure distal to the obstruction
o Kink in the aorta
 This causes the development of collateral circulation in the fetus
 Rapid deterioration and death may occur with severe acidosis and
hypotension
 Will need ventilator and BP support
 Risk for hypertension, ruptured aorta, aortic aneurysm, or stroke
 Clinical presentation:
o High BP in the arms
o Weak or absent femoral pulses
o Cool lower extremities with lower BP
o Signs of VHF
o Older children may experience dizziness, headaches, fainting,
nose bleeds
 Treatment:
o Infants and children: balloon angioplasty (recommend surgery in
infants < 6 months old)
o Adolescents: placement of stents

Aortic Stenosis

 Characterized by obstruction of Left ventricular outflow

 Aortic valve is normally tricuspid, but due to defect is bicuspid
 Usually asymptomatic
 To assess, think about where you hear the aortic valve BEST ->
reduced intensity of second heart sound
o Loudest: 2nd intercoastal space and right sternal border
o ONLY ONE HEARD FROM THE RIGHT STERNAL BORDER
 Clinical presentation (Infants):
o Weak pulses
 o Hypotension
o Tachycardia- due to increased blood volume in the heart because
it cannot pass through the obstructed valve
o Poor feeding
 Clinical presentation (children):
o Exercise intolerance
o Chest pain
o Dizziness when standing
 Treatments:
o Valve replacement
o Norwood procedure

Pulmonary Stenosis

 Narrowing of pulmonary valve that obstructs blood flow to the lungs

 Can develop right ventricular hypertrophy due to the obstructed flow
from right ventricle to the lungs
 Blood flow to pulmonary artery is obstructed -> R ventricular
hypertrophy
 Mild stenosis -> asymptomatic
 Moderate to severe stenosis -> dyspnea and fatigue on exertion,
possible cyanosis
 Treatment:
o Nonsurgical: Balloon angioplasty with cardiac catheterization
o Infants: brock procedure
o Children- Pulmonary valvotomy
 Systolic ejection murmur
 May have cyanosis if severe
 CHF
 Cardiomegaly
 Clog in pulmonary artery

Congestive Heart Failure

 There are two primary causes of heart failure in children and

adolescents
o “Over-circulation failure”
  Occurs when blood mixes inside the heart due to
congenital heart defect
 ASD/VSD
o Pump Failure
 Occurs when the heart muscle becomes damaged and is
no longer able to process the blood flow
 Hyper/Hypoplasia
 Heart cannot supply enough oxygenated blood to meet the metabolic
needs of the body tissues either at rest or at work
 Left sided failure decreases blood flow to kidneys (activates the renin
angiotensin aldosterone system) -> fluid retention in the heart -> fluid
buildup in the lungs
o Right: deoxygenated
o Left: oxygenated

Congestive Heart Failure 2 Types

 The inability of the heart to pump an adequate amount of blood into

the pulmonary or systemic circulation
 In children, occurs as result of structural abnormalities
 Heart muscle may become damaged if left untreated
 Right sided
o Defined as: unable to pump much blood to the lungs. Because of
the congestion in the right side of the heart, blood flow begins to
back up into the veins. Eventually, swelling is noticed in the feet,
ankles, lower legs, eyelids, and abdomen due to fluid retention.
o Right ventricle is unable to pump blood effectively into the
pulmonary artery
o Results in increased pressure in the right atrium and systemic
circulation
o Systemic hypertension causes hepatosplenomegaly and edema
o Enlarged liver, enlarged spleen, HTN, multi-organ failure, a lot
more edema on the right side of heart failure.
 Left Sided
o Unable to pump blood to the body. Blood begins to back up into
the vessels in the lungs, and the lungs become stressed.
Breathing becomes faster and more difficult. Also, the body does
not receive enough blood to meet its needs, resulting in fatigue
and poor growth in children.
 o Left ventricle is unable to pump blood into the systemic
circulation
o Results in increased pressure in the left atrium and pulmonary
veins
o Lungs become congested with blood, resulting in increased
pulmonary pressures and edema
o Pulmonary edema, crackles, peripheral edema

Assessments

 Impaired Myocardial function:

o Tachycardia, sweating, decreased urine output, fatigue,
weakness, restlessness, anorexia, pale or cool extremities, weak
peripheral pulses, decreased BP, gallop rhythm cardiomegaly
 Pulmonary congestion (left sided):
o Tachypnea, dyspnea, retractions (infants), flaring nares, exercise
intolerance, orthopnea, cough hoarseness, cyanosis, wheezing,
grunting
 Systemic Venous Congestion (Right sided):
o Weight gain, heptamegaly, peripheral edema, especially
periorbital, ascites, neck vain distention (children)

Congestive Heart Failure Nursing Care

 Maintain oxygen levels

 Elevate HOB
 Monitor I/Os
 Daily weight
 Supplemental oxygen
 Cluster care to decrease oxygen demands
 High calorie diet/formula; small frequent feeds
 Diuretics (maximizes cardiac output and eliminates excess fluids)
 ACE inhibitors (dilate blood vessels)

Acquired Cardiac Conditions

Pulmonary Artery Hypertension
  If infant is born premature, the already high resistance in the lungs
does not do them any favors
 Increased pressure due to right ventricle hypertropia
 Resistance in the lungs is highest after birth
 Backs up into the heart and body
o Right ventricular hypertrophy -> heart failure
 Causes:
o Prematurity
o Chronic lung disease
o Left heart failure
 Clinical presentation:
o Dyspnea with exercise
o Chest pain
o Syncope
 Treatment:
o Vasodilator therapy
o Oral calcium channel blockers
o Lung transplantation if severe
 Nursing care:
o Promote rest
o Small, frequent feedings

Rheumatic Fever

 Acquired autoimmune disorder that occurs 1-6 weeks after untreated

group A Beta-hemolytic strep infection
 Caused by the production of antibodies against the streptococci toxin;
these antibodies attack the heart valves
 New jones criteria for diagnosis established in 2015 for low risk and
high-risk populations (criteria to the right is for low risk)
 Jones criteria
o Major manifestations (2 or more):
 Carditis
 Polyarthritis
 Chorea
 Subcutaneous nodules
 Erythema marginatum (disc-shaped reddened macules)
o Minor manifestations: 1-6 weeks
  H/ O RF
 Fever greater or equal to 101.3
 Sed rate greater or equal to 60
 c-reactive protein (CRP) greater or equal to 3.0 mg/dl
 Prolonged PR interval (unless carditis is present)
 Clinical Manifestations:
o Fever
o Painful and tender joints- most often in the knees, ankles,
elbows, and wrists (polyarthritis)
o Red, hot, or swollen joints
o Nontender subcutaneous nodules over bony prominences
o Chest pain
o Tachycardia, heart murmur
o Friction rub/ pericardial rub
o Fatigue
o Non-pruritic macular rash on trunk and extremities (erythema
marginatum)
o Jerky, uncontrollable body movements (chorea)
o Outburst of unusual behavior, such as crying or inappropriate
laughing
 Therapeutic Management
o Treat strep infection
o Salicylates trat inflammatory process
 aspirin
o Prophylaxis:
 Penicillin IM injections once a month
o May require valve replacement
 Nursing Care
o Bed rest
o Promote good nutrition
o Assess for CNS involvement
 Can occur weeks to months after illness
o Educate regarding risk for recurrent infection
o Life-long cardiac follow-up with cardiology

Kawasaki Disease

 Acute systemic vasculitis of unknown origin

  Self-limiting (resolves in 6-8 weeks)
 Mainly affects children < 5 years of age
 20-25% develop acquired heart disease
 Warm Cream
o Fever (warm) lasting longer than 5 days +4 out of 5 of the
following:
 C: conjunctivitis (non-exudative)
 R: Rash (polymorphous non-vesicular)
 Hands and feet; changes through stages
 E: edema (or erythema of hands or feet)
 Erythema: desquamation of hands and feet occurs in
the subacute phase
 A: Adenopathy (cervical, often unilateral)
 M: mucosal involvement (erythema or fissures or crusting)
 Treatment:
o IVIG should be given within 10 days of symptoms
o High dose aspirin (during initial febrile phase)
 Considerations:
o Monitor for side effects of aspirin (Bleeding, Gi upset)
o IVIG is a blood product
 Monitor for infusion reaction
 Complications of disease:
o Without treatment 25% of kids will suffer permanent cardiac
sequelae
o Coronary artery aneurysm
o Myocarditis
 Muscle of the heart is inflamed
o Echocardiogram is key
o If IVIG vaccine is given. It cannot be given with other live
vaccines MMR and ______.

Supraventricular Tachycardia (SVT)

 HR over 22o bpm

 May be present with or without heart defect
 Infants
o Poor feeders, irritable
 Older children
o Palpitations, chest pain, c/o dizziness, SOB
 Treatment:
o Vagel stimulation (increases intrathoracic pressure)
o Adenosine
o Synchronized cardioversion: external (pads) or internal (catheter
placed inside)
o Beta blockers or calcium channel blockers can prevent future
episodes