NCM 109 LEC Care of Mother and Child at Risk or with Problems (Acute or Chronic)

CRDIOVASCULAR DISORDER
Mary Jane Rigor

CONGESTIVE HEART FAILURE These include:

• It is the inability of the cardiovascular system to provide o Cardiomyopathy (ds. Of the heart muscle resulting in
adequate cardiac output to meet the metabolic demands poor pump function)
of the body. o Endocarditis (infection of the inner lining of the heart)
o Heart fails to pump enough blood to support o Rheumatic fecer
the body’s functions o Myocarditis (inflammation of the heart muscle)
o Types of CHF depend on which part of the heart o These diseases results in impaired myocardial
fails: the left half that pumps to the body, or the contractility with a subsequent fall in cardiac output. This
right half that pumps to the lungs phenomenon causes overload and resultant pulmonary
o Etiology – the absolute incidence of the CHF in and systemic venous congestion
infants and children is unknown because of the o Tacchyarryhtmias (abnormally fast heart muscles)
wide range of causes. o Bradyarrythmias (abnormally slow heart rates)
• Congenital heart defects are the most common causes.
SIGNS AND SYMPTOMS
• Defects with left or right shunt (ventricular septal defect)
• Tires easily during feeding
impose a volume load.
• Periorbital edema, weight gain
• Left sided obstructive defects (hypoplastic left heart
• Rales and rhonchi
syndrome, aortic stenosis, coarctation of the aorta)
impose a pressure load as there is obstruction to forward • Dyspnea, orthopnea, tachypnea
flow of blood. • Diaphoretic/sweating
• Excessive volume and pressure can contribute to • Tachycardia
pulmonary edema. • Failure to gain weight
• Acquired heart disease is the most common cause in
TREATMENT OF CONGESTIVE HEART FAILURE
older children and adolescents.
• The inability of the myocardium to circulate enough
oxygenated blood to meet the demands of the body. MEDICATION THERAPY
• When the heart fails, cardiac output is diminished. Heart
rate, preload, contractility, and afterload are affected. 1. DIGITALIS
• Peripheral tissue is not adequately perfused. - increases contractility and decreases heart rate. (ex:
• Congestion in lungs and periphery develops. digoxin)
- Nursing responsibilities:
→ BP and HEART RATE monitoring

2. ACE-inhibitors – Arterial vasodilator/afterload reducing agent.

3. DIURETICS
- enhance renal secretion of sodium and water by
reducing circulating blood volume and decreasing
preload. (ex: furosemide {Lasix})
- Nursing Responsibility:
→ measure urine output
→ if there is still no urine output, report to the
physician.

4. BETA BLOCKER – increases contractility.

TREATMENT

➢ DIET – low sodium, small frequent feedings (be sure you can
CLINICAL MANIFESTATIONS pick the right foods for a low NA diet)
• Tachypnea ➢ NURSING CARE:
• RR greater than or equal to 60 in infants and toddlers • Measure intake and output – weighing diapers.
and greater than or equal to 40 in children over 2 years • Observe for changes in peripheral edema and
old. circulation.
• Retractions, flaring or rapid shallow respirations • If ascites present – take serial abdominal
• Restlessness in neonates and infants measurements to monitor changes.
• Older children (dyspnea) with exertion and orthopnea • Skin care
• Rales and rhonchi • Turning schedule
• Pulmonary congestion
FINDINGS OF LEFT CHF AND RIGHT CHF
• Pulmonary edema
• Systemic venous congestion indicates right ventricular HEART FAILURES
failure. Sings of this include: LISTED IN ORDER OF EARLIEST TO LATER FINDINGS
o Hepatomegaly, jugular venous distention, RIGHT BILATERAL LEFT
peripheral edema, periorbital edema, ascites
• Nocturia • fatigue in • Restlessness,
• Cardiac symptoms of CHF include:
• Bulging neck adults irritability,
o Tachycardia, gallop rhythms, diaphoresis, and
veins • decreased play hostility,
decreases peripheral pulse, cool mottled and agitation
• ankle and foot activity in
threaduy pulse indicate poor perfusion, edema children • Anxiety
hypotension is a late sign, growth failure and • liver • tachycardia • Cough, often
poor weight gain – is very common, respiratory enlargement • hypotension dry initially
difficulties especially during feeding. called • Shortness of
hepatomegaly breath
• Tachypnea

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 NCM 109 LEC Care of Mother and Child at Risk or with Problems (Acute or Chronic)
CRDIOVASCULAR DISORDER
Mary Jane Rigor
• Crackles
• Pulmonary
edema • Many complex defects require staged repairs that is more
• ‘frothy’ than 1 surgery w/c is usually require for final correction.
sputum – may • Completion of stage repairs occurs by aged 2-4
be blood • Repair of defects that is impose little pairs or no
tinged
hemodynamic alteration may be deferred until the age 2
• Diaphoreses
or 3.
• Cyanosis
• Weight gain • Mild isolated defects may never require surgery.
• CPB (Cardiopulmonary bypass is implemented w/c is
used for the pair of many congenital defects)
• CPB is a mechanical pump and artificial oxygenator that
provides for a short period substitution for heart and
DIAGNOSTIC FINDINGS lung.
• the primary goal is to determine the underlying cause of
CBP Principle include the removal of unoxygenated blood via a
the heart failure.
venous cannula and the delivery of the oxygenated blood back to
o History and physical exam
the patient via an aortic cannula
o CXR – to determine heart size and pleural
effusions ETIOLOGY: usually not known – associated with maternal factors:
o EKG for changes, arrythmias
o Echocardiogram to measure valvular o Infection
abnormalities o Alcoholism
o Nuclear imaging – to determine myocardial o Age over 40 years
contractility, myocardial perfusion, and acute o Diabetes mellitus, type one
cell injury o Genetics, chromosomal changes
o Hemodynamic monitoring of arterial blood
pressure, pulmonary artery pressure, GENERAL FINDINGS OF CONGENITAL HEART DEFECTS
pulmonary artery wedge pressure and cardiac • Child small for age
output. • Physiological failure to thrive
• Exercise intolerance
TREATMENT AND NURSING MANAGEMENT
• Dyspnea while feeding
• Objective: to restore balance between myocardial oxygen • Squatting position
supply and demand
• Clubbing of fingers
• Treatments: oxygen, digitalis, vasodilators, nitrates
antihypertensives, cardiac glycosides, diuretics, intra- Physical consequences of cardiac problems
aortic balloon counter pulsation, ventricular assist
pumping, etc. • Increased workload.; pulmonary hypertension; decreased
systemic output; cyanotic defects
NURSING INTERVENTIONS • Can lead to hypoxemia and polycythemia
• Administer medications as ordered • Concern: formation of thrombus with embolus
• Administer oxygen as ordered – to prevent tissue
hypoxia 1. ACYANOTIC DEFECT – infant/child is “pink”
• monitor hemodynamic indicators
• monitor for findings of hyponatremia, hypokalemia Pathology: hole in the heart’s internal wall
• restrict fluids and assess for findings of fluid retention - Blood flows from the heart’s internal wall
• client and family teaching - Blood flows from heart’s arterial (left) to venous (right)
o medications and side effects side or a “left to right shunt”, not systemically, but only
o how to conserve energy and thus oxygen within heart itself
o teach client relative to report - Size of defect will determine severity of condition
▪ weigh gain of more than two pounts - Four common types: all with increased pulmonary blood
in 24 hours (equals 1 liter) flow
▪ dsypnea
▪ decreased exercise tolerance TYPE FINDINGS
o importance of sodium-restricted diet. Atrial Septal Defect (ASD) Asymptomatic or mild heart
o Medication directed at improving contractility failure (HF)
are referred to as positive inotropes. There are
three classes of agents Ventricular Septal Defect HF to a degree that depends
▪ Cardiac glycosides (VSD) on the size of defect; murmur
▪ Sympathomimetics
Asymptomatic during infancy;
▪ Phosphodiesterase
mild HF; machinery-like
o DIGOXIN – is a cardiac glycoside and is Patent Ductus Arteriosus murmur; increased pulse
currently the first line inotrope used in the (PDA) pressure; dyspnea, bounding
infant or child. It improved ventricular
rapid pulse on exertion
contraction, a reduction in heart rate and a
reduction of cardiac work. It is frequently used Increased BP in head and
in combination with diuretics. arms; lower BP in feet & legs;
Coarctation: Obstructive cooler temperature in both
CONGENITAL HEART DEFECTS IN GENERAL Defect legs; mild CHF. Occasional
increased BP in older children,
• Occurs in approximately 8 in 1000 live births (AHA)
who complain of headache,
• There are minimum of 35 types of recognized defects.
dizziness, and fainting.
• Such as patent ductus arteriosus to more serious and
complex anomalies such as hypoplastic left heart
syndrome.

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 NCM 109 LEC Care of Mother and Child at Risk or with Problems (Acute or Chronic)
CRDIOVASCULAR DISORDER
Mary Jane Rigor

2. CYANOTIC DEFECT: infant/child is “blue” ATRIAL SEPTAL DEFECT (ASD)

Pathology • Higher pressure exists in t he left side of the heart

• Right atrium gets congested initially
- Unoxygenated blood mixes with oxygenated, via a “right
• Muscles will compensate due to hypertrophy by
to left shunt”
increasing the heart contractility.
- Decreases oxygenation to the entire system
- Results far more severe than acyanotic CLINICAL MANIFESTATIONS
- Thrombus formation is always a concern
• Asymptomatic
TYPE FINDINGS • Often soft systolic murmur
Tetralogy of Fallot (TOF): VSD, Cyanosis, depending on • More classically split S2 unaffected by respiratory
Pulmonic Stenosis, Overriding degree of obstruction or of system.
Aorta, Right Ventricular blood flow from right
Hypertrophy ventricle; murmur; failure to DIAGNOSIS
thrive; clubbing; exertion • Murmur is detected during routine health examination
causes dyspnea and cyanosis • CXR demonstrate increase heart size
• Echocardiogram demonstrate the location and size of the
Transposition of the Great Cyanosis, depending on type defect.
Vessels (TOGV) and size of associated defects;
cardiomegaly TREATMENT
• Diuretics for CHF
• Surgical repair – performed in the preschool age because
NURSING CARE OF THE CHILD WITH A CONGENITAL HEART there is possibility of closure in the first two years of life
DEFECT
• Surgery is often performed via a median sternotomy
• Emotional, physiological, and psychological interventions (vertical incision along the sternum). Defect is repaired
• Assisting the child and family to adjust to special needs via stitch closure or patch through an incision made at
• Goals of treatment: the right atrium.
o Child will maintain adequate oxygenation and
physiological stability MAIN COMPLICATIONS OF SURGERY
o Family will understand signs and symptoms of ATRIAL ARRYTHMIAS
the condition, and how to manage each of them
o Child will attain milestone of normal growth and • heart block secondary to edema around a surgical
development interruption of the conduction system
o When child has surgery, child and family will be • For the results so f many years of increased pulmonary
prepared, know prognosis, and know how to blood flow often leads to severe pulmonary
give home care afterward. hypertension.

NURSING INTERVENTIONS VENTRICULAR SEPTAL DEFECT

• Abnormal connection between the R & L ventricles

• Recognize CHF
• Monitor height, weight, vital signs, pulses, pulse
oximeter, intake and output
• Give medications: digoxin (Lanoxin), furosemide (Lasix) or
chlorothiazide (Diuril); monitor for desired outcomes and
side effects
• Recognize and treat pain appropriately: pharmacological
and nonpharmacological interventions
• Maintain a safe environment
• Conserve energy
• Maintain proper nutrition, with small, frequent feedings
• Support and discuss treatment with parents
• Place in proper position – slanting position with head
elevated, older babies in infant seats, occasional knee-
chest.
DEFECTS WITH INCREASE PULMONARY BLOOD FLOW
• Are caused by a shunting of the blood from the left of
the heart to the right side through an abnormal
connection (L to R shunt). The blood flows from the left
to the right side because the pressure are greater on the
left side of the heart.
• The increase amount of blood in the right side leads to
increased pulmonary blood flow
• Infants leads to:
o CHF, Atrial Septal Defect, Ventricular Septal
defects, patent ductus arteriosus,
antrioventricular septal defects and truncus
arteriosus.
• Defects can be located in various positions along the
septum
INCIDENCE: common among CHD
• Right chamber of the heart has more than the usual
amount of blood volume, therefore congestion of the
right side of the heart happens
• The myocardium stretches beyond the normal size
• Tachycardia, earliest sign, which is normal while in the
nursery, reason why it is not always diagnosed upon
delivery
• The heart gets tired, the cardiac output decreases
• Cardiac output is the direct proportion of heart rate and
stroke volume of the heart
• Organ perfusion decreases, organ malfunctions sets in
• Glomerular filtration rate decreases
• Multi-organ malfunction due to congestive heart failure
because of inadequate blood supply due to the worn out
heart muscles.
1. Oxygenated blood is shunted from left to right side of the
heart via defect
2. A larger volume of blood than normal must be handled by the
right side of the heart -> hypertrophy
3. Extra blood then passes through the pulmonary artery into
the lungs, causing higher pressure than normal in the blood
vessels in the lungs -> congestive heart failure.
DIAGNOSIS
• Loud holosystolic murmur
• CXR moderate defect shows cardiomegaly
• Echocardiogram

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 NCM 109 LEC Care of Mother and Child at Risk or with Problems (Acute or Chronic)
CRDIOVASCULAR DISORDER
Mary Jane Rigor

CLINICAL MANIFESTATIONS
• Asymptomatic
• CHF
o Tachypneic
o Diaphoretic
o Fatigue easily
o Underweight
o Cyanotic is not usually present
o Feeding history will usually reveals an infant
tires before a feeding is completed.

PATHOPHYSIOLOGY
1. Increase pressure on the left side of the heart, blood
flow through VSD is L-R
2. Blood flow will recirculate through the pulmonary artery
to the lungs
3. Increase pulmonary blood flow to heart enlargement
and pulmonary venous congestion

Degree of the L-R shunting depends on two major factors:

✓ The size of the defect and

✓ The child’s pulmonary resistance

TREATMENT
• Small VSD who does not demonstrate signs of CHF do
not require treatment as approximately 70-75% of
defects will close spontaneously (Miyake et al 2004)
• May close by two years
• Digoxin and diuretics
• High calorie formula (NGT)
• Surgical repair – Indicated between 3 and 12 months

POST-OP COMPLICATIONS

• Atrial arrhythmias
• Complete heart block
• Ventricular arrythmias
• Residual shunt of leaking on the site

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