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Changes in the heart of the newborn

First breath, lungs inflate, decrease in pulmonary vascular resistance, pulmonary artery pressure drops, R atrium pressure decrease. Blood flow to L heart increased pressure in L atrium, closure of foramen ovale. The decrease in pressure of the pulmonary artery leads to closure of the ductus arteriosus (between aorta and pulmonary artery). Ductus venosus (between L umbilical vein and IVC) closes because of lack of blood flow and vasoconstriction.


Heart rates

Infant 90-160
Toddler-Preschooler 80-125
School age 70-100
Adolescents 60-100



Normal BP

Infant 80/40
Toddler 80-100/64
School age 94-112/56-60
Adolescents 100-120/50-70



Give regular intervals about every 12 hours. One hour before or two hours after a meal. NOT WITH FOOD If it is missed and more than four hours have passed withhold the dose. Do not give a second dose if the child vomits. Monitor potassium levels which cause toxicity. Digitalizing the first dose is dividing it into several doses over 24 hours to reach maximum effect. Watch for prolonged PR interval, and decreased ventricular rate. S&S of toxicity: N&V, diarrhea, lethargy, bradycardia

Apical pulse for 60 seconds. Withhold if:
Infant <90



Clubbing of fingers and toes (usually after 1 year) indicated chronic hypoxia due to CHD. First sign is softening of the nail bed, rounding of the fingernails, shininess and thickening of ends.



Abnormal heart enlargement. Often has a prominence of the precordial chest wall


Murmur evaluation

relation to the heart cycle
Grade I soft and hard to hear,
Grade II soft and easily heard
Grade III loud without a thrill
Grade IV loud with precordial thrill
Grade V loud, precordial thrill, audible with stethoscope partially of chest
Grade VI very loud, audible with the naked ear
Quality: harsh, musical or rough; high, medium, or low pitch
Variation with position: sit, lye, stand


Cardiac Catheterization info

Diagnostic: structural defects
Interventional: treatment to dilate occluded or stenotic structure of vessels or close some defects.
Electrophysiologic: electrodes ID abnormal rhythms and destroy sites of abnormal electrical condudtion.

R-side: femoral vein to the R atrium
L-side: into the aorta and heart via an ARTERY
Contrast material is injected into the heart and images taken.


Cardiac Catheterization nursing care

No iodine or shellfish allergy
No anticoagulants
Mark the location of pedal pulses for easy finding later
Inform they may feel heart racing, and warmth or stinging with contrast.
Complications: bleeding, low grade fever, loss of pulse in the extremity used for catheterization, development of arrhythmia. Leg will need to be straight for 4-8 hours with bed rest.

Post op: check the pressure dressing frequently. If bleeding occurs, apply pressure 1 inch above the site. I&O. Contrast is diuretic.

Instructions: Change pressure dressing day after, keep covered and do not get wet for several days. Report S&S infection. Compare extremities. take temp 1xday for 3 days, report if over 100.4. No bath for 3 days. No strenuous activity for 3 days. Tylenol or ibuprofen for pain


Categories of congenital heart defects

Disorders with decreased pulmonary bloodflow (cyanotic): tetralogy of fallot and tricuspid atresia

Disorders with increased pulmonary bloodflow (acyanotic): patent ductus arteriosus PDA, atrial septal defect, ventricular septal defect VSD

Obstructive disorders (acyanotic): coarctation of the aorta, aortic stenosis, pulmonary stenosis

Mixed disorders (cyanotic): transposition of the great vessels, total anomalous pulmonary venous return, truncus arteriosus, hypoplastic left heart syndrome


Disorders decreased pulmonary bloodflow

Pressure in the right side of the heart increases becoming greater than the left side. Deoxygenated blood mixes with the oxygenated blood on the left side and is pumped throughout circulation. This causes low oxygen saturation levels from 50 to 90%. The kidneys compensate for low oxygen, releasing EPO and increasing red blood cells called polycythemia. This can thicken the blood and increase the workload of the heart. Tetralogy of Fallot and tricuspid atresia


Tetralogy of fallot pathophysiology

Four defects:
1. pulmonary stenosis: narrowing of the pulmonary valve and outflow tract, creating obstruction from R ventricle to the pulmonary artery. Decrease in blood flow to the lungs for O2 and amount returning from lungs. This increases pressure in the R-ventricle. Shunted thru VSD
2. VSD ventricular septal defect allows O2 blood to mix with unO2 blood and is pumped thru
3. Overriding aorta of the VSD: enlargement of the aortic valve so much that it appears to arise from the right and left ventricles rather than the correct left ventricle,
4. R ventricular hypertrophy due to continued overuse while attempting to overcome the high pressure.

Dx occurs first few weeks life due to cyanosis and murmur. Most have a PDA (patent ductus arteriosus) at birth, decreasing the initial severity of cyanosis. Hypoxia is the primary problem


Tetralogy of Fallot treatment

Notice color changes associated with eating, activity, or crying. If cyanosis is to severe and persistent infant may come become unresponsive. As an infant gets older they can use specific postures such as bending the knees, assuming the fetal position to relieve a hypercyanotic spell. The walking child may squat periodically which helps increase pulmonary bloodflow by increasing systemic vascular resistance. In an infant, the nurse may put them in the knee chest position

May have loud harsh murmur, clubbing, decreased O2 sat

Labs: increased H&H, RBC; ECG, cardiac catheterization

Management: prostaglandin E1, dilate the ring around the ductus arteriosus, prophylactic antibiotics, propranolol to decrease myocardial irritability (prevent hypercyanotic spells), morphine to lower 02 demand, sodium bicarb to treat acidosis.

Surgical: palliative create a shunt from the aortic arch to the pulmonary artery to have blood going to lungs. Definitive is to repair stenosed valve, fix the septal defect, make sure aorta is only coming off the L ventricle.


Tricuspid atresia

The valve between the right atrium and the right ventricle fails to develop. There's no opening to allow blood flow from the right atrium to the right ventricle and then through the pulmonary artery and lungs. Deoxygenated blood passes through the atrial septum thru a defect for a patent foramen ovale and into the L atrium. Deoxygenated blood mixes with oxygenated blood and travels through the lungs.

Infants will have cyanosis a few days later when the ductus arteriosus closes. They will have rapid respirations, difficulty feeding, cyanosis, poor sucking, crackles or wheezes, murmur, clubbing if older.


Disorders with increased pulmonary flow

Normally left-sided pressure is higher. With certain defects it will cause the right side of the heart pressure to rise. This causes a greater amount of blood to move through the heart. If the amount of blood flowing to the lungs is large, it could cause heart failure. It will cause R ventricle hypertrophy. Deoxygenated blood can mix with oxygenated blood.
Tachypnea will increase calorie use leading to feeding problems. tachycardia. Poor weight gain, decreased growth and development, sodium and fluid retention, increased risk for pulmonary infections, vasoconstriction decrease in pulmonary bloodflow. Pulmonary hypertension.. Oxygen is not helpful. It acts as a pulmonary dilator which will increase pulmonary bloodflow even more causing tachypnea, increasing lung fluid retention, and causing more problems. Early surgical correction is essential.


Atrial Septal Defect

A hole in the wall of the septum that divides the right atrium from the left atrium. There are three types based on location.
1. Ostium primum ASD1: opening is at the lower portion of the septum
2. Ostium secundum ASD2: opening is near the center of the septum
3. Sinus venosus defect: opening is near the junction of the SVC and the R atrium

If small, 80% spontaneous closure in 18 months.

There is increased blood volume in the right atrium, increase blood flow to the lungs. It can cause pulmonary hypertension, heart failure, atrial arrhythmia, or stroke. Most children are asymptomatic.

Possible difficulty growing, hyperdynamic precordium, systolic ejection murmur, R ventricular heave

ECG, x-ray shows enlarged heart


Ventricular septal defect

Opening between the right and left ventricular chambers. One of the most common heart defects. Spontaneous closure occurs in half the children by age 2. The opening vary in size. Children with Small defect may be asymptomatic. A left to right shunt happens when pulmonary vascular resistance is low. There is increased blood in the right ventricle and then pumped to the pulmonary circulation, increasing pulmonary vascular resistance leading to increased pulmonary artery pressure and right ventricular hypertrophy. If Pulmonary vascular resistance exceeds systemic, right to left shunting of blood occurs resulting in Eisenmenger syndrome(pulmonary HTN and cyanosis). Heart failure commonly occurs with moderate to severe unrepaired ventricular septal defect. At risk for aortic valve regurgitation and infective endocarditis.

No initial S&S. Signs of heart failure around 4-8 wks. Tire easily, difficulty thriving, color change or sweating when feeding, edema, tachypnea, holosystolic harsh murmur at L sternal border, possible thrill or adventitious lung sounds
MRI, ECG with color flow doppler, cardiac catheterization,

Management: may close on its own; medical management such as prophylactic antibiotics (to prevent bacterial endocarditis), digoxin and diuretics for mild CHF. Surgically can repair the hole with a patch or suture it.


Atrioventricular canal defect

Includes: atrioventricular septal defect AVSD, AV canal, or endocardial cushion defect. 40% of downsyndrome kids have this.

AV canal failure of endocardial cushions to fuse. These are needed to separate the central parts of the heart near the tricuspid and mitral AV valves. In a complete AV Canal defect, oxygenated blood from the lungs enters the left atrium and ventricle, crossing over the septum and returning to the lungs. This recirculation problem is inefficient. The left ventricle pumps two to three times more blood than normal. Causes a left to right shunt.

Frequent respiratory infections, difficulty gaining weight, cyanosis, retractions, tachypnea, nasal flaring, rales and loud murmur. Signs of heart failure.



Patent Ductus Arteriosus

Fails to close within the first weeks of life. There's a connection between the aorta and pulmonary artery. Occurs more frequently in premature infants and in infants born and high altitudes. Blood flows from the aorta through the PDA and back to the pulmonary artery and lungs, causing an increased left ventricular work load and increased pulmonary vascular congestion. This is often seen with other congenital heart defects so that some oxygenated blood will reach systemic circulation. Blood enters the aorta then travels to the pulmonary artery instead of entering systemic circulation. This increases the workload of the left side of the heart. Eventually you will see right ventricular hypertrophy. Symptoms depend on the severity.

Heart failure, respiratory infections, Fatigue, poor growth and development, tachycardia, tachypnea, bounding pulses, widened pulse pressure, low diastolic blood pressure, rails, harsh continuous murmur (machinery like) loudest under the left clavicle, metabolic acidosis,

Management: endomethacin (prostaglandin inhibitor) because decreased prostaglandins help close the ductus arteriosus. Watch for GI and intracranial bleeding with it; only give 2 doses. If that doesn't work, surgery


Coarctation of the aorta

Narrowing of the aorta which carries highly oxygenated blood from the left ventricle to the rest of the body. 'Restricted blood flow increases pressure on the L ventricle and causes dilation of the proximal aorta and L ventricle hypertrophy' It is seen more often in males. Blood pressure is increased in the heart and upper portions of the body, and decreased in lower areas. Can lead to heart failure. At risk for aortic rupture, aortic aneurysm, and CVA.

Irritability, epistaxis, leg pain and cramps with activity, dizziness, fainting, and headaches. Bounding pulses in upper extremities, weak or absent in lower. Measure blood pressure in all four extremities. Soft or loud systolic murmur at the base of the heart. X-ray may show left-sided enlargement and rib notching
May be asymptomatic, depending on the size.
ECG, x-ray, MRI, CT,
Management: repair before age 4 to avoid permanent HTN, balloon aortaplasty (not usually done because it renarrows), resection and anastamosis, or resect and patch the narrowing area.


Aortic Stenosis

Obstruction of blood flow between the L ventricle and aorta. More often in males. Muscle obstruction, valve obstruction, or narrowing of the aorta above the valve. Most common is obstruction of the valve: aortic valve stenosis. L ventricle hypertrophy and possible failure, backup of pressure in pulmonary circulation, pulmonary edema, heart failure.

Often asymptomatic. The child may fatigue easily, complaint of chest pain when active, dizziness, difficulty eating, faint pulses, thrill at the base of the heart, systolic murmur at L sternal border.

ECG, possible exercise stress test if fatigue and pain


Pulmonary Stenosis

Causes obstruction in the bloodflow between the right ventricle and the pulmonary arteries. Often associated with other heart anomalies. Often asymptomatic but if severe they may have dyspnea and fatigue with exertion. It may happen because of a muscular obstruction below the pulmonary valve, obstruction at the valve, or narrowing of the pulmonary artery above the valve. Valve obstruction is the most common. It causes right hypertrophy and decreased pulmonary bloodflow. Pressure in the right atrium could cause a reopening of the foreman ovale.

Mild dyspnea or cyanosis with exertion. Palpate the sternal border for a thrill. There may be a high-pitched click after the second heart sound and a systolic ejection murmur.


Transposition of the great vessels/arteries

The pulmonary artery and the aorta are transposed. The aorta arises from the right ventricle instead of the left and the pulmonary artery arises from the left ventricle instead of the right. Not compatible with life unless another defect. Usually diagnosed in the first few days. It gets worse after the ductus arteriosus closes. Surgery is performed by 4 to 7 days old.

May not see cyanosis if VSD or if the ductus arteriosus remains open. *Significant cyanosis without a murmur is indicative. Cyanosis. Loud 2nd heart sound. Possible heart failure (edema, tachypnea, adventitious lung sounds). Polycythemia, poor feeding, metabolic acidosis, exercise intolerance

ECgraphy and and cardiac catheterization - Palliative Rashkind procedure (opens back up the foramen ovale with balloon).

Management: Prostaglandin E1 to keep ductus arteriosus open.

Surgical is an arterial switch, coronary arteries have to be reimplanted and can cause MI


Total Anomalous Pulmonary Venous Connection

The pulmonary veins do not connect normally the left atrium, they connect to the right atrium often via the superior vena cava. Oxygenated blood that would normally flow into the left atrium now enters the right atrium into the right ventricle, increasing pressure on the right side leading to R hypertrophy. No chance for life unless there is another defect such as a patent foramen ovale or an ASD to get blood to the left atrium. If this happens there will be pulmonary hypertension and pulmonary edema. Cyanosis will vary depending on severity. Other findings depend on associated anomalies.

Cyanosis, Tiers easy, difficulty feeding, chest prominence of the right ventricular impulse, retraction, tachypnea, splitting of the second heart sound, hepatomegally.

ECG, x-ray, cardiac catheterization


Truncus arteriosus

One major artery leave the heart and supply blood to the pulmonary and systemic circulation. It is positioned over both the left and right ventricles. There is usually increased blood flow to the lungs and decreased to systemic.

Observe for cyanosis, tiring easily, difficulty feeding, poor growth, possible increased respiratory rate, nasal flaring, grunting, retractions, restlessness, lung sounds, and a murmur.


Hypoplastic Left Heart Syndrome

Congenital defect in which all the structures on the left side of the heart are severely underdeveloped. The mitral and aortic valve are completely closed or small, the left ventricle is nonfunctional and is unable to supply blood to the systemic circulation. Treatment includes palliative care, cardiac transplant within first few weeks, or palliative reconstructive surgery in 3 stages from days to weeks.

They may be asymptomatic for a few days until the ductus arteriosus closes. They will get circulatory collapse-shock and must be resuscitated.

Vitals tachycardia, tachypnea, hypothermia, cyanosis, Increased work to breathe, decreased O2 and pallor, single 2nd heart sound, murmur. Usually found on ultrasound prenatally.


Relieving hyper cyanotic spells

Use a calm and comforting approach. Place in a knee to chest position, provide supplemental oxygen, administer morphine, supply IV fluids, administer propranolol.


How to improve oxygenation with a congenital heart defect

Suction as needed,
position in Fowler or semi Fowler position
monitor vitals closely and oxygen saturation
observe for tachypnea and respiratory distress
listen for lung sounds
Chest physiotherapy
provide humidified oxygen as ordered, warming it if needed
Anticipate the need for ventilation


Promoting nutrition for a child with congenital heart disease

They need increase nutrition due to the increased energy expenditure with increased cardiac and respiratory workloads. Formulas may need additives such as polycose or vegetable oil.
Make sure nipple is large enough to decrease work load, no more than 20 minutes per feeding. Possible enteral or pareneteral nutrition. Offer small frequent feedings. Breast-feeding before and after cardiac surgery can help with the immune system. It may be given by a bottle or tube.

150 cal-kg-day


Cardiac tamponade

abrupt cessation of the chest tube output accompanied by an increase in heart rate and increased filling pressure (R atrial) may indicate cardiac tamponade