Cardiac Dysfunction Revised \'17 PDF

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Cardiovascular Dysfunction

Fetal Circulation – In utero, the purpose of the heart is to develop the muscles. The placenta does all the work and provides oxygen to perfuse all the organs (once they cut off fetal circulation, the heart is expected to work 100%). Therefore, the lungs aren’t needed and are nonfunctional. The blood is detoured away from the lungs through two abnormal openings called shunts. In utero, since the heart doesn’t need to work, pressures of both sides are equal. Upon the first breath, the pressure on the left side ↑ and closes the flaps of the shunts. Foramen ovale – a straight pathway across the right atrium to the left atrium, and then into the left ventricle. Blood then flows into the aorta and systemic circulation. The ↑ pressure of the LA stimulates the closure of the foramen ovale within several weeks of birth. Ductus arteriosus – the vascular channel between the pulmonary artery and the aorta. When the blood is pumped through the pulmonary artery, a major portion is shunted to the descending aorta through this shunt. Closes within several days (10-15 hours) after birth. If it’s been a week and you hear a machine-like murmur, it’s abnormal. Ductus venosus – connects the umbilical artery to the superior or inferior vena cava. Constricts within 48 hours.

Congenital Heart Defects – most develop during the first 8 weeks of gestation. Etiology: - Fetal drug exposure – phenytoin, ACE inhibitors, lithium, warfarin, Dilantin - Maternal alcoholism - Maternal viral infections – rubella - Maternal metabolic disorders – phenylketonuria, DM, and hypercalcemia - Maternal complications of pregnancy – if mom has bleeding, hypertension - ↑ maternal age - Genetic patterns - Chromosomal abnormalities – Turner, trisomy 21 (Down’s) - X-ray exposure Clinical Manifestations – the presence of a heart murmur is often the first indication. A murmur is when blood flows with higher pressure to get through an abnormal opening, either through a narrowed valve or vessel or through a shunt.

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Cardiovascular Dysfunction Assessment focuses – the nurse is the first person who comes in contact with the child. Ask about activity and behavior. Ask about nutrition status, if they tire easily while eating, or exercise intolerance. Note diaphoresis. Lethargy, restlessness, irritability. Do they play like they’re supposed to? Ask about weight. Gaining weight too quickly indicates edema. Not enough weight is lack of calories. 24-hour calorie recall. Observe overall color. What does the child look like when they’re upset? Ask for any chest deformities (enlarged chest). Signs of respiratory effort. Clubbing indicates long-term hypoxemia. If you palpate the PMI and it feels like a cat is purring, it is a thrill. Heaves is lifting of the chest wall during contractions. It is abnormal. Auscultate heart sounds and grade murmurs. Classification of Defects Acyanotic defects (LR)  ↑ Pulmonary Blood Flow (PDA, ASD, VSD) – tachypnea, dyspnea, tachycardia, poor weight gain, diaphoresis, periorbital edema, murmur, CHF, recurrent URIs  Blood Flow Obstruction (COA, AS) – diminished pulses, poor color, delayed cap refill, ↓ urine output, CHF with pulmonary edema Cyanotic defects (RL)  ↓ Pulmonary Blood Flow (PS, TOF or tricuspid atresia) – cyanosis, dyspnea, loud murmur, mottled skin, chronic hypoxemia includes fatigue, clubbing of fingers and toes, and delayed developmental milestones, hypoxic spells, poor weight gain, polycythemia, diaphoresis  Mixed defects (TGA) – cyanosis, poor weight gain, pulmonary congestion

Defects with ↑ Pulmonary Blood Flow (Acyanotic) • When a connection occurs between the left and right side of the heart, the blood is shunted from the left to the right side of the heart (LR) and ↑ the amount of blood pumped to the lungs. • Clinical Manifestations  HR, RR, and metabolic rate ↑  Sucking to feed takes energy and diaphoresis may occur  Poor weight gain if unable to take enough calories  CHF  dyspnea, tachypnea, intercostal retractions, and periorbital edema  Frequent URIs Examples of defects with ↑ pulmonary blood flow include PDA, ASD, and VSD.

Patent Ductus Arteriosus (PDA) • Abnormal opening between the aorta and the pulmonary artery; failure of the fetal ductus arteriosus to close after a whole week of life. • Clinical Manifestations – Dyspnea; tachypnea; tachycardia; full, bounding pulses; widened pulse

pressure (difference between systolic and diastole usually less than 30-35); hypotension; CHF; intercostal retractions; hepatomegaly; and poor growth. A continuous “machinery” murmur and a thrill in the pulmonic area

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Cardiovascular Dysfunction Frequent URIs Pulmonary hypertension – lungs getting overfilled with blood. Parents say their child always has a cold, runny nose, sound congested, phlegm in their chest, etc. • Clinical Therapy Administration of NSAIDS (IV ibuprofen [Motrin]) or indomethacin, a prostaglandin inhibitor, often stimulates closure of the ductus arteriosus. Only on preterm infants! Not for full-term.

Video-assisted thoracoscopic surgery with clip ligation – for in term infants. Burn off opening to cause the flap to close.

Transcatheter closure by obstructive device is the standard therapy – closure by an umbrella or coil device

Atrial Septal Defect (ASD) • An abnormal opening between the two atria (foramen ovale never closed), allowing blood from the higher pressure LA to flow into the lower pressure RA. Back into the pulmonary artery to the lungs to get re-oxygenated again. • Clinical Manifestations – o May be asymptomatic with small or moderate-size ASDs o May have CHF with large ASDs; fatigue, easy tiring, and poor growth o Systolic murmur with a fixed split second heart sound o Cardiac enlargement; frequent URIs • Clinical Therapy – Conservative treatment – Spontaneous closure of some small ASDs occur within the first 4 years of life Closure with a septal occluder during cardiac catheterization. Aspirin at 81 mg per day is prescribed for 6 months after the procedure Surgical patch closure (pericardial patch/Dacron patch). Arrhythmias may develop postoperatively.

Ventricular Septal Defect (VSD) • Abnormal opening between the two ventricles results in ↑ pulmonary blood flow. Blood is shunted from the LV directly across the open septum into the pulmonary artery. Most common congenital heart defect. • Clinical Manifestations o Asymptomatic in small VSDs o Moderate or large VSDs – CHF, poor growth, ↓ exercise tolerance, ↑ # of URIs, and pulmonary hypertension o Left and right ventricular hypertrophy

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Cardiovascular Dysfunction o o

Dyspnea, ↑ RR, ↓ in development, feeding difficulties Loud, harsh, pansystolic murmur (during the entire systole) auscultated at 3rd or 4th left intercostal space; thrill may be present. Louder the murmur, the smaller the VSD hole. If a faint murmur is heard, the VSD is getting larger

• Clinical Therapy Conservative treatment – Most small VSDs spontaneously close within the first 6 months of life. Gives the body a chance to fix itself. VSD surgical closure (patch) is performed after 1 year of age (before 2) if they have no symptoms. If they are symptomatic and CHF cannot be managed medically then surgery for these infants is performed within the first 6 months of life. For instance, if you have a 2-month old with a VSD going into HF, they will repair it right away. If you have a 2-year-old with a VSD, no HF, they can wait it out. • Complications – Arrhythmias, right bundle branch block, and complete heart block. May need a pacemaker • Prognosis – respond well to surgery and experience substantial catch-up growth

Obstructing Defects (Acyanotic) • An anatomic stenosis causes obstructed blood flow and results on a pressure load on the LV and ↓ CO. The greater the narrowing, the more obstructed the blood flow is to the circulation. • Clinical Manifestations –  Low CO, diminished pulses, poor color, delayed cap refill time, ↓ urinary output  CHF and pulmonary edema  Leg cramps, cooler feet than hands, and stronger pulses in the arms than the legs.  ↓ blood flow suppy to the GI tract may lead to necrotizing enterocolitis Examples of obstructing defects include AS, COA, and PS.

Aortic Stenosis (AS) • Narrowing of the aortic valve obstructs blood flow from the LV to the systemic circulation. The LV must work harder to force blood past the narrowed valve opening. The prominent anatomic consequence of AS is the hypertrophy of the left ventricular wall. This stricture in the aortic outflow tract causes resistance to ejection of blood from the LV. The extra workload on the LV causes hypertrophy • Clinical Manifestations o ↑ Left ventricular hypertrophy and ↑ in the LV pressure o ↓ CO; tachycardia (extra workload) o Significant AS causes CHF o Weak and thready peripheral pulses (lower extremities) o Chest pain after exercise; exercise intolerance o Feeding intolerance o Fainting and dizziness (syncope)

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Cardiovascular Dysfunction o o o

Systolic blood pressure may be higher in the right arm than the left Systolic ejection heart murmur (ejection click may be heard) and thrill; high-pitched diastolic decrescendo murmur Splitting of S2 may be noted

• Complications – chest pain, syncope, and sudden death can occur during vigorous exercise. Bacterial endocarditis • Clinical Therapy

PGE1 (Prostaglandin E1) given to maintain a patent ductus arteriosus (PDA), as well as dopamine and diuretics to treat CHF Balloon dilation during cardiac catheterization to dilate the narrowing. Surgical valvotomy (surgical cutting of a constricted valve to relieve obstruction) Aortic valve replacement is performed when the stenosis is severe. Lifelong anticoagulant therapy (aspirin or warfarin)

Coarctation of the Aorta (COA) • Narrowing or constriction anywhere along the aorta. This obstructs the systemic blood outflow. • Clinical Manifestations o ↑ BP in the upper extremities (arms, neck, and head) with bounding brachial and radial pulses o ↓ BP in the cool lower extremities (legs) with weak or absent femoral and leg pulses o Infants with open fontanelles, head expands due to the higher blood flow o Older children complain of headaches because the pressure is so high o Weakness, pain and cramping in the legs after exercising due to the ↓ blood flow o Pale; poor feeding; failure to thrive, and ↑ respiratory effort o CHF o Severe constriction: cyanosis in the lower extremities, HF, and shock. o Renal failure and necrotizing enterocolitis o S2 is heard as a loud single sound; systolic ejection murmur and thrill may be present o Dizziness, fainting, & epistaxis (nose bleeding) resulting from hypertension • Complications – increased risk for aneurysms • Clinical Therapy PGE1 is given to reopen the ductus arteriosus to promote blood flow to the kidneys and lower extremities To prevent CHF, give inotropic meds, diuretics, and oxygen Balloon dilation during cardiac cath for mild cases Surgical resection with either a patch or end-to-end anastomosis (shortening the aorta).

Defects with ↓ Pulmonary Blood Flow (Cyanotic)

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Cardiovascular Dysfunction Pulmonic Stenosis (PS) • Stenosis obstructs blood flow into the pulmonary artery and results in right ventricular hypertrophy. • Clinical Manifestations o Cyanosis o Dyspnea and fatigue on exertion (can’t walk or run or meet sucking needs without stopping to breathe) o Signs of CHF, HF, and chest pain on exertion o Loud systolic ejection murmur with a widely split S2 and thrill o Enlarged pulmonary artery • Complications – bacterial endocarditis. Lifelong infective endocarditis prophylaxis may be needed. • Clinical Therapy – balloon dilation during cardiac cath Surgical valvotomy is performed when balloon dilation is unsuccessful On occasion, pulmonary valve is replaced

Tetralogy of Fallot (TOF) • "Gift that keeps on giving." Four defects  Pulmonic stenosis  Right ventricular hypertrophy  VSD  Overriding aorta • Clinical manifestations o ↑ RR and depth of breathing, tachycardia, irritability o Polycythemia o Hypoxic spells, or “Blue/Tet” spells – acute episode of cyanosis and hypoxia. Their oxygen requirements exceed the blood supply. Usually caused by stress, pain, crying, illness, defecation, or feeding. Toddlers tend to instinctively squat as a way to reoxygenate the lungs, the heart, and the brain. Infants need to be put in a knee-to-chest position. Treatment includes: administer O2, knee-chest position, and calm the child. Administer morphine for pain if needed. Change the diaper if that is what is causing them to be upset. o Metabolic acidosis o Poor growth o Clubbing o Exercise intolerance o Systolic murmur and thrill • Clinical Therapy Most corrective surgery is done by 1 or 2 years of age, unless symptomatic (3-4 months). Blalock-Taussig shunt (palliative) – creation of aortopulmonary conduit to ↑ pulmonary blood flow.

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Cardiovascular Dysfunction Tricuspid Atresia • Tricuspid atresia valve fails to develop (no valve or opening exists), consequently there is no communication from the RA to the RV. The RV is hypoplastic (small and nonfunctional). Blood flows through an ASD (or a patent foramen ovale) to the left side of the heart. The ductus arteriosus provides the only flow of blood to the pulmonary artery and lungs. • Clinical Manifestations o Left ventricular hypertrophy o Cyanosis o Tachypnea o Poor feeding o CHF o Pulmonary edema o Hepatomegaly o Acidosis o Hypoxic spells o Clubbing o Polycythemia o Growth delays o Continuous murmur in pulmonic area. A single S2 in the aortic area. A harsh systolic murmur • Clinical Therapy – Prostaglandin E1 is given immediately to maintain a PDA. A balloon atrial septostomy is performed to increase the atrial opening size. A Fontan procedure is performed for the single ventricle defect. Can also do palliative procedures (Blalock-Taussig shunt or pulmonary artery banding). Prophylaxis for thromboembolism and infect endocarditis is recommended. Digoxin and diuretics may be needed longterm.

Mixed Defects

Transposition of the Great Arteries (TGA) • The pulmonary artery leaves the left ventricle, and the aorta exits from the right ventricle with no communication between the systemic and pulmonary circulations (vessels are switched). All the deoxygenated blood from the body is going back to the body. Cyanosis may be less apparent when a large VSD is present. • Clinical Manifestations – Cyanosis (blue baby). Progresses to hypoxemia and acidosis. o Infants take frequent rest periods during feeding o Rapid RR and fatigue o Growth failure o Systolic murmur if a VSD is present. S2 is loud and heard as a single sound o Right ventricular hypertrophy o ↑ H&H or polycythemia

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Cardiovascular Dysfunction • Clinical Therapy – (Therapeutic Management) The administration of IV prostaglandin E1 may be initiated to keep the ductus arteriosus open to temporarily ↑ blood mixing and provide an oxygen saturation of 75% or to maintain CO. Palliative procedure is a balloon atrial septosotomy, meaning you make an ASD to permit oxygenated and unoxygenated blood to mix. To stabilize the patient. (Surgical) An arterial switch procedure is the procedure of choice in the first few weeks of life. The advantage of the arterial switch procedure is the reestablishment of normal circulation.

Procedures for Cardiac Diagnoses 1. Chest X-Ray – provides information on heart size (cardiomegaly) and pulmonary blood flow patterns (lung infection). 2. ECG – graphic measure of the electrical activity of the heart. To see if their heart rhythm is normal and regular (e.g. problems with SA firing). 3. Echo – ultrasound of the heart to produce an image of cardiac structures. Size of heart chambers, movement of valves, defects. 4. Cardiac Catheterization – an invasive diagnostic procedure in which a radiopaque catheter is introduced through a large bore needle into a peripheral vessel and then guided into the heart with the aid of fluoroscopy. Sites used are femoral artery/vein, brachial artery/vein, SVC, or IVC. Injects a dye. Purpose – Can measure pressure in all 4 chambers, analyze heart structures, and blood flow pattern. Can be used for intervention purposes. Dilating stenotic valves with a balloon catheter. Nursing Care Management Pre-Cardiac Cath - Complete nursing assessment includes: accurate height (essential for correct catheter selection), weight, history of allergic reactions (some contrast agents are iodine based), look for signs of infection (severe diaper rash may be a reason to cancel if femoral access is required), assess and mark the pulses, baseline oxygen saturation, etc. - NPO (1 feed before if breast feeding, 4-6 hours if formula fed, 6-8 hours regular feeding) - Methods of sedation include oral or IV. - A bolus of Heparin, to thin their blood so they don’t throw a clot. Post-Cardiac Cath - Assess pulses for equality and symmetry. Expected weakness of pulses for 1-2 hours. - Temperature and color of the affected extremity - VS every 15 mins for the first hour. Every 30 mins for another hour. Every hour for the remaining 8 hours. BP, especially for hypotension which may indicate hemorrhage. - Dressing may indicate bleeding or hematoma formation. - Fluid intake, both IV and oral. Because of the blood loss, the child’s NPO status, and diuretic actions of dyes used during the procedure, put children at risk for hypovolemia and dehydration.

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Cardiovascular Dysfunction -

Blood glucose levels for hypoglycemia in infants. They should receive dextrose-containing IV. Maintain the affected extremity straight to maintain healing of the cannulated vessel.

Complications • Nausea & vomiting – from sedation. Adjust diet slowly. Zofran. • Hemorrhage – from the heparin. Immobilize leg and maintain straight for 8 hours. Do not remove the bandage. Just reinforce it with another bandage if it becomes saturated. • Blood clots – from the entry through an artery. Temp, color, cms checks in legs, size • Arrhythmias – placed on a cardiac monitor for an apical pulse

Congestive Heart Failure (CHF) • Heart function is impaired and CO is inadequate to support the body’s circulatory and metabolic needs. May result from a congenital heart defect that either ↑ pulmonary blood flow or obstructs the systemic blood outflow tract. Pulmonary blood volume overload. In other words, the heart becomes overloaded, does not pump effectively enough, therefore it’s not able to meet the needs of the whole body. Causes include: Coronary vascular disease, acidosis, dysrhythmias, severe anemia, sepsis. Left-sided heart failure – the LV is unable to pump blood into the systemic circulation, instead it back flows. Resulting in ↑ pressure in the LA and pulmonary veins, congesting the lungs with blood, causing elevated pulmonary pressure and pulmonary edema. Manifests with respiratory symptoms. Frequent URIs, pulmonary congestion, tachypnea, or orthopnea. Right-sided heart failure – the RV is unable to pump blood effectively into the pulmonary artery, resulting in ↑ pressure in the RA and systemic venous circulation. The right side pumps blood forward into the lungs, instead it back flows into the systemic circulation. Manifests with systemic symptoms. Periorbital edema in infants. Lower extremity edema in older children. Hepatosplenomegaly. • Clinical Manifestations – cardiomegaly, tachypnea (L), hepatosplenomegaly (R) 1. Impaired myocardial function  Tachypnea  Tachycardia and weak pulses  Pallor, cool extremities  Oliguria  Diaphoresis  Fatigue, weakness, restlessness, irritability  Anorexia  Hypotension  Capillary refill time >2 secs 2. Pulmonary Venous Congestion  Tachypnea  Wheezing, crackles  Retractions; nasal flaring  Pulmonary edema  Cough, grunting  Poor feeding; ↑ tachypnea and diaphoresis with feeding

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