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75 Cards in this Set
- Front
- Back
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Signs and Symptoms of Congenital Heart Disease
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Heart murmur
Repiratory difficulties: tachypnea, dyspnea, shortness of breath Failure to thrive Cyanosis Presence of other congenital defects Exercise intolerance and fatigue |
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Diagnostic Evaluation-Cardiac Catherization: Pre-procedure care
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Pre-procedure care
Nursing assessment Obtain height/weight History of allergic reactions Assess diaper area Assess and mark dorsalis pedis, posterior tibial pulses Baseline O2 sat Patient/parent teaching Maintain NPO status for 4-6 hours prior to procedure |
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Diagnostic Evaluation-Cardiac Catherization: Post-procedure care
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Post-procedure care
Pulses, especially below cath site Temperature and color of extremity Vital signs Blood pressure Dressing for bleeding or hematoma FLAT FOR 4-6 HOURS Fluid intake Hypoglycemia Apply direct continuous pressure 2 fingerbreaths above the site to depress artery and stop bleeding Keep area clean and dry Pressure dressing may be removed day after cath. |
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Newer Classification of CHD: Hemodynamic characteristics
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Increased pulmonary blood flow
Decreased pulmonary blood flow Obstruction of blood flow out of the heart Mixed blood flow |
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Increased Pulmonary Blood Flow Defects
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Abnormal connection between two sides of heart
--either the septum or the great vessels Increased blood volume on right side of heart Increased pulmonary blood flow Decreased systemic blood |
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Lesions with Increased Pulmonary Blood Flow
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Infants born with CHD that causes an increase in pulmonary blood flow are at increased risk for CHF and pulmonary vascular disease
Blood flows from the higher pressure left side of the heart to the lower pressure right side Left--to--right shunt |
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Increased Pulmonary Blood Flow Defects
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Atrial septal defect
Ventricular septal defect Patent ductus arteriosus |
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Atrial Septal Defect
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Abnormal opening between the atria, allowing blood from the higher pressure left atrium to flow into the lower pressure right atrium.
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Atrial Septal Defect: pathophysiology
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Because left atrial pressure slightly exceeds right atrial pressure, blood flows from the left to the right atrium, causing an increased flow of oxygenated blood into the right side of the heart. Despite the low pressure difference, a high rate of flow can still occur because of low pulmonary vascular resistance and the greater distensibility of the right atrium, which further reduces flow resistance. This volume is well tolerated by the right ventricle because it is delivered under much lower pressure than in a ventricular septal defect. Although there is right atrial and ventricular enlargement, cardiac failure is unusual in an umcomplicated ASD. Pulmonary vascular changes usually occur only after several decades if the defect is unrepaired.
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Atrial Septal Defect: Clinical manifestations
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Patients may be asymptomatic. They may develop congestive heart failure (CHF). There is a characteristic murmur. Patients are at risk for atrial dysrhythmias (probably caused by atrial enlargement and stretching of conduction fibers) and pulmonary vascular obstructive disease and emboli formation later in life from chronic increased pulmonary blood flow.
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Atrial Septal Defect: management
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spontaneous closure
surgical repair |
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Atrial Septal Defect
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If large or persistent surgery to close defect occurs 1-5 years of age
Interventional cardiac cath Pericardium patch (cardiopulmonary bypass) If done open heart child at risk for endocarditis |
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Ventricular Septal Defect (VSD)
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Abnormal opening between the right and left ventricles. May vary in size from a small pinhole to absence of the septum, resulting in a common ventricle. Frequently associated with other defects, such as pulmonary stenosis, transpostion of the great vessels, patent ductus arteriosus, atrial defects, and coarctation of the aorta. Many VSDs (20% to 60%) are thought to close spontaneously. Spontaneous clsoure is most likely to occur during the first year of life in children having small or moderate defects. A left-to-right shunt is caused by the flow of blood from the higher pressure left ventricle to the lower pressure right ventricle.
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Ventricular Septal Defect (VSD): pathophysiology
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Because of the higher pressure within the left ventricle and because the systemic arterial circulation offers more resistance than the pulmonary circulation, blood flows through the defect into the pulmonary artery. The increased blood volume is pumped into the lungs, which may eventually result in increased pulmonary vascular resistance. Increased pressure in the right ventricle as a result of left-to-right shunting and pulmonary resistance causes the muscle to hypertrophy. If the right ventricle is unable to accommodate the increased workload, the right atrium may also enlarge as it attempts to overcome the resistance offered by incomplete right ventricular emptying.
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Ventricular Septal Defect (VSD): Clinical manifestations
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CHF is common. There is a characteristic murmur. Patients are at risk for bacterial endocarditis and pulmonary vascular obstructive disease. In severe defects, Eisenmenger syndrome may develop.
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Patent Ductus Arteriosus (PDA)
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Failure of the fetal ductus arteriosus (artery connecting the aorta and pulmonary artery) to close within the first weeks of life. The continued patency of this vessel allows blood to flow from the higher pressure aorta to the lower pressure pulmonary artery, causing a left-to-right shunt.
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Patent Ductus Arteriosus (PDA): pathophysiology
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The hemodynamic consequences of PDA depend on the size of the ductus and the pulmonary vascular resistance. At birth the resistance in the pulmonary and systemic circulations is almost identical, thus equalizing the resistance in the aorta and pulmonary artery. As the systemic pressure exceeds the pulmonary pressure, blood begins to shunt from the aorta, across the duct, to the pulmonary artery (left-to-right shunt).
The additional blood is recirculated through the lungs and returned to the left atrium and left ventricle. The effect of this altered circulation is increased workload on the left side of the heart, increased pulmonary vascular congestion and possibly resistance, and potentially increased right ventricular pressure and hypertrophy. |
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Patent Ductus Arteriosus (PDA): Clinical manifestations
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Patients may be asymptomatic or show signs of CHF. There is a characteristic machinery-like murmur. A widened pulse pressure and bounding pulses result from runoff of blood from the aorta to the pulmonary artery. Patients are at risk for bacterial endocarditis and pulmonary vascular obstructive disease in later life from chronic excessive pulmonary blood flow.
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Patent Ductus Arteriosus (PDA)
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May be attributed to stimulation of prostaglandins (PGE)
Administer IV indomethacin (indocin), a prostaglandin inhibitor = lower PGE and leads to ductus closure If fails interventional cardiac cath 6m-1y (occluder device or coil) Exceptionally large - ductal ligation (thoracotamy - open chest) |
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Obstructive Defects
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Coarctation of the aorta
Pulmonic stenosis |
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Lesions obstructing blood flow to the ventricles
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Pressure in the ventricle and in the great artery before the obstruction is increased and the pressure in the area beyond the obstruction is decreased.
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Coarctation of the Aorta (COA)
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Localized narrowing near the insertion of the ductus arteriosus, resulting in increased pressure proximal to the defect (head and upper extremities) and decreased pressure distal to the obstruction (body and lower extremities).
Incidence: 4th most common lesions with a slight male dominance Frequently associated with other defects |
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Coarctation of the Aorta (COA): Clinical manifestations
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There may be high blood pressure and bounding pulses in arms, weak or absent femoral pulses, and cool lower extremities with lower blood pressure. There are signs of congestive heart failure (CHF)in infants. Often these patients' hemodynamic condition deteriorates rapidly and they are admitted to the ICU near death, usually severly acidotic and hypotensive. Mechanical ventilation and inotropic support are often necessary before surgery. Older children may experience dizziness, headaches, fainting, and epistaxis resulting from hypertension. Patients are at risk for hypertension, ruptured aorta, aortic aneurysm, or stroke.
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Coarctation of the Aorta (COA)
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HTN, epistaxis, H/A, dizziness
May not be picked up until later during BP screen Balloon angioplasty or surgical end to end anastamosis Long term antihypertensives |
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Pulmonic Stenosis (PS) and Catheter Placement
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Balloon angioplasty in the Cardiac Cath Lab to dilate the valve. A catheter is inserted across the stenotic pulmonic valve into the pulmonary artery, and a balloon at the end of the catheter is inflated and rapidly passed through the narrowed opening. The procedure is associated with few complications and has proved to be highly effective. It is the treatment of choice for discrete PS in most centers and can be done safely in neonates.
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Pulmonic Stenosis (PS)
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Pathophysiology: narrowing at the entrance to the pulmonary artery
Clinical signs: maybe asymptomatic, mild CHF, murmur, cardiomegaly |
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Pulmonic Stenosis (PS): management
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Dependent of the severity of stenosis
Balloon valvuloplasty - via cardiac cath relieves stenosis Moderate to severe - valvotomy |
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Decreased Pulmonary Blood Flow Defects: Tetralogy of Fallot
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The classic form includes four defects: (1) ventricular septal defect, (2) pulmonic stenosis, (3) overriding aorta, (4) right ventricular hypertrophy
Incidence: One of the most common defects (10% of all CHD) |
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“Tet spells”
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Related to increased need for O2 in face of limited PBF
Crying and persistent irritability with increasing cyanosis may be first sign Spell may occur spontaneously or with feeding, bathing, IV insertion etc. Treatment: Morphine Oxygen #1 KNEE CHEST POSITION fluids |
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Transposition of the Great Arteries-mixed defect
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Pathophysiology:
pulmonary artery arises from the morphologic left ventricle and the aorta arises from the morphologic right ventricle (+/- VSD) Incidence: accounts for 10% of all CHD 75% male predominance Clinical signs depends on size of defect-often cyanotic at birth Treatment: If no defects occur PGE will be administered to keep ductus arteriosus open Balloon atrial septum pull through to widen the foramen ovale (creates an artificial ASD) Arterial switch performed at 1 week to 3 months |
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Hypoplastic Left Heart Syndrome
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Underdevelopment of the left side of the heart, resulting in a hypoplastic left ventricle and aortic atresia. Most blood from the left atrium flows across the patent foramen ovale to the right atrium, to the right ventricle, and out the pulmonary artery. The descending aorta receives blood from the patent ductus arteriosus supplying systemic blood flow.
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Hypoplastic Left Heart Syndrome
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Pathophysiology:
underdevelopment of left heart. Requires ASD or patent ductus which allows mixing of blood Clinical Signs: mild cyanosis with CHF, shock, hypotension Requires maintenance of PDA with prostaglandins for survival in absence of ASD |
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Congestive Heart Failure (CHF)
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Clinical Manifestations:
TACHYCARDIA TACHYPNEA respiratory distress respiratory infections failure to thrive pulmonary edema periorbital edema hepatomegaly gallop rhythm irritability oliguria cool skin diaphoresis cardiomegaly cyanosis weight gain |
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CHF in Children
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Impaired myocardial function
Tachycardia, fatigue, weakness, restless, pale, cool extremities, decrease BP, decrease urine output Pulmonary congestion Tachypnea, dyspnea, respiratory distress, exercise intolerance, cyanosis Systemic venous congestion Peripheral and periorbital edema, weight gain, ascites, hepatomegaly, neck vein distention |
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Management of the child with CHF
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Improve cardia function:
Digoxin Ace Inhibitors Remove Accumulated fluid and Sodium: Lasix Diuril Aldactone Improve tissue oxygenation Fluid Restriction Maximize nutrition Treat upper respiratory infections Decrease cardiac demands |
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Nursing Care - Administration of Cardiac Medications
KNOW THIS SLIDE |
Check apical pulse for one minute
Hold meds if pulse below 90-110 in infants and young children; 70 beats/min in older children Obtain rhythm strip-assess for prolonged P-R interval and dysrhythmias Signs and symptoms of digoxin toxicity-therapeutic range (0.8-2.0 micro grams/L) nausea/vomiting CLASSIC SIGN Anorexia Bradycardia Dysrhythmias |
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Nursing Care-Decreasing Cardia Demands
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Assessment: Signs and symptoms of Early CHF
rest and conservation of energy Plan care according to infant's sleep wake cycle Feed on demand-small frequent Monitor temperature-avoid extremes Assess for areas of skin breakdown |
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Nursing Care-Reducing Respiratory Distress
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Assessment, positioning, and oxygen administration
Elevate HOB to 45 degree angle Humidified oxygen Monitor for signs and symptoms of respiratory infection |
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Nursing Care-Maintaining nutritional status: FTT
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Several factors related to CHD interfere with normal growth
FTT major problem in infants with CHD Feed on demand-usually q3 hours May require gavage supplementation Increasing caloric content of feedings |
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Cyanosis: Respiratory vs Cardiac Cause
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Cardiac:
cyanosis increases with crying does not improve significantly with oxygen CLASSIC SIGN: TACHYPNEA Respiratory: Cyanosis decreases with crying Improves with oxygen Respiratory distress |
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Consequence of Long Term Cyanosis
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Polycythemia
hemorrhage Bacterial endocarditis clubbing Brain abscess, CVA, DD Pulmonary HTN Hypercyanotic spells (tet spells) |
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Endocarditis
KNOW THIS SLIDE |
BE: bacterial endocarditis
IE: infective endocarditis SBE: subacute bacterial endocarditis Strep Staph Fungal infections PROPHYLAXIS: 1 hr before procedures (IV) OR MAY USE PO IN SOME CASES |
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Rheumatic Fever
Rheumatic Heart Disease KNOW THIS SLIDE |
RF - Rhematic Fever
Inflammatory disease occurs after Group A B-hemolytic streptococcal pharyngitis Infrequently seen in U.S.; big problem in Third World Self-limiting-a disease that eventually goes away even if untreated Affects joints, skin, brain, serous surfaces, and heart Rhematic Heart Disease Most common complication of rheumatic fever (RF) Damage to valves as result of RF |
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Epidemiology
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Peak risk group: 5-15 years
Girls affected more often than boys Increased incidence in blacks Increased prevalence in socially and economically deprived population groups |
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Pathophysiology
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Group A beta hemolytic strep-environmental trigger
Host suseptibility Immune Response |
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Hypoplastic Left Heart Syndrome
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Underdevelopment of the left side of the heart, resulting in a hypoplastic left ventricle and aortic atresia. Most blood from the left atrium flows across the patent foramen ovale to the right atrium, to the right ventricle, and out the pulmonary artery. The descending aorta receives blood from the patent ductus arteriosus supplying systemic blood flow.
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Hypoplastic Left Heart Syndrome
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Pathophysiology:
underdevelopment of left heart. Requires ASD or patent ductus which allows mixing of blood Clinical Signs: mild cyanosis with CHF, shock, hypotension Requires maintenance of PDA with prostaglandins for survival in absence of ASD |
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Congestive Heart Failure (CHF)
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Clinical Manifestations:
TACHYCARDIA TACHYPNEA respiratory distress respiratory infections failure to thrive pulmonary edema periorbital edema hepatomegaly gallop rhythm irritability oliguria cool skin diaphoresis cardiomegaly cyanosis weight gain |
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CHF in Children
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Impaired myocardial function
Tachycardia, fatigue, weakness, restless, pale, cool extremities, decrease BP, decrease urine output Pulmonary congestion Tachypnea, dyspnea, respiratory distress, exercise intolerance, cyanosis Systemic venous congestion Peripheral and periorbital edema, weight gain, ascites, hepatomegaly, neck vein distention |
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Management of the child with CHF
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Improve cardia function:
Digoxin Ace Inhibitors Remove Accumulated fluid and Sodium: Lasix Diuril Aldactone Improve tissue oxygenation Fluid Restriction Maximize nutrition Treat upper respiratory infections Decrease cardiac demands |
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Nursing Care - Administration of Cardiac Medications
KNOW THIS SLIDE |
Check apical pulse for one minute
Hold meds if pulse below 90-110 in infants and young children; 70 beats/min in older children Obtain rhythm strip-assess for prolonged P-R interval and dysrhythmias Signs and symptoms of digoxin toxicity-therapeutic range (0.8-2.0 micro grams/L) nausea/vomiting CLASSIC SIGN Anorexia Bradycardia Dysrhythmias |
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Nursing Care-Decreasing Cardia Demands
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Assessment: Signs and symptoms of Early CHF
rest and conservation of energy Plan care according to infant's sleep wake cycle Feed on demand-small frequent Monitor temperature-avoid extremes Assess for areas of skin breakdown |
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Nursing Care-Reducing Respiratory Distress
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Assessment, positioning, and oxygen administration
Elevate HOB to 45 degree angle Humidified oxygen Monitor for signs and symptoms of respiratory infection |
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Nursing Care-Maintaining nutritional status: FTT
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Several factors related to CHD interfere with normal growth
FTT major problem in infants with CHD Feed on demand-usually q3 hours May require gavage supplementation Increasing caloric content of feedings |
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Cyanosis: Respiratory vs Cardiac Cause
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Cardiac:
cyanosis increases with crying does not improve significantly with oxygen CLASSIC SIGN: TACHYPNEA Respiratory: Cyanosis decreases with crying Improves with oxygen Respiratory distress |
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Consequence of Long Term Cyanosis
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Polycythemia
hemorrhage Bacterial endocarditis clubbing Brain abscess, CVA, DD Pulmonary HTN Hypercyanotic spells (tet spells) |
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Endocarditis
KNOW THIS SLIDE |
BE: bacterial endocarditis
IE: infective endocarditis SBE: subacute bacterial endocarditis Strep Staph Fungal infections PROPHYLAXIS: 1 hr before procedures (IV) OR MAY USE PO IN SOME CASES |
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Rheumatic Fever
Rheumatic Heart Disease KNOW THIS SLIDE |
RF - Rhematic Fever
Inflammatory disease occurs after Group A B-hemolytic streptococcal pharyngitis Infrequently seen in U.S.; big problem in Third World Self-limiting-a disease that eventually goes away even if untreated Affects joints, skin, brain, serous surfaces, and heart Rhematic Heart Disease Most common complication of rheumatic fever (RF) Damage to valves as result of RF |
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Epidemiology
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Peak risk group: 5-15 years
Girls affected more often than boys Increased incidence in blacks Increased prevalence in socially and economically deprived population groups |
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Pathophysiology
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Group A beta hemolytic strep-environmental trigger
Host suseptibility Immune Response |
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Treatment: KD
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High dose intravenous immunoglobulin and oral ASA
Treatment should be initiated within the first 10 days of onset Continue treatment until Afebrile for several days ASA for 6-8 weeks or indefinitely if cardiac abnormalities present |
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Therapeutic management: KD
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Prevent or reduce coronary artery disease
IV gamma globulin at a dose of 2g/kg over 12 hour infusion High dose ASA therapy begun at same time Initially dose is 80-100 mg/kg/day until fever resolves Dose increased to 3-5 mg/kg/day through weeks 6-8 of illness If coronary artery damage identified, dose is continued indefinitely |
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Nursing Care: KD
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Monitor cardiac status-signs of CHF
Daily weight, including I&O Supportive care-cool cloths, nonscented lotions, mouth care, clear liquids, soft solids ENCOURAGE REST: IRRITABILITY IS A HALLMARK OF KD |
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Discharge: KD
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Follow-up monitoring
Support family: irritability can last up to 2 months Teach regarding desquamation Address arthralgia (warm baths) Defer live immunizations for 3 months 2-3 month follow-up for serial EKG, CXR, ECHO |
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Systemic Hypertension
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Primary: No known cause
Secondary: Identifiable cause Pediatrics: HTN generally secondary to structural abnormality or underlying pathology Renal disease CV disease Endocrine or neurologic disorders KIDS DO NOT GET HTN UNLESS: CONGENITAL HEART DEFECT OR KIDNEY DISEASE |
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BP Screenings for Children
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Start at age 4
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Hyperlipidemia
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Identify kids at risk and treat early
Treatment: dietary restrict intake of cholesterol and fats If no response to diet: Rx colestipol (Colestid) cholestyramine (Questran) |
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Medication Moments: Digoxin
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Treatment of CHF
Action: Increases the force of myocardial contraction S/E: arrhythmias, bradycardia, fatigue, anorexia, n/v |
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Medication Moments: Captopril
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Indications: Alone or with other agents in the management of HTN
Action: ACE Angiotensin-converting enzyme inhibitors block the conversion of angiotensin I to the vasoconstrictor angiotensin II. S/E: agranulocytosis, angioedema, cough, hypotension, taste disturbances |
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Medication Moments: Enalapril
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indications: alone or with other agents in the management of HTN
action: ACE inhibitor, net result is systemic vasodilation S/E: cough, hypotension, proteinuria, angioedema |
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Medication Moments: Furosemide (Lasix)
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indications:
edema due to: CHF, Hepatic or renal disease Hypertension Action: Inhibits the reabsorption of sodium and chloride from the loop of Henle and distal renal tubules Increases renal excretion of water, sodium, chloride, magnesium, hydrogen, and calcium S/E: dehydration, hypochloremia, hypokalemia, hypomagnesemia, hyponatremia, hypovolemia, metabolic alkalosis |
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Medication Moments: Spironolactone (Aldactone)
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indications: Management of edema associated with CHF, cirrhosis and nephrotic syndrome
Treatment of hypokalemia (counteracts potassium loss caused by other diuretics) Action: Causes loss of sodium bicarbonate and calcium while saving potassium and hydrogen ions by antagonizing aldosterone. S/E: hyperkalemia |
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Medication Moments: Indomethacin (indocin)
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indications: IV: Alternative to surgery in the management of patent ductus arteriosus in premature neonates
action: Administer IV indomethacin (indocin), a prostaglandin inhibitor = lowers PGE and leads to ductus closure. S/E: allergic reactions including anaphylaxis |
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Medication Moments: gamma globulin (as related to Kawasaki Disease [KD])
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intravenous innumoglobulin: ABBR: IVIG. A solution containing concentrated human immunoglobulins (antibodies), primarily IgG. IVIG has numerous uses in health care, including as replacement therapy for patients with immune deficiencies; as a treatment for Kawasaki disease
S/E: renal failure, allergic reactions including anaphylaxis |
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ASA (as related to Kawasaki Disease [KD])
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indications: prevent or reduce coronary artery disease
Action: decreases platelet aggregation S/E: GI bleeding, exfoliative dermatitis, stevens-johnson syndrome, toxic epideermal necrolysis, allergic reactions including anaphylaxis and laryngeal edema |
