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75 Cards in this Set

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Signs and Symptoms of Congenital Heart Disease
Heart murmur
Repiratory difficulties: tachypnea, dyspnea, shortness of breath
Failure to thrive
Cyanosis
Presence of other congenital defects
Exercise intolerance and fatigue
Diagnostic Evaluation-Cardiac Catherization: Pre-procedure care
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
Diagnostic Evaluation-Cardiac Catherization: Post-procedure care
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.
Newer Classification of CHD: Hemodynamic characteristics
Increased pulmonary blood flow
Decreased pulmonary blood flow
Obstruction of blood flow out of the heart
Mixed blood flow
Increased Pulmonary Blood Flow Defects
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
Lesions with Increased Pulmonary Blood Flow
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
Increased Pulmonary Blood Flow Defects
Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus
Atrial Septal Defect
Abnormal opening between the atria, allowing blood from the higher pressure left atrium to flow into the lower pressure right atrium.
Atrial Septal Defect: pathophysiology
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.
Atrial Septal Defect: Clinical manifestations
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.
Atrial Septal Defect: management
spontaneous closure
surgical repair
Atrial Septal Defect
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
Ventricular Septal Defect (VSD)
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.
Ventricular Septal Defect (VSD): pathophysiology
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.
Ventricular Septal Defect (VSD): Clinical manifestations
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.
Patent Ductus Arteriosus (PDA)
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.
Patent Ductus Arteriosus (PDA): pathophysiology
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.
Patent Ductus Arteriosus (PDA): Clinical manifestations
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.
Patent Ductus Arteriosus (PDA)
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)
Obstructive Defects
Coarctation of the aorta
Pulmonic stenosis
Lesions obstructing blood flow to the ventricles
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.
Coarctation of the Aorta (COA)
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
Coarctation of the Aorta (COA): Clinical manifestations
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.
Coarctation of the Aorta (COA)
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
Pulmonic Stenosis (PS) and Catheter Placement
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.
Pulmonic Stenosis (PS)
Pathophysiology: narrowing at the entrance to the pulmonary artery
Clinical signs: maybe asymptomatic, mild CHF, murmur, cardiomegaly
Pulmonic Stenosis (PS): management
Dependent of the severity of stenosis
Balloon valvuloplasty - via cardiac cath relieves stenosis
Moderate to severe - valvotomy
Decreased Pulmonary Blood Flow Defects: Tetralogy of Fallot
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)
“Tet spells”
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
Transposition of the Great Arteries-mixed defect
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
Hypoplastic Left Heart Syndrome
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.
Hypoplastic Left Heart Syndrome
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
Congestive Heart Failure (CHF)
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
CHF in Children
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
Management of the child with CHF
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
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
Nursing Care-Decreasing Cardia Demands
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
Nursing Care-Reducing Respiratory Distress
Assessment, positioning, and oxygen administration
Elevate HOB to 45 degree angle
Humidified oxygen
Monitor for signs and symptoms of respiratory infection
Nursing Care-Maintaining nutritional status: FTT
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
Cyanosis: Respiratory vs Cardiac Cause
Cardiac:
cyanosis increases with crying
does not improve significantly with oxygen
CLASSIC SIGN: TACHYPNEA
Respiratory:
Cyanosis decreases with crying
Improves with oxygen
Respiratory distress
Consequence of Long Term Cyanosis
Polycythemia
hemorrhage
Bacterial endocarditis
clubbing
Brain abscess, CVA, DD
Pulmonary HTN
Hypercyanotic spells (tet spells)
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
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
Epidemiology
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
Pathophysiology
Group A beta hemolytic strep-environmental trigger
Host suseptibility
Immune Response
Hypoplastic Left Heart Syndrome
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.
Hypoplastic Left Heart Syndrome
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
Congestive Heart Failure (CHF)
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
CHF in Children
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
Management of the child with CHF
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
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
Nursing Care-Decreasing Cardia Demands
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
Nursing Care-Reducing Respiratory Distress
Assessment, positioning, and oxygen administration
Elevate HOB to 45 degree angle
Humidified oxygen
Monitor for signs and symptoms of respiratory infection
Nursing Care-Maintaining nutritional status: FTT
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
Cyanosis: Respiratory vs Cardiac Cause
Cardiac:
cyanosis increases with crying
does not improve significantly with oxygen
CLASSIC SIGN: TACHYPNEA
Respiratory:
Cyanosis decreases with crying
Improves with oxygen
Respiratory distress
Consequence of Long Term Cyanosis
Polycythemia
hemorrhage
Bacterial endocarditis
clubbing
Brain abscess, CVA, DD
Pulmonary HTN
Hypercyanotic spells (tet spells)
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
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
Epidemiology
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
Pathophysiology
Group A beta hemolytic strep-environmental trigger
Host suseptibility
Immune Response
Treatment: KD
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
Therapeutic management: KD
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
Nursing Care: KD
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
Discharge: KD
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
Systemic Hypertension
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
BP Screenings for Children
Start at age 4
Hyperlipidemia
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)
Medication Moments: Digoxin
Treatment of CHF
Action: Increases the force of myocardial contraction
S/E: arrhythmias, bradycardia, fatigue, anorexia, n/v
Medication Moments: Captopril
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
Medication Moments: Enalapril
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
Medication Moments: Furosemide (Lasix)
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
Medication Moments: Spironolactone (Aldactone)
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
Medication Moments: Indomethacin (indocin)
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
Medication Moments: gamma globulin (as related to Kawasaki Disease [KD])
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
ASA (as related to Kawasaki Disease [KD])
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