Cardiovascular System Flashcards
An invasive procedure that can be used to diagnose a congenital heart defect and repair certain heart defects by inserting a catheter into the femoral artery and threading it up to the heart
Cardiac catheterization
Cardiac Catheterization pre-op nursing care
NPO for 6-8 hrs, assess for allergies to iodine or shellfish, assess kidney function (BUN, creatinine), assess and mark distal pulses
Cardiac catheterization post-op nursing care
Check insertion site for bleeding, check extremity distal from insertion site to ensure adequate circulation (pulses, cap refill, color, temp), increase fluid intake to flush contrast dye, position patient in supine position with affected extremity straight for 4-6 hours**
Anatomic abnormality of the heart that causes altered blood flow
Congenital heart defect
Risk factors for increased risk of CHD
Exposure to teratogen during pregnancy, maternal smoking and alcohol use, maternal medical conditions such as diabetes
S/S of CHD
Depends on defect present. However, many of the defects cause: HF, hypoxemia, murmurs
CHD nursing care
Provide frequent rest periods and small, frequent meals, provide O2 and high calorie formula as ordered by provider
CHDs that increase pulmonary blood flow
Atrial septal defect (ASD), ventricular septal defect (VSD), AV canal defect, patent ductus arteriosus (PDA)
CHD characterized by a hole in the septum that separates the left and right atria
Atrial septal defect (ASD)
S/S of ASD
May be asymptomatic, but can cause S/S of HF and murmur
A systolic murmur with a wide fix splitting of S2 may be present with what CHD?
ASD
ASD treatment
Closure of hole through cardiac cath or surgical patch
Hole in the septum between the left and right ventricles
Ventricular septal defect (VSD)
S/S of VSD
S/S of HF, murmur
A loud systolic murmur at the left sternal boarder is present with which CHD?
VSD
Treatment for VSD
Surgery to suture or patch the hole
A hole in the center of the heart that allows blood to flow between all four chambers; instead of a mitral and tricuspid valve, there is a single AV valve
Atrioventricular (AV) canal
S/S of AV canal
S/S of HF, loud systolic murmur
Treatment of AV canal
Surgical patch closure and valve reconstruction
CHD in which the fetal artery that connects the aorta and the pulmonary artery fails to close after birth
Patent ductus arteriosus (PDA)
S/S of PDA
Machine-hum murmur, bounding pulses, wide pulse pressure
PDA treatment
Indomethacin, coils to occlude PDA during cardiac catheterization
CHDs that result in decreased pulmonary blood flow
Tetrology of fallot, tricuspid atresia
CHD that is a combination of four different defects PROV: pulmonary stenosis, right ventricular hypertrophy, overriding aorta, ventricular septal defect
Tetrology of fallot (TOF)
S/S of TOF
Cyanosis, hypercyanotic “tet” spells, systolic murmur
Intervention for tet spells
Place child in knee-chest position to increase blood flow to lungs
PDA treatment
Surgical repair within first year of life
CHD in which the tricuspid valve fails to develop
Tricuspid atresia
S/S of tricuspid atresia
Cyanosis, tachycardia, dyspnea, clubbing
Treatment for tricuspid atresia
Multiple surgeries including shunt placement, glen procedure, fontan procedure
Congenital heart defects that cause obstructed heart flow
Coartation of the aorta, aortic stenosis, and pulmonary stenosis
Narrowing of the aorta that occurs after blood is supplied to the upper extremities, but blood flow to the lower extremities is impaired
Coarctation of the aorta
S/S of coarctation of the aorta
Upper extremity HTN and bounding pulses, poor lower extremity perfusion causing weak pulses, cool skin, and pallor
Coarctation of the aorta treatment
Balloon angioplasty and stent placement, surgical removal of narrowed section of aorta, Antihypertensives
Narrowing of the aortic valve that decreases blood flow to the whole body
Aortic stenosis
S/S of aortic stenosis
Hypotension, decreased pulses, tachycardia, poor feeding, exercise intolerance
Aortic stenosis treatment
Balloon dilation or valvotomy
narrowing of the pulmonary valve which obstructs blood flow to the lungs
Pulmonary stenosis
S/S of pulmonary stenosis
Systolic ejection murmur**, cyanosis, cardiomegaly, HF
Pulmonary stenosis treatment
Balloon dilation of valvotomy
Congenital heart defects that result in mixed blood flow
Transposition of the great arteries (TGA), total anomolous pulmonary venous connection, truncus arteriosis, hypoplastic left heart syndrome
Congenital heart defect in which the aorta and pulmonary artery connections to the heart are reversed resulting in PDA or septal defect
Transposition of the great arteries (TGA)
S/S of TGA
HF, SOB, cardiomegaly, cyanosis, hypoxia, murmurs, fatigue, poor growth
TGA treatment
Prostaglandins to keep PDA open, surgery within 1st week of life to reverse connections and correct defect
Congenital heart defect in which the pulmonary veins are connected to the right side of the heart instead of the left atrium resulting in oxygenated blood being pumped right back into lungs; this defect requires ASD in order for patient to survive
Total anomalous pulmonary venous connection (TAPVC)
S/S of TAPVC
Cyanosis, dyspnea, poor feeding
TAPVC treatment
Surgical repair to connect pulmonary veins to left atrium
Congenital heart defect in which there is a single vessel or trunk rather than a separate pulmonary artery and aorta. Patient will also have VSD causing mixing of blood.
Truncus arteriosis
S/S of truncus arteriosus
HF, murmurs, cyanosis, poor feeding
Truncus arteriosis treatment
Surgical repair within first few months of life
Congenital heart defect in which the left side of heart and associated structures are underdeveloped resulting in PDA and ASD
Hypoplastic left heart syndrome
S/S of hypoplastic left heart syndrome
Cyanosis, HF, cold extremities, lethargy
Hypoplastic left heart syndrome treatment
Prostaglandins to keep PDA open until surgery. Surgery done in three different stages (Norwood procedure, Glenn shunt, fontan procedure)
General S/S of HF
Poor feeding, tachycardia, activity intolerance, pallor, weak pulses, cardiomegaly
S/S of L sided HF
Tachypnea, dyspnea, nasal flaring, retractions, wheezing
S/S of R sided HF
Peripheral edema, ascites, hepatomegaly, JVD
Labs associated with HF
Elevated hBNP
HF treatment
Digoxin, diuretics (furosemide), beta blockers, ACE inhibitors
HF nursing care
Ensure child is upright when feeding, use a nipple with enlarged opening (decreases energy used while feeding), provide high-calorie formula, provide frequent rest periods, take pulse before administration of digoxin (Hold if below 90 bpm for infant, hold if below 70 bpm for older children)***, monitor for S/S of digoxin toxicity (N/V, bradycardia, dysrhythmias), closely monitor serum digoxin levels (therapeutic range between 0.8-2)
S/S of hypoxemia
Cyanosis, tachypnea, dyspnea, clubbing, polycythemia (elevated RBC production)
Hypoxemia treatment
O2, morphine, IV fluids, knee-chest position for cyanotic episodes to improve blood flow to lungs
Infection of the inner layer of the heart
Infective endocarditis (IE)
S/S of IE
Fever, malaise and lethargy, loss of appetite, splinter hemorrhages**, petechiae, murmur, muscle and joint pain
Labs associated with IE
Elevated ESR and CRP
IE treatment
IV antibiotic therapy via PICC line over 2-6 weeks, valve repair or replacement if IE resulted in valve damage
IE family teaching
Prophylactic antibiotics will be needed prior to dental work or invasive procedure/surgery
Inflammatory disorder of the heart, blood vessels, and joints
Rheumatic fever
Rheumatic fever key risk factor
Partially treated or untreated strep throat infection
Labs associated with rheumatic fever
(+) GABHS, (+) ASO titer, elevated ESR and CRP
Diagnosis of rheumatic fever
Jones criteria; diagnosis requires two major criteria present OR one major and two minor criteria present
Jones major criteria for diagnosis of rheumatic fever
- Carditis (inflammation of heart — can lead to murmurs, pericardial friction rub, cardiomegaly, arrythmias, and CHF), polyarthritis (painful swelling of joint), 2. erythema marginatum (non-pruritic rash on the trunk and limbs), 3. chorea (involuntary muscle movements, 4. non-tender subcutaneous nodules
Jones minor criteria for diagnosis of rheumatic fever
Fever, arthralgia (joint pain), elevated ESR or CRP, prolonged PR interval
Rheumatic fever treatment
Long-term penicillin administration, bed rest
The systemic inflammation of the blood vessels in the body (vasculitis)
Kawasaki disease
What are the three phases of Kawasaki disease?
Acute, subacute, and convalescent phase
S/S during the acute phase of Kawasaki disease
High fever (over 102 F) lasting for 1-2 weeks and will be unresponsive to antipyretics, various areas of erythema on body (eyes, chapped and cracked lips, oral mucosal membrane, palms and soles), arthritis, enlarged cervical or neck lymph nodes, cardiac symptoms such as dysrhythmias and myocarditis
S/S of subacute phase of Kawasaki disease
Fever resolves but patient has arthritis, peeling skin around nails, palms, or soles.
S/S during convalescent phase of Kawasaki disease
No clinical manifestations, but abnormal labs may be present
Abnormal labs associated with Kawasaki disease
Elevated CPR and ESR, decreased albumin levels
Criteria for diagnosis of Kawasaki disease
Fever for over five days and four of the five symptoms including: conjunctivitis, rash, extremity changes (redness of hands and feet, peeling skin), adenopathy (enlarged lymph nodes), mucosal changes (red cracked lips, red mucus membranes, strawberry tongue) — hint: remember CREAM
Kawasaki disease treatment
IV immunoglobulin, high dose aspirin
Kawasaki disease nursing care
Monitor cardiac function (d/t carditis), monitor daily weights and I&Os, educate family that live immunizations should NOT be administered to child for 11 months (varicella, MMR)
Disorder characterized by decreased hemoglobin due to insufficient intake of iron or some kind of malabsorption syndrome that results in decreased absorption of iron
Iron deficiency anemia
Key risk factor for iron deficiency anemia in children
Excess intake of cows milk
S/S of iron deficiency anemia
Fatigue, pallor, SOB, tachycardia
Labs associated with iron deficiency anemia
Decreased Hgb, Hct, RBCs, MCH, MCV, and ferritin
Iron deficiency anemia treatment
Iron supplementation: iron sulfate (PO), iron dextran (IV or IM; use z-track method for IM administration to prevent leakage of med into subq tissue)
Iron deficiency anemia family teaching
Increase child’s intake of iron-rich foods (green veggies, meat, raisins, iron fortified foods), vitamin C INCREASES absorption of iron while calcium DECREASES absorption of iron (take with iron supplements with OJ, but avoid taking them with milk)
Family teaching for child who takes liquid iron
Use straw and brush teeth after to prevent staining of teeth; green or tarry-like stools are expected
An autosomal recessive genetic disorder that results in chronic anemia, pain, infection, and organ damage
Sickle cell anemia
Sickle cell anemia risk factors
Family hx, African American, middle eastern or Mediterranean descent
S/S of sickle cell anemia
Pain, fatigue, swollen hands and feet, jaundice
Sickle cell crises can be brought on by
Infection, stress, or dehydration
Sickle cell crisis characterized by severe pain
Vaso-occlusive
Treatment of vaso-occlusive sickle cell crisis
Around-the-clock opioid administration
Sickle cell crisis that occurs when sickle cell blood vessels become trapped in the spleen which lead to enlargement of spleen and severe anemia
Splenic sequestration crisis
Sickle cell crisis usually caused by a viral infection (fifth disease) in which bone marrow stops producing RBCs leading to severe anemia
Aplastic crisis
Labs associated with sickle cell anemia
Decreased Hct
Increased reticulocytes, WBCs, and bilirubin
T or F: all newborns are screened for sickle cell anemia
True
Blood test that measures Hgb levels and assesses for abnormal types of Hgb
Hemoglobin electrophoresis
Sickle cell anemia treatment
Pain management (opioids), antibiotics (infection), IV fluids, blood products, oxygen therapy, hydroxyurea (can reduce sickling of blood cells and prevent vaso-occlusive crisis)
Sickle cell anemia family teaching
Encourage adequate fluid intake, prevent infection (hand hygiene, avoid crowds, stay up to date with vaccines), seek immediate medical attention if child has fever or S/S of infection
Group of genetic disorders characterized by defective hemoglobin formation and anemia
Thalassemia
S/S of thalassemia
Pallor, jaundice, decreased appetite and growth rates, enlarged liver and spleen, deformed facial bones
Thalassemia treatment
Frequent blood transfusions, chelation therapy to decrease build-up of iron from blood transfusions
X-linked recessive disorder that causes deficiency in clotting factors
Hemophilia
Hemophilia ___ results in a deficiency of clotting factor 8 and hemophilia ___ results in a deficiency of clotting factor 9
A; B
S/S of hemophilia
Excess bleeding and bruising, joint pain and swelling, decreased ROM
Labs associated with hemophilia
Elevated aPTT, decreased factor 8 or 9; NOTE: platelet count and PT will NOT be affected
Hemophilia treatment
Factor replacement
Hemophilia family education
Prevent bleeding (no NSAIDs or aspirin, avoid IM injections), engage in PT to maintain ROM, NO contact sports, RICE acute bleeding (rest, ice, compression, elevation)
Interventions for epistaxis (nose bleed)
Lean head forward, maintain pressure with thumb and finger on soft spot of nose for 10 minutes, apply ice pack to bridge of nose; packing with epinephrine or cauterization may be indicated for persistent bleeding
Epistaxis family teaching
Keep nose lubricated and use cool mist humidifier in room, avoid blowing nose forcefully
