Pedi CV Flashcards
4th-8th week of gestation. Major cause of death related to birth defects 0-1y. Associated with certain syndromes: Trisomy 21, DeGeorge, Apert, Cri du chat, Noonan
Congenital CV Disorders
Common causes: Infection Autoimmune response Environment? Heredity
Acquired CV Disorders
Maternal: infection, substance use in pregnancy, diabetes.
Genetic: History of CHD in other family members, syndromes, other anomalies, congential or chromosomal
Risk factors of Pediatric Cardiovascular Disorders
Gas exchange shifts to lungs. Umbilical cord cut. Lungs inflate (PVR decreases), SVR increases, Blood to LA increases. Flow through fetal shunts reversed: PFO closes d/t L sided pressure. PDA closes within 24-48 hours
Newborn (pulmonary) Circulation
INCREASED PULMONARY BLOOD FLOW. ACYANOTIC. Ductus arteriosus fails to close (usually 2-3 days). Blood from aorta to PA. Common; 5-10% of infants with CHD.
Treatment: IV ibuprofen, indomethacin to stimulate closure in premature infants. Surgical ligation of PDA.
Goals: Prevent pulmonary hypertension, vascular issues
Patent Ductus Arteriosus (PDA)
INCREASED PULMONARY BLOOD FLOW. ACYANOTIC. L TO R SHUNT. Hole in atrial septum. Oxygenated blood from L atrium mixes with non oxygenated blood with R atrium. Common; 6-10% of CHD. May hear murmur. Echo may show dilated R ventricle.
Treatment: Rest, nutrition, surgical repair: patch placed.
Goals: Prevent adult complciations; stroke, arrythmias, pulm htn
Atrial Septal Defect (ASD)
INCREASED PULMONARY BLOOD FLOW. ACYANOTIC. L TO R SHUNT. Hole in ventricular septum. Oxygenated blood from L ventricle to non-oxygenated blood in R ventricle. Common; 20-25% of CHD.
Treatment: Digoxin- controls rate and rhythm. Lasix- diuresis. ACE inhibitors- decrease SVR, aortic pressure and shunting. Surgical: temporary branding of pulmonary vessels (reduce flow to lungs), patch at 3-12 mo.
Goals: Prevent heart failure and pulm htn (in moderate to large VSDs)
Ventricular Septal Defect (VSD)
OBSTRUCTED BLOOD FLOW. ACYANOTIC. Narrowing of the descending aorta. 5-8% of CHD. Once PDA closes, perfusion to lower extremeties impaired. 4-extremity Bps (higher in arms than legs). Treatment: Prostaglandin to keep PDA open (perfuse kidneys and lower extremities). Diuretics, O2, inotropes. Surgical repair- end to end anastomosis.
Goals: Prevent shock, heart failure, renal failure, NEC
Coarctation of the Aorta
OBSTRUCTED BLOOD FLOW. ACYANOTIC. Narrowing of the aortic valve. Systemic blood flow compromised.
Treatment: Surgical repair/balloon valvuloplasty/Ross, bacterial endocarditis prophylaxis, exercise restrictions
Aortic Stenosis
OBSTRUCTED BLOOD FLOW. ACYANOTIC. L side of the heart severely underdeveloped (mitral & aortic valves ascending aorta). Decreased force of L ventricle contraction. Reduced systemic blood flow. Open PDA allows R-L shunting; mixing in R ventricle. Most common cause of death among neonates with CHD. R ventricle dilation/hypertrophy.
Treatment: Prostaglandin to keep PDA open and maintain systemic perfusion. Surgical repair- Norwood- 3 stage repair. 1) RV converted to systemic effects. 2.) Separate pulm/systemic circulation
Hypoplastic Left Heart Syndrome
DECREASED PULMONARY BLOOD FLOW. CYANOTIC. OBSTRUCTION OF FLOW TO LUNGS. R TO L SHUNT. Most common cyanotic heart defect in infants. Four (sometimes five) defects: Pulmonic stenosis, right ventricular hypertrophy, VSD (sometimes ASD), overriding aorta. Progressive cyanosis “tet spells” - knee to chest (decreases return to heart). 10% of CHD.
Treatment: Surgical repair- BT shunt. Close VSD/ASD. Relieve pulmonary stenosis.
Goals: Manage hypercyanotic episodes, prevent metabolic acidosis.
Tetralogy of Fallot
DECREASED PULMONARY BLOOD FLOW. CYANOTIC. OBSTRUCTION OF BLOOD FLOW TO LUNGS (R to L SHUNT). Flow from R ventricle to pulmonary artery obstructed. 3 types, severity can vary: subvalvular, valvular, supravalvular. 2nd most common CHD, 5-10%.
Treatment: Surgical repair: (depend on type). Valvuloplasty via cardiac cath; patch angioplasty. Lifelong prophylaxis for infective endocarditis. Goals: prevent heart failure.
Pulmonic Stenosis
DECREASED PULMONARY BLOOD FLOW. OBSTRUCTION OF BLOOD FLOW TO LUNG. CYANOTIC. Pulmonic valve underdeveloped or closed. Blood cannot get to lungs for oxygenation. Cyanosis immediately. RV and tricuspid valve small, dysfunctional. ASD usually present (R-L shunting)
Treatment: Must be managed at birth- Prostaglandins immediately to keep PDA open. Goals: Manage hypercyanotic episodes. Prevent metabolic acidosis.
Pulmonary Atresia
DECREASED PULMONARY BLOOD FLOW. CYANOTIC. OBSTRUCTION OF BLOOD FLOW TO LUNGS. Tricuspid valve did not form- no flow from R atrium to R ventricle (CYANOSIS). ASD present (R-L shunt). R ventricle hypoplastic; R atrium enlarged/hypertrophic. L ventricle overloaded- enlarged, fx decreases. 1 in 10,000 babies. Treatment: PGA immediately to keep PDA open. 3 surgeries to establish pulmonary circulation: BT shunt, Glenn, Fontan. Prophylaxis for endocarditis. May require anticoaglant treatment.
Goals: Prevent hypoxemia
Tricuspid Atresia
Gas exchange in the placenta. Oxygenated blood via the umbilical vein. High PVR (lungs not used yet). Placenta and PDA = low SVR. IVE to RA to Foramen Ovale to LA. SVC to RA to RV to Ductus Arteriosus to descending aorta (lungs are bypassed)
Fetal Circulation
ability to produce contraction
Contractility
Amount of blood pumped from L ventricle each minute
Cardiac Ouput
How much blood pumped with each beat
Stroke Volume
How much blood in heart/ventricle at end of diastole
Preload
How much pressure in great vessels
Afterload
Cardiac Output formula
Heart Rate x Stroke Volume
Maintain adequate oxygenation Maintain adequate cardiac output and tissue perfusion Maintain adequate hydration and nutrition Promote comfort/pain relief Administer and manage meds Monitor for/prevent complications Promote growth and development Provide support to child and family
Nursing Interventions for Cardiac Disorders
Disorders with Increased Pulmonary Blood Flow, Obstructive Disorders
Acyanotic
Disorders with Decreased Pulmonary Blood Flow, mixed flow disorders
Cyanotic
Asymptomatic if small defect Tachypnea Tachycardia Murmur Diaphoresis Poor weight gain Frequent respiratory infections Hypotension/Heart Failure
S/s of acyanotic disorders
MIXED BLOOD FLOW. CYANOTIC.
Aortia and pulmonary arteries connected to the wrong ventricles. Oxygenated blood from L ventricle back to lungs. Non-oxygenated blood from body back to R atrium. PDA, ASD, or VSD also present, allowing shunting. Common 5% of all newborns with CHD. 50% mortality rate in 1st month, 90% in 1st year if untreated.
Treatment: PGE immediately, Surgery- arterial switch procedure within 2 weeks of life
Goals: Prevent heart failure
Transposition of Great Arteries
MIXED BLOOD FLOW. CYANOTIC. No division of aorta and pulmonary artery (one common great artery). VSD. Aortic and pulmonic valves fused together. Cyanosis common. Overcirculation to lungs, decreased to body. Activity/exercise limitations
Treatment: Diuretics, digoxin, Surgery- separate PA and aorta, close VSD, conduit from RV to pulm arteries.
Goals: Prevent HF and pulm htn
Truncus Arteriosus
MIXED BLOOD FLOW. CYANOTIC. No connection of pulmonary veins and L atrium. Must have PFO or ASD for blood from R atrium to get to body. Cyanosis present. 1% of CHD; surgery for survival.
Treament: PGE immediately, maintain PDA. Surgery- reconnect pulmonary veins to L atrium; create ASD if not present
Goals: Prevent compression of pulmonary veins
Total Anomalous Pulmonary Venous Return (TAPVR)
MIXED BLOOD FLOW. CYANOTIC. Aorta and pulmonary artery exit from R ventricle. Unoxygenated blood goes to body from R ventricle through aorta without going to lungs. Only outlet through VSD (required to survive). Often additional defects.
Treatment: Surgery- Make VSD bigger if necessary
Modified BT shunt. Arterial switch, Rastelli or Fontan. Prophylaxis for endocarditis
Goals: Prevent HF
Double Outlet Right Ventricle (DORV)
Structural of functional impairment of the ventricles. Acquired.
3 categories:
Ventricular dysfunction- structural abnormalitites
Volume overload- cardiac or non cardiac
Pressure overload- obstruction
S/s vary based on age, cause, severity
Heart Failure
Decreased cardiac output.
Pulmonary venous congestion: cough, tachypnea, labored breathing and diaphoresis while feeding, crackles, grunting, cyanosis
Systemic venous congestion: peripheral edema/fluid retention, ascites, enlarged liver, JVD.
Impaired CO: tachycardia, pallor, cool periphery, weak pulses, hypotension, delayed cap refill, oliguria, tiring with activity.
Increased metabolic demand: diaphoresis, poor weight gain or weight loss, FTT.
Heart Failure S/S
Collaboration with multidisciplinary team
Maintain oxygenation and cardiac output
Monitor fluid balance/weight
Heart Failure Interventions
Autoimmune, inflammatory. 2-4 weeks after untreated infection with Group A streptococcus (prevented with antibiotics for strep pharyngitis) Highest incidence ages 5-15y. S/s subtle or distinct: Low grade fever, joint pain (arthralgia)/ polyarthritis, red truncal rash, nodules on elbows/knees, carditis/valvulitis (murmur), chorea, CRP/ESR. Jones criteria for diagnosis. long hospitalization
Treatment: Prevent- full course of antibiotics for strep. Antibiotics, anti-inflammatory meds. Pain relief.
Acute Rheumatic Fever
Prevention of future strep Proper use of antibiotics S/s of heart failure Prevention of infective endocarditis F/U care (prevent rheumatic heart disease)
Teaching of Acute Rheumatic Fever
Most cases are bacterial (staphylococci and streptococci - most common). Infection of endocardium (inner lining) and possibly valves. Vegetations grow causing dysfunction. Variety of s/s. Risk factors: CHD, CVC, intra-cardiac devices, rheumatic heart disease, IV drug use. Duke criteria for diagnosis
Treatment: Support cardiovascular system. Rest/comfort/meds (antibiotics)
Teach: Prophylactic antibiotics before dental or respiratory procedures/surgeries
Infective/Bacterial Endocarditis
Disease of heart muscle. Affects size of heart chambers, wall thickness and contraction. 3 types.
Treatment: HF treatment. Frequent visit; monitor for disease progression; prevent/slow. Beta blockers. Heart transplant?
Cardiomyopathy
Disease of heart muscle. Heart muscle thins, L ventricle dilated, decreased squeeze (lower CO). Caused by myocarditis (virus, chemo, Duchenne muscular dystrophy)
Dilated cardiomyopathy
Disease of heart muscle. Hypertrophy of L ventricle and septum, walls become rigid. Obstruction of outflow, dysfunction of L ventricle, myocardial ischemia. Caused by genetic mutations/malformation syndromes
Hypertrophic cardiomyopathy
Acute, idiopathic systemic vascular inflammatory disorder. Usually less than 5y. Exact cause unknown. 3 phases.
Treatment: Comfort, rest. Fluids, pain relief. IVIG, aspirin.
Kawasaki disease
1st stage. Abrupt onset of fever, not responsive to antipyretics; widespread inflammation of small and medium sized arteries. Lasts 1-2 weeks, fever over 5 days, maculopapular rash, edema, joint pain, strawberry tongue, cracked lips, tachycardia, decreased LV function, cervical lymphadenopathy, red conjunctiva, swollen feet/hands
Acute stage of Kawasaki Disease
2nd stage. Fever subsides. Desquamation of fingers/toes; high PLT count (aneurysm risk)
Subacute phase of Kawasaki disease
3rd stage. Compete resolution of s/s. Usually 3 months after onset
Convalescent phase of Kawasaki disease
Increase in cardiac output or peripheral vascular resistance leads to increase in BP.
Primary- no identifiable cause, most common in pediatrics
Secondary- identifiable cause (renal, renovascular, endocrine)
3 visits: Bp over 95th percentile or over 130/90
Risk factors: Overweight, male, african-american or mexican american
Treatment: Labs, lipid profile. Anti hypertensives. Low sodium, low fat diet. Weight control; developmentally appropriate activity; decrease screen time
Hypertension
Prevents PDA closure
Prostaglandin E (PGE)
used in conditions that require an open PDA for mixing
Ibuprofen/NSAIDS
Indomethacin
Used to close PDA; inhibits PGE
Alters force or strength of heart muscle contractions to increase cardiac output
Used in HF
Ex: Digoxin
Inotropes
Decrease peripheral resistance, afterload & preload (can cause cough)
ACE inhibitors (“pril)
Blocks beta-adrenergic receptors to decrease excitability in heart (check pulse and BP before giving)
beta blockers (lol)
Medication: sodium rich diuresis (monitor u/o and K+)
Loop diuretics (Lasix)
Inotropic effect, negative chronotropic effect (avoid giving with meals, monitor for toxicity
Cardiac glycosides (Digoxin)
