Exam 2 Blueprint Cardiac Flashcards

1
Q

What are the mixed defects?

A

Transpositional of the great vessels (TGV), total anomalous pulmonary venous return (TAPVR), Truncus arteriosus, and hypoplastic L heart syndrome (HLHS)

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2
Q

what is important to know about mixed defects?

A

Survival depends on mixing of blood from the pulmonary and systemic circulation within the heart, variable S/S depending on defect, cyanosis (although not always visible), CHF, and may require multiple surgeries (many times in the 1st week of life)

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3
Q

what is TGV?

A

the Aorta exits off the R ventricle and the pulmonary artery off the L ventricle, no communication between the pulmonary and systemic circulations, incompatible with life unless another defect is present that allows the mixing of blood, rapid and sustained cyanosis, surgical repair (immediate), and IV prostaglandin E may be admin to maintain ductal patency until surgery (to force the PDA and ASD to stay open)

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4
Q

what is TAPVR?

A

R atrium receives all the blood that normally would flow into the L atrium, R side of the heart hypertrophies, is overworked, and may cause a backup of blood in the lungs, L side of the heart, especially the L atrium, may remain small, generally have other defects, such as ASD or PDA, that will help the child by allowing more blood to get from the R side of the heart to the L side and out to the body, and if no other defects, immediate and progressive cyanosis and immediate surgical repair.

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5
Q

what is Truncus arteriosus?

A

during fetal development, failure of the pulmonary artery and aorta to divide, resulting in one single vessel that opens into both R and L ventricles. Resistance is less to pulmonary blood flow than to systemic blood flow, so more blood flow to the lungs. Moderate to severe CHF with variable cyanosis. Surgical repair in the 1st month of life, VSD is usually repaired 1st.

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6
Q

what is HLHS?

A

second most common CHD, severe underdevelopment of the L side of the heart, aortic valve, aorta, L ventricle, and mitral valve. Pulmonary congestion and edema. Child will be asymptomatic until ductus arteriosus closes, then poor perfusion with cyanosis, tachypnea, and dyspnea. IV prostaglandin E to keep ductus arteriosus open until taken to surgery.

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7
Q

what are the obstructive defects?

A

Coarctation of the aorta
Aortic stenosis
Pulmonic stenosis

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8
Q

infection of valves and inner lining

A

bacterial endocarditis

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9
Q

what is important to know about bacterial endocarditis?

A

Sequalae of bacteremia
Strep Viridians
Low grade, intermittent fever, malaise, arthralgias, new murmur

Increased ESR, vegetation on ECHO
TX: Penicillin

Prevention: give ABX b4 dentistry/procedures and TEACH!

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10
Q

inflammatory disease of the heart, joints, skin, and CNS

A

rheumatic fever

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11
Q

what is important to know about rheumatic fever?

A

Group B hemolytic strep (+ ASO)

Aschoff bodies: the lesions of rheumatic fever found around blood vessels in the myocardium

Mitral valve carditis, murmur, CHF possible

Polyarthritis

Rash: erythema marginatum (trunk/ext)

SubQ nodules

Chorea

TX: prevention of strep, cardiac damage prevention, recurrence prevention, and PenG

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12
Q

what is Kawasaki Disease?

A

systemic vasculitis, ectasia (dilation of coronary artery leads to aneurysm (giant)), S/S = high fever, red eyes, ring around iris, strawberry tongue, rash (desquamates), and serious = MI, TX = high dose IVIG and salicylate therapy, and NC: grumpy kids, symptomatic, supportive.

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13
Q

what have increased pulmonary blood flow?

A

ASD (atrial), VSD (ventricle), PDA, and AV canal

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14
Q

what is patent ductus arteriosus?

A

fetal duct between the pulmonary artery and the aorta fails to close. May have no symptoms, but a murmur may be heard, and the child may develop CHF. May close spontaneously, if not, it may be closed medically with the admin of Indomethacin (Indocin), a prostaglandin inhibitor. If med is unsuccessful, surgery may be needed.

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15
Q

what is atrial septal defect (ASD)?

A

hole between the atria. May be a foramen ovule that has not closed at birth or a defect unrelated to the fetal duct. Most have no symptoms, but may develop CHF, if the ASD is large. A murmur may be heard. May ASDs close spontaneously. If not, surgery or interventional cardiology may be performed.

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16
Q

what is ventricular septal defect (VSD)?

A

most common congenital heart defect. Hole between the ventricles. May have no symptoms, but a murmur may be heard, and the child may develop CHF. May close spontaneously, if not, it may be close medically with admin of Indomethacin (Indocin). If med is unsuccessful, surgery may be needed.

17
Q

what is atrioventricular canal (AVC)?

A

a large hole in the middle of the heart. S/S of progressively worsening CHF. Surgical repair is required.

18
Q

what have decreased pulmonary blood flow?

A

Tetralogy of Fallot (TOF) and Tricuspid Atresia

19
Q

what is important to know about decreased pulmonary blood flow?

A

Clinically not enough blood flow to the lungs – blood is shunted from the R to the L side of the heart. Blood bypasses the pulmonary system.

20
Q

what is ToF?

A

Most common decreased pulmonary blood flow defect. Four defects: VSD, overriding aorta, pulmonary stenosis, R ventricular hypertrophy. R ventricular hypertrophy develops over time because the ventricle is working extra hard to circulate the blood.

21
Q

what are the S/S of ToF?

A

TET spells (child becomes cyanotic especially when crying and while eating (infancy), and during play (older kids). Polycythemia (greater than normal # of circulating RBC). Clubbing of the fingers (may develop due to chronic hypoxia)

22
Q

what are the TX of ToF?

A

surgical repair (MUST)  don’t have to have it right away, few different surgeries because they cannot repair at the same time. Cyanosis that develops during a TET spell can be relieved when the legs and knees are bent, resulting in reduced blood flow to the lower body and improved blood flow to the vital organs. Infants should be placed in a knee-chest position. If defect has not been repaired, older kids usually squat instinctively.

23
Q

what is tricuspid atresia?

A

a closed tricuspid valve after birth. No movement of blood from the R atrium to the R ventricle. Incompatible with life unless another defect is present that allows mixing of the blood. Rapid and sustained cyanosis. Immediate surgical repair.

24
Q

what is the normal blood flow through the heart?

A

Body > IVC: or head > SVC > R atrium > tricuspid valve > R ventricle > pulmonic valve > pulmonary artery > lung > pulmonary veins > L atrium > mitral valve > L ventricle > aortic valve > aorta > body

25
Q

what is important to know about digoxin?

A

Half-life is short -1 ½ days to work
Increases PRI
50 mcg/mL, IV, PO
HIGH TOXICITY
Preemies more susceptible
Need therapeutic range (0.8-2.0 mcg/L)

K+ levels decrease = digoxin effects increase (take apical rate 1M)

NEVER give more than 1mL to an infant/ check 1 H b4, 2 H after meals (Q12H)

If missed dose, give if within 4 H, if > 4 H give next dose at normal time

26
Q

When should you NOT give a dose of digoxin?

A

NO GIVE IF HR < 90 (small kid) and NO GIVE IF HR < 70 (older kid)

27
Q

what are the S/E and toxicity of digoxin?

A

Bradycardia, dysthymia, anorexia, N/V (if kid vomits dose, do not give another dose, instead give next dose at scheduled time), and visual disturbances.

28
Q

Coarctation of the Aorta (CoA)

A

a narrowing of the aorta, usually distal to the ascending vessels. markedly higher BP and pulses in upper extremities. Surgical repair.

29
Q

Aortic Stenosis (AS)

A

narrowing of the aorta or aortic valve. surgical repair or balloon angioplasty. Murmur, CHF

30
Q

Pulmonic stenosis (PVS)

A

narrowing of the pulmonary artery or valve. surgical repair or balloon angioplasty. cyanosis during activity or CHF.