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med/surg 2 > class 10 congenital heart defects, kawasaki disease > Flashcards

class 10 congenital heart defects, kawasaki disease Flashcards

1
Q

what side of the heart is oxygenated

A

left

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2
Q

what circulatory system has the highest resistance

A

systemic

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3
Q

on what side of the heart is the pressure the highest

A

left

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4
Q

the ______ the pressure gradient the _______ the rate of flow

A

higher
greater

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5
Q

why does blood flow from high pressure to low pressure

A

it takes the path of least resistance

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6
Q

the (higher/lower) the resistance the (higher/lower) the rate of flow

A

higher
lower

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7
Q

pulmonic resistance is (less/more) than systemic resistance

A

less

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8
Q

what is preload

A

the amount of blood returning to the heart (the volume of blood in a ventricle before systole)

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9
Q

what is afterload

A

the amount of pressure the heart needs to exert to eject blood during ventricular contraction

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10
Q

what is contractility

A

the efficacy of the heart muscles to pump (contract)
-assessed by looking for cyanosis in extremities

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11
Q

what are congenital heart defects

A

mild to severe defects arising from abnormal formation of heart or major vessels
-50% show s&s during 1st year of life

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12
Q

what is stenosis

A

narrowing or obstruction of the valves

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13
Q

what is atresia

A

abnormal (missing/malformed) valves

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14
Q

mild CHD:

A

common
may be asymptomatic & caught later in life

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15
Q

moderate CHD:

A

may be symptomatic, will need treatment

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16
Q

severe CHD:

A

discovered in utero
needs treatment once born

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17
Q

maternal risk factors for CHD

A

-medications (warfarin, antiepileptics, oral tretinoin)
-infections/illness(rubella)
-diabetes/lupus
-alcohol/drug use

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18
Q

infant risk factors for CHD

A

high or low birth weight

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19
Q

genetic risk factors for CHD

A

specific syndromes
-family hx

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20
Q

inspection findings for CHD

A

-failure to thrive (FTT)
-cyanosis
-pallor
-chest configuration
-pulsations (in neck veins)
-respirations
-clubbing

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21
Q

palpation and percussion findings for CHD

A

-crackles
-dim peripheral pulses
-hepato/splenomegaly

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22
Q

auscultation findings for CHD

A

-HR and rhythm (murmur)
-heart & chest sounds abnormal

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23
Q

CXR for CHD looks for

A

-heart size
-pulmonary blood flow

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24
Q

ECG for CHD looks for

A

-electrical activity
-conduction abnormalities
-heart rate/rhythm

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25
Q

echocardiography for CHD looks for

A

anatomy and structure (valves)

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26
Q

cardiac cath for CHD looks for

A

-diagnostic and interventional
-pressures & saturations
-monitor for complications

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27
Q

pre op for cardiac cath

A

-HT & WT
-allergies
-baseline o2
-pulses

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28
Q

post op from cardiac cath

A

-assess site
-monitor bleeding
-pulses
-o2
-extremity assessment
-vitals Q1
-hypoglycemia d/t NPO

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29
Q

Acyanotic defects with increased pulmonary flow

A

-atrial septal defect
-ventricular septal defect
-patent ductus arteriosus
-atrioventricular canal
“A-VAP”

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30
Q

Acyanotic defects with obstructive ventricular flow

A

-coarctation of the aorta
-aortic stenosis
-pulmonic stenosis
“CAP”

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31
Q

increased pulmonary blood flow

A

-connections along the septum or great arteries -> higher left-sided pressure causes left-to-right flow (shunt)-> increasing pulmonary blood flow causing increased pressure and stress in the lungs

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32
Q

acyanotic defects causes shunting from:

A

left to right

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33
Q

what is patent ductus arteriosus

A

the ductus arteriosus connecting the aorta and pulmonary artery fails to close after birth

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34
Q

what is ventricular septal defect

A

a hole in the septum seperating the ventricles allows blood to mix
-good prognosis
-loud murmur

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35
Q

what is atrial septal defect

A

a hole in the septum between the atrias allows blood to mix
-patched in cath lab then aspirin until 6m post-op
-s3 murmur

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36
Q

what is atrioventricular canal defect

A

a defect in which there is a hole between the 4 chambers of the heart

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37
Q

clinical manifestations ASD/VSD

A

-heart failure is common (left to right shunting)
-loud murmur at base of left sternal border
-risk for infective bacterial endo carditis

38
Q

what is infective bacterial endocarditis

A

an infection of the inner lining of the heart in the endocardium, generally involves the valves which can potentially destroy heart valves
-all children with CHD are at risk

39
Q

prevention of infective bacterial endocarditis in kids with CHD

A

-prophylactic antibiotic 30-60 mins before and up to 2 hours after procedures (surgical, dental, invasive)
-broad spectrum (amoxicillin, ampicillin, azithromycin)

40
Q

what are patho of obstructive defects

A

narrowed valves or vessels obstruct blood from exiting heart->increased pressure on ventricules->decreased cardiac output

41
Q

acyanotic obstructive defects in CHD

A

-aortic stenosis (AS)
-Pulmonic stenosis (PS)
-coarctation of aorta (CoA)
“CAP”

42
Q

what is aortic stenosis

A

narrowing of the aortic valves (triple lumen becomes double lumen)
-blood backs up into the lungs

43
Q

what is pulmonic stenosis

A

narrowing of the pulmonic valve due to malformation
-increases pressure, dc blood to the lungs and may be cyanotic at birth
-may give IV prostaglandins to keep PDA open to dec pressure
-surgery: stent

44
Q

what is coarctation of aorta

A

narrowing defect in aorta

45
Q

clinical manifestations of coarctation of aorta

A

-increased BP in arms but dec in legs (will have cool and weak pulses)
-may have bounding upper pulses, headaches, nosebleeds, and inc risk for stroke
-rt side has inc pressure= enlarged liver, heart, edema, and ascites
-could be asymptomatic but cyanotic

46
Q

treatment for acyanotic defects

A

-surgery often indicated, infants must be minimum 10lbs before surgery
-FTT is common->can takes months to have surgery
-nutrition supplementation is primary tx until big and stable for surgery
-HTN is managed with beta blockers, angiotensin converting enzyme inhibitor (ACE) but can cause renal issues & drop bp
-medical management of HF
-may need o2

47
Q

what is heart failure (HF)

A

-results from structural or functional cardiac disorders that impair the ability of the ventricles to fill or eject blood
-defects that cause obstruction or result in increased blood volume and pressure within the heart will eventually lead to HF

48
Q

heart failure is characterized by

A

-ventricular dysfunction
-reduced exercise tolerance
-diminished quality of life
-shortened life expectancy

49
Q

clinical consequences of rt sided heart failure

A

-increased pressure in RA & systemic venous circulation
-hepatosplenomegaly, peripheral edema, ascites

50
Q

clinical consequences of lt sides heart failure

A

-increased pulmonary pressure, pulmonary congestion, dyspnea, cough
-inc risk for resp infection

51
Q

3 major s&s groups of heart failure manifestations

A
  1. impaired myocardial function
    2.pulmonary congestion
    3.systemic venous congestion
52
Q

how does impaired myocardial function present

A

-increased heart rate (+160)
-gallop on ascultation
-diaphoresis
-irritable
-FTT
-dec CO
-pallor

53
Q

how does pulmonary congestion present

A

-difficulty expanding lungs
-inc resp (+60)
-SOB
-nasal flaring
-hypoxemia/cyanosis
-costal retractions
-inc metabolic demand=FTT
-orthopnea->HOB elevated

54
Q

how does systemic venous congestion present

A

-rt sided failure
-hepatomegaly
-generalized edema
-ascites
-weight gain (early sign)
-distended neck veins

55
Q

goals of treatment for CHD

A

-improve cardiac function (inc contractility and dc afterload) (digoxin, ACE inhibitors, beta blockers
-remove accumulated fluids and sodium (diuretics)
-decrease cardiac demands
-improve tissue oxygenation/decrease oxygen consumption
-dec stimuli in room, warm room,

56
Q

medications for chronic heart failure

A

-digitalis
-angiotensin converting enzyme (ACE) inhibitors (dec afterload=dec BP. dc urine output d/t renal damage)
-beta blockers
-diuretics

57
Q

digitalis toxicity s&s

A

-do not give to babies w heart rate less than 90-110 or kids less than 70
-EKG monitor
-dec heart rate
-nausea
-given in Mcg not Mg or babies

58
Q

nursing considerations for HF

A

-possible fluid and sodium restriction, K + supplementation
-provide neutral thermal environment
-reduce work of breathing (o2, positioning)
-minimize rest, promote rest
-prevent/tx infections
-prevent skin breakdown from edema

59
Q

cyanotic defects that decrease pulmonary flow

A

-tetralogy of fallot
-tricuspid atresia

60
Q

cyanotic defects that mixes blood flow

A

-transposition of the great arteries
-total anomalous pulmonary venous return
-truncus arteriosus
-hypoplastic left heart syndrome

61
Q

patho of decreased pulmonary blood flow

A

obstruction of blood flow-> decreased pulmonary blood flow-> increased pressure on the right side of heart-> right to left shunt

62
Q

what is a tricuspid atresia (TA)

A

underdeveloped valve leads to underdeveloped right ventricle (no right valve)

63
Q

what is tetralogy of fallot (ToF)

A

4 defects: Ventricular septal defect, pulmonic stenosis, aorta overriding ventricular septal defect, right ventricle hypertrophy

64
Q

clinical manifestations in tetralogy of fallot

A

-may be acutely cyanotic at birth or mild cyanosis that progresses over first year
-characteristic systolic murmur; moderate in intensity
-acute episodes of hypercyanosis and hypoxia (tet spells) or anoxic spells (cyanosis during crying/feeding)

65
Q

what is a mixed defect (cyanotic)

A

combined anomalies of heart structures - complex defects with abnormal connections and pressures = mixing of saturated and unsaturated blood

66
Q

what are the 4 cyanotic mixed defects

A

-transposition of great vessels (TGA)
-total anomalous pulmonary venous return (TAPVR)
-truncus arteriosus (TA)
-hypoplastic left heart syndrome (HLHS)

67
Q

what is transposition of great vessels (TGA) cyanotic

A

aorta comes off the RIGHT ventricle (deoxygenated blood being circulated) and pulmonary artery comes off the LEFT ventricle (oxygenated blood going to the lungs)

68
Q

what is total anomalous pulmonary venous return (TAPVR) cyanotic

A

pulmonary veins return blood to the RIGHt side of the heart (oxygenated and deoxygenated blood mixing in the right atrium)

69
Q

what is truncus ateriosus (TA) cyanotic

A

a ventricular septal defect and fusion of the aorta and pulmonary artery to be a single vessel (mixed blood going to both systemic and lungs)

70
Q

what is hypoplastic left heart syndrome (HLHS)

A

the left side of the heart is underdeveloped at birth

71
Q

clinical manifestations of transposition of the great arteries (TGA)

A

-s&s will depend on type and size of defect. infants with minimal communication are severely cyanotic and critical
-if a large septal defect or PDA is present they will have sone oxygenation but have s&s of hF
-heart sounds vary
-cardiomegaly is present a few weeks after bith

72
Q

therapeutic management of Transposition of the great arteries (TGA)

A

-prostaglandins iV may be initiated to keep a PDA to allow for some oxygenation
-balloon septostomy may allow for cardiac mixing of blood done under cardiac cath
-surgical arterial switch procedure performed in the first few weeks of life

73
Q

what does the paO2 need to be for cyanosis to be present

A

<80-85%

74
Q

what is hypoxemia

A

decreased arterial oxygen saturation

75
Q

what is hypoxia

A

reduction in tissue oxygenation results in impaired cellular processes

76
Q

what is cyanosis

A

blue discolouration in mucus membranes, skins, nail beds with reduced o2 saturations

77
Q

what is polycythemia

A

-clinical manifestation of hypoxemia
-increased # of RBC, increases o2 carrying capacity of the blood

78
Q

what is clubbing

A

-clinical manifestation of hypoxemia
-thickening and flattening of tips of fingers and toes

79
Q

infants with mild hypoxemia s&s

A

-may be asymptomatic
-mild cyanosis
-delayed or no growth and development

80
Q

infants wth severe hypoxemia s&s

A

-fatigue with feeding
-poor weight gain
-tachypnea
-dyspnea
-tissue hypoxia and poor perfusion

81
Q

hypoxemia management

A

-re-establish pulmonary blood flow
-treat hyper cyanotic episodes (tet spells)
-monitor for worsening hypoexmia, anemia
-maintain hydration
-prevent and tx infections

82
Q

nursing care for cyanotic defects

A

-may always have low o2, may need o2 supp, HOB 45
-ensure adequate hydration( I&O, dehydration= inc risk of stroke)
-daily weight
-tx infections &prevent (i.e vaccines)
-nutritional support w NG
-cardiac and resp monitoring
-encourage rest and dec stimuli
-parent education

83
Q

what is kawasaki disease (KD)

A

-systemic vasculitis of unknown cause (peak in toddlers)
-self limiting without treatment, 20-25% develop cardiac sequelae

84
Q

cardiovascular systemic in kawasaki disease

A

-coronary arteries most susceptible
-dilation and/or aneurysm formation
-evident by day 7 - continued enlargement for 4-6 weeks
-potential for MI

85
Q

diagnostic criteria for KD

A

-no specific test
-critical lab values (CBC, CRP, ESR)
-echo
-prolonged elevated temperature (>5 days) that is not responsive to antibiotics & not attributable to another cause + 4/5 acute phase symptoms

86
Q

acute phase of KD

A

-high fever (unresponsive to antibiotics & antipyretics) and irritable
-develops conjunctivitis, polymorphous rash
-red cracked lips, “strawberry” tongue, rash
-edema/erythema of hands and feet
-single cervical lymphadenopathy
-early cardiac involvement

87
Q

subacute phase of KD

A

-begins with resolution of fever and lasts until all s&s have disappeared
-irritability persists
-greatest risk for coronary artery aneurysms
-peeling of fingertips and toes

88
Q

convalescent phase of KD

A

-begins when all clinical signs resolve
-ESR, CRP remain elevated, coronary complications
-phase ends when bloodwork is normal (6-8 weeks after onset)

89
Q

management of KD

A

-IVIG: dec fever and s&s, single infusion 2g/kg over 10-12h

-aspirin; anti-inflamm dose: 80-100mg/kg/d divded q6
anti-platelet dose: 3-5mg/kg/d

-family education: disease process
-aspirin administration and toxicity
-follow-up care (echo’s_

90
Q

nursing care of KD

A

-monitor cardiac and assess for HF
-I&O, daily weights, gallop rhythm, tachycardia, resp distress
-temperature
-monitor during IVIG
-symptom relief (dec skin discomfort, minimize mucosal inflammation (mouth care), promote rest to dec irritability (dec stimuli))

med/surg 2 (17 decks)

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