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NURS362 - Practice of Nursing III > Week 8: PEDS Cardiac > Flashcards

Week 8: PEDS Cardiac Flashcards

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1
Q

What parts of fetal circulation are unique to it specifically

A

Foramen Ovale

Ductus Arteriosus

Umbilical Vein

2 Umbilical Arteries

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2
Q

How does blood move in the fetus

A

Enters the baby from the umbilial vein –> umbilical vein joins the inferior vena cava –> goes to right atrium –> blood diverted from lungs through the foramen ovale –> left atrium then left ventricle –> aorta –> body gets O2

blood return to right atrium –> right ventricle –> pumped to pulmonary artery –> ductus arteriosus diverts blood to the aorta past where the carotids are, so oxygen poor blood goes back to the mom

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3
Q

Foramen Ovale

A

Hole between the L and R atria that will close after birth

it allows blood to move to the left atrium which allows blood to get around the body rather than go to the lungs (blood is already oxygenated)

So it connects the atria so that oygenated blood can get to the aorta and out to the body and brain

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4
Q

Ductus Arteriosus

A

connects the aorta and pulmonary artery so that deoxygenated blood gets to the right ventricle and then leaves via umbilical arteries or the lower half of the fetus

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5
Q

Umbilical Vein

A

1

sends oxygenated blood from the placenta to the fetus

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6
Q

Umbilical Artery

A

2

deoxygenated blood moves from fetus to placenta

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7
Q

We want to see how many vessels in the umbilical cord

A

3 - 2 UA and 1 UV

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8
Q

Fetal Circulation Path for oxygenated blood

A

oxygenated blood –> placenta –> umbilical vein –> shunted past fetal liver byductus venosa –> inferior vena cava to right atrium –> proceed through foramen ovale –> left atrium to left ventricle –> aorta –> brain and body

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9
Q

Fetal Circulation Path for poorly oxygenated blood

A

superior vena cava –> right atrium mixing with oxygenated blood –> right ventricle and then pulmonary tree (small amount to lungs which are nonfxnal and collapsed) –> ductus arteriosus –> aorta –> placenta via umbilical arteries

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10
Q

___ means blood away from the fetus

A

arteries

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11
Q

___ means blood to the fetus

A

vein

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12
Q

What forces the alveoli of the fetal lungs to open

A

when the infant takes the first breath, the dramatic increase in O2 and expansion of lungs leads to DECREASED PULMONARY VASCULAR RESISTANCE (PVR) which allows for increased pulmonary blood flow

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13
Q

When does the Foramen Ovale close

A

ideally closes at birth - can take a few days though

the blood is entering the right atrium from the top

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14
Q

When does the ductus arteriosus close

A

4 days after birth

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15
Q

What leads to increased systemic vascular resistance (SVR)

A

clamping the umbilical cord

this stops fetal circulation

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16
Q

Children are not just …

A

small adults

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17
Q

The child heart lies more where compared to adults

A

heart lies more horizontal and higher in the chest

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18
Q

The apex of a child’s heart is where

A

found at the 3rd or 4th intercostal space

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19
Q

How does child HR and BP differ

A

HR faster and BP lower

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20
Q

What is more common in child hearts

A

murmurs

regularly irregular HRs

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21
Q

What is never normal in neonates and what can it indicate?

A

Diaphoresis and/or nosebleeds (epistaxis) - never normal in neonates

can indicate heart defects or GI defects

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22
Q

2 types of Cardiac Dysfunction

A
  1. Congenital

2. Acquire

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23
Q

Congenital Cardiac Dysfunction

A

“Born with it”

Ex: Atrial septal defect, ventricular septal defect, patent ductus arteriosus, tetrology of fallot, hyperplastic left heart, etc.

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24
Q

Acquire Cardiac Dysfunction

A

“Develops after birth”

ex: CHF, HTN, Rheumatic Heart Dx
* CHF is sometimes congenital but not always

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25
Q

When in gestation does the heart form

A

4-6 weeks

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26
Q

__ to ___ occurence of congenital heart anomalies occur per 1000 births

A

4-10

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27
Q

If someone has a congenital heart anomaly what is more likely to occur

A

other body system effects too like downs syndrome, TE fistula, hernias (inguinal, umbilical)

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28
Q

Causes of Congenital Heart Defects

A
  1. Genetic (Downs, Trisomy, 18, 21, Family Hx)
  2. Drugs (mom took)
  3. Infections
  4. Maternal Conditions (IDDM, Lupus, Seizure Disorder, Cocaine and Alcohol, Abuse, >40).
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29
Q

The first three weeks are important to heart development, but…

A

women usually learn they are pregnany much later and their actions could have made an impact

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30
Q

If mom says there is something wrong…

A

then something is probably wrong

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31
Q

Ways to Diagnose and Detect Heart Defects

A

Fetal Ultrasound

Fetal Echo

X Ray

Echo and Electro Cardiograms

MRI

Cardiac Cath

H&P!!! - If mom says there is something wrong like they are sweating, not feeding or falling asleep during, then something is probably wrong

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32
Q

Important Assessments to make for babies before and after birth

A

Health promotion and health management of baby and mother

Hx of maternal illness

Family Hx

Presence of other anomalies

Poor growth and development

FTT

Issues related to chronicity

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33
Q

S/S of a Congenital Heart Defect

A

Poor Feeding

Murmur

Poor Weight Gain (FTT)

Cyanosis - not always right away - often after 2nd day of life or more

Tachycardia

Tachypnea

Clubbing

Polycythemia

Squatting

Frequent URIs

Crackles (CHF Major Complication)

Central Edema

Activity Intolerance

Low O2 Saturation

JVD (may be hard to see)

Activity Intolerance

Periorbital Edema in babies

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34
Q

Why is there a push to advocate for non-quick discharge after births?

A

To try and see if cyanosis occurs after a few days and prevent an infant from having cardiogenic shock

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35
Q

Clubbing occurs as a result of

A

chronic hypoxia

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36
Q

Polycythemia

A

increased Hct as a defensive mechanism - increased RBC production - can be an issue with dehydration

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37
Q

What is squatting with heart defects

A

It is squatting occurring to increase and maintain oxygenation and icnrease blood flow to tissues

seen a lot with Tetralogy of Fallot

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38
Q

Why are URIs more common with heart defects

A

because there is increased breathing and effort of breathing

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39
Q

___ is a major complication of CHF

A

crackles

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40
Q

3 Categories of Heart Defect Etiology

A

Acyanotic

Cyanotic

Obstructive Systemic Blood Flow

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41
Q

Acyanotic Heart Diseases

A

Increased Pulmonary Blood Flow (Red Coloring) - too much

ex: CHF, PDA, ASD, VSD, Atrioventricular Canal (AV Canal or AVC)

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42
Q

Cyanotic Heart Diseases

A

Decreased pulmonary blood flow (Blue coloring) too little

Cyanosis occuring from increased concentration of reduced Hgb (no O2 on it)

ex: Tricuspid atresia (TA), Pulmonary atresia (PA), Transposition of the great arteries (TGA), Teralogy of Fallot

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43
Q

Is blue coloration always a sign of cyanotic heart disease

A

no its not always a sign but usually is

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44
Q

Obstructive Systemic Blood Flow Heart Diseases

A

Blood cannot get to where it needs to go - lungs or body

ex: Coarctation of the aorta, aortic stenosis, hypoplastic left heart

also can see blue coloration

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45
Q

Acyanotic means…

A

increased pulmonary blood flow

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46
Q

S/S of Acyanotic Defects

A

Murmurs - get louder with CHF from turbulent blood flow

Pulmonary Edema

Rales(crackles from fluid) and Rhonchi

Widening pulse pressure

Tachycardia (too much fluid in CHF)

thrill possible

FTT

recurrent resp infections

poor weight gain - feed poorly

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47
Q

Nursing Interventions for Acyanotic Heart Defects

A

Keep O2 Sats up - NC, HFC, Vent

Digitalize - IV, precautions done (Digoxin)

Diuretics and Fluid Restrictions - Lasix, high calorie formula to dec amt fed

Accurate I&O

Frequent breaks w feeding, lavage feeds or IV feeds - less work

All of this done before surgeyr is done

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48
Q

Patent Ductus Arteriosus (PDA)

A

Failure of the Ductus Arteriosus to close soon after birth (which joins the pulmonary artery and aorta)

Symptoms dependent on the amount of shunting and degree of pulmonary HTN

Flow higher pressure of aorta to the lower presusre of the pulm artery so more blood flow here increases issues of CHF due to shunting

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49
Q

You often see what as low in PDA

A

low diastolic BP

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50
Q

PDA is more common in…

A

premature infants

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51
Q

Treament for PDA

A
  1. Pharmacological - Indocin - for premies or those too ill for surgery
  2. Surgery - for term infants or those who indocin doesnt work - cath lab
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52
Q

What surgery is done to close a PDA

A

lateral incision

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53
Q

Why is it important to monitor UO, BUN, and Cr when taking Indocin to close PDA

A

because it can cause kidney damage

54
Q

What category is PDA

A

acyanotic

55
Q

Atrial Septal Defect (ASD)

A

Defect in the septum between the right and left atrium

similar s/s but not the same as patent foramen ovale

oxy blood moves L atrium to R atrium which causes PVR to decrease and LVP increases leading to the shunting from L to R from high to low pressure

56
Q

Why may you hear murmurs from ASD

A

from the shunting of blood

57
Q

WHy does CHF occur with ASD

A

increased blood flow to lungs from more blood in R atrium going to lungs

58
Q

What category is ASD

A

Acyanotic

59
Q

Treatments for ASD

A

If asymptomatic - watch and wait for spon closure

If ASD w/ CHF (RHF) treat CHF and delay surgical repair

If ASD w/ intractible CHF - early surgical repair

Cath lab pulls flap closed

60
Q

Ventricular Septal Defect (VSD)

A

Abnormal opening between ventricles

Blood will flow L ventricle to R ventricle

61
Q

What is the most common congenital heart defect

A

ventricular septal defect (VSD)

62
Q

What is the size of the opening between ventricles for VSD

A

size of a pinhole all the way to lack of a septum

63
Q

S/S of VSD

A

CHF - FTT, fatigue, tachypnea

Murmur

pulmonary HTN

64
Q

Category of VSD

A

Acyanotic

65
Q

Treatment for VSD

A

IT WILL CLOSE ITSELF 30-50% OF THE BED!!!!!!

If not closing, but asymptomatic - no treatment

Intractable CHF (RHF) from VSD - needs to be closed early –> diruetics, high calorie feedings to tune up for surgery and then get them into surgery

66
Q

Symptoms of VSD increase…

A

with the size of defect and amount of shunting

67
Q

Remember Cyanotic heart disease means…

A

decreased pulmonary blood flow

68
Q

S/S of Cyanotic Heart Diseases

A

Cyanosis (which does not respond as expected to O2 tx)

Tachycardia

Dyspnea

Hepatomegaly

FTT

Polycythemia

Clubbing

Diaphoresis w/ feeding

Tet Spell / Hypercyanotic Spell

69
Q

What is a Hypercyanotic Spell (Tet Spell)

A

Increased rate and depth of breath, increased HR, cyanosis, pallor, poor tissue perfusion, diaphoresis, irritability, crying, seizures, LOC - BLUE HANDS AND MOUTH

Happens when waking from sleeping, with feedings, crying, and defecating, constipation and agitation

70
Q

Tet Spells are treated…

A

aggressively:

calm child, delay procedure, morphine to knock them out, give O2, propanolol, kne chest (prone), IV fluids, dopamine or phenylephrine

71
Q

Why can hepatomegaly occur from cyanotic heart defects

A

because heart failure can lead to an enlarged liver

72
Q

NIs for Cyanotic Heart Defects

A

Prostaglandin E1

O2 management

Bicarbonate

Keep calm and keep procedures to minimum - cyanosis increases with crying and feeding

Gavage feeding or IV feeding - less work

Knees to chest - squat

Antibiotic prophylaxis for dental work or invasive procedures is needed

73
Q

Prostaglandin E1 is used in cyanotic heart defects why

A

to keep a patent ductus arteriosus open

74
Q

Why is bicarb given for cyanotic heart defects

A

to manage metabolic acidosis

75
Q

Why do knees to chest (squat) for cyanotic heart defects

A

to decrease systemic blood flow return to the heart

76
Q

Why is antibiotic prophylaxis given for cyanotic heart defects

A

to prevent myocarditis from occurring

77
Q

If someone has a TET spell what should be done immediately

A

pull knees to chest (squat) to decrease systemic blood flow to the heart and improve oxygenation

78
Q

Transposition of the Great Vessels

A

Cyanotic Heart Defect

Noncommunicating systemic and pulmonary system

Caucses circulation to be reversed and is non conductive to life

79
Q

How is circulation reversed in Transpotition of the Great Vessels

A

pulmonary vessel comes out of left ventricle instead of R

aorta comes out of right ventricle instead of L

Often has ASD or VSD (cannot survive without these)

80
Q

Transposition of the Great Vessels is …

A

non conductive to life w/o intervention

81
Q

If the ductus closes in Transpotition of the Great Vessels what can occur

A

cardiogenic shock

82
Q

Treatment for Transposition of the Great Vessels

A

Survival depends on early aggressive management!!!:

PGE_1 infusion to keep PDA open to prevent cardiogenic shock

Create a septal defect to allow access

Correct vessels surgically later

Surgical correction w/ in a week age

83
Q

___-___% of survival with repair for transposition of the great vessels

A

90-95%

84
Q

What surgery is done for Transposition of the Great Vessels

A

Arterial Switch

They used to do conduits to correct circulation but there is risk for clotting in these

85
Q

Tetrology of Fallot

A

Cyanotic Heart Defect

Combo of 4 defects that causes Tet Spells

Leads to chronic problems even after fixing it

86
Q

What is the most common cyanotic heart lesion

A

Tetrology of Fallot

87
Q

What are the 4 defects in Tetrology of Fallot

A

Pulmonic Stenosis - Obstruction of Outflow to the lungs d/t narrow vessel

  1. VSD
  2. Overriding aorta - aorta sits between R and L venticle so blood comes from both and goes out systemically causing cyanotic effect
  3. Right ventricular hypertrophy (rarer)
88
Q

What defect can lead to Pentology of Fallot

A

VSD

89
Q

Treatment for Tetrology of Fallot

A

Knee to Chest (Squat) - decreases systemic vascular resistance

Surgery in stages

90
Q

What is the morality rate of terology of fallot

A

10% - very high

91
Q

Someone who had their tetrology of fallot treated still…

A

may never be symptom free - chronic issues occur

92
Q

Obstructive systemic blood flow heart defects means…

A

decreased blood flow to body

93
Q

S/S of Obstructive Systemic Blood Flow

A

diminished pulses - radial and pedal

poor color - blue

delayed capilary refill

decreased UO - because of poor blood flow to kidneys

CHF w/ pulmonary edema

pressure increase in lower extremities

Poor feeding/weight gain = FTT

94
Q

BP is generally what way in obstructive systemic blood flow

A

BP generally decreased in lower extremity - but normal is higher in LE than UE

take a 4 limb blood pressure

95
Q

NIs for Obstructive Systemic Blood Flow

A

depending on defect and symptoms: follow interventions for increased pulmonary blood flow or decreased pulmonary blood flow

If incr: treat systemic heart failure

If decr: look at tx for tetrology of fallot or knee to chest to increase blood flow

96
Q

Coarctation of the Aorta

A

Obstructive Heart Defect

Presents in 2nd week of life

May or may not be symptomatic

it is narrowing of the aorta (aortic arch) either before or after the ductus arteriosus (after is most common)

97
Q

Coarctation of the Aorta leads to increased risk for what

A

CVA - decreased systemic blood flow leading to strokes

AAA - abdominal aortic aneurysm

98
Q

The most common location for coarctation of the aorta occurs before or after the ductus arteriosus?

A

After

99
Q

S/S of Coarctation of the Aorta

A

HA

Epistaxis

Dizziness

BP increase in UE, Decreased in LE

CHF (LHF) w/ Hepatomegaly from CHF

Decreased pulses and pressures in LE

Gallops, thrills, murmurs - depend on VSD for mumurs and gallop heard in CHF

100
Q

The discrepancy of BP between UE and LE in Coarctation of the Aorta is

A

almost 10 points which is huge

101
Q

What category of heart defect is coarctation of the aorta

A

Obstructive Systemic Blood Flow

102
Q

Tx for Coarctation of the Aorta

A

Medically manage CHF

Prostaglandin E1 - keep PDA open if symptomatic early on

Delay surgical correction via balloon dilation to buy time, then resect subclavian artery to the aorta past the constriction

103
Q

What keeps the PDA open when needed to prevent cardiogenic shock

A

Prostaglandin E1 - PE1

104
Q

What does survival from coarctation of the aorta depend on

A

depends on the complexity of coarct (VSD present? pre or post ductal) and recurrence - depends on complexity

105
Q

The 3 categories of heart defects are what kinds of heart disease

A

Congenital

106
Q

What are the 4 important Acquired Heart Disease to know

A

CHF

Rheumatic Fever

Kawasaki’s

HTN

107
Q

Why do we see more HTN nowadays

A

increased incidence of obesity in children

108
Q

Rheumatic Fever

A

Acquired Heart Disease - Autoimmune disease caused by Group A Infection (strep in rare cases)

109
Q

S/S of Rheumatic Fever

A

Fever

Painful/tender Joints

Red Hot or Swollen Joints

Chest Pain

Palpitations

Fatigue

SOB

Chorea

Erythema Marginatum

110
Q

Chorea

A

poor muscle coordination

111
Q

Erythema marginatum

A

Papular rash on the body

112
Q

We diagnose rheumatic fever with…

A

the Jones Criteria

113
Q

Jones Criteria

A

criteria of required, major, and minor s/s that determine if someone has Rheumatic fever

114
Q

What are the requirements needed in the Jones Criteria

A

1 required, 2 major s/s and no minor s/s

OR

1 required, 1 major, 1 minor

115
Q

What is teh required symptom for rheumatic fever/jones criteria

A

Recent Strep Infection

116
Q

What are the major s/s used in the jones criteria

A

polyarthritis

carditis

chorea

erythema marginatum

subq nodules

117
Q

What are the minor s/s used in the jones criteria

A

fever

arthralgia

previous RHD or RF

Increased CRP

Increased ESR

prolonged PR interval

118
Q

What increases CRP

A

inflammation

119
Q

What increases ESR

A

inflammation because of fibrinogen

120
Q

Complications occurring in the heart from Rheumatic Fever

A

Valve Stenosis

Valve Regurgitation

Damage to heart muscle

A Fib

Heart Failure

121
Q

Labs and Tests to look for with Rheumatic Fever

A

Elevated ESR

Elevated CRP

leukocytosis (increased WBC)

Prolonged PR interval

122
Q

Tx for Rheumatic Fever

A

anti infectives

anti inflammatories

tx of CHF if occurring - digoxin and diuretics

prophylactic antibiotics everyday until 18 yo and with dental care/surgery as adults

123
Q

Kawasaki Disease

A

A type of acquired heart dsiease

a multisystem inflammatory disese leading to aneurysms, ischemic heart disease, and infarcts

124
Q

What is the etiology of Kawasaki Disease

A

etiology unknown but likely infection triggers to certain susceptible people

125
Q

How serious is Kawasaki Disease

A

self limiting and gets better but without treatment 25% of people develop cardiac sequelae

126
Q

S/S of Kawasaki Disease Stage 1

A

High fever unresponsive to treatment > 5 days

Reddened Conjunctiva

Pharyngitis - strawberry tongue

Rash varies with child - red palms and peeling on hands and feet

Cervical lymphadenopathy

Labs - elevated ESR

127
Q

S/S of Kawasaki Disease Stage 2

A

cracking lips and fissures

peeling fingers and toes

joint pain

cardiac disease - coronary blood vessel inflammation aneurysms, MI d/t coronary blood vessel inflammation

s/s similar to multi system inflmmatory disease

128
Q

Tx for Kawasaki Disease

A

Hospitalized >3 days usually yo treat fever and potential cardiac issues: high dose IV gamma globulin, coumadic, salicylate therapy, and steroid use (controversial)

follow up for several weeks to months

129
Q

How long is the hospital stay usually for kawasaki disease

A

greater than or equal to 3 days

130
Q

How long is follow up for kawasaki disease usually

A

several weeks to months

131
Q

If there is no cardiac involvement with Kawasaki’s Disease in the first month…

A

they are usually going to be ok

NURS362 - Practice of Nursing III (13 decks)

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