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Fall - Pediatrics > Cardiac > Flashcards

Cardiac Flashcards

1
Q

What occurs with perfusion if you do not have enough pressure?

A

Blood will be shunted to the central part of the body
Extremities will lack perfusion

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2
Q

What are the goals regarding hemodynamic stability?

A

Prevent cardiogenic shock/failure
Bridge to surgery
Transplant

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3
Q

What are the goals regarding limiting secondary complications?

A

Respiratory failure
G&D delays
Infections
Kidney Disease

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4
Q

What age is myocardial tissue less effect? What does this put the child at risk for?

A

Under 2 myocardial tissue is less effective

Increased risk of cariogenic shock
Decompensated quickly

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5
Q

What is CO dependent on in children?

A

HR - fast
Ca, glucose (keep heart pumping) and volume
Less reserve to meet increase metabolic demands
ISWL increased
Unstable fluid shifts

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6
Q

What is one of the reason children have such a fast baseline HR?

A

The heart muscle is not very strong so it does not pump blood efficiently enough therefore needs a faster HR to get enough blood to the body

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7
Q

How do you assess the cardiac function in a child?

A

Listen to apical pulse for 1 minute
Cap refill at midline such as ear, forehead, sternum
Brachial and femoral pulses

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8
Q

What should you remember in regards to pulse ox with children?

A

May need a central probe because extremities aren’t as reliable
Pulse ox on hands will end up in the childs mouth (can put on toes but not reliable)

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9
Q

What is CO?

A

HR x SV (volume of blood per beat)

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10
Q

What is after load?

A

Resistance in the vessels

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11
Q

What is preload?

A

Maximum expansion of ventricle before ejection

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12
Q

What if the workload of heart is excessive?

A

Leads to strain on the ventricles

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13
Q

What is a septum in the heart?

A

Fibrous tissues that divide the ventricles

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14
Q

What is shunting

A

Abnormal pathway for blood to flow through the heart
Blood follows the path of least resistance over a septum or vascular wall

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15
Q

What is going on with the lung in utero? How do babies in utero get oxygen?

A

Lungs are filled with fluid so they do not work for O2 exchange

Blood comes from mom via the umbilical cord and bypasses the lungs by using the ductus arterioles to get to the body

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16
Q

At what are is the circulatory system normal?

A

2 months

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17
Q

When do you diagnose heart diseases in babies?

A

Prenatal
Newborn in nursery (can be difficult because changes are happening during this time)
2 months well baby visit (usually thin and sweaty)

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18
Q

Which side of the heart is strong while in fetus? Which side of the heart is strong once baby takes first breath?

A

Fetal: Right side stronger
After 1st breath: Left side strong

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19
Q

What are the type of high pulmonary blood flow disease?

A

Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Patent ductus arteriosis (PDA)

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20
Q

What is a low pulmonary blood flow disease?

A

Tetrology of fallot

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21
Q

What is a ventricular septal defect? What is the blood flow?

A

Opening in the intraventricular septum that separates the two ventricles of the heart
Blood flow is shunted from left to right

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22
Q

What are the S/S of VSD?

A

Fatigue
SOB
Difficulty feeding
Poor growth
Turbulence –> heart murmur (loud harsh systolic murmur)
Palpable thrill

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23
Q

How do you diagnose SVD

A

Echocardiogram

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24
Q

What is the treatment for VSD?

A

Surgical closure for a large defect

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25
Q

What is patent ductus arteriosis (PDA)?

A

When the ductus arteriosis does not close after birth –> on contraction blood flow form the left ventricle to the aorta and back to the pulmonary arteries by going through the PDA –> overloading the lungs

** blood should go from aorta into body**

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26
Q

What is the treatment for PDA? When can this be preformed?

A

Patent ductus arteriosis occlusion: insert catheter in groin –> feed through heart –> angiogram is taken of PDA to measure it so appropriate sizure occlusion device can be inserted to close PDA

After a few weeks

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27
Q

Is blood still going to the body with a PDA?

A

Yes, it is the least harmful because only a little blood is baking up into the pulmonary arteries instead of going to the body

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28
Q

When should the ductus arteriosus close?

A

in 48-72 hours of life

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29
Q

What s/s would you expect with a high pulmonary blood flow heart defect?

A

NO cyanosis
Pulmonary HTN
Crackles
R sided heart failure (see edema in the body)

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30
Q

What is the shunt that is expected to be seen with a high pulmonary blood flow heart defect? Where do you see blood increase?

A

Left to right shunt

Increased blood to the lungs

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31
Q

Why do you see right sided heart failure with a high pulmonary blood flow heart defect? Why do you see edema?

A

Blood is backing up into the lungs and causing pulmonary HTN –> the right ventricle to have to work really hard –> right sides HF

Edema is seen because the R atria is letting blood flow back into the body

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32
Q

Why is it concerning when a baby with a heart defect sweats? What about with feeds?

A

Babies shouldn’t sweat until 1 year because they don’t have sweat glands that are developed
Sweating with feeds is a neuro/hormonal response to heart failure

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33
Q

If a child is gaining weight rapidly but still looking thin, what should you be worried about?

A

FLuid volume overload

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34
Q

What are some s/s of poor perfusion?

A

Increase HR
Increase RR
Cool/clammy extremities
Cap refill over 2 seconds
Cyanosis
Mottling
Pale
Weak/thready pulses

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35
Q

Where do children that are fluid overloaded hold their fluid? How do you measure this?

A

Belly - abdominal girth
Extremities - pitting edema over a bony prominence

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36
Q

What are complications r/t to neuro with reduced CO?

A

Irritable with long term cognitive delays

37
Q

What are some complications r/t GI with reduced CO?

A

Hepatomegaly
Poor feeding and weight Gian
GERD

38
Q

What are some complications r/t renal with reduced CO?

A

Decreased UOP
Chronic kidney disease

39
Q

How should you monitor CO?

A

Monitor PEWS
Cardiac monitor
Pulse ox: 88-90

40
Q

What medications can help to increase CO and reduce workload?

A

Digoxin
Inotropes
Vasopressors
Diuretics
ACEi/ARBS

41
Q

What are some nursing interventions to increase CO and reduce workload?

A

IV access with or w/o fluids
Oxygen
Strict I&Os
Daily AM weight
Weight all diapers
Conserve energy by dressing stimuli and clustering care

42
Q

What are some feeding considerations to increase CO and reduce workload?

A

Small and frequent feedings
Limting feeding to 20 minutes
High calorie
Anything that can’t be ate within 20 minutes should be given via a Gtube

43
Q

What are some assessment cues of impaired gas exchange?

A

Tachypnea
Pulmonary congestion
Abnormal lung sounds
Retractions
Increased work of breathing
Diaphoretic
SpO2 less than 88%
Increased HR
irritable

44
Q

What are some intervention that should be taken to improve gas exchange?

A

Oxygen
Pulse ox
Clear upper airway with suction (especially before feeds)
HOB elevated
Conserve energy by clustering care and decreasing environmental stimulation

45
Q

Why should you be cautious of a new dry cough?

A

Early sign of respiratory distress

46
Q

What is digoxin? What does it do? What is the therapeutic window? What does toxicity look like? What electrolyte should you watch for?

A

Ionotropic med

Helps heart contract with greater force to move blood

0.5-2.0ng/ml

Vomiting

Potassium but can be hard to monitor if on diuretic and peeing out potassium

47
Q

What are some considerations for digoxin administration?

A

Hold for a pulse less than 80-90
2 RN dose verification
Every 12 hours NOT BID
Do not give with food or formula

48
Q

How do you administer medication for infants?

A

Syringe between the lower cheek and gums
Little bit of medication at a time
Blow on face to make them swallow
Give right before feeding because will initiate sucking

49
Q

Can the patent ductus ateriosus be manipulated? How? Why would you want open vs. closed?

A

Can be forced open or closed with medical management

Indomethacin - vasoconstrcits (closes duct) - given if causing a lot of pulmonary issues

Prostaglandin - vasodilators (opens duct) - bring blood flow to lung b/c in low blood flow disorders can have difficult time getting BF to lungs

50
Q

What are the 4 defects in tetralogy of Fallot?

A

Overrding aorta
Ventricular septal defect (VSD)
Pulmonary stenosis
Right ventricular hypertrophy

51
Q

What is going on with the blood flow in tetralogy of fallot? What does this cause?

A

Right to left shunt

Blood is not going to the lungs instead, unoxygenated blood is getting pushed out into the body and causing extreme cyanosis

52
Q

What is an overriding aorta? Treatment?

A

Aorta moves forward directly over the VSD allowing oxygen poor blood form the right ventricle to flow into the aorta

Shunt placed between branch of the aorta and right pulmonary artery –> provide another path for blood to get to the lungs to get oxygenated

53
Q

What is pulmonary stenosis? Treatment?

A

Pulmonary artery (gets blood to the lungs) is narrowed and pulmonary valve doesn’t open all the way resulting in less blood going to the lungs

Patch used to widen the pulmonary artery and valve

54
Q

What is right ventricular hypertrophy? Treatment?

A

Wall of right ventricle is thicker than normal d/t right ventricle working harder than normal to pump blood through the narrowed pulmonary valve

55
Q

How do you make sure the surgery worked in Tetrology of Fallot?

A

During surgery, you can take saturation levels in each of the chambers

56
Q

Does the loudest murmur mean to worst defect?

A

No, intensity does not indicate severity

A tiny VSD can sound really loud d/t increased pressure
A large VSD can sound quiet d/t less pressure

57
Q

What are the complications of a low pulmonary blood flow defect?

A

Extreme cyanosis
Polycythemia (body produces more hemoglobin to get more oxygen to the body)

58
Q

What are the cues for impaired gas exchange?

A

Increased WOB
Increased RR
Oxygen use
Retractions
Adventicious breath sounds
Decrease baseline pulse ox
Cyanosis
Clubbing
Polycythemia (>14-16 g/dL)
Severe activity intolerance

59
Q

What is a hyper cyanotic spell or a “tet” spell? What is it caused by?

A

Decreased pulmonary blood flow d/t increased resistance
Increased need for oxygen

Caused by stress d.t crying, feeding or tantrum

60
Q

What are the nursing interventions for a “tet” spell?

A

FIRST: Knee to chest/tripod (forces blood back to heart into pulmonary artery)
Oxygen
Morphine (relax patient and relax pulmonary vascular spasm)

61
Q

What are complications of polycythemia r/t low pulmonary blood flow disorder?

A

Risk for thrombosis d/t sludge like blood
Stroke
DVT
Cognitive delays

62
Q

What are the nursing interventions to prevent complications r/t polycythemia?

A

Hydration
Anticoagulation with baby aspirin

63
Q

What are the risks of giving a child aspirin?

A

There is an increase of Reyes syndrome (liver failure/encephalitis) when a child has a viral disease

64
Q

What are complications r/t to all congenital heart defects?

A

Poor weight gain d/t imbalanced nutrition, GERD, fussy eaters, puking
Developmental delays
Immunosupression

65
Q

How do you prevent complications r/t all congenital heart defects?

A

Feeding support - balance nutrition and stress
Playing
Vaccinate

66
Q

What is an obstructive lesion (coarchication of the aorta)?

A

Coractation of the aorta (pinching of the aorta) –> decreased pulses and perfusion
Decrease blood supply below the obstruction

67
Q

What is the consequences of an obstructive lesion?

A

Poor distal pressure –> poor pulses and perfusion –> difference in contralateral pulses upper vs. lower or left/right extremity

68
Q

What if an obstructive lesion occurs before the beaches of the aorta? After?

A

Before: all limbs are affected
After: just lower limbs are affected

69
Q

What is the surgical care for congenital heart defects?

A

Correct underlying defect
If there is failed medical management –> surgical staging and Interventional Cardiac Cath

70
Q

What should you be watching post cardiac Cath? interventions?

A

Bleeding
Vascular compromise of extremities

Check pulses and compare both sides
Lay flat - give pain control, swaddling and comfort hold to keep flat

71
Q

What do you use a band for r/t CHD?

A

Restricts extra blood flow in high pulmonary blood flow disorders –> decrease in pulmonary congestion

72
Q

What is discharge teaching all parents should know for all heart defects? (9)

A

CPR
Apnea/cardiac monitor training
S/S of HF
How to respond to tet spells
Nutrition/feeding
Medication instructions
How to check pulse, BP and SpO2
Infection prevention
Support groups

73
Q

What are the different kind of acquired heart diseases?

A
  1. Arrhythmia : CHD
  2. Infectious: endocarditis
  3. Collagen vascular disease (autoimmune disorder): rheumatic fever and Kawasaki disease
74
Q

What is the concern regarding infectious endocarditis and CHD?

A

It causes an increase risk because they have implantable devices and cause have valve diseases

75
Q

What is the cause of rheumatic fever? Can it be prevented? What age group does it most commonly affect?

A

Group A strep that goes untreated

Can be prevented if strep is recognized and treated correctly

5-15 years old

76
Q

What are the s/s of rheumatic fever?

A

MAJOR:
C: carditis
A: arthritis
S: subcutaneous nodules
E: erythema marginatum (rash)
S: sydenhams chorea (neuro disorder - rapid irregular movements of arms and legs)

MINOR
F: fever
R: raised ESR/CRP
A: arthralgia (joint pain)
P: prolonged PR interval
P: previous RF

77
Q

When do rashes blanch? When do they not blanch?

A

Blanch: inflammation
Not blanch: vascular

78
Q

How do you treat rheumatic fever?

A

Acute: treat strep with antibiotics (PNC V or amoxicillin) and symptomatic treatment

Life long: monthly PNC G, daily ASA, cardiac follow ups

79
Q

Why do you need life long treatment with rheumatic fever?

A

Relapses are common

80
Q

What is Kawasaki disease? How do you treat it?

A

Over active immune system

Treatment is IVIG and ASA

81
Q

What age does Kawasaki disease affect most? What is the worst complication r/t this?

A

Less than 5 years old

Coronary artery aneurysms

82
Q

What are the 3 phases of Kawasaki disease?

A

Acute: high fever (above 104) for 5-10 days which is only window to diagnose to prevent complication
Subacute: acute s/s start to go away, peeling of skin, arthritis and arthralgia and become at risk coronary aneurysm
Convalescent: lifelong management and high risk for coronary events

83
Q

What is the criteria for Kawasaki disease?

A

Fever for more than 5 days and 4 out of 5 of the following

C: conjuntivitis (non-exudative)
R: rash (non-vesicular)
E: edema (or erythema of hands and feet)
A: Adenopathy (cervical usually unilateral)
M: Mucosal involvement (inflamed, cracked, fissures or crusting, erythema)

84
Q

Which side of heart is strong in adults/chidlren? Which side is strong in a fetus?

A

Adults and children: left side is strong

Fetus: right side is strong

85
Q

How do you treat Pulmonary HTN?

A

Correct the underlying defect 6 months
Oxygen
Manage HF
Pulmonary vasodilators like Nitric oxide or PDE5 inhibitors (viagra)

86
Q

When does cyanosis usually occur? What are the complications? What is the baseline SVO2?

A

with right to left shunting

Polycythemia

Baseline: 75-85%

87
Q

S/S of HF?

A

Early:
Cough
Poor weight gain and poor appetite
Difficulty feeding/fatigue/gerd
Abdominal pain d/t lack of perfusion
Fussy and developmental delays

Late:
Respiratory distress (nasal flaring, SOB, retractions, grunting)
Fatigue and poor activity intolerance
Diaphoretic and clammy
Decreased UOP
End of s/s d/t lack of perfusion (CKD, neuro/cognitive delays, growth failure)

88
Q

Why is the a heart with CHD more at risk for endocarditis?

A

Normal heart: smooth lining, bacteria can’t stick
CHD: rough area on heart d/t pressure from an abnormal opening/leaky valve. Even w/ surgery, rough areas may remain d/t scarring, patching inviting bacteria to build up and multiply

89
Q

What are long term complications of HF?

A

Growth and development delays/FTT
End organ damage (brain, kidney, skin, GI, heart, liver)

Fall - Pediatrics (15 decks)

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