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Pediatrics > Cardiologic Disorders > Flashcards

Cardiologic Disorders Flashcards

1
Q

What are the signs of a cardiac disorder (9)?

A

cyanosis
irregular HR
edema
clubbing
fever
retractions/work of breathing
prominent precordial chest wall
abnormal pulses
abdominal distention

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2
Q

What are some diagnostic tests for cardiac disorders (8)?

A

arteriogram
ECG
CXR
Holter/ambulatory ECG
ECHO
Stress test
Hcg/Hct
pO2

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3
Q

What are some nursing goals/interventions for children with cardiac disorders and their families?

A

Improving oxygenation
Promoting adequate nutrition
Assisting the child and family with coping
Providing postoperative nursing care
Preventing infection & family education
Providing child and family education

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4
Q

What is the therapeutic range of digoxin?

A

0.8-2 ng/mL

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5
Q

What are the parameters for digoxin administration?

A

infants: <90 bpm
children: <70 bpm
adults: <60 bpm

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6
Q

What are the S/Sx of digoxin toxicity?

A
  • N/V
  • dysrhythmia
  • decreased UO
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7
Q

What is the antidote for digoxin?

A

Digibind

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8
Q

How does the cardiac circulation change after birth?

A

With the first breath, alveoli begin to open. Increase alveoli decreases pulmonary pressure, causing the pressure gradient of the heart to change to LT>RT from RT>LT. Pulmonary pressure normalizes 6-8 wks after birth. Increased LTA pressure closes the foramen ovale. The ductus arteriosus closes.

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9
Q

What are the signs and symptoms of poor perfusion?

A
  • cyanosis
  • clubbing
  • cold, clammy skin
  • edema
  • fatigue
  • dyspnea with exertion
  • difficulty feeding
  • decreased UO
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10
Q

What are some complications of poor perfusion?

A
  • edema
  • ventricular hypertrophy
  • tachypnea
  • tachycardia
  • ischemia
  • renal impairment
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11
Q

What are the signs and symptoms of hypercyanotic spells?

A

increased cyanosis
hypoxemia
dyspnea
agitation

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12
Q

What are the interventions for hypercyanotic spells?

A
  • knee to chest position
  • supplementary oxygen
  • morphine sulfate
  • fluids
  • propanolol
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13
Q

What are the four structural defects that make up Tetralogy of Fallot?

A
  • ventricular septal defect
  • right ventricular hypertrophy
  • overriding aorta
  • pulmonary stenosis
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14
Q

What are the signs and symptoms of Tetralogy of Fallot?

A
  • Tet spells
  • difficulty feeding
  • cyanosis
  • dyspnea, SOB, decreased O2
  • clubbing
  • adventitious lung sounds/HF
  • tripod position or squatting
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15
Q

What are some management interventions for Tetralogy of Fallot?

A
  • morphine sulfate = vasodilation
  • provide oxygen
  • knee to chest position
  • fluids
  • correction of metabolic acidosis
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16
Q

Explain how Tetralogy of Fallot causes its signs and symptoms.

A

Pulmonary stenosis decreases blood flow into the pulmonary arteries. As a result, pressure in the RTV increases, causing right ventricular hypertrophy, eventually resulting in HF. Decreased blood flow into the pulmonary arteries also decreases oxygenation of the blood. Ventricular septal defect causes LT to RT shunting of blood, and overriding aorta both allow deoxygenated and oxygenated blood to mix. Blood in circulation is deficient in oxygen, resulting in poor perfusion. Poor perfusion causes hypercyanosis; difficulty feeding as fatigue and difficulty breathing occurs; dyspnea as the body tries to compensate for hypoxia; clubbing. Children will squat or adopt tripod position to help circulation back to the lungs and heart.

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17
Q

What is the pathophysiology of tricuspid atresia?

A

The tricuspid fails to form, preventing blood from entering the pulmonary arteries. Instead, blood is shunted through the patent ductus arteriosus and foramen ovale, resulting in mixing of blood and insufficient oxygenation of the system. Tricuspid atresia also may consist of VSD.

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18
Q

What are the two diseases that decrease pulmonary blood flow?

A

Tetralogy of Fallot and Tricuspid Atresia

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19
Q

What are the signs and symptoms of Tricuspid Atresia

A

cyanosis
tachypnea
work of breathing
difficulty feeding
HF: crackles, wheezing
cool, clammy skin
clubbing
compensatory polycythemia

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20
Q

What are some complications that may occur even after Tricuspid atresia is corrected?

A

atrial arrhythmia, LTV dysfunction
may require pacemakers

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21
Q

What are some disorders of increased pulmonary blood flow?

A

Patent ductus arteriosus, atrial septal defect, ventricular septal defect, atrioventricular canal defect

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22
Q

Describe the pathophysiology of a patent ductus arteriosus.

A

When the ductus arteriosus fails to close after birth, mixing of blood between the pulmonary arteries and aorta (RT to LT*) occurs, causing increased blood flow to the lungs and insufficient oxygenation of the system. Pulmonary congestion and RTV hypertrophy occurs.

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23
Q

What are signs and symptoms of patent ductus arteriosus?

A

CALL
Cardiac: bounding peripheral pulses, increased HR, low DBP
Activity intolerance
Lungs: HF w/ tachypnea, dyspnea, SOB; edema
Loss of weight: difficulty feeding

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24
Q

What are the treatment medications for patent ductus arteriosus?

A

prostaglandin inhibitors: indomethacin and ibuprofen

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25
Q

What is the pathophysiology of atrial septal defect?

A

The foramen ovale fails to close, causing a LT to RT shunt in the atria. This causes mixing of blood and increased blood flow to the lungs. RTV hypertrophy, pulmonary HTN/congestion, and decreased perfusion result.

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26
Q

What are the signs and symptoms of atrial septal defects?

A

activity intolerance
cyanosis, clubbing, HF, tachycardia
pleural effusion: crackles, dyspnea, pneumonia
loss of weight/impaired growth

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27
Q

Describe the pathophysiology of ventricular septal defects.

A

Holes in the septum allow LT to RT shunting of blood into the RTV. RTV volume/pressure increases, increasing blood flow into the pulmonary arteries and causing pulmonary congestion and HTN. Pulmonary HTN causes damage to pulmonary arteries. Blood is also mixed, causing poor perfusion. LTV hypertrophy occurs as the heart attempts to meet systemic demands for blood volume and oxygen.
Untreated VSD will lead to Eienmenger syndrome, where shunting reverses.

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28
Q

What are the signs and symptoms of VSD?

A

HOLE
HF - dyspnea, fatigue, edema, crackles, diaphoresis, clamminess, frequent lung infections
Often fatigued - difficulty feeding
Low growth rate
Extra heart sounds - holosystolic murmur

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29
Q

What are the medications typically ordered for prevention or management of CHF?

A
  • digoxin
  • diuretics
  • ACE inhibitors (captopril)
  • beta blockers
  • anticoagulants
30
Q

Describe the pathophysiology of atrioventricular canal defects.

A

The AV valves fail to form, basically causing a large VSD. Blood from all chambers mix and enter the pulmonary artery and aorta. Increased blood flow to the pulmonary arteries occur. Increased blood volume causes LTV hypertrophy as the LTV does most of the work.

31
Q

What are the signs and symptoms of AV canal defect?

A

Cyanosis, difficulty feeding, work of breaking, retractions, tachypnea, nasal flaring, rales, murmur, signs of HF

32
Q

What are some complications of AV canal defects?

A

complete heart block
mitral regurgitation and future valve replacement

33
Q

What are three obstructive congenital heart disorders?

A

Coarctation of the aorta, aortic stenosis, pulmonary stenosis

34
Q

Describe the pathophysiology of coarctation of the aorta.

A

Narrowing of the aorta interrupts blood flow. Pressure before the coarctation increases, and often causes headaches, nosebleeds, heart failure, stroke, increased upper extremity SBP, and bounding upper extremity pulses. Lower extremities experience poor perfusion, decreased SBP, and weak pulses.

35
Q

What are signs and symptoms of coarctation of the aorta?

A

HF
HA, epistaxis, bounding UE pulses, elevated UE BP, posterior LT sided murmur
rib notching
HTN
diminished LE pulses, decreased LE BP, Raynaud’s syndrome

36
Q

What are some medications used in the treatment or management of coarctation of the aorta?

A

alprostadil (prostaglandins to keep DA open)
digoxin

37
Q

What are some complications of coarctation of the aorta?

A

HF
aortic aneurysm
aortic rupture
CVA

38
Q

Describe the pathophysiology of aortic stenosis.

A

The aorta is obstructed due to valve/muscle/vessel issues. Stenosis decreases CO and increases LTV pressure, resulting in LTV hypertrophy and eventually HF.

39
Q

What are some signs and symptoms of aortic stenosis

A

fatigue, dizziness
difficulty feeding
chest pain
faint pulses
murmur
HF

40
Q

Describe the pathophysiology of pulmonary stenosis.

A

Obstruction of the pulmonary arteries due to valve/muscle/vessel issues. Obstruction causes increased pressure in the RT side of the heart may cause the FO to reopen. PDA may relieve pulmonary stenosis by allowing more blood flow to the lungs.

41
Q

What are the signs and symptoms of pulmonary stenosis?

A
  • dyspnea
  • activity intolerance
  • hypercyanotic spells
  • HF
  • thrill at sternal border
  • high pitched click after S2
  • murmur
42
Q

What are some mixed congenital heart disorders?

A

Transposition of the great vessels, total anomalous pulmonary venous return, truncus arteriosus, hypoplastic LT heart syndrome

43
Q

Describe the pathophysiology of transposition of the great vessels.

A

The pulmonary artery and aorta are transposed, resulting in a closed loop circulatory system. Deoxygenated blood is unable to reach the lungs and get oxygenated. Instead, it reenters the systemic circulation via the aorta, causing poor perfusion. Fatal if no PDA/VSD/ASD or left untreated.

44
Q

What are the signs and symptoms of transposition of the great vessels?

A

worsening cyanosis
difficulty feeding
tachypnea, tachycardia
prominent ventricular impulse

45
Q

What medication can be given to manage transposition of the great vessel until surgical intervention?

A

alprostadil (prostaglandins)

46
Q

Describe the pathophysiology of total anomalous pulmonary venous return.

A

The pulmonary veins connect to the RTA or SVC instead of the LTA. Oxygenated blood enters the RTA, increasing pressure and remains in the pulmonary loop. Fatal if no ASD. Complications include RTV hypertrophy, pulmonary HTN, and pulmonary edema.

47
Q

What are the signs and symptoms of TAPVR (total anomalous pulmonary return)?

A
  • cyanosis
  • fatigue, difficulty feeding
  • work of breathing, tachypnea
  • S2 splitting, murmur
  • hepatomegaly
48
Q

Describe the pathophysiology of truncus arteriosus.

A

The pulmonary artery and aorta are fused due to an embryonic development defect. Blood is completely mixed, but more blood enters the lungs due to pressure being lower in the lungs. LTV hypertrophy occurs d/t LTV strain. Poor perfusion occurs due to mixing of blood. Pulmonary HTN, stenosis, and edema occur. Systemic BP is low.

49
Q

What are signs and symptoms of truncus arteriosus?

A
  • cyanosis
  • fatigue
  • work of breathing, difficulty feeding, tachypnea
  • HF
  • holosystolic murmur
50
Q

What are the medication that can be given for management of truncus arteriosus?

A

digoxin, ACE inhibitors, diuretics

51
Q

Describe the pathophysiology of Hypoplastic LT heart syndrome.

A

The LT side of the heart is underdeveloped, and therefore cannot sufficiently supply blood to the systemic circulatory system. It is often fatal unless a heart transplant can be performed.

52
Q

What are the signs and symptoms of hypoplastic LT heart syndrome?

A
  • cyanosis
  • fatigue, difficulty feeding, tachypnea, dyspnea
  • tachycardia
  • gallop rhythm
  • only P2 sound
  • holosystolic murmur
  • circulatory shock
53
Q

Describe the pathophysiology of heart failure.

A

Increased demands of the heart cause hypertrophy of the ventricles, and when CO decreases and the heart cannot meet these demands, heart failure occurs. Most common is congestive heart failure, where increased pressure outside of the heart (afterload) or pooling of blood in the heart increases the workload of the heart.

key words: CO, hypertrophy, afterload

54
Q

What are the signs and symptoms of HF?

A
  • difficulty feeding
  • fatigue, dizziness, irritability, exercise intolerance
  • SOB, syncope
  • decreased UO, edema, diaphoresis
  • cyanosis, cold/clammy skin
  • adventitious breath sounds
  • tachycardia, tachypnea, work of breathing
  • weak, thready pulses
  • abd distention or organomegaly

key: lungs, cardiac, abd, fluid retention

55
Q

What are the interventions for HF?

A
  • airway: Fowler’s position, suction, O2
  • medications: digoxin, diuretics, ACE inhibitors, beta blockers, anticoagulants
  • nutrition : higher calorie intake
  • decrease metabolic needs
56
Q

Describe the pathophysiology of infective endocarditis.

A

Cardiac tissue damage d/t other diseases cause increased platelet and thrombi aggregation, forming vegetations that foster bacterial/fungal growth.

57
Q

What are signs and symptoms of infective endocarditis?

A
  • fever
  • fatigue, weight loss
  • flu-like symptoms
  • petechiae
  • extra-cardiac emboli or hemorrhagic lesions
  • prolonged PR interval
  • dysrhythmia
  • adventitious breath sounds
  • splenomegaly
58
Q

Describe the pathophysiology of acute rheumatic fever.

A

Acute infection causes an antibody response in which antibodies end up damaging cardiac tissue, joints, and muscles.

59
Q

What are the signs and symptoms of acute rheumatic fever?

A
  • fever
  • joint pain
  • flu-like symptoms
  • rash, erythema, subQ nodules
  • prolonged PR interval
  • chorea
  • carditis
60
Q

What are the medications used for treatment/management of acute rheumatic fever?

A
  • ibuprofen
  • penicillin
  • corticosteroids
  • haloperidol
61
Q

Describe the physiology of cardiomyopathy.

A

Damage to the myocardium caused by CHD, genetics, or unknown etiology.
Restrictive cardiomyopathy causes atrial relaxation.
Dilated cardiomyopathy causes ventricular relaxation. Hypertrophic cardiomyopathy causes ventricular hypertrophy

62
Q

What are the signs and symptoms of cardiomyopathy?

A
  • chest pain
  • syncope, fatigue, poor growth
  • tachypnea, work of breathing, respiratory distress
  • fluid retention
  • tachycardia, dysrhythmia
  • pleural effusion
63
Q

What are some complications of cardiomyopathy?

A
  • heart failure
  • blood clots
  • arrhythmia
  • cardiac arrest
64
Q

What are the parameter for HTN in children?

A

12mmHg over the 95% percentile or >130/89 and >140/90 for children >13 YO

65
Q

Describe the pathophysiology of Kawasaki disease.

A

Acute systemic vasculitis caused by autoimmune response in medium-sized arteries. Inflammation and edema leads to coronary dilation or aneurysms.

66
Q

What are the signs and symptoms of Kawasaki Disease?

A
  • fever, chills, HA, malaise
  • N/V, diarrhea, abd pain
  • joint pain, edema
  • dry, cracked lips
67
Q

What are the treatment/management options for Kawasaki Disease?

A
  • aspirin
  • immunoglobulin therapy
  • tylenol (NOT NSAIDs)
  • maintain fluids
  • monitor for I&O, signs of HF or RD, aspirin toxicity
  • no live vaccines after immunoglobulin therapy
  • cardiology follow ups
68
Q

What are some possible complications of cardiac catheterization?

A
  • bleeding
  • low-grade fever
  • loss of pulse in extremity distal to site
  • arrhythmia
  • thrombus
  • infection
69
Q

What are some possible complications of cardiac surgery?

A
  • atelectasis
  • bacterial endocarditis
  • cardiac tamponade
  • CVA, HF, hemorrhage
  • PE, pneumonia, pneumothorax, pulmonary edema
  • post-perfusion syndrome
  • post-cardiac surgery syndrome
  • seizure
  • infection
70
Q

What are the steps for nursing care in cardiac catheterizations?

A

Preop
- obtain parental consent forms, assessment
- provide education
- NPO 4-6 hrs
- contrast dye solution
Postop
- monitor vitals Q15 min, 30 min
- keep extremity straight for 4- hr, bed rest
- monitor dressing, I&O
- education

71
Q

What educational points should nurses teach for post-op care of cardiac catheterization?

A
  • cardiac f/u
  • monitor for fever, bleeding, N/V, infection, skin changes
  • tylenol and ibuprofen for pain
  • avoid showering and exercise for 3 days post-op

Pediatrics (10 decks)

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