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Pediatrics > Alterations in Cardiac Function/Cardiac Anomalies > Flashcards

Alterations in Cardiac Function/Cardiac Anomalies Flashcards

1
Q

Role of Clinical Perfusionist

A

Operates cardiopulmonary bypass apparatus during cardiac surgeries

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2
Q

What is cardiopulmonary bypass + its 2 main components?

A

Provides a motionless, bloodless field for the surgeon to work on

  1. an artificial blood pump, which continuously propels blood forward
  2. an artificial oxygenator and then to the patient’s tissues while the surgeon repairs the anomaly within the heart.
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3
Q

What is a cardioplegia pump?

A

Used to introduce a high potassium solution directly to the heart to induce and maintain cardiac arrest.

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4
Q

Describe normal blood flow through adult heart

A
  1. Periphery
  2. SVC/IVC
  3. RA
  4. Tricuspid
  5. RV
  6. Pulmonary
  7. PA
  8. Lungs
  9. PV
  10. LA
  11. Mitral
  12. LV
  13. Aortic
  14. Aorta
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5
Q

Systole

A

when the heart contacts with ejection of blood

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6
Q

Diastole

A

when the heart relaxes and fills with blood

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7
Q

End Diastolic Volume

A

volume of blood in the heart after filling

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8
Q

End Systolic Volume

A

volume of blood left in the heart after contraction

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9
Q

Cardiac Output

A

The volume of blood ejected from the left ventricle each minute

Equal to HR x SV`

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10
Q

Normal Stroke Volume of Infant

A

0.032ml

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11
Q

Normal CO for infant

A

77ml/kg/min

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12
Q

In children CO is almost completely dependent on ________

Until age _____

why?

A

Heart Rate

5

This is when the heart muscle is fully developed and can better contribute to stroke volume

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13
Q

Tachycardic and Bradycard heart rates can compromise:

A

Cardiac Output

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14
Q

How does a tachycardic HR compromise cardiac output?

A

ventricular filling time and end-diastolic volume are lowered, and myocardial oxygen consumption is increased

Therefore, improper filling leading to sub-adequate output and increased workload of ventricle

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15
Q

How does a bradycardic HR compromise CO?

A

blood is not being perfused in timely manner

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16
Q

When does myocardial perfusion occur?

What are the implications of a tachycardic HR on this?

A

Diastole

Because there is
1. inadequate output/return in tachycardic HRs and
2. need for myocardial oxygenation increase

cardiac ischemia and ventricular dysfunction can occur

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17
Q

Stroke Volume

A

Volume of blood ejected per beat

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18
Q

What 3 factors influence stroke volume

A

Preload Afterload and Contractility

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19
Q

Preload

A

the amount of blood filling the ventricles during diastole

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20
Q

What effect does increased preload have on stroke volume?

A

Increase stroke volume to a maximum value, but beyond this stroke volume falls (unable to compensate)

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21
Q

In what conditions is an increased preload seen?

A

Hypervolemia

Regurgitation of valves

Heart failure

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22
Q

Afterload

A

is the load that the heart must eject against

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23
Q

What alterations to afterload increase stroke volume?

A

Reductions in afterload increase stroke volume if other variables remain constant.

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24
Q

In what conditions in an increased afterload seen?

A

Hypertension

Vasoconstriction

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25
Q

An increased afterload means an ______ cardiac workload

A

increased

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26
Q

Contractility

A

Force of contraction

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27
Q

An increase in contractility produces an ________ in stroke volume if:

A

increase

preload and afterload are unchanged

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28
Q

What 3 interventions can produce clinically significant alterations to preload, afterload, and contractility?

A
  1. vasoactive agents
  2. inotropic agent
  3. changes in blood volume
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29
Q

Direction of fetal circulation from placenta

A
  1. Placenta
  2. Umbilical Vein
  3. Ductus Venosus: bypass liver
  4. IVC
  5. RA
    a) some blood continue to RV - pulmonary trunk, lungs, pulmonary veins, LA

i) From pulmany trunk some blood is shunted away from lungs through ductus arterious to aorta

b) some blood is shunted through foramen ovale to LA

  1. LA
  2. LV
  3. Aorta
  4. Circulation
  5. Umbilical artery
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30
Q

Ductus Venosus

A

a fetal blood vessel that shunts oxygenated blood from the umbilical vein directly to the inferior vena cava, bypassing the liver.

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31
Q

Foramen Ovale

A

an opening between the 2 atria in the fetal heart that allows blood to bypass the pulmonary circulation (lungs).

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32
Q

Ductus Arteriosus

A

s a fetal blood vessel connecting the pulmonary artery to the aorta, enabling blood to bypass the lungs.

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33
Q

What is persistence of fetal circulation?

A

Shunts do not close in 48-72 hours as they should.

Become PFO (patent foramen ovale) or PDA (patent ductus arteriosus)

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34
Q

What occurs to the umbilical arteries at birth?

A

tretching umbilical arteries results in arterial constriction and reduced venous return through the umbilical vein.

35
Q

What changes occur to the ductus venosus at birth and what is its remnant?

A

Ductus venosus gradually closes (over a period of days)
Ligamentum teres hepatis remnant of the ductus venosus

36
Q

What triggers constriction of the ductus arteriosus at birth and what is its remnant?

A

Increased O2 [ ] in blood triggers constriction of the ductus arteriosus
Ligamentum arteriosum- fibrous remnant of the DA

37
Q

What triggers closure of the foramen ovale?

A

Increased BF to the lungs and LA equalizes pressure in the two atria which results in closure of the foramen ovale

38
Q

Causes of Heart Defects (non closure of shunts)

A

o Multifactorial Causes:
 Teratogenic
 Chance
 Familial Link
* Chromosomal Abnormalities
o Deletion at Chromosome 22 (DiGeorge Syndrome
o Down’s Syndrome (Trisomy 21)
o Turner’s Syndrome (X chromosomes is missing)
o Trisomy 13 (3 copies of 13)

39
Q

7 Signs and Symptoms of Congenital Heart Defects

A
  1. cyanosis (peripheral or central)
  2. respiratory distress
  3. congestive heart failure
  4. decreased cardiac output
  5. abnormal rhythms
  6. cardiac murmur
  7. failure to thrive
40
Q

What does an echocardiogram assess?

A

Ultrasound to generate image

location and relationship of intra cardiac and extra cardiac structures
cardiac function
measures sizes of cardiac chambers
valve functions
size of defects
estimates gradient and blood flow direction.

41
Q

What is cardiac catherization?

A

o Involves the insertion of a catheter through an peripheral artery/vein which is then advanced into the heart.
o Performed under fluoroscopy (cath-lab)

42
Q

What 4 pieces of information are obtained in cardiac catherization?

A

o Pressures within the heart
o Oxygen saturations
o Blood flow patterns
o Structural information (valves, chambers, great vessels)

43
Q

How are congenital cardiac diseases classified

A

By degree of pulmonary blood flow

44
Q

In lesions of increased pulmonary blood flow, which direction is blood shunted and why?

A

From left to right

High to low pressure

45
Q

Major complication of lesions of increased pulmonary blood flow and why

A

Congestive heart failure

Oxygenated blood is being forced back through pulmonary circulation repeatedly

46
Q

3 Lesions with increased pulmonary blood flow

A
  1. Patent Ductus Arteriosus
  2. Atrial Septal Defect
  3. Ventricular Septal Defect
47
Q

Who is PDA seen in?

A
  • Occurs in premature infants (< 28 weeks) – 80%
  • 5-10% of all defects, 1/2000 of term infants
48
Q

Where is the communication between in patent ductus arteriosus?

A

From aorta back through pulmonary artery

49
Q

Management of PDA?

A
  1. Oxygen
  2. Fluid restriction
  3. Diuretics
  4. Indomethacin
  5. Trans-catheter closure in children over 18mon
  6. Surgical ligation
50
Q

Why is oxygen management necessary in those with PDA?

A

Oxygenated blood that should be perfusing tissues is being shunted back from aorta through pulmonary artery (left to right shunt)

51
Q

Why is fluid restriction and diuretics necessary in PDA?

A

Increased blood continues circulating through pulmonary circulation

52
Q

Why is indomethacin used in management of PDA?

A

Vasoconstrictor to close off PDA

53
Q

What is an atrial septal defect and what shunt would not be closed for this to occur?

A

Communication between left and right atrium

Can be PFO but other defect types exist

54
Q

Treatment of atrial septal defect

A

Cath lab or heart surgery

Asymptomatic: monitored without medication

Symptomatic: treated with diuretics and digoxin

Sometimes not discovered until adulthood

55
Q

What is a ventricular septal defect and describe blood flow?

A

Communication between left and right ventricles

Some blood circulates into aorta, but some is shunted through defect back into pulmonary circulation

56
Q

What 2 things are you assessing for in lesions with increased pulmonary blood flow

A
  1. decreased perfusion to periphery
  2. congestive heart failure
57
Q

What medications are used in treatment of lesions with increased pulmonary blood flow?

A

indomethacin

diuretics

oxygen

58
Q

Result of lesions with decreased pulmonary blood flow

A

Delivery of deoxygenated blood to periphery resulting in hypoxia or decreased volume of flow

Blood flow from right to left, skipping pulmonary circulation

59
Q

2 Types of Lesions with Decreased Pulmonary Blood Flow

A
  1. tetralogy of fallot
  2. tricuspid atresia
60
Q

Four components of Tetralogy of Fallot

A
  1. Large Ventricular Septal Defect
  2. Pulmonary Artery Stenosis
  3. Right Ventricular Hypertrophy (secondary to stenosis)
  4. Overriding aorta (deoxygenated blood from RV goes through VSD because its easier than going through stenotic PA)
61
Q

What is a tet spell?

A

Extreme, potentially fatal hypoxemia occuring in children with TOF

Severe cyanosis, seen ON EXERTION because child is receiving high quantities of deoxygenated blood

62
Q

Why will children resume a squatting/fetal position during a tet spell?

A
  1. Increased systemic vascular resistance: forcing blood into pulmonary circulation
  2. Improved pulmonary blood flow
  3. reduced right to left shunting by increasing venous return
  4. enhanced ventilation
63
Q

Signs and Symptoms of TOF

A
  1. clubbing
  2. increased megakaryocytes further contribute to clubbing
  3. central cyanosis
64
Q

Treatment of TOF

A
  1. beta blockers
  2. morphine
  3. prostaglandin (vasodilator)
  4. surgery/shunt from subclavian to PA
65
Q

What is tricuspid atresia?

A

imperforate tricuspid valve - no opening between right atrium and ventricle

66
Q

What must be present in order for blood flow to occur in tricuspid atresia

A

Presence of other heart defects

  1. ASD/PFO
  2. VSD
    and/or
  3. PDA
67
Q

What are the effects on the heart muscle in tricuspid atresia

A
  • Right atrial hypertrophy
  • Right ventricle hypotrophic
68
Q

What are the symptoms of tricuspid atresia and when do they begin to arise?

A

cyanosis
acute respiratory failure
hypoxemia
acidosis

When the DA starts to close at 12-24 hours

69
Q

How is tricuspid atresia treated?

A
  1. palliative creation of shunts
    - balloon septostomy (between atria)
    - BT shunt (between subclavian and PA)
    - central shunt (AO to PA)
70
Q

Complications of Catheterization

A
  1. arrhythmias
  2. bleeding
  3. cardiac perforation
  4. CVA
  5. contrast reaction
  6. hypercyanotic spells
  7. local vascular complications
  8. infection
71
Q

Nursing care post catherization

A

Monitor for
- extremitiy perfusion compromise
- venous obstruction
- infection risk
- bleeding
- respiratory compromise
- renal function
- pain
- hypothermia

72
Q

Bialock Taussig Shunt

A

Shunt from subclavian artery to pulmonary artery for palliation of lesions with decreased pulmonary blood flow

Do not take BP in arm

73
Q

Purpose of fetal position in TOF

A

increases systemic vascular resistance (afterload) and decreases VSD shunting, forcing blood through PA

Aim to decrease pulmonary vascular resistance

74
Q

If a child’s oxygenation does not improve with oxygen supplementation, what should be suspected?

A

Heart defect

75
Q

Post cardiac cath procedure focusses on:

A

evaluation of vital signs, distal pulses, pressure dressing

76
Q

Decreased Pulmonary Blood Flow disorders result in:

Increased Pulmonary Blood Flow disorders result in:

A

Cyanosis

Pulmonary Edema

77
Q

Prostaglandin Use in TOF vs Tricuspid Atresia

A

Tricuspid Atresia: keep PDA open until surgical repair

TOF: increase dilation of the pulmonary artery and increase the amount of blood flowing to the lungs to be oxygenated

78
Q

Goal of Treatment of a TET Spell

A
  1. to slow the heart rate
  2. raise the systemic pressure in order to push blood into the stenotic pulmonary artery

The increase in systemic pressure will increase the amount of blood being oxygenated and help reduce the hypercyanotic spell.

79
Q

r u awesome and beautiful

A

yes

80
Q

Signs of Extremity Perfusion Compromise vs Venous Obstruction Post Cath

A

Perfusion: ARTERIAL
- pallor, mottling, diminished pulses, cool temp

Obstruction: VENOUS
- edema, dusky, normal cap refill

81
Q

General Management of lesions with decreased pulmonary blood flow

A
  1. prostaglandins
  2. hydration
  3. oxygen
  4. surgery
82
Q

Which congenital heart anomalies utilized vasoconstrictors vs vasodilators

A

VS: increased

VD: decreased

83
Q

Tricuspid Atresia can be exacerbated during ________ of may require _______

A

times of feeding

full resusitation

Pediatrics (12 decks)

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