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Pediatrics > Alterations in Cardiac Function/Cardiac Anomalies > Flashcards

Alterations in Cardiac Function/Cardiac Anomalies Flashcards

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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
An increased afterload means an ______ cardiac workload
increased
26
Contractility
Force of contraction
27
An increase in contractility produces an ________ in stroke volume if:
increase preload and afterload are unchanged
28
What 3 interventions can produce clinically significant alterations to preload, afterload, and contractility?
1. vasoactive agents 2. inotropic agent 3. changes in blood volume
29
Direction of fetal circulation from placenta
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 6. LA 7. LV 8. Aorta 9. Circulation 10. Umbilical artery
30
Ductus Venosus
a fetal blood vessel that shunts oxygenated blood from the umbilical vein directly to the inferior vena cava, bypassing the liver.
31
Foramen Ovale
an opening between the 2 atria in the fetal heart that allows blood to bypass the pulmonary circulation (lungs).
32
Ductus Arteriosus
s a fetal blood vessel connecting the pulmonary artery to the aorta, enabling blood to bypass the lungs.
33
What is persistence of fetal circulation?
Shunts do not close in 48-72 hours as they should. Become PFO (patent foramen ovale) or PDA (patent ductus arteriosus)
34
What occurs to the umbilical arteries at birth?
tretching umbilical arteries results in arterial constriction and reduced venous return through the umbilical vein.
35
What changes occur to the ductus venosus at birth and what is its remnant?
Ductus venosus gradually closes (over a period of days) Ligamentum teres hepatis remnant of the ductus venosus
36
What triggers constriction of the ductus arteriosus at birth and what is its remnant?
Increased O2 [ ] in blood triggers constriction of the ductus arteriosus Ligamentum arteriosum- fibrous remnant of the DA
37
What triggers closure of the foramen ovale?
Increased BF to the lungs and LA equalizes pressure in the two atria which results in closure of the foramen ovale
38
Causes of Heart Defects (non closure of shunts)
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
7 Signs and Symptoms of Congenital Heart Defects
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
What does an echocardiogram assess?
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
What is cardiac catherization?
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
What 4 pieces of information are obtained in cardiac catherization?
o Pressures within the heart o Oxygen saturations o Blood flow patterns o Structural information (valves, chambers, great vessels)
43
How are congenital cardiac diseases classified
By degree of pulmonary blood flow
44
In lesions of increased pulmonary blood flow, which direction is blood shunted and why?
From left to right High to low pressure
45
Major complication of lesions of increased pulmonary blood flow and why
Congestive heart failure Oxygenated blood is being forced back through pulmonary circulation repeatedly
46
3 Lesions with increased pulmonary blood flow
1. Patent Ductus Arteriosus 2. Atrial Septal Defect 3. Ventricular Septal Defect
47
Who is PDA seen in?
* Occurs in premature infants (< 28 weeks) – 80% * 5-10% of all defects, 1/2000 of term infants
48
Where is the communication between in patent ductus arteriosus?
From aorta back through pulmonary artery
49
Management of PDA?
1. Oxygen 2. Fluid restriction 3. Diuretics 4. Indomethacin 5. Trans-catheter closure in children over 18mon 6. Surgical ligation
50
Why is oxygen management necessary in those with PDA?
Oxygenated blood that should be perfusing tissues is being shunted back from aorta through pulmonary artery (left to right shunt)
51
Why is fluid restriction and diuretics necessary in PDA?
Increased blood continues circulating through pulmonary circulation
52
Why is indomethacin used in management of PDA?
Vasoconstrictor to close off PDA
53
What is an atrial septal defect and what shunt would not be closed for this to occur?
Communication between left and right atrium Can be PFO but other defect types exist
54
Treatment of atrial septal defect
Cath lab or heart surgery Asymptomatic: monitored without medication Symptomatic: treated with diuretics and digoxin Sometimes not discovered until adulthood
55
What is a ventricular septal defect and describe blood flow?
Communication between left and right ventricles Some blood circulates into aorta, but some is shunted through defect back into pulmonary circulation
56
What 2 things are you assessing for in lesions with increased pulmonary blood flow
1. decreased perfusion to periphery 2. congestive heart failure
57
What medications are used in treatment of lesions with increased pulmonary blood flow?
indomethacin diuretics oxygen
58
Result of lesions with decreased pulmonary blood flow
Delivery of deoxygenated blood to periphery resulting in hypoxia or decreased volume of flow Blood flow from right to left, skipping pulmonary circulation
59
2 Types of Lesions with Decreased Pulmonary Blood Flow
1. tetralogy of fallot 2. tricuspid atresia
60
Four components of Tetralogy of Fallot
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
What is a tet spell?
Extreme, potentially fatal hypoxemia occuring in children with TOF Severe cyanosis, seen ON EXERTION because child is receiving high quantities of deoxygenated blood
62
Why will children resume a squatting/fetal position during a tet spell?
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
Signs and Symptoms of TOF
1. clubbing 2. increased megakaryocytes further contribute to clubbing 3. central cyanosis
64
Treatment of TOF
1. beta blockers 2. morphine 3. prostaglandin (vasodilator) 4. surgery/shunt from subclavian to PA
65
What is tricuspid atresia?
imperforate tricuspid valve - no opening between right atrium and ventricle
66
What must be present in order for blood flow to occur in tricuspid atresia
Presence of other heart defects 1. ASD/PFO 2. VSD and/or 3. PDA
67
What are the effects on the heart muscle in tricuspid atresia
* Right atrial hypertrophy * Right ventricle hypotrophic
68
What are the symptoms of tricuspid atresia and when do they begin to arise?
cyanosis acute respiratory failure hypoxemia acidosis When the DA starts to close at 12-24 hours
69
How is tricuspid atresia treated?
1. palliative creation of shunts - balloon septostomy (between atria) - BT shunt (between subclavian and PA) - central shunt (AO to PA)
70
Complications of Catheterization
1. arrhythmias 2. bleeding 3. cardiac perforation 4. CVA 5. contrast reaction 6. hypercyanotic spells 7. local vascular complications 8. infection
71
Nursing care post catherization
Monitor for - extremitiy perfusion compromise - venous obstruction - infection risk - bleeding - respiratory compromise - renal function - pain - hypothermia
72
Bialock Taussig Shunt
Shunt from subclavian artery to pulmonary artery for palliation of lesions with decreased pulmonary blood flow Do not take BP in arm
73
Purpose of fetal position in TOF
increases systemic vascular resistance (afterload) and decreases VSD shunting, forcing blood through PA Aim to decrease pulmonary vascular resistance
74
If a child's oxygenation does not improve with oxygen supplementation, what should be suspected?
Heart defect
75
Post cardiac cath procedure focusses on:
evaluation of vital signs, distal pulses, pressure dressing
76
Decreased Pulmonary Blood Flow disorders result in: Increased Pulmonary Blood Flow disorders result in:
Cyanosis Pulmonary Edema
77
Prostaglandin Use in TOF vs Tricuspid Atresia
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
Goal of Treatment of a TET Spell
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
r u awesome and beautiful
yes
80
Signs of Extremity Perfusion Compromise vs Venous Obstruction Post Cath
Perfusion: ARTERIAL - pallor, mottling, diminished pulses, cool temp Obstruction: VENOUS - edema, dusky, normal cap refill
81
General Management of lesions with decreased pulmonary blood flow
1. prostaglandins 2. hydration 3. oxygen 4. surgery
82
Which congenital heart anomalies utilized vasoconstrictors vs vasodilators
VS: increased VD: decreased
83
Tricuspid Atresia can be exacerbated during ________ of may require _______
times of feeding full resusitation

Pediatrics (12 decks)

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