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Pediatrics > Exam 3: Cardio > Flashcards

Exam 3: Cardio Flashcards

1
Q

Patent Ductus Arteriosis

A

In fetal circulation, this is where blood comes to from the pulmonary artery (because blood in fetal circulation bypasses the lungs) and then it brings the blood to the descending aorta which provides blood to the lower extremities and organ

*This normally closes after birth, but with some congenital heart defects you may want to keep it open after birth

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2
Q

Fetal Circulation: Descending Aorta

A

Provides blood to organs and lower extremities

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3
Q

Fetal Circulation: L Aorta

A

provides blood to head and upper extremities

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4
Q

Superior vena cava

A

Where blood from head and upper extremities drains in to in order to get perfused

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5
Q

Fetal Circulation

A

All through umbilical circulation!! Gas exchange of fetus occurs via fetal circulation from umbilical cord

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6
Q

Foramen Ovale

A

A hole that allows blood to pass from right to left atrium

*Normally closes after birth, but may want to keep it open with certain congenital heart defects

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7
Q

Changes That Occur After Birth (3)

A
  1. Foramen ovale closes
  2. Closing of patent ductus arteriosis (doesn’t always close right away)
  3. Lungs expand and gas exchange now occurs in lungs
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8
Q

Neonate and Infant Hearts (5 facts)

A
  1. Heart and great vessels develop during first 3-8 weeks of gestation
  2. Heart sounds in the neonate are higher pitched and of greater intensity than adults
  3. Have faster heart rates
  4. Are dependent on adequate HR and rhythm to maintain CO because they cannot increase their stroke volume
  5. Myocardial muscle is less efficient and has fewer organized myocardial fibers, so they are very dependent on calcium, glucose, and volume
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9
Q

How do neonates and infants increase CO?

A

By increasing HR!

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10
Q

AV canal surgery

A

Can cause conduction system problems secondary to the surgery due to proximity of surgery to the AV node
*May lead to arrhythmias or pace maker

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11
Q

Cardiac Output

A

Volume of blood ejected by heart in 1 min.

  • In infants, good CO is dependent on adequate volume
  • Only way for infant to increase CO is to increase HR
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12
Q

Preload

A

Volume of blood returning to the heart

*At risk for decreased preload with fluid loss and dehydration

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13
Q

Afterload

A

resistance against which ventricles pump when ejecting blood

*Congenital heart defects may increase afterload

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14
Q

FETAL CIRCULATION

A

1st: Blood returns from placenta to ductus venous
2nd: Inferior vena cava

3rd: Right atrium
* Goes through foramen ovale
4th: Left atrium

5th: Left ventricle
6th: out the aorta, which provides blood to head and upper extremities
* Blood from upper extremities drains through SUPERIOR VENA CAVA then goes to

A. Right atrium
*Through tricuspid valve
B. Right ventricle

C. Out the pulmonary artery
*Bypasses lungs
D. Patent Ductus Arteriosis

E. Descending aorta, which provides blood to organs and lower extremities

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15
Q

Adequate systemic circulation relies on (5)

A
  1. Adequate HR
  2. Adequate circulating volume
  3. Low pulmonary vascular resistance
  4. Capillary permeability
  5. Tissue utilization of O2
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16
Q

Mother’s Health History

A

Mother’s with Type I diabetes or lupus have increased risk of child having a heart defect or arrhtymia

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17
Q

Hydropsfetalis

A

Congenital heart defect where infant develops severe anemia and CHF

*Increased risk for infant getting hydropsfetalis if mother gets fifth disease (Parvo virus) during pregnancy

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18
Q

Cytomegalovirus

A

Causes mono in young children; if pregnant mother is exposed during pregnancy then there is increased risk that infant will be born with congenital heart defect

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19
Q

Pregnancy risk factors for Congenital Heart Defects in Infants (7)

A
  1. Parvo virus (Fifth disease)
  2. Cytomegalovirus
  3. Herpes
  4. Cox-sachi B
  5. Dilantin
  6. Acetaminophen
  7. Alcohol and drug use

*Always ask if mother was vaccinated for measles, mumps, and rubella

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20
Q

Birth history: meconium

A

If a baby passes meconium in utero, then they are at risk for aspiration which increases risk for pulmonary HTN, and that will increase the workload of the heart

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21
Q

Circamoral cyanosis

A

Color change around the lips; where you usually see first signs of cyanosis

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22
Q

Older Children Signs and Symptoms of Heart Defects (6)

A
  1. Exercise intolerance
  2. Edema
  3. Respiratory problems (SOB)
  4. Chest pain
  5. Palpitations
  6. Neurologic problems
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23
Q

PMI/Apical Impulse Locations

A
  1. In a child up to 7, it is at 4th ICS
  2. In a child older than 7, it is at 5th ICS
    * PMI tells you how well the LV is working!
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24
Q

Erb’s Point

A

Where you can hear innocent, valvular, and diastolic murmurs best

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25
Q

What to record with heart murmurs (5 things)

A
  1. Location (where the murmur is heard best)
  2. Time (when it is heard in S1 S2 cycle)
  3. Intensity (related to child’s position; heard when sitting up?)
  4. Loudness
  5. Grading (I-VI) *Murmurs IV-VI are accompanied by thrill
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26
Q

Grading of Murmurs: I

A

Very faint, often not heard if child sits up

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27
Q

Grading of Murmurs: II

A

Usually readily heard, slightly louder than grade I and audible in all positions

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28
Q

Grading of Murmurs: III

A

Loud, but not accompanied by a thrill

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29
Q

Grading of Murmurs: IV

A

Loud, accompanied by a thrill

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30
Q

Grading of Murmurs: V

A

Loud enough to be heard with a stethoscope barely touching the chest; accompanied by a thrill

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31
Q

Grading of Murmurs: VI

A

Loud enough to be heard with stethoscope not touching chest,, accompanied by a thrill

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32
Q

SVC and IVC

A

The two great veins; blood returning through them has lowest O2 saturation

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33
Q

Hemodynamic Principles (3)

A
  1. Blood flows from area of higher pressure to lower pressure and takes path of least resistance
    * Pressure in left side of heart > right side of heart
  2. Resistance in pulmonary artery is less than in systemic circulation
  3. Pressure in pulmonary artery is less than the pressure in the aorta
34
Q

Increased Pulmonary Blood Flow Classification of Heart Defects (4)

A
  1. Atrial spetal defect
  2. Ventricular spetal defect
  3. Patent ductus arteriosus
  4. Atrioventricular canal
35
Q

Obstruction to Blood Flow From Ventricles Classification of Heart Defects (3)

A
  1. Coarctication of aorta
  2. Aortic Stenosis
  3. Pulmonic Stenosis
36
Q

Decreased Pulmonary Blood Flow Classification of Heart Defects (2)

A
  1. Tetrology of Fallot

2. Tricuspid atresia

37
Q

Mixed Blood Flow Classification of Heart Defects (4)

A
  1. Transposition of great arteries
  2. Total anomalous pulmonary venous return
  3. Truncus arteriosus
  4. Hypoplastic left heart syndrome
38
Q

5 Characteristics of Defects with Increased Pulmonary Blood Flow

A
  1. Left to right shunting (because pressure is higher on left and blood goes to side of least resistance)
  2. Right atrial and ventricular enlargement (not very significant but it can occur)
  3. Unusual to have CHF
  4. May be totally asymptomatic except for auscultating a murmur
  5. Depending on the size of the hole, it can wait to be fixed (can close on it’s own by school age)
39
Q

3 places that Atrial Septal Defect can occur

A

ASD= hole between right and left atrium

  1. Primum – lower end of septum
  2. Secundum – center of septum
    * *This is the most common
  3. Sinus venus defect – junction of SVC & right atrium
40
Q

Symptoms of Atrial Septal Defect (3)

A
  1. May be asymptomatic
  2. May develop CHF
  3. Audible murmur
41
Q

Ventricular Septal Defect Characteristics (5)

A
  1. Most common defect causing increased pulmonary blood flow
    * This defect is causing increased pulmonary blood flow because it is going from the left to the right and then out the lungs
  2. It is an opening between right & left ventricle
    * Can be membranous or muscular
    * Muscular: multiple holes in the heart
  3. It is frequently found with other defects
  4. 20 – 60 % close spontaneously during first year of life
    * Depending on the size, may wait to do surgery during first year of life
  5. Overtime it can cause ventricular hypertrophy
    * ↑ pressure in right ventricle→ hypertrophy
  6. Eisenmenger syndrome may develop
42
Q

Eisenmenger Syndrome (4 steps)

A

1st: There is chronic increased pressure on the right side of the heart, which isn’t used to high pressure
2nd: As a result, children develop secondary pulmonary HTN, which adds more pressure to right side of heart
3rd: Pulmonary arterioles hypertrophy and become resistant to blood flow
4th: Pressure from back flow continuously increases and you get reverse shunt of blood, and now blood goes from right to left ventricle, causing a mixture of deoxygenated and oxygenated blood to go through aorta and into systemic circulation

43
Q

Symptoms of Ventricular Septal Defect

A
  1. CHF common

2. Audible murmur

44
Q

AV Canal Characteristics (5)

A
  1. Incomplete closure of endocardial cushions
  2. Low ASD continuous with high VSD
    * Can see there is a big hole in the middle of the heart
    * Can affect valves if severe
  3. Defects in mitral & tricuspid valve
  4. Blood flow between all 4 chambers of the heart
  5. Most common defect in children with Down’s syndrome
45
Q

AV Canal Symptoms (3)

A
  1. CHF
  2. Murmur audible
  3. Mild cyanosis that ↑ with crying
46
Q

AV Canal Complications (5)

A
  1. Heart block
  2. CHF
  3. MV regurgitation
  4. Arrhythmias
  5. pulmonary hypertension
  • All due to location of the AV canal
  • May need pacemaker due to heart block
47
Q

Patent Ductus Arteriosis (PDA) Characteristics (3)

A
  1. Failure of PDA to close within first weeks of life
  2. ↑ pulmonary blood flow; Increased pulmonary blood flow occurs with PDA because the pressure of the aorta is higher than in the pulm`onary artery, so you will have blood flow regurgitating back into the lungs which increases pulmonary blood flow
  3. May develop right ventricular hypertrophy
48
Q

Symptoms of PDA

A

May show signs of CHF, murmur

*Mortality rate is very low

49
Q

Medication Management of PDA (2)

A
  1. Indomethacin: A prostaglandin inhibitor that helps close the PDA
  2. NSAIDs can also be used to close it
    * Don’t want PDA to close during pregnancy, so pregnant women should never take NSAIDs!!
50
Q

Coarctation of the Aorta (COA)

A

Type of obstructive defect

When there is a narrowing of the aorta, about where the patent ductus arteriosis inserts into the aorta
*Localized narrowing near insertion of ductus arteriosis

  • There is extra circulation through collateral circulation, which are microvessels that are off branches of the heart
  • Collateral circulation can cause poor CO
51
Q

Symptoms of COA (6)

A
  1. ↑ upper extremities BP
  2. ↓ lower extremities BP
  3. Bounding upper extremities pulses
  4. Weak pulses in lower extremities
  5. CHF in infants
  6. Older children describe: headache, dizziness, leg pain
    * Leg pain because not getting adequate blood flow to legs
52
Q

Aortic Stenosis Characteristics (4)

A
  1. Type of obstructive defect; IT IS THE NARROWING OR STRICTURE OF THE AORTIC VALVE
  2. ↓ cardiac output
  3. Left ventricular hypertrophy
    * See this because LV has to work harder to push blood passed the obstruction
  4. Pulmonary vascular congestion
    * Because blood is backing up into the pulmonary veins
53
Q

Types of Aortic Stenosis (3)

A
  1. Valvular stenosis= Most common; when the valve itself is affected
  2. Subvalvular stenosis= a tissue in the aorta below the valve
  3. Supravalvular stenosis= Tissue in the aorta above the valve
54
Q

Aortic Stenosis Symptoms (7)

A
  1. Faint pulses
  2. Hypotension
    * Because narrowing is occurring further up in the heart
  3. Tachycardia
    * Compensating for low CO
  4. Poor feeding
  5. Exercise intolerance
  6. Chest pain and/or palpitations
  7. Dizziness with standing
55
Q

Pulmonic Stenosis Characteristics (6)

A
  1. Obstructive defect; Narrowing of entrance to pulmonary artery
  2. Right ventricular hypertrophy with ↓ PBF
  3. Could get pulmonary atresia - total fusion; no way for blood to come out of right atrium and then pulmonary artery (no blood going from heart to lungs)
  4. If PS severe, patients can develop CHF
  5. If very severe, patient can become cyanotic
    * But cyanosis isn’t usually associated
  6. PDA partially compensates for obstruction
    * PDA helps because it can increase blood flow to the lungs (since pressure is higher in the aorta)
56
Q

Symptoms of Pulmonic Stenosis (4)

A
  1. May be asymptomatic
  2. Mild cyanosis or CHF
  3. Newborns – cyanotic
  4. Murmur
57
Q

Tetrology of Fallot (TOF) Characteristics (6)

A
  1. Defect of decreased pulmonary flow
  2. VSD
  3. Pulmonic stenosis
    * In area of aorta below the valve that is narrowed
  4. Overriding aorta
  5. Right ventricular hypertrophy
    * Due to the pulmonary stenosis
  6. Depending on position of aorta, blood from both ventricles may be distributed systemically
    * Aorta pushed to right = increased cyanosis
    * Aorta pushed to left = decreased cyanosis
58
Q

TOF Symptoms (3)

A
  1. Cyanosis (increased if aorta is pushed to right)
  2. TET spells
  3. Murmor
59
Q

TOF Treatment

A

Need to get blood flow in the lungs, done using Blalock-Taussing shut

  1. Palliative: Blalock-Taussing shunt
    * Connection between subclavian and pulmonary artery
    * Increases blood flow to the lungs
    * Do this first, until the heart is ready for full correction
  2. Complete repair: close VSD, pericardial patch
    * Can do this once patient is 1 year old
    * Close VSD, shift aorta, etc.
60
Q

Tricuspid Atresia Characteristics (5)

A
  1. NO COMMUNICATION BETWEEN RIGHT ATRIUM AND RIGHT VENTRICLE
    * NO TRICUSPID VALVE!!!
    * If blood comes into the right atrium, it will just sit there
  2. To get the blood to go to lungs, may try to keep PDA open
    * If PDA stays open, some blood can go into lungs
    * Keep PDA open by giving Prostaglandin E
  3. Complete mixing of oxygenated and deoxygenated blood in systemic circulation
    * Child will be very cyanotic when born
    * Will be prepared for this when child is born, otherwise child won’t survive
  4. ASD or PFO necessary to create a hole to have somewhere for the blood to go
61
Q

Created defects to tx Tricuspid Atresia

A
  1. PDA –> allows blood to flow to pulmonary artery for oxygenation
    * Give Prosteglandin E to keep it open
  2. ASD —> allows blood flow to enter right ventricle and then to go into the lungs
    * or can be PFO
62
Q

Symptoms of Tricuspid Atresia (4)

A
  1. Cyanosis
  2. Tachycardia
  3. Dyspnea
  4. Clubbing
63
Q

Transposition of the Great Vessels Characteristics (2)

A
  1. Pulmonary artery leaves left ventricle and aorta leaves right ventricle with no connection (not compatible with life because totally deoxygenated blood is going into systemic circulation)
  2. Must keep PDA open and create PFO and/or ASD
    * PDA open to get blood out to extremities
64
Q

PFO and/or ASD in Transposition of Great Vessels

A

Created to have blood come into left side of heart, go over to the right side of heart (there is a mixing of oxygenated and deoxygenated), and then out into extremities

*Better to have some oxygenated blood in systemic circulation than none!

65
Q

Transposition of Great Vessels Symptoms (2)

A

cyanotic and cardiomegaly

66
Q

Transposition of Great Vessels Treatment

A
  1. Prostoglandin E to open PDA,
  2. Arterial switch with reimplanting coronary arteries
  3. Total correction will be done within first few weeks of life
    * Put Aorta on left side and Pulmonary artery on right side
67
Q

Hypoplastic Left Heart (3 characteristics)

A
  1. Underdevelopment of left side of heart
  2. Develops aortic atresia
  3. In order to survive to surgery, need other defects in place; Requires PDA and PFO or ASD immediately
    * NEED PROSTAGLANDIN E TO KEEP PDA OPEN!
68
Q

Hypoplastic Left Heart Symptoms

A

mild cyanosis with CHF, after PDA closes progressive deterioration

69
Q

Hypoplastic Left Heart Surgical Tx (3 steps)

A

1st Norwood – main pulmonary artery to aorta

  • Will occur early in infancy
  • Making the pulmonary artery the aorta and making right side of heart the left side of heart
  • All circulation to the lungs will be passive circulation

2nd: Bidirectional Glenn
* To make all circulation to lungs passive circulation

3rd: Modified Fontan
* To make all circulation to lungs passive circulation

~Will always require a transplant by mid-teens

~May only do palliative care and no surgery

70
Q

Reasons Patients Can Develop CHF (4)

A
  1. Volume overload – left to right shunts
  2. Pressure overload – obstructive defects
  3. ↓ contractibility – cardiomyopathy
  4. High cardiac output demands – sepsis, anemia, etc.
71
Q

Right Sided HF Symptoms (2)

A
  1. Edema

2. Hepatomegaly

72
Q

Left Sided HF Symptoms (2)

A
  1. Respiratory distress

2. Congestion

73
Q

Pediatric Symptoms of CHF (12)

A
  1. Tachycardia
  2. Diaphoresis
    * Usually seen on the bridge of the nose or scalp in children
  3. Easily fatigued
  4. Tachypnea
  5. Dyspnea
  6. Mild cyanosis
  7. Retractions, grunting
  8. Wheezing, cough
  9. Poor profusion
    * Prolonged capillary refill
    * Decreased urinary output
  10. Hepatomegaly
  11. Edema, weight gain
    * Weight gain from fluid retention
  12. Developemental delays
    * Clinical manifestations are due to ↓ myocardial contraction, ↑afterload & ↑preload
74
Q

DIGOXIN (7 pertinent info)

A

To treat CHF

  1. ↑cardiac output
  2. ↓ heart size by decreasing HR
  3. ↓venous pressure
  4. Relief of edema
  5. Before giving Digoxin, must take HR for full minute!!
  6. Symptom of toxicity in children: bradycardia, vomiting, arrythmias
    * For infants and toddlers, question HR lower than 110
    * For older children, question HR lower than 60
  7. Digoxin is usually given in liquid solutions; order in micrograms to ensure giving the right dose!!
75
Q

ACE INHIBITORS (two types and info)

A

To treat CHF

Captopril(Capoten) and Enalapril(Vasotec)

  1. Before giving ACE inhibitors, take BP!!
  2. Reduces blood pressure
76
Q

Diuretics to treat CHF

A
  1. Furosemide (Lasix)
  2. Spironoldactone (Aldactone)

*Possible fluid restriction and Na+ restriction

77
Q

Treatments to Decrease Cardiac Demands (4)

A
  1. Provide neutral thermal environment
    * Ensure patient isn’t too hot or too cold, as sweating and shivering can increase cardiac demands
  2. Treat existing infections
  3. Decrease effort to breath; Elevate HOB
  4. Provide rest periods
    * Organize care! Patient will get tired simply after washing
    * Do AM care, give rest period, then come back for feeding
78
Q

CHF Treatment: Nutritional Status (6)

A
  1. ↑BMR
  2. Well rested before feeding
  3. Every 3 hour feeds, ½ hr to finish feeding
    * May need to gavage after nippling if they only take a small amount by mouth
    * Don’t wait to put NG tube in until after feeding otherwise they will vomit
    * Small, frequent feedings; never take over 30 minutes to feed
  4. Soft preemie nipple
  5. Semi-upright position
  6. ↑calories/oz. instead of volume
    * Never give more volume, but increase calories!
79
Q

Hypoxemia and 2 changes that occur as a result

A

Decreased arterial O2 saturation

Over time, 2 physiologic changes occur in response to chronic hypoxemia

  1. Polycythemia – due to↑ RBC production
    * Polycythemia is an increase in RBC
    * Compensation to increase RBC for more oxygen
    * Check Hbg/Hct
    * Increase RBC puts you at risk for clots!
  2. Clubbing – thickening and flattening of tips of finger and toes
    * Children who are cyanotic since birth are smaller, poor weight gain, dyspnea on exertion and fatigue easily
80
Q

TET Spells

A

Hypeprcapnic spells (decreased O2, increased CO2)

  • Occurs with defects with obstructive pulmonary blood flow and communication between ventricles
  • Patient experiencing tet-spell can become very cyanotic
81
Q

TET Spell Interventions (5)

A
  1. Quickly put child in knee-chest position
    * This decreases venous return of desaturated blood from the legs and increases systemic pulmonary vascular resistance (diverting more blood flow into the pulmonary artery instead of out of the aorta, which would be desaturated blood)
  2. Calm child
  3. 100% O2
  4. Morphine IV push
    * Give morphine during tet-spell because there is an area with pulmonary stenosis that can go into a spasm
    * Morphine helps relax the spasm that occurs during tet spell
  5. IV replacement fluid

Pediatrics (13 decks)

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