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Cardiology > Embryologic Defects and diseases > Flashcards

Embryologic Defects and diseases Flashcards

1
Q

what are the 3 groups that have an increased incidence of persistent patent ductus arteriosus?

A
  • premature infants
  • babies born above 9,000 ft
  • maternal rubella infection
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2
Q

what is the incidence of PDA in infants that weight

A

70% incidence

1/3 spontaneous closure

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3
Q

when does functional closure of ductus arteriosus occur? anatomic closure?

A

functional: 10-15 hrs q birth
anatomic: 2nd -3rd weeks of life

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4
Q

how does the ductus arteriosus close?

A

thought to have more muscular fibers, when there is an increase in PaO2, contraction of the SPIRAL muscular fibers

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5
Q

why does ductus arteriosus stay open?

A

prostaglandins

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6
Q

how do you maintain an open ductus arteriosus?

A

administer IV PGE2

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7
Q

how do you maintain an open ductus arteriosus?

A

administer IV PGE2

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8
Q

how do you maintain an open ductus arteriosus?

A

administer IV PGE2

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9
Q

what is the incidence of congenital cardiovascular malformations in the US?

A

5-8 per 1000

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10
Q

what gender is more likely to have severe defects?

A

boys

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11
Q

what are the 2 main risk factors for congenital heart defects?

A
  • maternal diabetes 3 fold risk increase (recommend fetal US)
  • family history of cardiac defect in 1st degree relative
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12
Q

which type of heart defect is the most common?

A

VSD

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13
Q

what are systemic chambers? (4)

A

pulmonary veins, left atrium, LV, aorta

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14
Q

what are pulmonary chambers? (4)

A

systemic veins, RA, RV, pulmonary arteries

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15
Q

what is the clinical presentation of moderate/large PDA?

A
  • respiratory effects (diff weaning off ventilator, pulm edema)
  • CHF
  • feeding intolerance (necrotizing entrocolitis)
  • renal insufficiency
  • IV hemorrage or stroke
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16
Q

what is the classic presentation of PDA?

A

older infant or young child with large ductus shows hoarse cry, history of PNE, failure to thrive, increased work of breathing, and diaphoresis with activity/feeding

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17
Q

what are the physical exam findings of PDA?

A
  • wide pulse pressure
  • bounding pulses (palpable palmar pulses
  • increased work of breathing
  • hyperactive precordium
  • murmur (variable)
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18
Q

what is the classic presentation of murmur in PDA?

A
  • continuous or machinery soudning murmur along left upper sternal border
  • sometimes diastolic rumble if large
  • accentuated P2 component
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19
Q

what are xray findings of PDA?

A

increased pulmonary vascular markings, enlarged LA and LV

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20
Q

how do you treat a symptomatic neonate with PDA?

A

non-steroidal anti-inflammatory agents like indometacin or ibuprofen lysate

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21
Q

what if medical treatment in a symptomatic neonate fails?

A

surgical ligation through lateral thoracotomy

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22
Q

how do you treat a symptomatic older child with large ductus?

A

percutaneous occlusion

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23
Q

which NSAID has protection against intraventricular hemorrhage but results in decreased blood flow to the kidneys or brain?

A

indocin

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24
Q

which NSAID would you use for PDA in the setting of renal disease/insufficiency?

A

ibuprofen lysine

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25
Q

why do NSAIDs work in PDA?

A

they block prostaglandin synthesis from arachidonic acid and prostaglandins are known to keep DA open

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26
Q

what is the natural history of PDA?

A
  • pulmonary veno-occlusive disease (pulmonary hypertension) and/or Eisenmenger’s Disease
  • also increased risk of subacute bacterial endocarditis (SBE)
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27
Q

what is the natural history of PDA?

A
  • pulmonary veno-occlusive disease (pulmonary hypertension) and/or Eisenmenger’s Disease
  • also increased risk of subacute bacterial endocarditis (SBE)
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28
Q

what is the most common type of ASD?

A

secundum ASD

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29
Q

what are the 2 embryological basis of secundum ASD?

A
  1. too large a central hole (ostium secundum) in septum primum
  2. inadequate development of the septum secundum
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30
Q

what are the 2 embryological basis of secundum ASD?

A
  1. too large a central hole (ostium secundum) in septum primum
  2. inadequate development of the septum secundum
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31
Q

what structure do you compare the magnitude of the ASD to classify as a “large defect”?

A

“large defect” is a diameter equal to or greater than the MITRAL VALVE

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32
Q

what are the 2 criteria for ASD shunts being left to right?

A
  1. RV is thinner and higher compliance than LV (usual)

2. SVR higher than PVR (dependent shunt)

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33
Q

what are the 2 criteria for ASD shunts being left to right?

A
  1. RV is thinner and higher compliance than LV (usual)

2. SVR higher than PVR (dependent shunt)

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34
Q

True or False. ASD usually presents in infancy

A

False

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35
Q

What are the 2 classic physical exam findings of a large ASD?

A
  1. 2-3/6 systolic ejection murmur in upper left sternal border +/- diastolic rumble at LL sternal border
  2. 2nd heart sound is widely split (RV volume overload resulting in delayed RV emptying through all phases of respiration)
36
Q

What creates the murmur in ASD?

A
  • systolic ejection murmur = excessive blood flow across pulmonic valve
  • diastolic rumble = excessive blood flow in diastole across tricuspid valve
37
Q

Xray diagnosis of ASD

A
  • variable heart size depending on shunt size,
  • main pulmonary artery enlarged,
  • pulmonary vascular markings prominent
38
Q

what is the natural history of ASD?

A
  • development of pulmonary vascular disease
  • occurrence of atrial arrythmias
  • onset of cardiac failure
39
Q

what is the ASD management in INFANTS and why do you do this?

A

diuretic therapy because it can relieve breathlessness in most and hopefully shunt will close on its own

40
Q

what is the ASD management in older children who do not respond to medications?

A

CLOSE THE GOD DAMN HOLE HAOLE

41
Q

how many endocardial cushions appear during septation?

A

4

42
Q

when does ventricular septation occur?

A

days 28-42

43
Q

when does ventricular septation occur?

A

days 28-42

44
Q

what is the most common type of VSD and what causes it?

A

perimembranous VSD which is caused by deficiency or lack of membranous portion of the IV septum

45
Q

Superior endocardial cushion forms to ….

A
  • left surface of the outlet portion of the IV septum

- part of the mitral valve

46
Q

inferior endocardial cushion forms to…

A
  • inlet portion of the IV septum
  • membranous portion of the IV septum
  • parts of the tricuspid and mitral valves
47
Q

right endocardial cushion forms to…

A

parts of the tricuspid valve

48
Q

left endocardial cushion forms to…

A

posterior leaflet of the mitral valve

49
Q

a defect in which cushion would cause the most common type of VSD?

A

inferior endocardial cushion (forms the membranous portion of IV septum and perimembranous VSD is most common)

50
Q

when is a VSD considered a “large defect”?

A

defects that measure the same size as the aortic orifice

51
Q

explain the progression of physiological consequences of VSD

A
  • PVR is lower than SVR
  • pulmonary blood to the LA increases
  • increased EDV in LV
  • muscle fiber length increase and Frank-Starling causes increased LV contractility
  • increased LV output
52
Q

What valvular disorders would increase the magnitude of the VSD shunt?

A

pulmonary or aortic stenosis

53
Q

what is the clinical presentation of a large VSD?

A
  • respiratory distress and diaphoresis especially noted with feeds
  • failure to thrive
54
Q

what is the clinical presentation of a small VSD?

A

tachypnea, diaphoresis usually mild or absent

55
Q

what is the clinical presentation of a small VSD?

A

tachypnea, diaphoresis usually mild or absent

56
Q

a diastolic rumble heard in VSD is due to what?

A

increased blood flow across the mitral valve

57
Q

what is happening when a VSD murmur gets louder?

A
  • closing/restrictive VSD

- low PVR (pulmonary vascular resistance)

58
Q

what is happneing when the VSD murmur goes away?

A
  • large VSD with equalization of RV and LV pressure

- elevation in PVR

59
Q

what is the gold standard in diagnosing a VSD?

A

echocardiography

60
Q

what would an ECG show in large VSD?

A

RAD and increase in RV and LV voltages (combined hypertrophy)

61
Q

what is VSD management in infancy?

A
  • symptom based management

- diuretics are mainstay to treat “heart failure” symptoms such as tachypnea, diaphoresis, and pulmonary edema

62
Q

what are the indications for surgical closure of VSD?

A
  • pulm vasc changes in setting of large defect
  • persistent symptoms or poor growth despite med therapy
  • development of secondary complications (aortic insufficiency, double chambered RV)
63
Q

what is the natural history of VSD?

A

most defects close on their own but if left untreated EISENMENGER’S SYNDROME develops

64
Q

what is eisenmenger’s syndrome?

A

you get increased muscularization of the pulmonary arterioles which results in pulmonary hypertension. This increase RV pressure causing a shunt reversal. This leads to cyanosis and clubbing due to hypoxia and either a heart/lung transplant must occur or you will die

65
Q

what is eisenmenger’s syndrome?

A

L to R shunt causes increased pulmonary blood flow that leads to increased muscularization of the pulmonary arterioles which results in pulmonary hypertension. This increase RV pressure causing a shunt reversal. This leads to cyanosis and clubbing due to hypoxia and either a heart/lung transplant must occur or you will die

66
Q

what is the murmur physical exam of a large VSD?

A

2-3/6 harsh holosystolic ejection murmur heard best at LLSB (murmur is caused by flow across the shunt)

67
Q

what are the 4 criteria of tetraology of fallot?

A
  1. RV outflow tract obstruction
  2. RV hypertrophy
  3. Dextraposition of the aorta (aorta overrides the VSD
  4. VSD
68
Q

what is the most common cyanotic defect?

A

tetralogy of fallot

69
Q

what is the most common cyanotic defect?

A

tetralogy of fallot

70
Q

what is monology of fallot?

A
  • the embryological basis of TOF
  • abnl development of conal crests results in an outlet septum that is displaced anteriorly, rightward, and superiorly
  • this causes obstruction of the subpulmonary outflow tract
71
Q

where does most pulmonary blood flow come from in TOF?

A

ductus arteriosus flow

- size of ductus is primary determinant of magnitude of PBF

72
Q

what causes a “blue tetralogy”

A

R to L shunt if RV outflow resistance is higher than systemic vascular resistance leading to cyanosis

73
Q

what causes “pink tetralogy”

A

L to R shunt if RV outflow resistance less than systemic vascular resistance having no cyanosis

74
Q

what are tet spells precipitated by and what is their physical exam?

A
  • precipitated by prolonged crying, anemia, and dehydration

- BLUE, decreased intensity of murmur, and altered consciousness/sz on exam

75
Q

what is the treatment of a tet spell and how do you do it?

A
  • increase the PBF
  • knee chest position, phenylephrine, (both increase SVR) morphine for sedative effect, and volume expansion with IV fluids
76
Q

how do you prevent a tet spell and why?

A

beta blockers because theoretically decreases infundibular obstruction

77
Q

what would the precordial impulse show in LLSB of TOF?

A

RV dominance because displaced

78
Q

ECG findings of TOF

A

RAD with RVH

79
Q

how would you treat a ductal dependent PBF TOF?

A

prostaglandin infusion to maintain ductal patency until surgery can be performed

80
Q

how would you treat a ductal dependent PBF TOF?

A

prostaglandin infusion to maintain ductal patency until surgery can be performed

81
Q

what is natural history of TOF?

A

cyanotic, clubbing of fingers, soft teeth, limited exercise tolerance, CEREBERAL ABSCESSES

82
Q

how will a patient with prolonged TOF present in a school setting?

A

during physical exercise, patient will squat during exercise to increase SVR and push blood to PV circulation

83
Q

absent femoral pulses, you think…

A

coarctation of the aorta

84
Q

what congenital syndrome is associated with 15% having coarctation?

A

Turner’s syndrome

85
Q

what 3 areas suffer due to coarctation of the aorta?

A
  • bowel (necrotizing enterocolitis)
  • leg muscles (claudication)
  • kidneys (increased renin-angiotensin system activation)
86
Q

what is a common side effect of fixing coarctation?

A

rebound hypertension

87
Q

what are the classic findings on xray for coarctation?

A

rib notching from dilated intercostal arteries

- 3 sign (aortic knob, coarctation, post-stenotic dilation)

Cardiology (2 decks)

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