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Pediatrics > Peds CHD > Flashcards

Peds CHD Flashcards

1
Q

S1 sound is produced by?

A

closing of the AV valves

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2
Q

S2 is produced by?

A

closing of semilunar valves

-they close at different times depending on pt breathing so could be split sounds

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3
Q

rank of important things to listen for in a murmur

A
  1. timing - systolic, diastolic, continuous
  2. Pitch
  3. intensity - graded 1-6
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4
Q

which types of pitches indicate that the murmur is ALWAYS abnormal?

A

-high pitch
or
-diastolic murmurs

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5
Q

2 classifications that indicated SYSTOLIC murmur

A
  • ejection

- holosystolic

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6
Q

ejection murmurs

A
  • PS
  • AS
  • functional
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7
Q

holosystolic murmurs

A
  • VSD
  • MR
  • TR
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8
Q

Diastolic murmurs

A
  • AI
  • PI
  • MS
  • TS
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9
Q

continuous murmurs

A
  • PDA

- BT shunt or other aortopulmonary collateral

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10
Q

normal murmurs in kids

A
  • venous hums
  • pulmonary flow (RV to MPA)
  • MPA to branch PA
  • Still’s murmur
  • supraclavicular or carotid bruit
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11
Q

venous hum

A
  • continuous murmur
  • hearing the flow in the veins when they sit up and goes away when laying down
  • can hear better when head turns to one direction and goes away in opposite direction
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12
Q

Still’s murmur

A
  • blood flow across the cordae
  • don’t hear it sitting up but hear it laying down at mid sternal border
  • can vary w/ HR
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13
Q

Who to refer

A
  • murmur not clearly normal
  • abnormal EKG
  • Down’s or Marfan’s
  • high pitched or diastolic murmur
  • cardiac sx w/ or w/o murmur
  • fam hx of cardiomyopathy
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14
Q

CHF

A
  • heart is unable to pump enough blood to the body to meet its needs
  • not a good term - it’s actually working overtime
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15
Q

S/sx of CHF

A

-sweating, poor feeding, edema, increased sleeping, poor activity, FTT
-possible hepatomegaly, tachypnea, chest retraction, gallop
(different signs than in adults w/ CHF)

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16
Q

MC causes of CHF in infants

A

-volume overload from VSD, PDA, AV canal

big left to right shunts

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17
Q

Tx of CHF

A
  • diuretics: lasix/furosemide 1mg/kg BID - monitor K
  • inotropic agents: Digoxin 8-10mg/kg/day
  • ACE inhibitors: captopril start low and increase dose
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18
Q

when is captopril contraindicated?

A

in LVOT obstruction

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19
Q

types of ASD

A
  • secundum: MC; where the foramen ovale was
  • primum: lower down, part of an AVSD. Always have a cleft in MV
  • venous defect: always associated w/ APVR
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20
Q

ASD

A
  • isolated lesions that rarely cause problems

- many spontaneously close, if not closure is indicated at 3-5 yo

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21
Q

What is the MC cause of CHD?

A

VSD

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22
Q

VSD

A
  • most close spontaneously w/i the first year, sep. the muscular ones
  • severity depends on size
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23
Q

describe the VSD murmur

A
  • holosystolic
  • the pitch depends how big the hole is
  • isn’t always hear at birth b/c pressure on right side is still elevated so not flowing L->R as hard
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24
Q

AV canal consists of what abnormalities

A
  • primum ASD
  • single AV valve
  • VSD
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25
Q

AV canal is often associated w/ what condition?

A

Downs

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26
Q

S/s of AV canal

A

-HF w/i the first few months (worse in non-Downs pts)

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27
Q

murmur in AV canal

A
  • may be hard to hear

- if present: holosystolic and gallop may be present

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28
Q

What complication can occur if AV canal isn’t treated early enough in Downs?

A

Eisenmenger’s physiology

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29
Q

long term complications of AV canal

A
  • mitral valve function
  • AV block
  • sub aortic stenosis
30
Q

RVOT aka pulmonary stenosis MC location

A

at the valve

31
Q

RVOT (PS) murmur

A

typically a systolic ejection located left upper sternal that radiates to back/axilla**

32
Q

LVOT (AS) murmur

A

typically systolic ejection located RUSB and radiates to carotids

33
Q

Shone’s Complex

A
  • serial left heart obstructive lesions

- familial

34
Q

Coarctation of the aorta (COA)

A
  • hard to pick up prenatally b/c of PDA
  • can present in cardiogenic shock if PDA closes
  • difference in upper and lower pulses/BP (ALWAYS ck)
35
Q

COA murmur

A

systolic ejection murmur heard in the back as well

36
Q

tx of COA

A
  • typically surg repair in first few weeks of life by end to end anastomosis
  • if found at older age can be stented
37
Q

PDA

A
  • aortopulmonary collateral that connects the aorta and pulmonary artery
  • more common in premies
  • it’s lifesaving in ductal dependent CHDs
38
Q

uses of meds w/ PDA

A
  • prostaglandins keep them open

- indomethocin closes (if young enough)

39
Q

TGA

A
  • RV origin of the aorta
  • LV origin of the pulmonary artery
  • if no PFO or it’s too small, there’s no mixing of blue and red circulation
  • there’s plenty of pulmonary blood flow but still cyanotic b/c it’s all coming from the left ventricle
  • parallel circuits
40
Q

TGA is incompatible with life unless what types of communication are present?

A
  • ASD
  • VSD
  • PDA
41
Q

TGA intervention

A
  • if they have a small ASD, can do the Rashkind procedure –>
  • a balloon atrial septostomy to tear open the ASD to allow for more mixing
  • then preform an aterial switch operation
42
Q

what’s important to remember in a pt that has had the arterial switch operation to repair TGA?

A

the coronary arteries are moved in this operation so at risk for ischemic heart disease at younger age

43
Q

what is the MC cause of neonatal cyanosis?

A

tetralogy of fallot (TOF)

44
Q

4 abnormalities of TOF

A
  • aorta override
  • RVOT obstruction (PS)
  • VSD
  • RVH
45
Q

Tet spells

A
  • spasm of subpulmonary area
  • most likely to occur in am d/t dehydration
  • cyanosis that worsens and doesn’t resolve
  • increased R–>L shunting at VSD causing less pulmonary blood flow
  • a “misbalance” of pulmonary and systemic blood flow
46
Q

how to confirm a tet spell is happening

A

-listen - if murmur is quieter or not present, it’s a spell

47
Q

management of tet spell

A
  • knees to chest, O2, morphine
  • propanolol
  • increase SVR: phenylephrine, ketamine
  • push PRBC
48
Q

what’s CI in tet spell treatment?

A

beta agonists (albuterol, terbutaline, etc)

49
Q

surgery for TOF

A 
1st: palliative surg = BT shunt
then
-lillihei w/ cross circulation 
then 
-complete repair: close VSD and open RVOT
50
Q

long term effects of TOF

A
  • to and fro murmur from some PF and PI
  • RBBB
  • RV failure
51
Q

truncus arteriosus

A

-single artery comes from heart giving origin to coronaries, pulmonary arteries, and aortic arch

52
Q

complication of an untreated truncus arteriosus

A
  • uncontrolled pulmonary blood flow that leads to CHF uncontrollable w/ meds
  • eventual fixed PVR
53
Q

surgery for truncus arteriosus

A

VSD closure w/ RV-PA conduit done around 1-4 weeks of age

54
Q

TAPVR (total anomalous pulmonary venous return)

A

when all pulmonary veins drain via a venous channel into the RA or directly into the RA

55
Q

in TAPVR, all CO is via what?

A

a PFO or ASD

56
Q

3 types of TAPVR

A
  • supracardiac: rarely obstructive; present like ASD; MC
  • intracardiac: rare
  • infradiaphragmatic: important! obstructed at ductus venosus. EMERGENCY
57
Q

clinical presentation of an obstructed TAPVR

A
  • extremely ill from soon after birth and progressively worsen (blue and getting bluer)
  • severe pulmonary HTN secondary to pulmonary venous obstruction
58
Q

TAPVR surgery

A
  • “fillet” open confluence and attach to atrium then ligate descending vein
  • usually done w/i hours of diagnosis
59
Q

single ventricle physiology includes all anatomic arrangements requiring staged surgical repair. These 5 things are:

A
  • tricuspid atresia
  • pulmonary atresia
  • mitral atresia
  • aortic atresa
  • hypoplastic left heart syndrome (HLHS)
60
Q

other lesions leading to a single, functional ventricle

A
  • unbalanced AVSD
  • some forms of Ebstein anomaly (tricuspid valve anomaly)
  • some forms of DORV, DOLV
  • some heterotaxy syndromes
61
Q

HLHS presentation

A
  • often presents when PDA closes
  • no source of systemic blood flow so look terrible
  • need to give Prostin to keep PDA open
62
Q

PE in HLHS

A
  • sign of poor systemic perfusion if no PDA: poor femoral pulses, cyanotic
  • normal S1
  • single S2
  • non-specific murmur
63
Q

EKG and CXR in HLHS

A
  • EKG: little LV forces and RVH

- CXR: non-specific

64
Q

physiology of HLHS

A
  • pulm venous return MUST cross atrial septum and enter RA
  • pulm venous return and systemic venous return mix in the RA
  • from there it can take 2 routes: systemic outflow (Qs) or pulm outflow (Qp)
65
Q

what is the outcome of a pt w/ HLSH systemic outflow ratio (Qp:Qs) is 0.5:1

A

-the pt will have great systemic perfusion but O2 sats will be low

66
Q

outcome of a pt w/ HLSH systemic outflow ratio (Qp:Qs) is 2:1

A
  • pt will have great O2 sats and possible pulmonary edema

- but poor perfusion and poor BP and metabolic acidosis

67
Q

outcome of a pt w/ HLSH systemic outflow ratio (Qp:Qs) is 1:1

A
  • good systemic perfusion and acceptable O2 sats (80% is magic number)
  • pt is balanced
68
Q

HLHS surgery

A
  1. Sano operation
  2. Glenn
  3. Fontan
69
Q

Turner’s syndrome is associated w/ what CHD?

A

COA

70
Q

Downs is associated w/ what CHD?

A

-AV canal

71
Q

DiGeorge is associated w/ what CHD?

A

TOF

Pediatrics (9 decks)

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