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CM - Pediatrics > Cards, Pulm > Flashcards

Cards, Pulm Flashcards

1
Q

Upper Respiratory Tract pul infections

A

ØCroup

ØAcute Epiglottitis

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2
Q

LRTI

A

• Asthma : Diagnosis and Treatment

ØPertussis

ØBronchiolitis

ØCystic Fibrosis

ØHyaline Membrane Disease – Respiratory Distress Syndrome of the Newborn

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3
Q

sounds assoc w/

croup

epiglottitis

bronchiolitis

pertussis

A

Croup – cough and stridor

Epiglottitis- stridor

Bronchiolitis- wheeze

Pertussis- whooping cough

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4
Q

infecrtious vs noninfectious causes of Acute Epiglottitis

A

Infectious Causes:

  • Strep Pyogenes – remember this is what causes strep throat
  • Strep Pneumonia
  • Staph
  • less likely H Flu in pedi

Noninfectious causes:

thermal causes–

  • crack cocaine & marijuana smoking
  • throat burns of bottle-fed infants),

caustic insults–dishwasher soap ingestion

FB ingestion–ingestion & expulsion of a bottle cap

reaction to head & neck radiation therapy

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5
Q

define epiglotitis vs croup

A

epiglottitis - acute inflammation in the supraglottic region of the oropharynx with inflammation of the epiglottis, vallecula, arytenoids, and aryepiglottic folds

croup - Inflammation of the larynx, trachea- subglottic !

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6
Q

etiology of croup

A

Viral etiology (Distinguished from Bacterial Tracheitis)

  • Parainfluenza 1,2,3
  • Influenza A or B (A or B may be more severe depending on the year !)
  • Adenovirus, RSV
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7
Q

rare complication of croup

A

Bacterial Tracheitis- a

•Bacterial infection of the trachea -> complete respiratory failure by blockage of the trachea with swelling and purulent drainage….

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8
Q

si/sx of Bacterial Tracheitis-

A

develop over 1-3 days

  • Thick purulent exudate within trachea – may obstruct upper airway
  • ++Fever à pt appears TOXIC
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9
Q

si/sx of acute epiglottiti s

A

RAPID ONSET = mild s/t, fever = TOXIC appearance (resp. distress)

Muffled voice (“hot potato”)

Drooling, Pain

Labored breathing

TRIPODDING

  • •Neck hyperextended
  • •Mouth open
  • •Chin up- sniffing
  • •Leaning forward
  • •Outstretched arms

As illness worsens:

  • •Air Hunger
  • •Stridor is a LATE FINDING
  • •Restlessness
  • Pre apnea -> coma -> death
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10
Q

dx of acute epiglottitis

A

lateral neck film and look for THUMB PRINT SIGN

Direct visualization with intubation and endoscopy

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11
Q

tx of epiglottitis

A

Anesthesia Stat to the ED…

KEEP CHILD CALM – NO CRYING (EMS transport!!)

Use O2 if child will tolerate

Establish 2 lines IF the patient will TOLERATE

  1. Intubation (2-3 days)
  2. IV antibiotics
  3. Ceftriaxone or Cefotaxime x7-10 days
  4. Supportive care
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12
Q

family tx in epiglottitis

A

Tx of Family - NOT CONTAGIOUS !

  • if unimmunized or immunosuppressed family
  • or any child <6 mo without HIB vaccine complete—
  • THEN….consider Rifampin for ppx
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13
Q

age of epiglottitis vs croup

A

epi - <6 mo

croup - 3mo-5yr (2 y)

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14
Q

si/sx of croup

A

URI Si/Sx: Day 0-2

  • Rhinorrhea
  • Low grade temp
  • +/-Cough
  • +/- pharyngitis

Barking Cough: Day 0-5

  • +/- stridor insp/expir
  • WORSEN Day 2 and 3 of the Barking Cough (inform parents)
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15
Q

progression of croup

A

Typically occurs: 10p-4a

Resolves by day: 5-7

URI –> Barking cough—>resolution

(Day 1-2) - (2-3) ( 5-7)

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16
Q

tx of croup also define (mild, mod, severe)

mild

mild-mod

severe

A

Mild (at home)- If not seen in the office for

  • •Cold air, Open freezer door, Humidified air
  • •No abx

Mild-Moderate- seen in office barking cough w/ NO stridor at rest

  • •Decadron (IV solution given orally ) PO: 0.6mg/kg max 10-12+mg once
  • •HOME if comfortable
  • •Lasts 24-72 hours
  • •Remind family this gets worse day 2 and 3 !

Moderate-Severe in (office-clinic-ED): stridor at rest

  • •Decadron IV solution given PO:
  • •RACEMIC EPI by nebulizer : duration of action approx 2 hours- repeat as/if needed
  • •watch 2-3 hours for recurrence ..i
  • •if recurrence : call anesthesia = consider admission

no improvement :

  • After failed racemic epi –> continuous racemic epi, IM ep -> transfer to PICU
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17
Q

definition & etiology of bronchiolitis

A

Inflammation of the bronchioles, secretions into the inflamed bronchial tree kids < 2yo (LRI)

  • >50% caused by RSV
  • • (parainfluenza and adenovirus)
  • •bacterial- mycoplasma
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18
Q

si/sx of bronchiolitis

A

Begins with URI

  • •copious clear rhinorrhea
  • •congestion
  • •low grade fever (101/ 102F rectally)

Then develops WHEEZING +/- crackles (rales)

  • ↓ breath sounds – impending doom

Worsens day 2-5 of illness (vs croup day 2-3)

Average course of illness 10-12 days

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19
Q

Bronchiolitids worsens day ____of illness

croup worsens day ____ of illness

A

bronch Worsens day 2-5 of illness

croup day 2-3

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20
Q

dx and imaging of bronchiolitis

A

CXR: Findings :↑perihilar markings

  • •If first episode of wheezing
  • •If pneumonia is a consideration

Nasal Washings : PCR for RSV

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21
Q

tx of bronchiolitis

outpatient vs inpatient

A

Outpatient:

Bronchodilators: +/- helpful

  • Albuterol- can make worse !
  • Racemic epinephrine –rarely used…(vaponephrine) falling out of favor

Cool Mist +/- helpful –> Saline nebs

Steroids-PO (NO ICS) - Decadron, prednisolone (orapred)

Antibiotics= only if pneumonia superinfection

Inpatient: above +

Hospitalize if hypoxic :

  • •awake <91-93%
  • •if asleep <91%

If intubated / risk for intubation: needs a PICU available -> Impending respiratory failure

O2 to keep SpO2 above 94%

High flow 02 if sats <92% on 02

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22
Q

Vaccine pphx for bronchiolitis

A

Synagis(palivizumab)

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23
Q

Synagis(palivizumab) 0-6 mo indications

A
  • Premie < 35 wks
  • Chronic Lung Dz
  • Cerebral palsy / other neuro dz
  • CHD and/or heart transplant
  • Cystic Fibrosis (CF)
  • Severe immune compromise
  • possibly native American Indians or Alaskans
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24
Q

Synagis(palivizumab) 12-24 mo indications

A
  • Chronic Lung Dz with 02 requirement
  • Heart transplant during RSV season
  • Severe immune compromise
  • CF with certain findings (not all CF’ers)
  • Bronchopulmonary Dysplasia w/ hospitalization within 6 mo
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25
Q

Atopic Illnesses assoc. w/ asthma

A
  1. Atopic Dermatitis (AD) 80% have asthma or allergic rhinitis
  2. Food allergies: 30% have asthma
  3. Allergic Rhinitis
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26
Q

si/sx of asthma

A

Si/sx by age 5

Cough- dry

  • •Nocturnal, cold air, seasonal, exercise, lasts >3 wks

wheeze - Pitch varies, expiratory but can be inspiratory

  • Prolonged expiration is abnormal.

Could be: breathlessness, chest tightness, chest pain

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27
Q

Dx of asthma

A

Demonstration of variable/episodic expiratory airflow limitation that is reversible, w/ pre/post bronchodilators

  • •An improvement >8% of FEV1
  • •Must be able to perform peak flows

Exclusion of other reasons for this finding: CF, FB, RSV, etc….

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28
Q

first time wheezing differential

A

•Reactive Airway Disease (RAD)

•Bronchiolitis

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29
Q

tx of asthma 0-4

A

Mild -intermittent: SABA- Step 1

Persistent- step 2-6

  • (2)Low dose ICS or cromolyn/ montelukast
  • (3)Medium ICS
  • (4)Medium ICS + LABA or montelukast
  • (5)High dose ICS + LABA or montelukast
  • (6)Add oral steroid

CONSIDER Pedi Pulmonologist at step 2 or step 3 !

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30
Q

tx of asthma 5-11

A

Mild- intermittent – Step 1: (1) SABA

Persistent Step 2-6

  • (2) Low dose ICS or cromolyn, neocrodimil, montelukast or theophylline
  • (3) low dose ICS + LABA or LTRA, theo, med ICS
  • (4)medium ICS + LABA or Medium ICS + LTRA or theo
  • (5) high dose ICS + LABA or high dose ICS + LTRA/theo
  • (6) high dose ICS + LABA + oral steroid (or LTRA/theo and oral steroid

STEPS 2-4 consider allergy shots for allergic asthma patients

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31
Q

definition & etiology of pertussis

transmission??

A

coccobaccilus that colonizes the ciliated epithelium - airborne transmission

Bortadella Pertussis in US

Para pertussis causes Sporadic Pertussis (Europe

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32
Q

3 stages of pertussis

A

3-12 day incubation

Catarrhal stage: most contagious (common cold sx lasting 1-2 wks

  • •runny nose, sneezing, low-grade fever, and a mild cough

Paroxysmal stage: 1-6 weeks, up to 10 wks

  • The characteristic symptom is a burst, of numerous, rapid coughs.
  • patient suffers from a long inhaling effort characterized by a high-pitched whoop
  • Infants and young children often appear very ill and distressed -> may turn blue and vomit.

Convalescent stage: last for months.

  • cough usually disappears after 2 – 3 weeks, paroxysms may recur whenever the patient suffers any subsequent respiratory infection
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33
Q

dx of pertusssis

A

Nasopharyngeal swab - takes days –week to return

  • High clinical suspicion= Clinical Diagnosis !
  • TREAT and watch for results
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34
Q

si/sx of Children/infants w/ paroxysms in pertussis

A

Children/infants w/ paroxysms = Respiratory distress

  • Tongue protruding
  • Face purple
  • Eyes bulging & Eyes watery
  • Post tussive emesis and exhaustion
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35
Q

tx of pertusssis

A

Zithromax

Can use Erythromycin but 3 x per day for 10 days

Supportive care

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36
Q

complications of pertussis

A

Mild :

  • •Ear infection, loss of appetite, dehydration. pneumonia (up to 5% of cases)
  • •rib fracture from coughing (up to 4% of cases).
  • •loss of consciousness
  • •female urinary incontinence, hernias, angina, and weight loss

If hypoxic from paroxysm:

  • Encephalopathy
  • Seizures
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37
Q

Common Aspirated Objects

most common cause of FBA in infants vs older kids

A

•Peanuts! (approx 50% of all FBA )

•Seeds, nuts, popcorn, hardware, toys, batteries. Coins, hot dogs

  • Food most common cause of FBA in i_nfants and toddlers_
  • Non-food most common in older kids—> Coins, paper clips, pins, pen caps, coins
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38
Q

common causes of fatal FB aspirations

A
  • BALLOONS, gloves, similar expandable items
  • Balls
  • Marbles
  • toys
  • anything strong, round, unbreakable
  • Even ice cubes, cheese cubes
  • Clumpy, sticky foods, hard candies, lollipop pieces
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39
Q

where do FB aspirations occur in lungs of children vs adults

A

In adults ==== R mainstem

  • •Why: diameter of R mainstem and angle of departure from central mainstem

Kids ….proximal mainstem bronchus

  • •no preponderance of occurrence R over L
  • •R and L are close in diameter size and close in angle of departure

Then

bronchi Right and Left equally

Can be in larynx if large enough

•Laryngeal fb associated with higher morbidity/mortality –> no air passing

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40
Q

dx and tx tool for FBA

A

Bronchoscopy is diagnostic tool and treatment

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41
Q

describe 2 types of bronchoscopy for FBA and their uses

A

Flexible Bronchoscopy: used when FB dx is known

  • —Done with chronic or recurrent pneumonia
  • —Chronic cough

Rigid Bronchoscopy: If suspected FBA

  • —If non emergent
  • —Typically used but requires anesthesia
  • —Less risk of dislodgement
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42
Q

definition and etiology of CF

secretions viscous secretions in???

A

↑ salt content in sweat gland secretions viscous secretions in

  • • Lungs
  • • Pancreas
  • • Liver
  • • Intestine
  • • Reproductive Tract

Genetically driven disruption of the chloride channel

  • —Genetic mutation of CFTR *
  • —affects the transport of chloride
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43
Q

what is PATHGNOMONIC FOR CF

A

Meconium ileus - Kid doesn’t have their first poop by day 2 of life

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44
Q

CF patients have Colonization with:

in childhood-

young & adult?

A

•Colonization with

•Staph Aureus (and H flu) in childhood-

•pseudomonas can cause clinical disease in young CF patients!

•Pseudomonas Aeruginosa is ultimately found colonized in lungs of CF pts in adulthood

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45
Q

si/sx of CF:

name body areas affected

A

resp

sinuses

pancreas

billiary

MSK

psych

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46
Q

si/sx resp in CF

newborn , adults, suspicion raised with??

A

•Newborn :

  • Respiratory symptoms not typical in newborn but if respiratory distress of unclear etiology, keep a suspicion

•Infants and Children:

  • •Most likely presenting cc leading to dx of CF are respiratory sxs
  • •Persistant or chronic uri
  • •Wheezing of unclear etiology or recalcitrant

•Suspicion in setting of no CF dx should be raised with

  • •Chronic productive cough
  • •Recurrent Upper or Lower Resp Infections
  • •Hyperinflation on CXR
  • •PFT’s c/w obstructive disease
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47
Q

sinus si/sx in CF

A
  • Panopacification of sinuses by the age of 8 mo
  • Nasal polyposis found in approx 20 % of pts
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48
Q

pancreas si/sx in CF

A
  • Exocrine function typically insufficient in all newborns with CF
  • Insufficient digestive enzymes -> malabsorption–> failure to thrive, electrolyte abnl, anemia
  • May also develop endocrine function abnormality -> Glucose Intolerance or CF related DM
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49
Q

billiary si/sx CF

A
  • Focal biliary cirrhosis casused by inspissated bile
  • Hepatomegaly
  • Asymptomatic liver dz primarily
  • If progressive, in rare instances, can cause periportal fibrosis, cirrhosis, portal htn, variceal bleeding and require liver trnplnt
  • May see cholelithiasis (12% of pts with cf)
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50
Q

MSK si/sx in CF

A

•Reduced Bone Mineral Content

  • •Poor bone growth
  • •Higher bone loss
  • •Use of steroids increases risk of osteoporosis
  • •Poor absorption incr risk of osteoporosis

•Hypertrophic osteoarthropathy

•CLUBBING OF FINGERS AND TOES…..

  • Abnl proliferation of skin and osseous tissue at distal extremities
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51
Q

dx criteria for CF

A

Clinical sxs c/w CTF in at least 1 organ systems if older than newborn (newborn no organ involvement neccessary for dx)

AND

Evidence of CFTR *dysfunction by any one of the following tests

  • ↑Sweat chloride (over 60mmol/L) on 2 occasions
  • Presence of 2 disease causing mutations in the CFTR
  • Abnormal nasal potential difference
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52
Q

primary dx test for CF

2 reasons we do it?

A

Sweat Test

  • Dasxs(+) newborn screen, after 2 weeks of life and >2kg
  • •meconium ileus after Day Of Life 2 (DOL 2)

Measured and reported as : DX vs Possible CF vs CF unlikely

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53
Q

dx CF

+ Newborn screen –> _____ ?

based on results what other tests

A
    • Newborn Screening (IR)
  2. Chloride Sweat Test
    1. Intermediate (possible) = Molecular DNA (>2 mutations = CF)
    2. INconclusive sweat test or <2 gene mutations -= Nasal potential Difference
54
Q

dx methods for CF & when they are neccessary

A

•Newborn Screening - 50% of cases dxd

  • Possibly 7% cases dxd over the age of 18
  • Done on dried blood sample
  • Measuring levels of i_mmunoreactive trypsin (IRT)_
  • Must be done <8 weeks of life as IRT levels nlly fall
  • High false pos and neg rate, but pos must be confirmed
  • Confirmation done with DNA and/or sweat testing

Molecular DX

  • •DNA testing done on all pts w/ INTERMEDIATE (possible) sweat test result
  • •23 common mutations screened
  • T_WO mutations_ to be considered (+) for CF

•Nasal Potential Difference

  • Done on pts with <2 gene mutations and inconclusive sweat test
  • Measure chloride levels pre and post intranasal perfusions to alter chloride transport.
55
Q

classic vs non-classic dx of CF

A
56
Q

tx of CF

A

CFTR Modulators – (“older” treatments- 2012-2018)

  • Ivacaftor-
  • Tezacaftor/Ivacaftor

Triple Therapy: Trikafta, Symdeko, Orkambi

Oral Antibiotics: Azithromycin

Bronchodilators: daily albuterol q 4-6 hours

Inhaled Hypertonic Saline

Dnase

57
Q

name CTFR modulators & age group they are approved

A

Ivacaftor- G551D mutation (>6 m)

  • Restores function of mutant CF protein
  • First treatment approved to treat problem, not sequellae

Tezacaftor/Ivacaftor – F508del mutations (>6yo)

  • Improves lung function by 4 %
58
Q

name 3 types of triple therapy and their approved age groups

A

Trikafta= elexacaftor -ivacaftor - tezacaftor

  • > 12 years and older

Symdeko: tezacaftor and ivacaftor

  • >6 years and older

Orkambi: lumacaftor and ivacaftor

  • >2 years and older

Ivacaftor has been approved for kids 6 mo and older !

59
Q

CF tx for Airway secretion clearance enhancement

age group appropriate ??

A

Dnase

  • Cleaves long chains of proteins diminishing mucous viscousity
  • May be used daily but considering trials with QOD to cut cost

Inhaled Hypertonic Saline

  • •Hydrates inspissated mucous
  • •Used in kids OVER THE AGE OF 6
60
Q

inhaled txs for CF

A
61
Q

—Immunizations for CF

A
  • Influenza
  • Pneumoncoccal
  • Palivizumab (SYNAGIS) for RSV ppx if age appropriate !

Remember we talked briefly about Synagis on Friday!

62
Q

ultimate tx for CF

A

lung transplant

63
Q

dx imaging & Labs for ARDS

A

CXR:

  • • air bronchograms
  • • low lung volume
  • • ground glass appearance
  • •Pneumothorax

ABG- hypoxia

Hyponatremia from water retention

64
Q

ARDS

↑risk in infants born < ____wks

  • Formation of alveoli begins at ____wks…thus viability begins
  • 93% of RDS infants ____ wks

Also if ______ aspirations => increased risk

A

↑risk in infants born below age 30 weeks

  • Formation of alveoli begins at 24 wks…thus viability begins
  • 93% of RDS infants <28 weeks

Also if meconium aspirations => increased risk

65
Q

etiology of ARDS

A

surfactant deficency (quality & quantity)

leading to lung damage & pulm edema

66
Q

ARDS id different from TTN ???

A

TTN - (transient tachypnea of the newborn)

  • Seen in more mature newborns, less severe
67
Q

Interventions to prevent RDS

A

Administration of Antenatal Corticosteroids (to mom)

  • Given to Pregnant women at risk for delivery before 34 weeks

Administration of Exogenous Surfactant (to neonate)

  • Provision of Assisted Ventilation
68
Q

ARDS positive vs negatives of mechanical ventihlation

A
69
Q

describe fetal bF

A

Umbilical vein – delivers oxygenated blood from the placenta into the portal sinus in the liver and ductus venosus in the IVC

  • 2/3 of the blood that enters the _RA –> foramen oval_e to the LA, LV, aorta, –> head and upper extremities
  • 1/3 of blood that stays in the RA –> RV then PA –> ductus arteriosus –> aorta

Deoxygenated blood returns to the heart via the SVC –> mixes with oxygenated blood from the umbilical vein

Blood that doesn’t leave the aortic arch –> descending aorta where it leaves the fetus via the umbilical arteries –> placenta

Pulmonary artery pressure is higher than systemic pressure so

  • blood flow to the lungs is minimal
  • flow to the placenta is high
70
Q

LA pressure ___ RA pressure keeps the foramen ovale open

A

LA < RA pressure foramen ovale is open

71
Q

foramen ovale is

Open when ___< ____

closed when ____>____

A

foramen ovale is

Open when LA pressure < RA Pressure

closed when LA pressure > RA pressure

72
Q

fetal circulation 2/3 of the blood that enters the ___-> ___ ___ to the LA, LV, aorta –> head and upper extremities

A

fetal circulation 2/3 of the blood that enters the RA -> foramen ovale to the LA, LV, aorta --> head and upper extremities

73
Q

maternal fetal blood circ

PA –> ___ ____–> aorta

A

•PA –> ductus arteriosus –> aorta

74
Q

derivatives of fetal vasc structures

foramen ovale

umbilical v

ductus venosus

ductus arteriosus

A
75
Q

24-48 hours after birth

The ____ pO2 in the blood along with _____ pulmonary pressures causes the ___ ______ to close

A

24-48 hours after birth

The increased pO2 in the blood along with increased pulmonary pressures causes the ductus arteriosus to close

76
Q

after birth

With_____ blood returning to the LA from the lungs the LA pressure_____ and excessed the pressure in the RA, which closes the ____ ______

A

With increased blood returning to the LA from the lungs the LA pressure increases and excessed the pressure in the RA, which closes the foramen ovale

foramen ovale LA pressure > RA pressure

77
Q

define Acyanotic Heart Defects

how they shunt

name them

A

↑ blood flow to lungs (L->R shunt)

  • Patent ductus arteriosus**
  • Atrial septal defect**
  • Ventricular septal defect**
78
Q

Cyanotic Heart Defects definition

shunts

examples

A

↓ blood flow to lungs (R->L shunt)

  • Tetralogy of Fallot**
  • Transposition of great vessels
  • Tricuspid atresia
  • Total anomalous pulmonary venous connection
  • Truncus arteriosus
  • Hypoplastic left heart
79
Q

ex of Obstructive Heart Defects

A
  • Coarcation of aorta**
  • Aortic stenosis
80
Q

VSD causes ??

A

↑blood pressures in the right ventricle and the pulmonary arteries.

81
Q

ASD causes

A

•increasing the volume of blood that flows to the right side of the heart and lungs.

82
Q

define patent ductus arteriosus

A

Continued connection b/w the aorta and pulmonary a.

  • Allows oxygenated blood to flow from the aorta back to the pulmonary artery

Lungs, LA, LV, and aorta handles a larger volume of blood than normal

83
Q

a systolic continuous rough “machinery” murmur

dx???

A

Patent Ductus Arteriosus (PDA):

small grade 1-2

moderate 2-4

84
Q

si/sx of moderate PDA

A

Exercise intolerance

Murmur (grade 2-4)- Continuous rough “machinery” murmur (systolic

Hyperdynamic and displaced apical pulse

Wide pulse pressure, with low diastolic pressure

85
Q

si/sx of large PDA

A

Failure to thrive in infants

SOB and easy fatigue in older children

Murmur decrease (grade 1-2)

Diastolic apical murmur

Loud, split S2

Thrill

Bounding pulses, wide pulse pressure

LV failure

pHTN

Eisenmenger physiology

86
Q

define Eisenmenger physiology

dx?

A

PDA OR ASD

Eisenmenger physiology

  • Shunt switches from L-R to R-L
  • delivers oxygenated blood to the upper extremities
  • deoxygenated blood to the lower extremities
    • Hands are normal or less affected
    • toes are cyanotic and clubbed
87
Q

PDA closure

Premature infants

Term infants <6 kg

Term Infants >6kg

Adolescents and Adults

A

Premature infants

•First line: Inhibitors of prostaglandin synthesis – Indomethacin and Ibuprofen

•Second line: Medical management of HF symptoms

Term infants <6 kg

First line:

  • Asymptomatic – monitor and observe until >6 kg
  • Symptomatic –mgt of HF with Digoxin and Lasix

Second line: surgical ligation is the preferred, but percutaneous closure can be considered

Term Infants >6kg & Adolescents and Adults

First line: Percutaneous closure (coil vs devices closure)

Second line: Surgical ligation

88
Q

patent foramen ovale is not ASD bc ??

A

Technically not a ASD because there is no septal tissue missing

89
Q

si/sx of ASD

A

usually no murmur

Fixed split S2

pHTN

Heart failure

Right ventricle heave

Harrison’s grooves –transverse depression along the 6th and 7th costal cartilage due to RA enlargement

Eisenmenger syndrome

90
Q

types of ASD

A

Primum ASD (15-20%); Defect at the base, usually large

  • associated with another abnormality

Secundum ASD (70%): Located within the fossa ovalis

  • presents as isolated lesion

Sinus venosus ASD (5-10%): Malposition of the insertion of the SVC or IVC straddling the atrial septum

Coronary sinus ASD (<1%): Part or the entire common wall between the coronary sinus and the left atrium is absent

  • associated with persistent left SVC
91
Q

dx ECG & CXR ASD

A

Asymptomatic -> usually incidental finding on exam or echo

EKG- Usually normal

  • •Can have P-wave abnormalities or changes in V1 and V2 that look like a RBBB
  • •Can have a prolonged QRS

Chest x-ray- Normal

  • •Cardiomegaly
  • •Enlarged pulmonary artery

Echocardiogram

92
Q

tx of ASD

A

Medical management

  • Atrial arrhythmias
  • pHTN
  • Endocarditis prophylaxis

ASD closure

Percutaneous closure –secundum ASDs

Surgical closure

  • Secundum ASDs unamenable to percutaneous closure
  • Primum ASDs
  • Sinus Venosus ASDs
  • Coronary sinus ASDs
93
Q

Harrison’s grooves

define & dx?

A

• transverse depression along the 6th and 7th costal cartilage due to RA enlargement

ASD

94
Q

types of VSD

A

Type 1: Infundibular septum (10%): Asian population

  • associated with aortic valve prolapse

Type 2: Membranous septum (80%): Most common

  • Can also involve the muscular septum, which is then called a perimembranous VSD

Type 3: Inlet septum: not associated with MR or TR

  • associated with Down syndrome

Type 4: Muscular septum (trabecular) (5-20%)

  • Can be multiple and resemble swiss cheese

AV VSD (rare): Communication from LV to RA

  • acquired lesion after endocarditis or valve replacement
95
Q

most common type of VSD

A

Type 2: Membranous septum (80%)

• Can also involve the muscular septum, which is then called a perimembranous VSD

96
Q

si/sx of small VSD

A

Small VSDs asymptomatic and only present with a murmur

Murmur usually develops 4-10 days of life due to continued ↓ in PVR

97
Q

si/sx od mod- large VSD

A

Tachypnea, tachycardia

Poor feeding – may appear hungry but tires easily, sweats with feeding

Poor weight gain

Hepatomegaly

Pulmonary rales, grunting, and retractions

Pallor

Systolic murmur - Harsh or blowing holosystolic murmur

  • Mid-lower left sternal border
  • If the VSD is large and the ventricular pressures are equal there might be no murmur

Diastolic murmur

  • Diastolic rumble at apex
  • Diastolic decrescendo murmur at left sternal border

Thrill in the 3rd or 4th left intercostal space

Fixed split S2

98
Q

ECG & CXR VSD

A

EKG

  • LVH and RVH
  • Right atrial enlargement

Chest X-Ray

  • Increase pulmonary vascular marking
  • Cardiomegaly
99
Q

EKG & CXR ASD

A

EKG

  • P-wave abnormalities or changes in V1 and V2 that look like a RBBB
  • prolonged QRS

Chest x-ray

  • Cardiomegaly
  • Enlarged pulmonary artery
100
Q

CXR & EKG of PDA

A

Chest x-ray

  • Prominent main pulmonary artery
  • Prominent aortic knob
  • Cardiomegaly
  • Enlarge pulmonary markings

EKG

  • Biventricular hypertrophy
  • Left atrial abnormality
101
Q

Most ____ VSDs close during childhood and large VSDs tend to become _____.

More common in ____ and ____ defects

A

Most small VSDs close during childhood and large VSDs tend to become smaller

•More common in muscular and membranous defects

102
Q

Tx of

Small VSDs with no pHTN

Medium to large VSDs

  • No signs of pHTN or heart failure
  • signs of pHTN or heart failure
A

Small VSDs with no pHTN — Observation

Medium to large VSDs

  • No signs of pHTN or heart failure – observation vs VSD closure
  • signs of pHTN or heart failure – VSD closure
103
Q

VSD closure options

A

Surgical closure

Percutaneous closure

  • •Isolated, uncomplicated, muscular VSDs
  • •Membranous VSDs
104
Q

compications of VSD

A

Endocarditis

Aortic regurgitation

Seen in membranous VSDs

  • Subaortic stenosis
  • RV outflow obstruction

LV to RA shunting

105
Q

describe 4 malformations of the heart in ToF

A

RVOT obstruction = caused by multiple factors

  • Subvalvar obstruction from the infundibular septum
  • Hypertrophy of muscle bands
  • PV annulus is usually hypoplastic
  • PV itself is usually bicuspid and stenotic

Intraventricular communication (VSD)

  • a large, singular, subaortic defect located in the perimembranous region

Deviation of the origin of aorta to the right (over riding aorta)

  • Aorta is displaced to the right and is over the VSD
  • Leads to blood flow from both the RV and LV in the aorta

Concentric RV hypertrophy

106
Q

describe murmur in ToF

A

Systolic, crescendo-decrescendo murmur with a harsh ejection quality

• Also, possibly an early systolic click along the left sternal border can be present

107
Q

si/sx of ToF

A

Degree of RV obstruction is progressive so eventually patients will develop symptoms

Cyanosis

Respiratory distress

“Tet spells”

  • Hypercyanotic spells during times of excitement or stress
  • Usually seen in nail beds or lips

Murmur

  • Systolic, crescendo-decrescendo murmur with a harsh ejection quality
  • Also, possibly an early systolic click along the left sternal border can be present
108
Q

si/sx of ToF

Minimal obstruction –

Mild- MOd Obstruction

Severe obstruction –

A

Minimal obstruction –

  • asymptomatic at first
  • followed by pulmonary overload and HF symptoms within 4-6 weeks of life

Mild-moderate obstructions –

  • can be originally asymptomatic
  • can have cyanosis spells with excitement, agitation, or hypovolemia (Tet spells)

Severe obstruction –profound cyanosis at birth

109
Q

EKG and CXR in ToF

A

EKG

  • RA enlargement
  • RVH
  • Right axis deviation

Chest X-ray

  • Boot shaped heart
  • Upturned apex
110
Q

tx goal of ToF

A

Surgical repair

Goal is complete repair by 1 year of age, ideally by 6 months

111
Q

ToF Medical Management prior to surgery

A

Maintain ductal patency

  • Prostaglandin therapy – Alprostadil
  • Ductal stenting

Heart failure management

Prophylaxis antibiotics until surgical repair

112
Q

ToF Tet spell management

A

Tet spell management (step wise approach)

  1. Knee-chest position
  2. Oxygen
  3. IV fluids bolus (10-20 ml/kg)
  4. Narcotic (IV morphine or intranasal fentanyl)
  5. IV beta-blocker (propranolol, esmolol)
  6. IV phenylephrine
  7. Emergent surgery
113
Q

complications fo ToF

A
  • Pulmonary regurgitation
  • RV dysfunction
  • Residual RVOT
  • Aortic root and valve dilation
  • Arrhythmia
  • Sudden cardiac death
114
Q

F/u for ToF

echo

ekgs

holter

MRI

exercise

A

Regular echocardiograms -

  • •Yearly until 10 years of age
  • • Every other year throughout adulthood

Yearly EKGs

Holter monitor – every 3-4 years

Cardiac MRIs – every 3 years

Exercise testing – every 3 years

115
Q

define CoA

risk factors

A

Narrowing of the descending aorta, which is typically located at the insertion of the ductus arteriosus just distal to the subclavian

Genetic factors - Familial risk, Turner syndrome

Acquired CoA – rare (Takayasu arteritis, Severe atherosclerosis)

116
Q

CoA is usually accompanied by another cardiac lesion

A
  • Complex cardiac defects
  • Bicuspid aortic valve (most common in adults)
117
Q

Si/sx of CoA

Neonates:

Older infants & Children

Adults

A

Neonates: Asymptomatic

  • Absent or delayed femoral pulse compared to brachial
  • +/- murmur associated with other cardiac abnormality
  • Differential cyanosis (O2 sat in arms might be higher than legs)
  • Heart failure with shock – if PDA is closed
    • Pale
    • Irritable
    • Diaphoretic
    • Dyspnea
    • Absent femoral pulses
    • Hepatomegaly

Older infants & Children: Asymptomatic

  • Chest pain
  • Cold extremities
  • Claudication with physical exertion
  • Variability in BP , Variability in pulse
  • Hypertension

Adults: Asymptomatic

  • Hypertension
  • Variability in BP
  • Headaches
  • Epistaxis
  • Aortic dissection
118
Q

O2 sat in arms might be higher than legs

dx?

A

neonate CoA

119
Q

CoA si/sx of

Absent or delayed____ pulse when compared to____ pulse

O2 sat in arms might be_____ than legs

A

Absent or delayed femoral pulse when compared to brachial pulse

O2 sat in arms might be higher than legs

120
Q

CXR & EKG CoA

A

EKG- LVH +/- RVH

Chest X-ray

  • Cardiomegaly
  • ↑ pulmonary vascular markings
  • Notching of the posterior 1/3 of the 3 rd – 8 th ribs
    • apparent between ages 4-12
121
Q

Intervention for CoA should be considered for any patient with one of the following:

A
  • Critical CoA
  • CoA gradient > 20 mmHg
  • Radiological evidence of clinical significant collateral flow
  • Systemic hypertension
  • Heart failure
122
Q

tx of CoA

Neonates and infants:

Infants ≥ 4 months – children <25 kg

Children >25 kg and adults

A

Neonates and infants: open heart surgery is tx of choice

  • Prostaglandin (Alprostadil) along with inotropes are used to stabilize patient prior to surgery if critically ill

Infants ≥ 4 months – children <25 kg

  • either balloon angioplasty
  • or open heart surgery

Children >25 kg and adults: Transcatheter stenting

123
Q

TGA is caused when

Aorta arises from the ____ and PA arises from the ____

A

Aorta arises from the RV

and PA arises from the LV

124
Q

for TGA to be compatible w/ life what must occur?

A

At lest one communication between right and left side must exist to be compatible with life

  • VSD
  • ASD
  • PDA
125
Q

Characterized by absence of the TV resulting in no direct communication between the RA and RV

Associated lesions ???

A

tricuspid atresia

Associated lesions = ASD • VSD • TGA

126
Q

Total Anomalous Pulmonary Venous Connection

A

Failure of all 4 pulmonary veins to make their normal connection to the LA resulting in drainage of all pulmonary venous return into the systemic venous circulation

  • If all 4 pulmonary veins don’t connect to the LA then another abnormality needs to be present for right to left communication
127
Q

Cyanotic congenital heart defect that has a single truncal valve which then gives rise to the aorta and pulmonary arteries

A

Truncus Arteriosus

128
Q

Characterized by a diminutive LV and a small left sided structure incapable of supporting the systemic circulation

what must if have to be compatible w/ life??

A

Hypoplastic Left Heart

PDA and ASD to be compatible with life

129
Q

define stills murmur

A

Common type of benign or “innocent” functional heart murmur

  • It is not associated with any cardiac abnormality
  • Disappears as the patient moves into adolescence
130
Q

define sounds of stills murmur

A

Murmur across the aortic valve from high cardiac output

  • Soft or vibratory, systolic ejection murmur
  • Usually only grade 1-2/6
  • Best heard at the apex of the heart and LLSB
  • Heard best with the bell
  • Decreases with inspiration, sitting up, or standing
131
Q

describe murmurs assoc w/

Stills

ToF

VSD

PDA

A

Stills: Soft or vibratory, systolic ejection murmur

  • Best heard at the apex of the heart and LLSB
  • Decreases with inspiration, sitting up, or standing

ToF: Systolic, crescendo-decrescendo murmur with a harsh ejection quality

  • Also, possibly an early systolic click on LSB

VSD

Systolic murmur: Harsh or blowing holosystolic murmur

  • Mid-lower LSB

Diastolic murmur

  • rumble at apex
  • decrescendo murmur at LSB

PDA: Continuous rough “machinery” murmur (systolic)

  • late systole at the time of S2
  • Heard best at the Left 1st and 2nd ICS at LSB

CM - Pediatrics (3 decks)

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