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My Peds > Quiz 3- Pediatric Cardiology Part 2 > Flashcards

Quiz 3- Pediatric Cardiology Part 2 Flashcards

1
Q

An appropriate BP for a neonate should be:

A

65/40

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2
Q

What does CHF look like in children?

A
  • FTT, difficulty feeding
  • breathlessness
  • recurrent chest infections
  • tachycardia
  • heart murmur
  • hepatomegaly
  • cardiomegaly
  • pulmonary plethora
  • wheezing
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3
Q

Does the premature infant’s heart exhibit greater or lesser sensitivity to catecholamines?

A

Less sensitivity to catecholamines—> it is already near the maximum level of ß-adrenergic stimulation

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4
Q

The most common type of TEF is:

A

Type IIIB

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5
Q

In a patient with CDH, what should the peak inspiratory pressure be?

A

<30 cmH2O

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6
Q 
Which is not a manifestation of CDH?
A.) lab tests
B.) scaphoid abdomen
C.) decreased breath sounds
D.) arterial hypoxemia
A

A, I think…..

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7
Q

What are normal O2 sats for BT shunt, Fontan and Glenn shunts?

A

BT: 75%
Glenn: 85%
Fontan: 95%

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8
Q

A 12 lead of a newborn reveals upright T waves in all chest leads. Is this normal?

A

Yes- normal at birth
T wave then becomes isoelectric or inverted in leads V1-V4 by 1 week until adolescence, when it become upright
** failure of V1-V4 to invert by 1 week of age can indicated RVH

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9
Q

How does QRS axis appear at birth?

A

Right sided axis at birth d/t predominant RV during intrauterine development (QRS larger in leads looking at the right side of the heart)
—> shifts leftward ~ 1 month of age

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10
Q

How does normal CO of an infant compare to that of an adult?

A

A healthy full term infant has a CO 2-3 times that of an adult

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11
Q

What is the normal HR for a 1-3 year old?

3-6 year old?

A

1-3 yo: 70-110 BPM

3-6 yo: 65-110 BPM

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12
Q

What are the signs of DiGeorge/Velocardifacial syndrome?

A 
* 22q11.1 deletion syndrome
PATCH
- Parathyroid hypoplasia
- Abnormal faces
- Thymic hypoplasia: absence of T cells ****altered immunity 
- Cardiac defects (TOF and truncus arteriosus) and Cleft palate
- Hypocalcemia: seizures, cyanosis
Also, schizophrenia seems to correlate
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13
Q

What is the treatment for diGeorge syndrome?

A

No cure, just treat symptoms

  • infections—> abx, must use irradiated blood products
  • hypocalcemia—> vitamin D and Ca supplements
  • surgery—> thymus transplant, heart surgery
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14
Q

What is significant regarding Noonan Syndrome?

A

Similar to Turner’s syndrome

  • hearing loss and low set ears
  • slanted, sagging eyes
  • FTT—> feeding tube
  • neck webbing, chest deformities, short stature’
  • bleeding diathesis

** 50% have CHD—> pulmonary valve dysplagia and pulmonary stenosis*** THIS IS SIGNIFICANT

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15
Q

What is Marfan syndrome?

A
  • mutation of fibrillen gene
  • CV: MVP, MVR, ascending aorta dilation, main pulmonary artery dilation, arrhythmias,
    • AORTIC DISSECTION LIKELY AT ANY SIZE: usually >5 cm
  • ventricular dilation, abnormal systolic function
  • pulmonary disease: chest wall deformities, progressive scoliosis—> restrictive lung disease
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16
Q

What is the treatment for Marfan syndrome?

A

Ăź-blockers/BP control

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17
Q

What is VATER association? (VACTERL)

A

A group of non-random anomalies
- Vertebral (hemivertibrae->half of ribs not developed)
- Anal atresia: will need a colostomy (no way to get stool out)
- CV: ASD, VSD, TOF—> ductal dependent lesions
- Trans-Esophageal fistula
- Renal anomalies- incomplete formation of 1 or both kidneys
- Limb defects- absent or misplaced thumbs, etc
( a diagnosis is made if pt has 3 or more of these)

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18
Q

What are anesthetic considerations of a pt with VACTERL?

A
  • CV: ASD, VSD, TOF- ductal dependent lesions require patency
  • vertebral/tracheal anomalies—> difficult airway management and difficulty with regional
  • hypoplastic vertebrae—> scoliosis
  • limb defects—> difficult vascular access
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19
Q

What is CHARGE association?

A
  • Coloboma (pupils misshapen)
  • Heart defects
    -choAnal atresia (nasal septum defect)
  • Retardation of growth and development
  • Genitourinary problems
  • Ear abnormalities
    Also, conotruncal and aortic arch abnormalities, upper airway abnormalities
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20
Q

What is important we do with a patient who has CHARGE association?

A

Think “have they had their cardiac work up?”

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21
Q

What are conotruncal abnormalities?

A

Congenital cardiac outflow tract abnormalities

—> TOF, pulmonary atresia with VSD, double outlet RV, truncus arteriosus, transposition of the great arteries

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22
Q

What happens during cyanosis?

A
  • body compensating for hypoxia
  • increased erythropoiesis—> increased circulating blood volume
  • increased 2.3.DPG —> HGB less affinity for O2 in the lungs
    • greater O2 delivery to the tissues
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23
Q

What are anesthetic implications for cyanosis?

A
  • cyanotic kids should not be NPO any longer than needed per guidelines
  • if dehydrated—> increased blood viscosity can lead to renal, pulmonary and cerebral thrombosis
  • with increased Hct: PVR increases more than SVR, which further decreases pulmonary blood flow
  • viscosity increases the longer they are NPO
24
Q

How does cyanosis affect coagulation?

A

Hct > 65% impairs microvascular perfusion

—> coagulopathies

25
Q

What happens to a right-to-left shunt versus a left-to-right shunt when PVR and SVR change?

A
  • Right-to-left—>will increase when SVR decreases or PVR increases
  • left-to-right —>will increase when SVR increases or PVR decreases
26
Q

T/F a left to right shunt will cause systemic hypotension, increasing acidosis, insufficient coronary perfusion.

A

True

27
Q

What is a common occurrence in premature infants, that could be the reason the require mechanical ventilation?

A

PDA

28
Q

What are problems that might occur during a PDA closure?

A
  • difficulty ventilating or Hgb desat. D/t lung retraction
  • tear PDA with massive hemorrhage
  • inadvertent ligation of the aorta and pulmonary artery
  • ** pre-op—> crossmatch blood, antibiotics, vitamin K
29
Q

What are standard monitors for the closure of a PDA?

A
  • pulse ox X2–> one on the right hand, one of lower limb
    • if pulse ox lost on lower limb- may indicate aorta being clamped—> check for correct clamping
  • IV line just for fluids and drugs
  • high dose opioids, muscle relaxant, +/- ketamine
  • ETT should only have a small air leak d/t difficulty ventilating with lung retraction
  • keep glucose containing solutions running
30
Q

What is the most common cyanotic CHD, and what are the main characteristics?

A

TOF

  1. ) RV outflow tract obstruction (RVOTO)
  2. ) RVH
  3. ) VSD
  4. ) overriding aorta
31
Q

What takes place during a tet spell?

A

Dynamic narrowing—> hypercyanotic episodes—> increased right to left shunt

32
Q

In TOP, what determines the degree of hypoxemia?

A

The relationship between RVOTO and SVR

33
Q

What genetic disorders are associated with TOF?

A

DiGeorge syndrome and trisomy 21

34
Q

What causes a hypercyanotic (Tet) spell?

A 
Crying
Feeding
Anesthetics
Metabolic acidosis
Increased PaCO2
Catecholamines
Surgical stimulation
35
Q

A tet spell requires URGENT INTERVENTION. What types of interventions would you employ?

A
  • aggressive use of vasoconstrictors
    • phenylephrine: 0.5-1 mcg/kg- repeat as needed
    • Norepinephrine: 0.5mcg/kg bolus
  • IVF bolus
  • 100% FiO2
  • sedation/analgesia: fentanyl or morphine
  • NaHCO3
  • Ăź-blockers: relaxes spasm at pre-pulmonic level and decreases HR
36
Q

What is the surgical intervention for TOF?

A
  1. ) palliative BT shunt until pt is an infant
    • BT shunt: subclavian artery attached to PA-avoids pulm valve and VSD- gets blood to the lungs where it can be oxygenated
  2. ) complete repair
    • closure of VSD, relief of RVOTO
    • transannular patch, right ventriculotomy will lead to RV dysfunction and a degree of pulmonary regurgitation
37
Q

When does a congenital diaphragmatic hernia (CDH) usually occur?

A

In the first 5-10 weeks of fetal life

38
Q

What happens during a congenital diaphragmatic hernia?

A
  • the gut herniates into the thorax, via right or left posterolateral foramen of bochdalek or the anterior foramen of morgagni
    • the left side is the most common
  • 50% mortality rate d/t respiratory insufficiency and PPHN
39
Q

What are s/s of CDH?

A
  • hypoxia
  • scaphoid (sunken in) abdomen
    Dx made by sonography
40
Q

Prior to surgery, how is CDH treated?

A
  • immediate stabilization with sedation, paralysis and moderate hyperventilation
  • ECMO
41
Q

What are anesthetic concerns with CDH?

A
  • decrease gastric distention (bowels are in thorax, limited space)
  • low O2 delivery- use pressure limited modes
  • concern for right side pneumothorax
  • awake intubation
  • do not use N2O
  • peak pressures: keep <30cmH2o
42
Q

What is a tracheoesophageal fistula (TEF), and how is it diagnosed?

A
  • most common type is IIIB: blind pouch at lower esophagus that connects to trachea
    Dx: made by failure to pass catheter into stomach, confirmed by visualization of catheter coiled in a blind pouch
  • aspiration is common, seen in VACTERL
43
Q

What are anesthetic considerations with TEF?

A
  • frequent auctioning, copious pharyngeal secretions
  • no positive pressure ventilation prior to intubation
  • awake intubation without muscle relaxants
  • pt will be dehydrated and malnourished
  • do not extend the neck or instrument the esophagus—> may disrupt esophageal repair
44
Q

What are potential complications of TEF repair?

A
  • PNA
  • congenital anomalies
  • atelactasis
  • SQ air
  • RLN injury
  • esophageal stricture
  • anostomotic leaks
45
Q

What is the principle cause of death with TEF?

A

Pulmonary complications
Anastomatic leaks
Associated anomalies

46
Q

What is hypoplastic left heart syndrome?

A

Under-developed left heart

  • hypoplastic LV (tiny LV)
  • aortic and mitral valve atresia or stenosis
  • ASD: necessary to survive- Left- to- right shunt
  • PDA: mixed oxy/deoxygenated blood to aorta
  • elevated RA pressures
  • cyanosis and cardiogenic shock—> death if untreated
  • hypoplastic aortic arch
47
Q

What symptoms are seen at birth in hypoplastic left heart syndrome?

A
  • tachycardia
  • tachypnea
  • cyanosis
  • systolic murmur
48
Q

What is the treatment for hypoplastic left heart syndrome?

A
  • Initially prostaglandins to keep DA open
  • Heart transplant
  • Surgical repair—> goal of surgery is single ventricle type circulation
    • RV becomes single ventricle—> pulmonary blood flow supplied. Passively from SVC and IVC
49
Q

What takes place from a surgical standpoint in Norwood stage I, II, and III repair?

A

(Remember, all of this stems from a bad/absent pulmonic valve)

Norwood stage I: (neonatal period)

  • reconstruct aortic arch so that is arises from the pulmonary trunk
    • pulmonary valve becomes aortic valve
    • BT shunt: from subclavian artery to PA

Norwood stage II:

  • BT shunt disconnected
  • Glenn shunt created: connect SVC to PA

Norwood stage III:

  • Fontan shunt created: SVC and IV both connected to right PA
  • sometimes a fenestration made from shunt to RA, so blood can still get to RV

May have one large ventricle in all 3 of these stages

50
Q

What causes PVR to increase?

A 
PEEP
High airway pressures
Atelactasis
Low FiO2
Respiratory/metabolic acidosis

Increased Hct
SNS stimulation
Direct surgical manipulation
Vasoconstriction—>phenylephrine

51
Q

What causes PVR to decrease?

A 
No PEEP
Low airway pressure
Lung expansion to FRC
High FiO2 
Resp/metabolic alkalosis

Low Hct
Blunted stress response
N2O
Vasodilators: milrinone, prostacyclin

52
Q

How is CO affected in Noonan’s syndrome?

A
    • CO depends on adequate preload and low PVR—> everything is passively flowing into the pulmonary system
    • if PVR is high, no blood will flow
  • absent RV preload reserve
  • single ventricle limits contractility
    • ventricle may be overloaded and dilated or under filled and hypertrophied
  • HR blunted in response to exercise
    • need normal rhythm or they lose ventricular filling
  • afterload is increased as a physiological response to decreased CO
53
Q

What is an arterial switch?

A

Arterial trunk transacted above level of semi-lunar valves—> relocated to appropriate ventricles, coronary arteries re-implanted into aortic root

54
Q

What takes place during an AV defect repair?

A
  • patch closure of atrial and ventricular communications
  • reconstruct AV valves
  • eliminates intracardiac shunt
55
Q

What takes place in the repair of truncus arteriosus?

A
  • closure of VSD
  • establish RV to PA with a homograft
    • abolishes intracardiac shunting and restores normal functions
56
Q

What is important regarding milrinone?

A
    • excellent in sick neonatal hearts ♥️
  • inhibits cAMP hydrolysis —> PDE3 blocker
    • increases Calcium available in SR—> positive inotropy
  • restores efficiency of Ăź-agonists in isolated myocytes after a period of reperfusion
  • vasodilators peripheral smooth muscle
  • effective in treatment of low CO syndrome
  • long term use causes hypotension

***** its an inotrope that promotes diastolic relaxation and decreases peripheral vascular resistance

My Peds (6 decks)

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