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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
What happens to a right-to-left shunt versus a left-to-right shunt when PVR and SVR change?
- Right-to-left—>will increase when SVR decreases or PVR increases - left-to-right —>will increase when SVR increases or PVR decreases
26
T/F a left to right shunt will cause systemic hypotension, increasing acidosis, insufficient coronary perfusion.
True
27
What is a common occurrence in premature infants, that could be the reason the require mechanical ventilation?
PDA
28
What are problems that might occur during a PDA closure?
- 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
What are standard monitors for the closure of a PDA?
* 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
What is the most common cyanotic CHD, and what are the main characteristics?
TOF 1. ) RV outflow tract obstruction (RVOTO) 2. ) RVH 3. ) VSD 4. ) overriding aorta
31
What takes place during a tet spell?
Dynamic narrowing—> hypercyanotic episodes—> increased right to left shunt
32
In TOP, what determines the degree of hypoxemia?
The relationship between RVOTO and SVR
33
What genetic disorders are associated with TOF?
DiGeorge syndrome and trisomy 21
34
What causes a hypercyanotic (Tet) spell?
``` Crying Feeding Anesthetics Metabolic acidosis Increased PaCO2 Catecholamines Surgical stimulation ```
35
A tet spell requires URGENT INTERVENTION. What types of interventions would you employ?
* 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
What is the surgical intervention for TOF?
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
When does a congenital diaphragmatic hernia (CDH) usually occur?
In the first 5-10 weeks of fetal life
38
What happens during a congenital diaphragmatic hernia?
- 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
What are s/s of CDH?
- hypoxia - scaphoid (sunken in) abdomen Dx made by sonography
40
Prior to surgery, how is CDH treated?
- immediate stabilization with sedation, paralysis and moderate hyperventilation - ECMO
41
What are anesthetic concerns with CDH?
- 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
What is a tracheoesophageal fistula (TEF), and how is it diagnosed?
- 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
What are anesthetic considerations with TEF?
- 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
What are potential complications of TEF repair?
- PNA - congenital anomalies - atelactasis - SQ air - RLN injury - esophageal stricture - anostomotic leaks
45
What is the principle cause of death with TEF?
Pulmonary complications Anastomatic leaks Associated anomalies
46
What is hypoplastic left heart syndrome?
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
What symptoms are seen at birth in hypoplastic left heart syndrome?
- tachycardia - tachypnea - cyanosis - systolic murmur
48
What is the treatment for hypoplastic left heart syndrome?
- 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
What takes place from a surgical standpoint in Norwood stage I, II, and III repair?
(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
What causes PVR to increase?
``` PEEP High airway pressures Atelactasis Low FiO2 Respiratory/metabolic acidosis ``` Increased Hct SNS stimulation Direct surgical manipulation Vasoconstriction—>phenylephrine
51
What causes PVR to decrease?
``` No PEEP Low airway pressure Lung expansion to FRC High FiO2 Resp/metabolic alkalosis ``` Low Hct Blunted stress response N2O Vasodilators: milrinone, prostacyclin
52
How is CO affected in Noonan’s syndrome?
* * 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
What is an arterial switch?
Arterial trunk transacted above level of semi-lunar valves—> relocated to appropriate ventricles, coronary arteries re-implanted into aortic root
54
What takes place during an AV defect repair?
- patch closure of atrial and ventricular communications - reconstruct AV valves - eliminates intracardiac shunt
55
What takes place in the repair of truncus arteriosus?
- closure of VSD - establish RV to PA with a homograft - abolishes intracardiac shunting and restores normal functions
56
What is important regarding milrinone?
* * excellent in sick neonatal hearts ♥️ - inhibits cAMP hydrolysis —> PDE3 blocker - increases Calcium available in SR—> positive inotropy - restores efficiency of ß-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

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