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Neonatal-Perinatal Boards Review > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Tetralogy of Fallot defects

A

VSD

Overriding aortic arch

Pulmonary stenosis/obstruction

Right ventricular hypertrophy

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2
Q

Tetralogy of Fallot embryonic cause

A

Incomplete rotation of conotruncus—leads to malalignment of conal and ventricular septum

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3
Q

Five T’s of cyanotic heart disease

A

Tricuspid atresia

Truncus

Transposition

Tetralogy of Fallot

TAPVR

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4
Q

Two genes responsible for cardiac left-right differentiation

A

Shh

Pitx2c

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5
Q

Vascular defects that present as congestive heart failure (include other findings with each)

A
  1. AVM—liver (hepatomegaly)
  2. AVM—cerebral (diminished pulses, pulmonary edema—like PDA but “steal” is up carotid)
  3. Vein of Galen aneurysm (cranial bruit/bounding carotid, irritability/seizures, high RA PO2 from highly oxygenated blood shunting thru aneurysm, DIC)
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6
Q

Gene responsible for RVOT development

A

Tbx1

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7
Q

Two cardiac abnormalities highly associated with 22q11

A

Tetralogy of Fallot

Interrupted aortic arch type B (most common type overall, 60% have 22q11 deletion)

(type B is after left carotid artery (before left subclavian))

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8
Q

Two things associated with supravalvar pulmonic stenosis

A
  1. Williams syndrome
  2. Congenital rubella
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9
Q

Milronone mechanism and indications

A
  1. Phosphodiesterase 3 inhibitor—increased cAMP
  2. Improved ventricular function
  3. Decreased peripheral vascular resistance

Indications: RV dysfunction, improving function in cardiac patients coming off bypass (especially if need decreased SVR)

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10
Q

What is the Delta wave and what’s it associated with?

A

Preexcitation of ventricles (a wave preceding the R)

(Preexcitation is via accessory pathway, causes WPW)

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11
Q

Antiarrhythmic drug classes and where they work on phases

A

I: active depolarization (Na block eg procainamide, lidocaine)

II and III: sustained depolarization phase (beta- and K-block, respectively eg propranolol, amiodarone)

IV: repolarization (Ca-block)

*Do not use Ca-channel blockers (verapimil) in neonates

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12
Q

Associations with Ebsteins anomaly

A

Lithium

Wolff-Parkinson-White and SVT (or RBB–think things that may be affected by a displaced node)

Very enlarged right heart on CXR

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13
Q

Starling forces

A

Hydrostatic: Pressure fluid (ie solvent) exerts outward from capillaries

Oncotic: Pressure solutes exert that pulls fluid into capillaries

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14
Q

Physiologic factors that close ductus arteriosus

A

1) increased PaO2
2) decreased prostaglandins (PGE2)

(Both these occur 2-2 sudden lung inflation at birth)

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15
Q

Mechanism of action in PDA closure for indomethacin or ibuprofen

A

Prostaglandin synthesis inhibition by cyclooxygenase enzyme (COX) inhibition (binds so arachidonic acid cannot)

Success rate equal (75%) between two medications

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16
Q

How do glucocorticoids impact ductus arteriosus closure

A

Potentiate its sensitivity to oxygen (which promotes closure)

Lack of maternal betamethasone is a risk factor for PDA

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17
Q

Name the three pathways that affect pulmonary vasoregulation

A
  1. Endothelin (think bosentan AKA Remodulin, endothelin antagonist)
  2. Nitric oxide (think iNO, sildenafil)
  3. Prostacyclin (think milrinone, epoprostenol AKA Flolan)

(NEJM.org)

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18
Q

What is the end effect of bosentan?

A

Endothelin receptor antagonist, preventing endothelin-receptor complex from causing endothelial constriction and proliferation

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19
Q

What is the mechanism of action of sildenafil?

A

Phosphodiesterase-5-inhibitor

Prevents breakdown of vasodilatory cGMP (nitric oxide pathway)

20
Q

Mechanism of action of milrinone

A

Phosphodiesterase-3 inhibitor, prevents cAMP breakdown (prostacyclin pathway)

  1. Pulmonary vasodilation
  2. Reduces afterload (arterial relaxation)
  3. Improves myocardial [ventricular] function
21
Q

What effects do corticosteroids have in relation to pulmonary hypertension

A
  1. Reduce reactive oxygen species
  2. Increase cGMP synthesis
  3. Reduce cGMP metabolism
    * Net pulmonary vasodilation (via nitric oxide pathway)*
22
Q

What characteristic of the blood vessels most significantly impacts blood flow?

A

Vessel diameter (AKA radius)

Think of Poiseuille’s Law–inverse, where because:

Q=P/R

Q=P x (πr4 / 8nL)

23
Q

What are the main substrates of the 1) fetal and 2) adult myocardium?

A
  1. Fetal - glucose and lactate
  2. Adult - fatty acids
24
Q

Characteristic cardiac findings in glycogen storage diseases

A

Short PR interval

Biventricular hypertrophy

25
Q

Conotruncal lesions should make you think of what genetic syndrome?

A

22q11, AKA DiGeorge

26
Q

Mechanisms of hydrocortisone on increasing blood pressure (four groups of action)

A
  1. Inhibits nitric oxide synthase (NOS) and prostaglandin release - inhibits vasodilation
  2. Increases Ca++ concentration - contractility
  3. Upregulates adrenergic receptors and decreases catecholamine metabolism - vasoconstriction and contractility
  4. Upregulates angiotensin-II receptors - vasoconstriction
27
Q

Cardiac defects associated with elfin facies, open mouth, transient hypercalcemia

A

Supravalvar aortic OR pulmonic stenosis

(Rubella is also associated with supravalvar pulmonic stenosis)

28
Q

Cardiac defects associated with Rubella

A

Patent ductus arteriosus (PDA)

Supravalvar pulmonic stenosis

29
Q

Oxygenation index equation

A

OI= (what you’ve put in) / (what you get out)

(MAPxFiO2) / PaO2

OI>40 is considered the threshold for ECMO

30
Q

How does PCO2 influence pulmonary vs cerebral blood flow

A

A low PCO2 vasodilates pulmonary vasculature

A low PCO2 vasoconstricts cerebral vasculature

Reason that patients with head injuries used to be hyperventilated, and patients with PPHN would be overventilated

31
Q

What percentage of infants with BPD develop pulmonary hypertension

A

1/3

Reason to do screening echocardiography, and theoretically consider cardiac catheterization

32
Q

The congenital heart defect variants known for a reverse saturation differential

A

dTGA with aortic coarctation

dTGA with pulmonary hypertension

33
Q

Two ECG abnormalities seen in Pompe disease

A

Short PR interval

Bilateral ventricular hypertrophy

Can also have preexcitation (all from their hypertrophic cardiomyopathy)

34
Q

Hydrocortisone ________ catecholamine metabolism

A

decreases

  • So they “stick around” longer*
  • It also decreases NOS expression and prostaglandin action*
35
Q

The first- and second-line agents for fetal SVT

A

Digoxin and amiodarone

Digoxin first-line mainly 2-2 safety profile, while amiodarone’s 90% effective for AV reentry

36
Q

Normal QRS axis for term neonates

A

+55 to +200

Remember it’s right-axis deviation that’s normal

37
Q

Frequency of chromosomal abnormalities in fetus with congenital heart defects

A

1 in 8 fetuses

Most commonly the Trisomies (21, 18 and 13) or DiGeorge

38
Q

The most common brain abnormalities in CHD

A

White mattery injury and infarction

Including on preoperative MRI

39
Q

Four genes associated with HLHS

A

NKX2-5

GJA1

NOTCH1

HAND1

Sibling’s likelihood of ANY CHD with prior infant with HLHS is 22% (8% for HLHS in particular)

40
Q

Most commonly affected gene in Long QT Syndrome (LQTS)

A

KCNQ1

Both LQTS and KCNQ1 have a _Q__

41
Q

The typical timeframe for symptomatic hypertrophic cardiomyopathy 2-2 maternal diabetes to resolve

A

1 month

NeoReviews

42
Q

The amount of desaturated hemoglobin needed for cyanosis

A

3-5g/dL

Since it’s an absolute amount, that’s why the higher your Hb the less desaturation’s needed to appear cyanotic (e.g. 80% saturated with a Hb 15 vs. 70% when Hb 10)

43
Q

The risk of CCHD in siblings of a person with HLHS (hypoplastic left heart syndrome)

A

22% for any CHD, 8% for HLHS specifically

44
Q

Metabolic side effects (usually transient) of epinephrine infusion

A

Lactic acidosis

Hyperglycemia

Hypocarbia (low HCO3)

45
Q

In HLHS, the best echocardiographic way to assess adequate atrial communication (i.e. blood flow)

A
46
Q

The most common cause of neonatal SVT (supraventricular tachycardia)–multiple names

A

AVRT (atrioventricular reentrant tachycardia OR reciprocating tachycardia)

“Orthodromic reciprocating tachycardia”

An accessory pathway that can bypass AV node; differs from the most common cause when older, which is AV_N_RT

Neonatal-Perinatal Boards Review (11 decks)

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