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congenital heart disease Flashcards

1
Q

purpose of umbilical vein and how many

A

carries oxygenated blood from mother to fetus
1 umbilical vein

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2
Q

purpose of umbilical artery and how many

A

carries deoxygenated blood from fetus to mother
2 umbilical arteries

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3
Q

purpose of ductus venosus

A

shunts blood from umbilical vein to IVC (bypasses liver)

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4
Q

purpose of foramen ovale

A

shunts blood from RA to LA (bypasses lungs)

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5
Q

purpose of ductus arteriosus

A

shunts blood from pulmonary artery/trunk to aorta (bypasses lungs)

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6
Q

how ductus arteriosus closure is facilitated

A

decreased PVR reverses flow form ductus arteriosus, which exposes DA to increased PO2, and closes DA.

decreased circulating PGE1 (usually released from placenta) also facilitates DA closure

functionally closes with SVR > PVR

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7
Q

murmur that you’d hear if ductus arteriosus remained open

A

systolic and diastolic murmur

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8
Q

how foramen ovale closure is facilitated

A

first breath expands lungs and deceases PVR,
placenta separates from cord wall and increases SVR,
this creates LA pressure > RA pressure and PFO closes

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9
Q

drugs that can close and open PDA

A

closure can be facilitated with indomethacin, a prostaglandin synthase inhibitor

it can be opened with PGE1

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10
Q

how long does it take PFO to close

A

3 days

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11
Q

how long does it take PDA to close

A

several weeks via fibrosis

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12
Q

cardiac circulation in fetus versus adults

A

adults: circulation in parallel
fetus: circulation in series

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13
Q

right to left shunt occurs when

A

PVR is > SVR
(blood bypasses the lungs. “blue baby”)

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14
Q

left to right shunt occurs when

A

SVR > PVR
(oxygenated blood recirculates through right heart and lungs. “pink baby”)

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15
Q

PVR equation and normal PVR

A

=(mPAP - PAOP)/CO * 80

normal: 150-200dynes/sec/cm^5

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16
Q

SVR equation and normal SVR

A

=(MAP - CVP) /CO * 80

normal: 800-1500 dynes/sec/cm^5

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17
Q

factors that increase and decrease PVR

A
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18
Q

factors that increase and decrease SVR

A
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19
Q

examples of right to left shunts

A

“five T’s”
TOF
Transposition of great arteries
tricuspid valve abnormality (Ebsteins anomaly)
Truncus arteriosus
Total anomalous pulmonary venous connection

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20
Q

hemodynamic goals for patients with right to left shunts

A

maintain SVR and decrease PVR
maintain contractility and HR

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21
Q

effect of right to left shunt on inhalation induction

A

volatile does not pass through lungs to rate of FA/FI is slowed and so is rate of induction

difference is more profound with less soluble agents (N2O and desflurane) and less profound with more soluble agents (iso)

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22
Q

effect of right to left shunt on IV induction

A

faster

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23
Q

pathophysiology of left to right shunt includes

A

decreased systemic BF which decreases CO and creates HoTN (bc blood is only recirculating through right heart and lungs, not out into the body)

increased pulmonary BF which creates pHTN and RV hypertrophy

24
Q

hemodynamic goals for a patient with a left to right shunt

A

avoid increased SVR
avoid decreased PVR by avoiding alkalosis, hypocapnia, high FiO2 and vasodilators

25
Q

examples of left to right cardiac shunts include

A

VSD
ASD
PDA
coarctation of aorta

26
Q

effect of L to R shunt on inhalation induction

A

negligible

27
Q

effect of L to R shunt on IV induction

A

possibly prolonged

28
Q

Eisenmenger Syndrome

A

when a patient with L to R shunt develops pulmonary HTN. increased right heart pressures cause a flow reversal through cardiac defect, likely leading to right to left shunt, hypoxemia, and cyanosis

29
Q

TOF is characterized by these 4 defects

A

VSD
aorta that overrides RV and LV (and receives blood from both ventricles)
pulmonic stenosis (obstruction to RV ejection)
RV hypertrophy

30
Q

RVOT obstruction/compensation and TOF

A

increased RVOT obstruction shunts more deoxygenated blood to VSD and out of the aorta
body compensates with erythropoiesis but that leads to polycythemia and increased risk of thromboembolism

31
Q

pathophysiology of a TET spell

A

precipitated by increased SNS activity which increases myocardial contractility and increases resistance at RVOT.
this shunts more deoxygenated blood to VSD which causes right to left shunt and hypoxemia

essentially a R->L shunt r/t increased PVR

32
Q

how the child will compensate for a TET spell

A

hyperventilate to compensate for hypoxemia
squat to increase intra abdominal pressure, which increases RV preload and SVR, and restores BF to pulmonary arteries which reverses ish the magnitude of right to left shunt

33
Q

perioperative treatment of a child in a TET spell

A

FiO2 100%
administer fluids to expand intra vascular volume
increase SVR with neo to augment SVR to PVR ratio
reduce SNS stimulation (deepen anesthesia, beta blockade with esmolol)
avoid inotropes (can worsen RVOT)
avoid excessive aw pressure
place infant in knee chest position to mimic squatting

34
Q

best induction agent for TOF baby

A

ketamine 1-2mg/kg IV or 3-4mg/kg IM
increases SVR and reduces shunting

35
Q

histamine releasing drugs and TOF baby

A

avoid them since it decreases SVR. this includes morphine, meperidine, atracurium

36
Q

most common congenital cardiac anomaly in children

A

VSD

37
Q

early signs of ASD

A

poor exercise tolerance, later could include atrial flutter, afib, CHF

38
Q

isolated ASD and abx

A

not indicated unless within 6mo of ASD repair

39
Q

what conditions is VSD usually associated with

A

trisomy 13, 18, 21
VACTERL (vertebral, vascular, anal, cardiac, tracheoesophageal fistula, renal, limb abnormalities)
CHARGE (coloboma, heart anomaly, choanal atresia, retardation, genital and ear abnormalities)

40
Q

how are VSD’s closed

A

usually close on their own by age 2 but if you need surgical intervention, they are an open approach via a patch (versus ASD is usually closed)

41
Q

isolated VSD and abx

A

not indicated for isolated VSD but is within 6 months of surgical repair

42
Q

pathophysiologic anatomy of coarctation of aorta

A

when aorta narrows in area of ductus arteriosus. LV must then generate higher pressure to overcome increased aortic resistance. Severe narrowing can limit blood delivered to lower half of body. Pink upper half, cyanotic lower half.

43
Q

SBP and coarctation of aorta

A

if it is proximal to left SCA take off, SBP in RUE will be > LUE
SBP is reduced in LE’s

44
Q

what does LE perfusion rely on with coarctation of aorta severe obstruction

A

relies on PDA

45
Q

management of BF to LE’s with patient that has coarctation of aorta

A

reduced BF facilitates organ and limb ischemia.
PGE1 is administered to facilitate DA potency until surgery can be performed (anastomosis)

46
Q

Ebsteins anomaly

A

downward (apical) displacement of tricuspid valve. Part of RV becomes part of RA which causes right atrial enlargement. This causes an ASD or PFO.

47
Q

pathophysiologic anatomy of transposition of great arteries

A

each vessel arises from wrong ventricle.
RV gives rise to aorta
LV gives rise to p. artery
RV circuit: systemic venous blood: RV–>aorta–>repeat
doesn’t go through pulmonary circulation
LV circuit: LV–>lungs–>repeat
doesn’t go through systemic circulation

48
Q

treatment for patient with transposition of great arteries

A

keep PDA open with PGE infusion (temporary fix)
Rashkind procedure allows some oxygenated blood to get to systemic circulation
intraartial baffle and arterial switch procedures are definitive tx

49
Q

anatomic features of hypo plastic left heart syndrome include

A

hypoplastic LV and aortic arch
mitral and aortic stenosis or atresia
ductal dependent circulation

50
Q

Goal of HLHS surgical correction: Norwood stage 1

A

when: neonatal period
goal: aortic reconstruction. aortic arch now rises from pulmonary trunk. p. arteries are disconnected from p. trunk and are used to create a shunt from SCA to RV

51
Q

Goal of HLHS surgical correction: Norwood stage 2

A

when: 3-6mo
goal: shunt from first procedure is taken down and new connection is made between SVR and p.arteries

52
Q

Goal of HLHS surgical correction: Norwood stage 3

A

when: 2-4 years (fontan procedure)
goal: conversion to fontan circulation: IVC is connected to p.artery with a conduit

53
Q

management of a patient after a fontan procedure

A

patient has a single ventricle that pumps blood into systemic circulation. pBF occurs passively from SVC/IVC to p.artery
BF to lungs is completely dependent on intrathoracic pressure. therefore pp ventilation is bad news bears. spontaneous ventilation is preferred.
preload dependent- give fluids

54
Q

pathophysiologic anatomy of truncus arteriosus

A

single artery that gives rise to pulmonary, systemic, and coronary circulations. mixed blood is pumped continuously. usually a VSD as well.
increasing PVR or p.BF can steal from systemic and coronary BF

55
Q

truncus arteriosus surgical intervention

A

can restore 2 ventricle arrangement by separating pulmonary from systemic BF by closing VSD

56
Q

which congenital heart defects are associated with ventricular outflow tract obstruction?

A

TOF
ebsteins anomaly
p. stenosis with ASD or VSD
eisenmengers syndrome

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