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congenital heart disease Flashcards

(56 cards)

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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

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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

Study These Flashcards
A

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

25
examples of left to right cardiac shunts include
VSD ASD PDA coarctation of aorta
26
effect of L to R shunt on inhalation induction
negligible
27
effect of L to R shunt on IV induction
possibly prolonged
28
Eisenmenger Syndrome
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
TOF is characterized by these 4 defects
VSD aorta that overrides RV and LV (and receives blood from both ventricles) pulmonic stenosis (obstruction to RV ejection) RV hypertrophy
30
RVOT obstruction/compensation and TOF
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
pathophysiology of a TET spell
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
how the child will compensate for a TET spell
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
perioperative treatment of a child in a TET spell
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
best induction agent for TOF baby
ketamine 1-2mg/kg IV or 3-4mg/kg IM increases SVR and reduces shunting
35
histamine releasing drugs and TOF baby
avoid them since it decreases SVR. this includes morphine, meperidine, atracurium
36
most common congenital cardiac anomaly in children
VSD
37
early signs of ASD
poor exercise tolerance, later could include atrial flutter, afib, CHF
38
isolated ASD and abx
not indicated unless within 6mo of ASD repair
39
what conditions is VSD usually associated with
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
how are VSD's closed
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
isolated VSD and abx
not indicated for isolated VSD but is within 6 months of surgical repair
42
pathophysiologic anatomy of coarctation of aorta
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
SBP and coarctation of aorta
if it is proximal to left SCA take off, SBP in RUE will be > LUE SBP is reduced in LE's
44
what does LE perfusion rely on with coarctation of aorta severe obstruction
relies on PDA
45
management of BF to LE's with patient that has coarctation of aorta
reduced BF facilitates organ and limb ischemia. PGE1 is administered to facilitate DA potency until surgery can be performed (anastomosis)
46
Ebsteins anomaly
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
pathophysiologic anatomy of transposition of great arteries
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
treatment for patient with transposition of great arteries
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
anatomic features of hypo plastic left heart syndrome include
hypoplastic LV and aortic arch mitral and aortic stenosis or atresia ductal dependent circulation
50
Goal of HLHS surgical correction: Norwood stage 1
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
Goal of HLHS surgical correction: Norwood stage 2
when: 3-6mo goal: shunt from first procedure is taken down and new connection is made between SVR and p.arteries
52
Goal of HLHS surgical correction: Norwood stage 3
when: 2-4 years (fontan procedure) goal: conversion to fontan circulation: IVC is connected to p.artery with a conduit
53
management of a patient after a fontan procedure
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
pathophysiologic anatomy of truncus arteriosus
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
truncus arteriosus surgical intervention
can restore 2 ventricle arrangement by separating pulmonary from systemic BF by closing VSD
56
which congenital heart defects are associated with ventricular outflow tract obstruction?
TOF ebsteins anomaly p. stenosis with ASD or VSD eisenmengers syndrome

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