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PEDS > Apex- neonates: congenital heart disease > Flashcards

Apex- neonates: congenital heart disease Flashcards

1
Q

In the fetus, where does gas exchange occur?

A

At the placenta

*organ of respiration

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2
Q

What are the 3 fetal shunts and where do they shunt blood and what do they bypass?

A
  1. Ductus Venous → shunts blood from the umbilical Vein to the iVc, bypassing the liVer

IVC → RA

  1. Foramen ovale → shunts o2 rich blood (from DV) from the RA to the LA, bypassing the lungs
  2. Ductus Arteriosis → shunts o2poor blood (from lower body, ivc, ra, rv) from the pulmonary Artery → Aorta , bypassing the lungs

(so i guess normally during systole, blood gets ejected from RV → PA → lungs → PVs → LA
fetus will go from RV → PA → PDA → Aorta)

-oxygenated blood from the ductus venouses and deoxygenated blood from the lower body coverge in the IVC where there is then 2 streams of blood traveling at different rates

> higher veloicy, oxygenated blood from the ductus venosus, flows across the flap of tissue (eustachian valve)- which preferentially diverts the oxygenated blood across the foramen ovale (RA > LA) to go and perfuse the myocardium and developing brain

> lower velocity (deoxygenated blood) is preferentially directed to the RV and pulmonary artery → ductus arteriosus → proximal descending aorta (immediately distal to the left subclavian artery) and perfuses the lower body and some of it returns to the placenta via its two umbilical arteries

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3
Q

What structure preferentially diverts oxygenated blood across the foramen ovale

A

Eustachian valve

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4
Q

What happens physiologically when baby takes first breath?

A

lungs expand, PaO2 increases, PaCo2 decreases

*lowers pulmonary vascular resistance

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5
Q

What happens when the umbilical cord is clamped?

A

theres an increase in SVR

-the decrease in PVR from first breaths + increase in SVR from cord clamp results in LA pressure climbing higher than RA pressure and then

  1. the flap of the foramen ovale closes and
  2. blood flow starts reversing from aorta (high pressue) back thru ductus arterosus and when that is exposed to increased O2 it closes
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6
Q

discuss prostaglandins and the ductus arterosis

A

prostaglandins released from the placenta help maintain a PDA
-when cord is clamped, there is decreased circulating levels of PGE1 which results in DA closure (+ exposure to oxygenated blood from backflow thru a newly pressurized aorta)

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7
Q

how would you know if a baby still has a PDA

A

they will have a continuous systolic and diastolic murmur

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8
Q

Functional vs anatomic closure of the Foamen ovale

adult remnant?

How many adults have a PFO? Problem?

A

Functional- cord clamping (LAP > RAP → increased SVR)
Anatomic closure = 3 days

fossa ovalis

30% ; increased risk of paradoxical embolism (embolism travels to brain instead of lungs)

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9
Q

Fuctional vs anatomic closure of the ductus arteriosus

adult remnant

A

functional - when SVR > PVR (increased PaO2 and decreased prostagladins from placenta)
anatomic closure = several weeks via fibrosus

ligamentum arteriosum

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10
Q

What can close vs open a PDA?

A

so think… prostaglandins from the placenta keep it open…. so it can be opened with:
→ Prostaglandin E1 (PGE1)

think NSAIDS block the syntehsis of praostaglandins by inhibiting COX 1 and COX 2 (the patheways where arachadonic acid gets converted to prostagladins and thromboxanes)
is so you can give **indomethacin (a porstaglandin synthase inhibitor) **

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11
Q

When does the ductus venous close?

adult remnant

A

when the umbilicar cord is clamped
(shunts blood flow from the umbilical cord to IVC, no blood from umbilical cord = no need for it)

ligamentum venosum

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12
Q

T/F- the ligamentum venosum cannot reopen

A

True

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13
Q

T/F- all the anatomic shunts essentially close functionally with umbilical cord clamping

A

True

FO bc the increase in SVR results in increased LAP > RAP
DA bc SVR > PVR = increased PaO2 and decreased prostaglandin release from placenta
DV bc no blood flow is coming from placenta now

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14
Q

When does the FO vs DA close anatomically?

A

FO - 3 days
DA - 3 weeks (“several” - just tryna keep it easy)

DV closes with cord clamping

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15
Q

the 4 big conditions that increase PVR

A

Hypercarbia
Hypoxemia
Hypothermia
Acidosis

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16
Q

What 3 things are the size and direction of a shunt depdendent on?

A
  1. ratio of PVR to SVR
    - R → L shunt occurs when PVR is higher than SVR
    - L → R shunt occurs wehn SVR is greater than PVR (isnt it always?)
  2. Pressure gradients between the cardiac chambers or arteries involved
  3. Compliances of the cardiac chambers
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17
Q

Calculation for PVR

normal

A
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18
Q

Calculation for SVR

normal value

A
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19
Q

increased or decreased SVR:

decreased SNS tone

A

decreased SVR

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20
Q

how does hemodilution affect PVR and SVR

A

decreases them both

no idea why - less viscosity? idk

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21
Q

Right to Left Cardiac Shunts
-Mneumonic x 2

A

“To the left, to the left, move your FEETTT”
Fallot (TOF)
Ebsteins anomaly (tricuspid valve abnormality)
Eisenmenger syndrome
Transposition of the great arteries
Truncus arteriosus
Total anaomalous pulmonary venous connection

5 T’s
1. TOF
2. Tricuspid valve abnormality (Ebstein)
3. Transposition of the great arteries
4. Truncus arteriosus
5. Total anamalous pulmonary venous connection

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22
Q

Left to Right shunts
Mneumonic

A

people of the VA are not “PC”

VSD
ASD
PDA
Coarctation of the Aorta

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23
Q

Hemodynamic goals of someone with a right to left shunt

A

Maintain SVR
Decrease PVR
→ hyperoxygenate
→hyperventilate
→avoid lung hyperinflation

-goals with shunts are always SVR and PVR related

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24
Q

How is inhalational induction affected with somone with a right to LEFT shunt? why?

A

decreased

  1. less blood going to lungs to pick up volatile agent
  2. shunted blood dilutes whatever blood is getting to the lungs and picking up the agent → gets diluted by the shunted blood
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25
Q

Is inhalational induction with a right to LEFT shunt most profoundly different with less soluable or more soluable agents

A

more profound with less soluable agents (N20 and desflurane)
-less difference noted with more soluble agents (isoflurane)

just remember, iso already takes forever , so if it takes a little longer- no one will notice; but someone will def notice nitrous and des taking longer

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26
Q

Faster or slower IV induction with right to LEFT shunt

what about a left to right shunt?

A

faster
-iv med bypasses lungs and directly enters systemic circulation → VRG

possibly prolonged as blood re-enters pulmonary circulation

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27
Q

how will a VSD affect your inhaltional induction

A

VSD = left to RIGHT shunt
-blood still gets to lungs
negligible effect

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28
Q

How do you want to manage your vent settings with someone with a VSD

A

low FiO2
don’t hyperventilate → keep CO2 normal

want to avoid decreases in PVR which would promote increased blood flow (o2 and hypocarbia dilate the vasculature)

so VSD = low systemic blood flow and high pulmonary blood flow
avoid decreasing PVR (which would encourage more pulmonary blood flow)
& avoid increasing SVR (which would make it harder for pulm blood flow to get out and make it back up and increase even further) + higher pressures in the left heart force blood to the right across the septal defect

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29
Q

Tetralogy of Fallot is characterized by what 4 defects?

4 goals

A
  1. RV outflow tract obstruction → pulmonary stenosis
  2. RV hypertrophy due to above
  3. VSD bc the septum get malaligned from the hypertrophy
  4. Overriding aorta that receives blood from both ventricles? - i guess RV > LV > aorta? idk

VAPoR

VSD
Aorta that overrides the RV and LV
Pulmonary Stenosis (obstruction to RV ejection)
RV hypertrophy

increase SVR
decrease PVR
maintain contractility and HR
increase preload

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30
Q

What’s the most common cyanotic congenital heart anomaly?

A

TOF

31
Q

Why are TOF kids at increased risk for thromboembolism and stroke?

A

bc the blood thats shunted thru the VSD and into systemic circulation is not oxygenated

-body senses this decrease in oxygenated blood in the systemic circulation and compensates with erythropoiesis - makes more blood cells to help carry o2; however this increase in RBCs increases the risk of thromboembolism and stroke

32
Q

What does a TET spell result in? (2)

A

hypoxemia and cyanosis

33
Q

What is a tet-spell precipitated by and what happens?

A

increased SNS activity (crying, agitation, pain, defication, fright, trauma)

-this increased SNS activity** increases myocardial contractility**, worsening the RVOT obstruction
-blood flows across path of least resistance, so increased resistance at the RVOT will force blood through the VSD → increased right to left shunting → hypoxemia

34
Q

T/F- only kids with unrepaired TOF can experience tet spells

A

True

35
Q

What 2 things will kids automatically do when having a TET spell?

A

hyperventilate and squat

  • they hyperventilate with the onset of hypoxemia to try and get more o2 to body
  • they squat → increases IAP → compresses abdominal arteries → increases RV preload, SVR, and blood flow through the RVOT
36
Q

3 things to do/increase for a TET spell

position to place infant in

3 things to avoid/decrease

A
  1. administer 100% fio2 - tx hypoxemia
  2. Give IVF - full ventricle will reduce RVOT obstruction
  3. increase SVR - neo → increasing SVR so blood has a harder time just sneaking across the VSD and more willbe directed towards the RVOT

knee to chest postion- to mimic squatting

  1. Avoid inotropes - the already hypertrophied RV will worsen RVOT obstruction if contracting harder
  2. Avoid excessive airway pressure → compresses pulm vessels and increases PVR
  3. Reduce SNS stimulation → deepen anesthesia, short-acting beta blocker - slow HR = more time for RV to fill + SNS stimulation increases PVR which will make it harder to get blood into lungs
37
Q

Anesthetic hemodynamic goals : TOF
SVR
PVR
HR
Contractility
Preload

A

SVR- increase
PVR - decrease
HR and CX - maintain (avoid increases)
Preload- increase

38
Q

What lab value would you want to look at if your kid has TOF and why

A

RBCs
-polycythemia will be proportional to the degree of chornic hypoxemia
-more rbcs = worse

39
Q

Induction agent for TOF and why

what opioid to avoid and why

A

Ketamine 1-2mg IV or 3-4mg IM

-increases SVR, reducing shunting

morphine (or any histamine releasing drugs) - decreases SVR, increas. sh

40
Q

TOF will result in what kind of axis devation on EKG?

what will the heart look like on CXR

A

right axis ( - I, + AVF)

due to RV hypertrophy

boot shaped

41
Q

Failure of the fossa ovalis to close results in what type of atrial septal defect?

A. Primum
B. Secundum
C. Sinus Venosus
D. Perimembranous

A

B. Secundum (occurs in the middle 1/3 of the atrial septum - represents 80% of all ASDs)

Primum ASDs occur in the lower region of the atrial septum, just above the tricuspid valve
Sinus venosus ASDs are located just below the IVC or less commonly just above the IVC

42
Q

What is the most common type of ventricular septal defect?

A

perimembraneous.

located in the middle of the ventricular septum, just below the septal leaflet of hte tircuspid valve

43
Q

is blood flow thru an ASD (ie PFO) usually cyanotic (right to left) or acyaonotic (left to right)

what about VSD?

A

PFO- usually acyantoic (left to right) (high pressure to low pressure)

same

44
Q

What is the most common congenital cardiac anomaly in kids?

what about adults?

A

VSD

* asignificant number of VSDs close by the kid is 2

bicuspid aortic valve = most common congenital cardiac defect in adults

45
Q

Hemodynamic mangement of ASD with anesthesia

A

hemodynamic effects of anesthetic agents are usually well tolerated

46
Q

How do they fix ASDs?

A

usually with a percutaneous transcatheter device

can also be done open with a suture or patch

47
Q

Which Trisomys are associated with VSDs

A

21
18
13

  • think cool years-
    21 drink
    18 adult
    13 teen
48
Q

if you hear your patient has a VSD, what do you want to know about it?

A

small or large

-if VSD is small- pulm blood flow is only slighlty increased and they tolerate anesthesia well
-if VSD large - RV and LV pressures equalize and then PVR and SVR will determine the direction of blood flow

49
Q

Goals with VSD

A

avoid decreases in PVR and increases in SVR
- will increase shunt flow

i guess if you decrease pressure on the right and/or increase pressure on the left, its going to send more blood back to the RV and less out the aorta? - AKA: increase shunt flow

50
Q

How are VSDs typically closed?

A

open repair with a patch

inotropic support may be needed afterwards

51
Q

Do patients with VSD tolerate anesthesia well?

A

usually the PPV that increases PVR + volatile agents that decrease SVR lead to stable hemodynamics as long as the balance doesnt favor right to left shunting

52
Q

Pt is undergoing surgical repair for coarctation of hte aorta. What is the BEST site to monitor the arterial blood pressure?

A

right arm

  • coarctation occurs when the aorta is narrowed in the area of hte ductus arteriosus
  • -LV much generate a higher pressure to overcome the increased aortic resistance and severe narrowing can limit hte amount of blood delivered to the lower half of the body
  • rarily, but possibly, the coarctation could be proximal to the left subclavian artery, reducing perfusion to the left upper extremity; so thats why the right would be best
53
Q

What is coarctation of the aorta?

what will be seen as symptoms?

A

its where the aorta narrows, usually around the level of the ductus arterosus
→obstruction of blood flow increases LV afterload

increased BP in upper extremities
decreased SBP in lower extremities +

pink upper body, blue/cyanotic lower body

54
Q

why would a kid be on Prostaglandin E1?

A

to keep the ductus arterosis open

-coarctation of the aorta can result in decreased blood flow to the lower extremities
-keeping the PDA open helps maintain blood flow to lower extremities until surgery can be done

pulm artery to aorta

55
Q

T/F- mild to moderate coarctation usually goes unnoticed for years

A

True

pts often develop collateral flow

56
Q

Pt scheduled for a Fontan procedure MOST likely has a diagnosis of:

A. truncus arteriosus
B. ebstein’s anomaly
C. transposition of the great arteries
D. hypoplastic left heart syndrome

A

D. Hypoplastic left heart syndrome

most common single ventricle lesion
-all patients with a single ventricle require surgical correction with the Fontan procedure

57
Q

What is characterized by a downward displacement of the tricuspid valve, right atrial dilation, and “atrialization” of the right ventricle

A

Ebstein’s anomaly

*there is usually an ASD or PFO

58
Q

What is transposition of the great arteries?

A

it’s when each great vessel arises from the wrong ventricle
→ RV gives rise to the aorta (poorly- oxygenated circuit)
→ LV gives rise to hte pulmonary artery (well oxygenated circuit)

Medical emergency!!!

59
Q

T/F transposition of hte great arteries is a medical emergency

A

True!
-cant send poorly oxygenated blood to a poorly oxygenated body and well oxygenated blood to the lungs.. dont do any good

60
Q

T/F= patients with hypoplastic left heart syndrome - we should aim to increase their PVR

A

false- this patient has a single ventricle that pumps blood into systemic circulation. Pulmonary blood flow is passive and anything that increases PVR should be avoided

61
Q

What is truncus arteriosus characterized by

A

a single artery that gives rise to the pulmonary, systemic, and coronary circulations.

there is usually a VSD

62
Q

What is this?

A

Ebsteins anomaly
-downward (apical) displacement of the tricuspid valve (atrialzation) causing right atrial enlargement, usually accompanied by an ASD or PFO

63
Q

What is hte most common congenital defect of the tricuspid valve?

A

Ebstein’s anomaly

64
Q

How will the onset of IV induction agents change in someone with Ebstein’s anomaly

A

-downward displacement of tricuspid valve allows RV to become apart of RA (atrialization)
→ increased RAP
→ IV induction may be prolonged due to pulling of drugs in the enlarged RA

65
Q

what is someone with ebstein’s anomaly at risk for?

what is the common dysrhythmia?

what is common in the postop period?

A

CHF *need to maintain RV function

SVT

RV vailure postop

66
Q

T/F- transposition of the great arteries is compatible with intrauterine life

A

True bc the flow thru the ductus arteriosus and foramen ovale allow communication between both ciruclations

*Medical emergency bc no chance of survival once born

67
Q

What is Rashkind procedure for?

what would be definitive surgical correction

A

transposition of the great arteries → creates an interarterial pathway to allow some oxygenated blood to reach the systemic circulation

intraatrial baffle and arterial switch

68
Q

in what condition is blood flow into the lungs completely dependent on negative intrathoracic pressure during spontaneous breathing and should make effort effort to maintain?

A

hypoplastic left heart syndrome

*increased PVR is detrimental to pulmonary blood flow

this patient has a single ventricle that pumps blood into systemic circulation. pulmonary blood flow occurs passively from the SVC/IVC > pulmonary artery

69
Q

T/F - pts with hypoplastic left heart syndrome are preload depdendent

A

True - dont let them get dry!

70
Q

What anamoly results in oxygenated and deoxygenated blood being pumped into both pulmonary and systemic ciruclations thats usually accompanied by a VSD?

A

Truncus arteriosus

single artery gives rise to pulmonary, systemic, and coronary circulations with no specific pathway for it to go to the lungs first

71
Q

why would you want to avoid decreasing PVR in a patient with truncus arteriosus

A

bc it will increase pulmonary blood flow and steal blood from systemic and coronary ciculations

single artery gives rise to pulmonary, systemic, and coronary circulations with no specific pathway for it to go to the lungs first

72
Q

Label

A
  1. Ebstein
  2. Transposition of the great arteries
  3. Hypoplastic left heart syndrome
  4. Truncus arteriosis
73
Q

Identify the featrues of TOF: (Select 2):

-Atrialization of the right atrium
-RVOT obstruction
-VSD
-Ductal-dependent circulation

what are the other 2

A

RVOT obstruction and VSD

+ RVH + Overriding aorta

atrialization is ebstein (usually ASD/PFO_
Ductal dependent circulation is hypoplastic left heart syndrome

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