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114 Cards in this Set

  • Front
  • Back
what are the 3 things in fetal circulation that go away when born
1-ductus venosus

2-foramen ovale

3-ductus arteriosus
what is ductus venousus
allow majority of oxygenated placental blood to bypass liver and enter IVC
what is foramen ovale
allows oxygenated blood from placenta to pass from RA to LA and into systemic circulation
what is ductus arteriosus
dexoygenated blood from SVC passes into RV & pumped into PA where much of it travels via DA into descending aorta to placenta to be oxygenated
what are the things that occur in the transition from fetal to neonatal circulation
*increased SVR
*decreased PVR
*closure of foramen ovale
*closure of ductus arteriosus
*closure of ductus venosus
why is there an increased SVR with transition from fetal to neonatal circulation
b/c of loss of low pressure placental circulation
why is there a decreased PCR with transition from fetal to neonatal circulation
b/c of
*expansion of lungs
*vasodilation d/t aeration
why is there closure of foramen ovale with transition from fetal circulation to neonatal circulation
due to flow reversal as SVR increases and PVR decreases
why is there closure of ductus arteriosus with transition from fetal circulation to neonatal circulation
flow reversal followed by constriction of the muscular wall
why is there closure ductus venosus with transition from fetal circulation to neonatal circulation
d/t muscular constriction of vessel wall
what is the incidence of congenital heart dz
7-10 / 1000 live births
what is the most common form of congential dz
congenital heart dz
what accounts for 10% of the cause of congential heart dz
chromosomal abnormalities
majority of chromosomal abnormalities are associated with what
trisomy 21
what accounts for 90% of the cause of congenital heart dz
multifactoral origin

(genetic +/- external factors)
what are some of the multifactoral origins of congenital heart dz
*maternal dm
*rubella
*ETOH abuse
*lithium use
what is the MOST often occuring congential heart dz problem
ventricular septal defect
what are the ACYANOTIC lesions
*ASD *VSD
*patent ductus arteriosus
*aortic stenosis
*pulmonic stenosis
*coarctation of the aorta
what type of shunt does an ACYANOTIC lesion produce
L to R
an ACYANOTIC results in what
*increased pulmonary blood flow
*pulmonary HTN
*R vent hypertrophy
*heart failure
when is repair best done on an ACYANOTIC lesion
at an early age
once PVR is what with an ACYANOTIC lesion sx may not produce significant benefit
> 1/3 SVR
atrial septal defect typically results from what
spontaneous genetic mutations
with atrial septal defects small lesions may do what
remain ASYMPTOMATIC throughout life
what is the threshold for closure with atrial septal defect
when pulmonary blood flow is >1.5x systemic blood flow
what are the symptoms of a large atrial septal defect
*DOE
*supraventricular dysrhythmias
*R heart failure
*paradoxical air embolus
*recurrent pulm infection
what are things that INCREASE L to R shunt
*increased SVR

*decreased PVR
what are things that decrease L to R shunt
*decreased SVR

*increased PVR
d/t increased pulm blood flow with atrial septal defect what might happen to IV drugs
possible dilution
d/t decreased systemic blood flow with atrial septal defect what might happen with inhalation induction
possible delay
what is the most common congenital HEART defect
ventricular septal defect
what heart defect often closes spontaneously in infancy
ventricular septal defect
what occurs with a large ventricular septal defect
*initial L to R shunt

*over time RVH occurs

*may become a R to L shunt
when should surgical correction occur with a ventricular septal defect
prior to PVR/SVR ratio reaching 0.7
with VSD L to R shunt what may IMPROVE the condition
volatile anesthetics and and positive pressure ventilation
with VSD late stage cyanotic R to L shunt what may WORSEN the shunt
volatile anesthetics and positive pressure ventilation
with VSD and late stage cyanotic R to L shunt what may IMPROVE the shunt
increased FIO2 and sympathetic stimulation
what causes patent ductus arteriosus
failure of spontaneous closure
what is the function of ductus arteriosus in the fetus
allows PA blood to bypass lungs and travel to placenta via aorta
when do symptoms develop with patent ductus arteriosus
most children remain asymptomatic until adolescence
what are the symptoms of patent ductus arteriosus
*pulmonary HTN

*heart failure
what is the tx for patent ductus arteriosus
medical tx
*non-selective inhibition of prostaglandin synthesis
-indomethacin
-ibuprofen
what do you WANT to do in the anesthetic management of patent ductus arteriosus
MINIMIZE L to R shunt
how would L to R shunt be MINIMIZED in the anesthetic management of patent ductus arteriosus
*VA (decrease SVR)

*positive pressure vent (increase PVR)
what would need to be AVOIDED in the anesthetic management of patent ductus arteriosus
*increased SVR

*decreased PVR
what medication would you AVOID in the anesthetic management of patent ductus arteriosus
ketamine

(d/t increased SVR and worsening of shunt)
what amt of the population has a BICUSPID aortic valve
2-3%
AORTIC stenosis is often associated with what
other CV abnormalities
severe AORTIC stenois may present as what in infancy
heart failure
symptoms of AORTIC stenosis typically do not develop until when
adulthood
symptoms of AORTIC stenois include what
*angina

*syncope

*heart failure
what are the initial symptoms of PULMONIC stenois
dyspnea on exertion
with the development of R heart failure the symptoms of PULMONIC stenosis are what
*peripheral edema

*ascites
if a foramen ovale is patent with PULMONIC stenosis what occurs
cyanosis d/t R to L shunting
what is the management of PULMONIC stenosis
*AVOID decreases in systemic blood pressure
*maintain SR w/ a normal HR
where is preductal coarctation of the aorta
just proximal to the L subclavian
where is postductal coarctation of the aorta
just distal to the L subclavian
what is the MOST common preductal or postductal
POSTDUCTAL
what are the general s/s of coarctation of the aorta
BP difference b/t upper and lower body
what are the s/s of coarctation of the aorta proximal to the lesion
*HA
*dizziness
*epistaxis
*palpitations
what are the s/s of coarctation of the aorta distal to the lesion
claudication in LE
what is the tx for coarctation of the aorta
resection or balloon dilation when pressure gradient reaches 30 mmHg
where should you measure BP with coarctation of the aorta
above and below the lesion
what are post-op concerns with coarctation of the aorta
*paradoxical HTN

*effects of decreased spinal cird blood flow during cross clamp

*abd pain
what are the CYANOTIC lesions
*tetralogy of fallot

*transposition of the great arteries
what type of shunt do CYANOTIC lesions produce
R to L
R to L shunts result in what
*decreased pulmonary blood flow

*arterial hypoxemia
what are the risks of a R to L shunt
*thromoembolism secondary to erythrocytosis d/t hypoxemia

*brain abscess
what is the survival like with a R to L shunt
*very limited in the absence of surgical correction

*takes communication of the systemic and pulmonary circulations
what is the most common cyanotic congential lesion
tetralogy of fallot
what are the components of tetralogy of fallot
1-large-single VSD
2-overriding aorta
3-R vent outflow obstruction
4-R vent hypertrophy
***********************************
with tetralogy of fallot a large VSD results in what
equilization of L and R vent pressures resulting in RVH
with tetralogy of fallot R to L shunting occurs d/t what
VSD, RVH and obstruction to the R vent outflow tract
with tetralogy of fallot resulting decrease in pulmonary flow produces what
arterial hypoxemia
with tetralogy of fallot a decreased SVR does what
increased R to L shunt worsening hypoxemia
with tetralogy of fallot an increased SVR does what
reduces R to L shunt
what are the s/s of tetralogy of fallot
*systolic ejection murmur
*cyanosis *squatting
*increased Hgb & Hct
*hypercyanotic attacks
*CVA
*cerebral abscess
*infective endocarditis
with a R to L shunt what are things that REDUCE the shunt
*INCREASED svr

*DECREASED pvr

*INCREASED pulm blood flow
what are ways to increase SVR with a R to L shunt
*ketamine (drug of choice)

*alpha agonism (phenyepherine)
what are ways to decrease PVR with a R to L shunt
increased FIO2
what are ways to increase pulmonary blood flow with a R to L shunt
beta blockade if outflow obstruction d/t infundibular spasm
with a R to L shunt what are things that WORSEN the shunt
*DECREASED svr

*INCREASED pvr

*INCREASED contractility

*hypovolemia
what are ways to decrease SVR with a R to L shunt
*VA

*histamine release

*alpha-blockade
what are ways to increase PVR with a R to L shunt
*positive pressure ventilation

*PEEP

*opening of the chest
what are ways that contractility are increased in a R to L shunt
increases in infundibular outflow obstruction
what is the pre-op management of tetralogy of fallot
*maintain hydration

*continue beta-blockers

*avoid precip of hypercyanotic attack
what needs to be AVOIDED in the induction of a pt with tetralogy of fallot
reduction in SVR
what agent is the preferred choice for the IV induction of a pt with tetralogy of fallot
KETAMINE
what may occur with mask induction of a pt with tetralogy of fallot
potential for decrease in SVR
what maintanence tech with tetralogy of fallot maintains SVR
ketamine + N2O
during maintenance of anesthetic on tetralogy of fallot pts what needs to be AVOIDED
VA
what type of muscle relaxant needs to be AVOIDED in a tetralogy of fallot pt
ones with histamine release
what needs to be AVOIDED in the ventilation of tetralogy of fallot pts
high inspiratory pressures and PEEP

**air embolism
what can be used in the HD management of tetralogy of fallot pts
*beta-blockers

*phenylephrine
what is eisenmengers syndrome
reversal of a L to R shunt d/t increases in pulmonary vascular resistance
when does shunt reversal occur with eisenmesengers syndrome
once the pulmonary vascular resistance exceeds systemic vascular resistance
what is the treatment for eisenmengers syndrome
*lung transplant with repair of VSD/ASD

*heart/lung transplant
what is transposition of the great arteries
failure of the spiraling of the truncus arteriosus during development
with transposition of the great arteries the aorta arises from where
the RV
with transposition of the great arteries the pulmonary artery arises from where
LV
transposition of the great arteries results in what
complete seperation of systemic and pulmonary circulation
what is required for survival with transpostion of the great arteries
VSD, ASD, patent foramen ovale or PDA
what is the mortality at 1yr without surgical tx with transposition of the great arteries
100%
what is the initial tx for transposition of the great arteries
maintenance &/or expansion of communications b/t systemic & pulmonary circulations
how is maintenance &/or expansion b/t systemic and pulmonary circulations kept with transposition of the great arteries
*prostaglandin E infusion
(maintain patency of PDA)
*balloon atrial septostomy
(increase atrial mixing)
*oxygen
(decrease PVR)
*diuretics and digoxin
(if heart failure present)
what type of surgical tx are done on transposition of the great arteries
*mustard or senning procedure (older adults)

*arterial switch (younger adults and children)
what is the mustard or senning procedure
creates a baffle of pericardium or atrial tissue that directs caval blood into the L atrium
what is the arterial switch procedure
*transect and switch the aorta and pulmonary artery

*reimplant coronaries on aorta
what must be done with IV drugs with transposition of the great arteries
must reduce dosages d/t lack of sig pulmonary circulation

(lack of pulm dilution)
what is a concern regarding inhaled drugs with transposition of the great arteries
delayed onset d/t mininal transfer to the systemic circulation
what are the goals in the anesthetic management of the pt with transposition of the great arteries
*avoid myocardial depression

*maintain high FIO2

*maintain hydration
what is truncus arteriosus
single arterial trunk overrides both ventricles
what is the survival with truncus arteriosus
very low
what is the tx for truncus arteriosus
*band pulm arteries if pulm blood is too high
*repair VSD so only LV ejects into arterial trunk
*create an artificial pulm artery w/ valve to feed the R & L PAs