Cardiovascular PowerPoint Flashcards
in utero what heart side is dominant
right
in utero why does the blood bypass the lungs
because it gets O2 from the placenta
what utero structures help shunt blood away from lungs
patent ductus arterosis
patent foramen ovale
normal blood flow
vena cava
right atrium
right ventricles
pulmonary artery
lungs
pulmonary veins
left atria
left ventricle
aorta
in children how is the heart compared to the body
larger compared to rest of body
heart muscle develops until
5years
under 5 years how does the child increase CO
increase HR
stroke volume
the volume of blood ejected by the ventricle with each contraction
3 factors affecting stroke volume
preload
afterload
contractility
preload
the end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions
afterload
the amount of resistance the heart must overcome to open toe aortic value and push the blood volume out into the systemic ciculation
some things to assess
skin color
cap refil
heart rate
blood pressure
JVD
thrills
murmur you can feel
S1
beginning of systole, AV valves close
S2
end od systole, closure of semilunar values
S3
normal in children
related to rapid filling of ventricle
S4
abnormal
heard late in diastole or early systole, heard in CHF and with decreased ventricular compliance
CCHD
pulse ox on pre ductal and post ducatal
pre: right hand
normal is >98% with less than 2-3% change
most defects occur during the first __ week of gestaion
8
congenital heart defects are categorized by their underlying path into 4 categroesi
increased pulmonary blood flow (acyanoitci)
decreased pulmonary flow (cyanotic)
obtructive
mixed
what is the first indication of congenital heart defect
murmur
a murmur indicates
turbulent blood flow with high pressure to get through a narrowed valve or through a shunt
increased pulmonary blood flow clinical manifestations
tachypnea, tachycardia, murmur, CHF, poor weight gain, diaphoresis, edema
decreased pulmonary blood flow clinical manifestations
cyanosis, hypoxic spells, poor weight gain, polycythemia
obstruction clinical manifestations
diminished pulses, poor color, delayed capillary refill, decreased urine output, CHF with pulmonary edema
mixed defects clinical manifestations
cyanosis, poor weight gain, pulmonary congestion
increased pulmonary blood flow
PDA
ASD
VSD
PDA
ASD
VSD
class
increased pulmonary blood flow
(acynanotic)
increased pulmonary blood flow cause the blood to flow to the
lungs instead of the body
PDA
- what is it
communication between left pulmonary artery and descending arota
pulmonary artery is a lower pressure system so oxygenated blood flows into the pulmonary artery
when does the PDA close functionally
12-24 hours
when does the PDA close structurally
2 weeks then turns into a ligament
PDA accounts for what percent of all infants with congenital heart disease
5-10%
PDA clinical manifesations
may be asymptomatic
dyspena
tachypnea
tachycardia
full bounding pulses
intercostal retractions
poor growth
murmur (KNOW THE TYPE)
PDA murmur claissifcation
machinery murmur during systole and diastole and a thrill in the pulmonary area
PDA have high risk for
frequent respiratory infections and pneumonia
PDA how will the left ventricle look
hypertrophic
clinical therapy of PDA
how to close
cardiac Cath by obstruction device
medication for PDA closure
IV Ibuprofen or indomethacin
- cannot be used if CHF is present
PDA prognosis
no long term sequelae if treated before pulmonary vascular disease
ASD what is it
opening in the atrial septum which permits left to right shunting of blood
ASD clinical manifestation s
- small to mod
asymtomatic
ASD clinical manifestations
- large
CHF, easy tiring, poor growth, mumur
large ASD murmur
soft systolic ejection murmur with fixed wide splitting of S2 may be heard
ASD what will the right ventricle look like
dilated
what is the most common cardiac defect
VSD
VSD what is it
opening in the ventricular septum results in left to right flow and then increased pulmonary flow
VSD small clinical manifestations
no symptoms
VSD mod to large
CHF, poor growth, decreased exercise tolerance, increased number of pulmonary infections
VSD murmur
systolic 3-4 left intercostal space
large vsd echo appearance
enlarged heart and pulmonary vascular margins on chest radiograph
post op Cath lab what to assess
vital signs, bleeding, infection, pressure dressing
decreased pulmonary blood flow
let of fallot
tet of fallot
dercreased pulmonary blood flow
(cyanotic)
4 defects of tet of fallot
stenosis of the pulmonary outflow tract or valve
right ventricular hypertrophy
ventricular septal defect
overriding aorta
let of allot how will the chest radiography show
BOOT SHAPTED HEARt
can metrology of fallout be dented by fetal echo
yes
TOF the child becomes hypoxic and cyanic as the
ductus artetosis closes
TOF s/s
polycytothemia
hypoxic spells
metabolic acidosis
poor growth
clubbing
exercise intolerance
systolic murmur
won’t eat well
delayed cap refil
right hand is different than left hand
what position do TOF toddlers go into
squat (knee to chest) to decreased the return of systemic venous blood to the heart = tetspells
how does squating help the TOF
increases peripheral vascular resistance and thus decreases magnitude of the right to left shunt across the VSD
what is the management for tetspells
place child in knee to chest
maintain calm enviornment
give O2
morphine or verssed
IV fluids
in obstructive lesions what type of blood flow is impared
systemic
examples of obstructive
COA
HLHS
COA
HLHS
type
obstructive
COA
narrowing of the descending aorta near the ductus arterioles or left subclavian artery
COA manifestations
many are asymptomatic
lower blood pressure in legs and higher in arms, neck and head
brachial and radial is bounding
femoral and leg pulses are weak
newborn with COA and severe constriction may have
cyanosis of lower extremities, heart failure, and shock as the PDA closes
chest radiography of COA will be
cardiomegaly, pulmonary venous congestion, indentation of the descending aorta
what med is given to newborns with COA
prostaglandin E to reopen the ductus arterosis
what might be a complication of COA
HTN and aneurysms
what is HLHS
mitral and aortic valves are either absent or stenosed along with a small left ventricle and aorta
where doe HLHS need to be born
level 4 NICU
s/s of HLHS
progressive cyanosis and signs of CHF
diminished pulses
pale color
delayed cap refill
decreased UO
no murmur
CXR HLHS
cardiomegaly and increased pulmonary vascular congestion
what med will you give for HLHS
PGE to keep PDA
tx for HLHS
transplant
mixed issues
TGA
TGA
mixed
TGA what is happening
pulmonary artery is the outflow tract for the left ventricle and the aorta is the outflow tract for the right ventricle
- pulmonary artery and aorta are switched
what do we need for survival of TGA
PDA
- so give PGE
in TGA does cyanosis improve with oxygen
no
CXR with TGA
egg shaped
tx of TGA
arterial switch
what is a complication of surgery
infective cardidis or endocarditis
what is Kawasaki syndrome
acute febrile systemic vascular inflammatory disorder that affects the small and midsize arteries including the coronary arteries
what is the leading cause of acquired heart. disease in children
Kawasaki
cause of Kawasaki
unknown but is thought to be an infectious trigger than leads to an autoimmune response
3 stages of kawaksai
acute
subacute
convalescent
acute Kawasaki
fever (5 days) >39
conjunctival hyperemia
cervical lymph node enlargement
strawberry tongue
cracked lips
rash on hands and face and trunk
subacute Kawasaki
no fever
cracking skin (lips, fingers, toes)
coronary artery aneurisms
treatment of Kawasaki
IVIG
- 2g/kg start slow
aspirin
what should we monitor for in Kawasaki
coronary artery answeusms
4 main cardio drugs
lasix
o2
dig
ACEI
s/s of dig tox in children
N/V
will still have blurry vision but may not report
what is cardiomyopathy affecting
the hearts muscle
what is the most common cardiomyopathy
dilated
dilated cardiomyopathy
enlargement of all cardiac chambers
systolic dysfunction
complication of dilated cardiomyopathy
blood clots
increase risk for embolism
treatment of dilated cardiomyopathy
CHF
- diuretics
- ACEI
- dig
hypertrophic cardiomyopathy
diastole dysfunction
risk of sudden death in young athletes
thickened left ventricular wall
tx for hypertrophic cardiomyopathy
beta blockers
calcium channel blockers
cardioverter
hypovolemic shock
clinical state of inadequate tissue and organ perfusion resulting from inadequate blood or plasma volume in the vascular space
s/s of hypovolemic shock
pale
cold
diaphoretic
increase hr
thready pulse
no blanching
what antibiotic class is dangerous to kidney
mycin
what tells us there is perfusion
UO
