Cardiology Flashcards
causes of increased pulm. blood flow
VSD large patent ductus arteriosus transposition of the great arteries truncus arteriosus tital anomalous pulmonary venous connect
CHD causes that result in obstructive lesions
severe aortic/pulm/mitral valve stenosis
coarcation of the aorta
interrupted aortic arch
hypoplastic left heart
causes of aq. heart disease - that lead to CHF
viral myocarditis
how does anemia cause CHF
increase to a high-output state
management of CHF in children
cardiac glycosides
loop diuretics
inotropic agent
digoxin - mechanism
increase efficency of Myocardial contraction and relieves tachycardia
furosemide - mechanism
reduce intravascular volume by maximizing sodium loss – leads to diminished ventricular dilation and improved function
dobutamine- mechanism
inotropic medication - given IV
when to use balloon valvuloplasty?
critical aortic and pulmonary valve stenosis
common innocent murmur at 2-7yrs
stills murmur
mid-left sternal border
sound of stills murmur
vibratory/twanging or buzzing
louder supine and when exercising
common innocent murmur at any age
pulmonic systolic murmur
pulmonic systolic murmur
upper left sternal border
blowing- high-pitched- loudes supine
louder with exercise
common innocent murmur at any age- but mainly school age
venous hum
venous hum
neck and below the clavicles
continous murmur
heard when sitting or standing
disappears if supine
ASD- classification
ostium primum
secundum
sinus venous
asd- ostium primum
lower portion
anterior mitral valve leaflet might cause mitral regurg
most common congenital hear lesion in Downs
ostium primum
ostium secundum
most common type of ASD
middle portion
sinus vinosus
high in the septum near the junction of the right atrium and superior vena cava
what are clinical features of ASD
minimal - only see them in osteum primeum
bc might develop mitral regurgitation and lead to CHF
PE for an ASD
increase ventricular impulse
systolic ejection murmur – best heard in the mid and upper left sternal borders
fixed split second heart sound
how to manage an ASD
closure by open heart surgery
vsd PE finding
holosystolic murmur LLSB
diastolic rumble at apex if pulmonary blood flow is high
EKG for VSD
if small: normal or LVH
if mod: LVH
RVH if pulm. hypertension
chest xray of VSD
if mod or large - cariomegaly and increased PVM
EKG of ASD
RAxis Deviation ,RVH, R atrial enlargement
xray of ASD
r atrial and ventricular enlargmenet
increased pul. vascular marking
patent ductus arteriosus PE
continous murmur at ULSB
machine like
brisk pulse
EKG of PDA
lvh
rvh if pulm. hypertension present
xray of PDA
cariomegaly with increased PVM
coarctation of the aorta pe
increased BP in right arm
reduced BP in legs
dampened and delayed femoral pulse
bruit left upper back
coarctation and EKG
normal or LVH
coarctation xray
rib notching
aortic stenosis PE
ejection clic
systolic ejection murmur at the base with radiation to the URSB and carotids
aortic stenosis EKG
normal or LVH
aortic stenosis xray
normal or mild cardiomegaly
prominent ascending aorta
pulm stenosis PE
ejection click
systolic ejection murmur at the ULSB
pulm stenosis EKG
RVH
pulm stenosis xray
normal
prominent main pulm artery
murmur intensity in VSD
as the sound increases the VSD is decreasing in size- as the blood is more forcefully traveling across
what happens when PVR becomes elevated in VSD
the second heart sound may be single and loud and noticible now
eisenmenger syndrome
condition in which the PVR becomes so high - that there is now a shift of R to L shunting
management of VSD
surgical closure if:
- hear dailure refractory to medical management
large VSDs with pulm. hypertension - close btw - 3-6 months
small to mod VSD - close btw 2-6 yrs
PDA
L to R shunt
– should have been closed after birth as the PaO2 rises - the ductus normally fibroses
high incidence in premis
clinical present of PDA
small - no symptoms
mod-large - CHF
wide pulse pressure >30mmHg
brisk ppulses
management of PDA
INDOMETHACIN
coarctation of the aorta
usually will be stenosis just below the left subclavian or just proximal to the ductus arteriosus
how do neonates survive the coarctation?
need to maintain a PDA to have some R to L shunting
these infants will be mild symptomatic but might develop CHF and worsen if the pDA closes
older kids with coarctation presentation
hypertension on R arm - and hypotension in the Lower extremities
femoral pulse is dampened and delayed
might lead to collateral formation - with the intercostal arteries
management of the coarcatation
IV PGE open the ductus
low dose dopa is given to maximize renal perfusion
might do surgery- but 50% might recurr
what to do if coarctation returns
balloon angioplasty
aortic stenosis and mI risk - why
increase O2 demand - and decrease perfusion - and increase demand since pumping so hard to feed the body
neonates with severe aortic stenosis - clinical
normal and then CHF at 12-14 hours of age
once PDA closes - all systemic flow must pass thru the stenosis -
aortic stenosis management
balloon valvuloplasty -
surgery - 5-10 yrs after valvuloplasty bc or recurrent stenosis or progressive insuffieciency
replace valve with either pulm valve(ross procedure) or prosthetic
pulm stenosis
might have some cyanosis - R to L shunt
management of pulm stenosis
balloon valvuloplasty if pressure gradient >35-40
non cardiac causes of central cyanosis
pulm. disease sepsis hypoglycemia polycythemia neuromuscular disease
cardiac causes of central cyanosis
tetrology of fallot transposition of great vessels tricuspid atresia truncus arteriosus total anomalous pulm. venous congestion
100% oxygen challenge test
if O2 doesnt raise despite 100% o2 then you know it is cyanotic CHD
tetralogy of fallot
most common cause of central cyanosis VSD Overriding aorta pulm stenosis RVH
tetralogy of fallot PE
systolic ejection murmur of pulm. stensosi
ekg of tetralogy
RVH
xray of tetralogy
boot shapped
transposition of the great arteries PE
no murmur
single S2
ekg of transposiion
normal or RVH
chest xray of transposition
small hear with narrow mediastinum - egg on a string
increase PVM
tricuspid atresia PE
no murmur -
single S2
if VSD systolic murmur of VSD
ekg of tricuspid
LAD, RAE, LVH
truncus arteriosus PE
single S2
systolic ejection murmur along left sternal border
truncus EKG
CVH - combined ventricular hypertrophy
xray truncus
enlarged heart
increased PVM
R aortic arch
total anomalous pulm venous connection PE
pulm ejection murmur along left sternal border
total anomalous pulm venous connection - EKG
RVH and RAE
total anomalous pulm xray
enlarged heart in older unrepaired childrean with supracardiac drainage
increased PVM a
how to increase SVR and decrease RVOT
volume infusion
systemic hypertension
valsalva
bradycardia
tet spells - what are they
sudden cyanosis and decreased murmur intensity
management of tetralogy
complete surgical repair at 4-8months
if really bad when born then might have initial procedure to improve systemic saturation and encourage pulm growth – blalock-taussig shunt
can give IV Na bicarb - to correct acidosis from prolonged hypoxia
transposition of great arteries -
they systems are parallel and need a VSD/AS/PDA
management of transposition
PGE
emergent balloon atrial septostomy
arterial switch operation
tricuspid atresia
ASD or PFO is always present
tricuspid atresia and no VSD
ventricular septum intact pulmonary atresia is also present –> therefore need PDA to be present
tricuspid atresia and VSD
L ventricle–> VSD –> pulm artery
tricuspid atresia is the only one with EKG findings remarkable for:
LAD and LVH
management of tricuspid atresia
fontan procedure - flow from the inferior vena cava is directed into the pulm arteries and means of extracardiac conduit or intra-arterial baffle or tunnel
glenn shunt
superior vena cava connected to pulm. artery
truncus arteriosum
VSD is almost always present
clinical of truncus arteriosum
CHF signs
diastolic murmur - across the mitral valve at the apex - from pulmonary blood flow that returns to the left atrium
management of truncus
CHF meds
surgery - close VSD and place homograft btween the rightventricle and pulm. artery
total anomalous pul. venous connection
there will be the return of pulm blood to the Superior vena cava - and they can only oxygenate through PDA
management of total anomalous
surgical - after diagnosis -
infective endocarditis - who gets it? what bug?
80% will be in kids w/ structural abnormalities
gram positive cocci - most common
gram negative - rare
fungal - rare unless chronically ill child
signs of infective endocarditis
murmur change/new splenomegaly hematuria splinter hemorrhage retinal hemorhage osler's node - janeway lesions roths spots - spots in retina
diagnsosis of infective endocarditis
blood culture -
ESR
rheumatoid factor will be elevated in 50%
echo- but transesophageal echo is best -
management of infective endocarditis
IV antimicrobial therapy
pericarditis - causes
infection, collagen vascular disease, uremia, inflammatory response after cardiac surgery
what is the most common cause of pericarditis
viral infection
Cozaski, echo, adeno, influenza, para, EBV
causes of purulent pericarditis
bacterial infection
staph and step. pneumoniae
symptoms of pericarditis
chest pain, intense while supine and relieved when sitting upright
friction rub
distant heart sounds
pulsus paradoxus >10mmhg reduction on systolic bP during inpiration
hepatosplenomegaly
diagnosis of pericarditis
think of it if underwent cardiac surgery and now dyspnea and fever
pericardiocentesis
ESR - elevated
management of pericarditis
antibiotics - anti-inflammatory agenet - asprin or steroid
drainage
myocarditis
common cause of sudden death in young athletes
follows URI
etiology of myocarditis
enterovirus - coxaskie bacteria (strep. pyogenes, diphtheria, staph TB) fungi - crypto/candida protozoa (typanosma cruzi (chagas )) autoimmune - SLE/rheumatic fever/sarcoid kawasaki
myocarditis PE
muffles heart sounds - resting tachy, hepatomegaly
diagnosis of myocarditis
elevated ESR
HIGH Cr
CRP
endomyocardial biopsy
ekg of myocarditis
T wave and ST changes
mangament of myocarditis
supportive
inotropic agents - diuretics - IVIG might help
dilated cardiomyopathy
ventricular dilation - and decrease cardiac function
dilated cardiomyopathy etiology
viral
mitochondrial abnormalities
carnitine defiency
nutritional deficiency – selenium and thiamine def.
management of dilated cardiomyopathy
medical management
treat underlying metab/nutrional issue
fix ALCAPA
cardiac transplant
hypertrophic cardiomyopathy
most typical: asymmetric septal hypertrophy
AD
hypertrophic cardiomyopathy pathophys
poor left ventricular filling –> LVOT obstruction – bc the mitral leaflet gets swept up into the subaortic region during systole
diagnosis of hypertrophic cardiomyopathy
LVH on EKG
echo
management of hypertrophic cardiomyopathy
calcium channel blocker- reduce LVOT
surgical myomectomy
antiarrhythmic meds
dual-chamber pacing
restrictive cardiomyopathy - etiology
amyloidosis
inherited infiltrative disorder (gauchers, fabry disease, hemosiderosis hemochromatosis
SVT- supraventricular tachy
most common dysrhythmia in childhood
AVRT
AVNRT
AVRT
retrograde conduction through an accessory pathway
AVNRT
the abnormality occurs in the different pathways within the AV node
WPW on EKG
delta waves
short P wave and then a slow rise on the QRS complex
WPW
when there is anterograde reentry
management of supraventricular tachy
vagal maneuvers or ice pack to the face iv adenosine synchronized cardioversion chronic medical management - digoxin or propanalol radiofrequency cather ablation
supraventricular tachy
rate; HR variation; P wave on EKG; predisposing factor; response to intervention
rate - >250 HR variation - none P wave- absent or abnormal axis predispose - none response - rapid
sinus tachy
rate; HR variation; P wave on EKG; predisposing factor; response to intervention
rate-
hear block or AV block
delayed or interrupted conduction of sinus or atrial impulses
ratio of atrial to ventricular impulses
1st degree av block
prolonged of the PR interval
2nd degree av block
type 1 - wenckebach – prolonged pR interval leading to failed AV conduction
type 2- abrupt failure of AV conduction without progressive prolongation of the PR interval
3rd degree av block
complete block - no conduction of atrial impulses to ventricles
etiology of av block
congenital third degree - children of moms with SLE
postsurgical av block - (especially VSD repair)
bacterial endocarditis
long qt syndrome etiology
50% AR jervell-lange-nielsen syndrome - associated with congenital deafness -
romano ward syndrome AD- not associated with deafness
drugs that prolong qt interval
TCA, erythromycin, terfenadine
diagnosis of prolonged qt
> .44sec
manage qt prolongation
b-blocker
