Flashcards in peds20 Deck (199):
def of CHF
inadequate ox delivery by the myocardium to meet the demands of the body
what do the kidneys do during CHF?
retain salt and water as an attempt to increase blood volume because the kidneys are being hypoperfused
catecholamines and CHF?
they are released to incr heart rate
how does incr pulm blood flow cause CHF?
it's just not what your heart is made to do; examples are VSD, PDA, transp of great arteries, truncus arteriosus, and total anomalous pulm venous conneciton
what obstructive lesions cause CHF?
severe aortic, pulm, and mitral valve stenosis, coarctation of the aorta, interrupted aortic arch, and hypoplastic left heart syndrome
infectious cause of CHF?
viral myocarditis (common in older kids), endocarditis, pericarditis,
evidence of pulmonary congestion
tachypnea, cough, wheezing and rales
evidence of impaired myocardial performance
tachycardia, sweating, pale or ashen skin, diminished urine output, and enlarged cardiac sillohuette on cxr
hepatomegaly and peripheral edema are evidence of what?
systemic venous congestion
late manifestations of CHF
cyanosis and shock
three types of drugs used for CHG
cardiac glycosides, loop diuretics, inotropes
how do cardiac glycosides work?
increase calcium-induced calcium release and therefore the force of contraction
example of cardiac glycoside
how do inotropes work?
increase heart contractility
examples of inoropes
how do phosphodiesterase inhib help CHF?
improve contractility and reduce afterload
balloon valvuloplasty used for what?
critical aortic and pulm valve stenosis
what percent of kids have an innocent heart murmur?
still's murmur age, location, and characteristics
age 2-7 years; mid-left sternal border; grade 1-3 systolic vibratory or buzzing; loudest supine and louder with exercise
pulmonic systolic murmur (systolic ejection murmur)
any age; upper left sternal border; grade 1-2, peaks in early systole; blowing, high-pitched, loudest supine and louder with exercise
venous hum- age, location, and characteristics
any age, but esp school age; neck and below the clavicles; continuous murmur, heard only sitting or standing; disappears if supine; changes with compression of the jugular vein or with neck flex or extension
ASD in the lower portion of the atrial septum. Often associated with cleft or division in the ant mitral valve leaflet and cause mitral regurg
ostium primum more common in what population?
ASD in the middle portion of the atral septum. Most common type of ASD
ASD high in the septum near the junction of the right atrium and SVC. The right pulm vein drains anomalously into the right atrium or SVC instead of into the left atrium
symptoms of acyanotic heart disease
minimal; incr RV impulse, systolic ejection murmur (from excessive pulm blood flow)at mid and upper left sternal borders; mid-diastolic murmur and fixed split second heart sound
how does acyanotic heart disease cause mid-diastolic filling rumble
excessive blood flow through the tricuspid valve
how does acyanotic heart disease cause fixed-split heart sound?
excessive pulm blood flow causes the the normal variation in timing of aortic and pulm valve closure with resp to be absent
high pitched holosystolic murmur at LLSB and thrill at LLSB; as the size of the VSD decreases, the intensity of the murmur increases
continuous "machinery like" murmur at ULSB; brisk pulses; diastolic rumble of blood across mitral st the apex;
phys exam fininds in coarctation of aorta
elevated BP in right arm, reduced BP in legs, delayed and dampened fem pulse; bruit left upper back
aortic stenosis murmur
ejection click; systolic ejection murmur at base with radiation to URSB, apex, suprasternal notch and carotids; thrill at URSB and suprasternal notch
murmur with pulm stenosis?
ejection click; systolic ejection murmur at ULSB
ECG findings in VSD
normal or mild LVH; RVH if pulm htn present
ecg findings in PDA
LVH; RVH if pulm htn present
ecg finding in coarctation of the aorta
normal or LVH
aortic stenosis findings on ECG
normal or LVH
pum stenosis finding on ecg
ASD finding on ecg?
right axis dev, rvh, and right atrial enlargement
small VSD prognosis?
may close spontaneously
what if VSD with 2:1 ul to systemic blood flow?
diastolic murmur of mitral turbulence (excess blood from lungs now passing through the mitral valve) heard at apex
ehn PVR exceeds SVR and shunting shifts to R to L
connects pulm art to aorta
management of PDA
indomethacin, can be closed surgically by coil embolization, thorascopic surgery, and ligation in a thoracotomy
coarctation of the aorta
narrowing of the aortic arch just below the origin of the left subclavian artery and typically at or just proximal to the ductus arteriosus
neonates with open PDA and coarctation
depend on R to L shuntthroug the PDA for perfusion of the lower thoracric and descending aorta; sx develop when the PDA closes
findings in older kids with coarctation of aorta
hypertension in right arm and bp reduced in lower extremities; radiofemoral delay
other findings in coarctation of the aorta
bicuspid aortic valve or aortic stenosis is present in half of kids (if either is present, you have systolic murmur); bruit through the coarctation may be heard at the LU back near the scapula
management of coarctation of the aorta
improve circulation to the lower body by IV prostaglandin E to open the DA, then inotropic meds; surgery but recurrence Is common so balloon angioplasty is the choice
aortic stenosis in the neonate may lead to what?
hypoplasia of the LV as a result of impaired fetal left ventricular development
initial management of aortic stenosis
balloon valvuloplasty, then surgery for aortic valve replacement (Russ procedure) after 5-10 yrs after palliative valvuloplasty bc of recurrent stenosis
aortic valve is replaced with the patient's own pulm valve
most common cardiac causes of central cyanosis
the 5 Ts: tetrology of fallot, tranposiiton of the great arteries, tricuspid atresia, truncus arteriosis, and total anomalous pulm venous connection
100% oxygen challenge test suggest cyanotic CHD when?
when PaO2 fails to rise despite administration of 100% ox
tetrology of fallot
VSD, overriding aorta, pulm stenosis, and RV hypertrophy
most common cause of central cyanosis
tetrology of fallot
murmor in tetrology of flalot?
systolic ejectrion murmur representing the pulm stenosis
what kinds of activities bring on cyanosis in a kid with tetrology of fallot?
things that decr SVR (exercise, vasodilation, volume depletion)or increase resistance through the RVOT (Crying, tachycardia)
sudden cyanosis and decr murmur intensity; caused by decr arterial ox sat, which increases resistance through the RVOT, resulting in incr R to L shunt
how does a kid deal with a tet spell?
squat; to incr venous return to the heart and incr SVR
management of tet of fallot?
surgical repair at 4-8 months old
some kids with tet of fallot who cannot undergo surgery right away get what?
palliative procedure to improve systemic saturation and encourage pulmonary growth; either modified Blalock-Taussig shunt or balloon pulm valvuloplasty
aorta arises from the RV and pulm art from the LV; in order to live, you must also have a VSD, ASD, PFO or PDA
physical exam in TGA
central cyanosis, single S2 and no murmur
management of TGA
initial management with PGE to improve ox sat by keeping the ductus patent; or emergent balloon atrial septostomy (rashkind procedure) that incr size of PFO or ASD
definitive repair of TGA
arterial switch operation; coronaries must also be incised and reimplanted
plate of tissue on the floor of the right atrium; ASD or PFO is always present; whether or not a vsd is present determines the direction of blood flow
clinical signs of pulm atresia
single S2 (if intacts ventricular septum)
ECG finding in tricsupid atresia
left axis deviation, LVH, and right atrial enlargmenet
flow from the IVC is directed into the pulm arteries; treatment for tricuspid atresia
SVC is anastamosed to the right pulm artery
treatment for tricuspid atresia
glenn shunt and then fontan
aorta and pulm artery originate from a common artery, the truncus; vsd is almost always present
pathophys of truncus
excessive blood flow to the lungs and CHF commonly develops; mixing of desat and sat blood occurs in the truncus so patients are mildly desat and sometimes cyanotic
murmur in truncus
systolic ejection mumur at the base from incr flow across the truncal vale; single S2; diastolic murmur across the mitral due to excessive pulm lood flow that returns to the LA
total anomalous pulm venous connection
pulm veins drain into the systemic venous side instead of the LA;
murmur in TAPVC
pulm murmur due to incr pulm blood flow
cardiomegaly with a snowman appearance
total anomalous pulm venous connection
most common cause of acquired heart disease in children in the US
most common cause of acquired heart disease worldwide
acute rheumatic fever
microbial infection of the endocardium (inside surface of the heart)
most endocarditis occurs in who?
80% in kids with anatomic defects of the heart; 50% of cases occur after cardiac surgery
bacteria that cause endocarditis
gram pos cocci (alpha hemolytic staph and strep)
rare causes of endocarditis
gram net and funghi
diagnosis of endocarditis
blood culture and ESR elevated
linear hemorrhages beneath the nails, seen in endocarditis
seen in endocarditis
small, raised pink or blue swollen tender lesions on the palms, soles, or pads of the toes or fingers; sign of endocarditis
small erythematous hemorrhagic lesions on the palms or soles; sign of endocarditis
ound or oval white spots seen in the retina; sign of endocarditis
found in 50% of patients with endocarditis
how to see vegetations?
transesophageal echo is more sens than transthoracic echo
management of endocarditis
IV anitbmicrobials fr 4-6 weeks; not a medical emergency, so therapy can be withheld until you do cultures
who should get antibiotic prophylaxis for endocarditis for surgery?
al patients with structural heart disease except secundum ASD; all post-op cardiac surgery patients for 6 months; all post-op cardiac surgerypatients for an indefinite pd of time if any hemodynamic residua of the lesion remain
inflamm of the pericardial space
causes of pericarditis
infection, collagen vascular disease, uremia, and inflamm response after cardiac surgery
most common cause of pericarditis in kids
viruses like coxsackievirus, echovirus, adenovirus, influenza, parainfluenza, and EBV
usually caused by bacterial infection like staph aureus and strep pneumo
patients with purulent pericarditis have a high incidence of what?
occurs in up to 1/3 of patients whose pericardium has been opened for surgery; thought to be an autoimmune response to viral infx
possible consequence of pericarditis
chest pain in pericardits?
most intense when supine and relieved when sitting upright
physical exam findingsin pericarditis
friction rub, distant heart sounds if effusion is large, pulsus paradoxus, hepatomegaly
pericarditis or MI
abnormally large decrease in systolic bp during inspir
ecg in pericarditis MAY show
ST changes or low-voltage qrs complexes in patients with pericardial effusion
treatment for bacterial or viral pericarditis?
antibiotics or steroids/aspirin
common cause of sudden death in young athletes
etiology of myocarditis
viruses, esp enterovirus like coxsackievirus; bacteria, fungi, protozoa, autoimmune disease, kawasaki disease
bacteria that cause myocarditis
diptheria, strep pyogenes, staph aureus, tuberculosis
symptoms of myocarditis
resting tachycardia and muffled heart sounds;
labs in myocarditis
elevated ESR, creatinine kinase MB fraction, and CRP
management of myocarditis
largely supportive; use of ionotropes, etc. as needed; heart transplant as last resort
prognosis of myocarditis
variable; mortality 10-20% and is esp high in young infants and those with ventricular dysrhythmias
most common cause of dilated cardiomyopathy
other causes of cardiomopathy
viral myocarditis, mitochondrial abnormalities, carnitine def, nutritional def (selenium and thiamine), hypocalcemia, chronic tachydysrhythmia, anomalous origin of left coronary artery from the pulm artery (ALCAPA), meds (doxorubicin)
eval of cardiomyopathy
viral serologies and serum carnitine
ALCAPA can cause what?
LVH in the absence of any disease known to cause it; most typical finidng is asymm septal hypertrophy
inheritance of hypertrophic cardiomyopathy
aut do n most cases
most common cause of sudden death in athletes
phys exam findings for hypertrophic cardiomyopathy
harsh systolic ejection murmur at the apex that is accentuated with maneuvers that reduce LV volume like valsalva or standing (by reducing LV volume, they worsen the outflow obstruction)
findings on ECG for hypertrophic cardiomyopathy
LVH, ST-seg and T wave changes, LAD and abnormally deep and wide Q waves in the inferior and lateral leads
management of hypertrophic cardiomyopathy
only treat patients w symptoms; beta blockers of CCBs reduce the LVOT obstruction; surgical myomectomy; antiarrhythmic medications; dual chamber pacing; participation in competitive sports prohibited
rigid ventricular walls that impair normal diastolic filling
etiology of restrictive cardiomyopathy
amyloidosis,inherited infiltrative disorders like Fabry disease, Gaucher disease, hemosiderosis, hemochromatosis
physical exam findings in restrictive cardiomyopahty
elevated central venous pressure leads to edema, hepatomegaly, and ascites
management of restrictive cardiomyopathy
reduce CVP with diuretics and improve diastolic compliance with beta blockers and CCBs
most common dysrhythmias of childhood
supraventricular tachy (most common), then heart block, and long QT syndrome
AV re-entrant tachycardia
retrograde conduction through an accessory path leads to SVT
AV node reentrant tachycardia
conduction abnormality occurs in diff pways within the AV node itself
Wolf-Parkinson white syndrome
when anterograde conduction occures through a bypass tract between the atria and ventricles
WPW associated with what?
sudden cardiac death
WPW on ecg?
delta wave (upslope of QRS with a short PR)
management of SVT
vagal maneuvers, IV adenosine, synchronized cardioversion, chronic med management, radiofrequency catheter ablation
vagal manuever that helps convert SVT to sinus rhythm
ice pack on face
primary med used to convert SVT to sinus rhythm
chronic medical management of SVT
digoxin or propanolol
radiofrequency cathether ablation
used to destroy the accessory pway in SVT
delayed or interrupted conduction of sinus or atrial impulses to the ventricles
first degree heart block
prolongation of the PR interval
second degree AV block
type 1 and type 2
type 1 second degree AV block
aka wenkebach; progressive prolongation of the PR interval leading to failed AV conduction
type 2 second degree AV block
abrupt failure of AV conduction without progressive prolongation of the PR interval
third degree av block
congenital third-degree block associated with what patient pop?
children born to mothers with SLE
post-surgical AV block
as a result of cardiac surgery
what infection may be associated with AV block?
treatment of asymp AV block
why is long QT bad?
increases the risk of lethal ventricular arrhythmias known as torsades de pointes
different inheritance patterns of long qt syndrome
autosomal recessive is jervell-lang-nielsen syndrome; autosomal dom is romano-ward syndrome
which cause of long qt is associated with congenital deafness
examples of drugs that prolong qt interval
phenothiazines, tricyclic antidepressants, erythromycin, tefenadine
most common cause of chest painin kids
rapid heart rate w absent p waves
difference between vesicles and pustules
vesicles are fluid filled and pustules are purulent filled
nodule filled with expressible material
cutaneous elevations caused by dermal edema
linear erosions into the epidermis caused by fingernail scratches
linear cracks into the dermis
configurated in a circle
in half circles
generalized, acral (hands, feet, buttocks), confined to a dermatme
how can we identify fungal hyphae
add 10% koh
how do we identify scabies
examine under a microscope looking for mites, eggs, or feces
absorption through the skin of a kid
same as through the skin of an adult except premature infants because they have a thinner stratum corneum
salicylic acids, urea, alpha hydroxy acids, and retinoic acid
destructive therapies (for warts, molluscum contagiosum)
high dose salicylic acid, podophyllin, 5-FU, cryotherapy, electrotherapy, and laser therapy
only low dose corticosteroids should be used where?why?
face and groin because these areas have thinner skin
local side effects of steroids
acne, hirsutism, folliculitis, striae (esp in axilla or groin), hyper- or hypopigmentation, atrophy, ecchymoses and telangiectasias, tachyphylaxis
immunomodulator used for atopic dermatitis
one to five percent sulfur
formulated with other meds, used for acne
used for eczema and psoriasis
inflamm of the epidermis and superficial dermis secondary to direct contact with the skin by a sensitizing substance
two types of contact dermatitis
allergic contact dermatitis and primary irritant contacst dermatitis
allergic contact dermatitis
T cell mediated
common causes of allergic dermatitis
poison ivy, oak or sumac; nickel containing jewelry and belt buckles; topical lotions and creams, perfumes, soap
clincial features of allergic dermatitis
erythematous papules and vesicles
treatment of allergic dermatitis
primary irritiant contact dermatiits
substance irritates the skin (not an allergic reaction); reaction is dose-dependent unlike allergic dermatitis
most common type of primary irritant dermatitis
secondary infection with what on diaper dermatitis?
clinical features of diaper dermaitis
erythema with papules on the upper thighs, buttocks, and genitourinary area WITHOUT involvement of the inguinal creases
involvement of the inguinal creases may suggest what
seborrheic dermaitits predominantly affects who?
infants and adolescnets
cause unknown maybe due to a yeast that lives in areas that overproduce sebum;
clinical features of seborrheic dermatitis
red scales and crust in areas with high numbers of sebaceous glands (scalp, face, chest, groin); skin lesions may be greasy
aka cradle cap dermatitis limited to the scalp
management of seborrheic dermatitis
low potency topical steroids, anti-fungals, sulfur, zinc, or salycilic acid shampoos
uncommon before 5 years old but extremely common in late childhood and adolescence
clinical features of pityriasis rosea
malaise/ache, then solitary large red lesion (herald patch) on the trunk or upper extremities present for 1-30 days; THEN oval red macules and papules erupt for 3-6 weeks from chin to midthigh in christmas tree distrib
are pityriasis rosea lesions pruritic?
in about 50% of cases
managemnet of pityriasis rosea
topical or systemic antihistamines; exposure to UV light may shorten the disease course