Transcript Cardiology Board Review - LSU School of Medicine

Cardiology Board Review
August 30th, 2011
Test Question
• The Saints will win the Superbowl this year.
A. True
B. False
CARDIAC HISTORY AND EXAM
Cardiac History
• Infants
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Gestation
FHx
Neonatal status
Growth and development
Feeding patterns
• Children
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Presence of palpitations
Chest pain
Lightheadedness or syncope
Activity level
Cardiac Exam
• Observation
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Respiratory distress?
Central cyanosis?
Clubbing?
Syndromic appearance?
• Palpation
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Hyperdynamic precordium?
Displaced PMI?
HSM?
Distal pulses equal? Bounding?
• Ausculatation
Heart Sounds
•S1: AV valve closure
•S2: Aortic and
pulmonary valve
closure (split)
•A2
•P2 (“hangout”
time)
•S3: rapid filling of
the ventricles
•Normal in kids!
•S4: pathologic,
heard with stiff
ventricles
Murmurs
Intensity
Placement in cardiac cycle
• Grade 1: Barely audible
• Grade 2: Audible and
constant
• Grade 3: Loud without thrill
• Grade 4: Loud with thrill
• Grade 5: Heard with
stethoscope just touching
the chest
• Grade 6: Heard with
stethoscope off the chest
• Systolic murmurs
– Pansystolic: begin with the
first heart sound
– Ejection: begin after the first
heart sound, have crescendodecrescendo quality
• Diastolic murmurs
– Immediate
– Early or medium
– Late
Question #1
• Which of the following accurately describes the
Still murmur?
– A: Mid-systolic murmur of low intensity heard at the
base of the heart, in the axillae, and over the back
– B: Systolic or diastolic murmur heard in the
infraclavicular region (usually right sided); disappears
when the patient is lying down
– C: Systolic murmur best heard above the clavicles, due
to turbulence in the carotid artery
– D: Musical or vibratory quality at the mid-to-lower
sternal border and toward the apex
– E: Loud continuous “machine-like” murmur
Innocent Murmurs
• Uniform characteristics
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Early systolic ejection
Short duration
Low intensity (grade 1&2)
Vibrating or musical quality
• Examples
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Still murmur
Venous hum
Supraclavicular bruit
PPS (peripheral pulmonary artery stenosis)
Pathologic Murmurs
• Longer and louder
• All diastolic (except venous hum) and pansystolic
murmurs are pathologic
• Systolic ejection murmur
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Ejection click?
Is S2 widely split?
Does the S2 split move? Normally?
Hyperdynamic precordium?
Distended neck veins?
Peripheral pulses normal?
CONGENITAL HEART DISEASE IN
NEONATE AND YOUNG INFANT
Clinical Presentations
• Recognize dysmorphic features as increased risk
for CHD
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Trisomy 21→ endocardial cushion defect
Trisomy 18→ VSD
Fetal alcohol syndrome→ ASD, VSD
22q11 microdeltion→ interrupted aortic arch,
Tetralogy of Fallot, truncus arteriosus, atrial or
ventricular septal defects, vascular rings
– 45 XO→ bicuspid aortic valve (16%), coarctation of
aorta (11%)
Clinical Presentations
• Bicuspid aortic valve
– Evaluated every 2 to 3 years
– 70% develop some degree of stenosis or
insufficiency by age 30
– Will require catheter-based or surgical
intervention at some point
Clinical Presentations
• Most have 1 of 4 presentations:
– 1) Asymptomatic murmur
– 2) Cyanosis (often without murmur)
– 3) Gradually progressing symptoms of heart failure
– 4) Catastrophic heart failure and shock
Asymptomatic with a Murmur
• Caused by regurgitant valves (mitral or
tricuspid) or by lesions producing turbulence
in a great artery (PS, AS, nonphysiologic
peripheral pulmonary stenosis, supravalvular
AS)
• Systolic murmur that obscures S1 is probably
VSD or AV valve regurg
Asymptomatic with a Murmur
• ASD = fixed split S2 (increased flow across the
pulmonary valve)
• Pulmonary stenosis = systolic click, heard best at
left sternal border, radiates to back and axilla
• Aortic stenosis = ejection click (does not change
with position), heard best at RUSB with radiation
to neck
• PDA = continuous “machinery” murmur, loudest
at left infraclavicular area
• VSD = holosystolic (if small, high-pitched and
heard along sternal border)
Asymptomatic with murmur
• PDA
– For preterm, can cause volume overload of right
heart
– Hyperdynamic precordium and wide pulse
pressure
– Dx by echo
– Treat with indomethacin x 3
– If fails to close, surgical ligation
Asymptomatic with murmur
• VSD
– For moderate-to-large, systemic pressure in right
ventricle leads to systemic pulmonary pressure
• CHF evolves over first 1 to 2 postnatal months
– Most surgical repair is at 4 to 6 months
– If the normal decrease in pulmonary vascular
resistance does not occur→ no left-to-right shunt→
could develop Eisenmenger’s and irreversible
pulmonary vascular changes→ now right-to-left shunt
(right heart failure, valve dysfunction, arrhythmias)
Question #2
• A 6-hour-old term male infant develops severe
cyanosis, but has no murmur on cardiac
ausculatation. He is in no apparent distress, and
CXR reveals prominent pulmonary vascular
markings.
• The next MOST appropriate step is:
A.
B.
C.
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E.
Start oxygen via nasal canula
Prostaglandin infusion
Atrial septostomy in cath lab
Echocardiogram
IV Furosemide
Cyanotic CHD
• Transposition of the
Great Arteries (TGA)
– Early severe cyanosis
(hours after birth)
• Oxygenated pulmonary
venous blood is unable to
reach systemic circulation
• Prostaglandin E1 given to
keep ductus open
• Balloon atrial septostomy
to ensure atrial-level
communication prior to
anatomic correction
Cyanotic CHD
• Pulmonary valve atresia
– Presents with early
severe cyanosis once the
ductus starts to close
– Start prostaglandin!
• Ebstein malformation
– Apical displacement of
the tricuspid valve
– Right to left shunting
(through PFO) results in
↓pulmonary blood flow
TGA
Ebstein’s
Pulm atresia
Cyanotic CHD
• Most commonly, the presence of serious CHD
is heralded by the identification of cyanosis in
an infant who is not in respiratory distress
(“happy cyanosis”)
Cyanotic CHD
• Tricuspid atresia
– Sytemic venous return
passes through PFO to LA
and LV where it mixes with
oxygenated blood entering
the LA
– The large single LV
conducts blood into both
great arteries
– VSD
• Large = minimal cyanosis
• Small = a loud murmur
• Absent = clinical cyanosis
Cyanotic CHD
• Total Anomalous
Pulmonary Venous
Connection
– PFO/ASD allows blood to
enter the left heart
– If pulm. vein connection
is above the diaphragm,
there is significant
volume load on the right
side of the heart, ↑
pulm blood flow, and
minimal cyanosis
Cyanotic CHD
• TAPV can be difficult to distinguish from ASD
– A palpable sternal lift, wide and fixed splitting of
S2 (due to RV overload), a pulmonary flow
murmur, a tricuspid valve diastolic flow rumble,
and tachypnea caused by pulm edema
– Only difference is presence of cyanosis
• When connection is below the diaphragm
– Infants are ill in newborn nursery with severe
pulm edema, pulm HTN, and cyanosis
Cyanotic CHD
• Truncus arteriosus
– Dilated aorta overrides a
large VSD
– Well developed PA arises
from aorta
– Mixing occurs in the
great artery
– Minimal cyanosis and no
significant murmur
Cyanotic CHD
• S2 is loud due to anterior position of truncal
aortic valve
• Ventricular lift is always palapable
• Ejection click (or multiple clicks) caused by a
valve that can have as many as 6 leaflets
• Commonly present with failure to thrive
several months after birth
Cyanotic CHD
• Review: Admixture lesions
– Tricuspid atresia, TAPV, truncus arteriosus
• Absence of pulmonary stenosis leads to minimal
cyanosis
• Sometimes transient cyanosis on first postnatal day
– Pulse ox below 95% are never normal in otherwise
healthy-appearing infants after the first 6
postnatal hours
Cyanotic CHD
• Hyperoxia test
– Cyanosis typically present with sats ≤ 85%
– Place the patient in a high-oxygen atmosphere
(FiO2 near 1.0)
– No increase in sats or PaO2 (≥150), cyanotic
congenital heart disease should be considered
Question #3
• A 4-month-old infant with unrepaired congenital heart
disease has had fever and URI symptoms since last
evening. Her mother brings her to clinic, and on
physical exam the patient is crying and unconsolable,
has marked cyanosis, a decrease in the loudness of her
murmur, and deep, rapid breathing.
• Of the following, the next MOST appropriate step is:
A. Echocardiogram
B. IVFs
C. Sedation with Morphine
D. Acetaminophen
E. IV Furosemide
Cyanotic CHD
• Tetrology of Fallot
– Usually are acyanotic at
birth, but often have
systolic murmurs
– If pulm atresia or severe
pulm stenosis, murmur
is less obvious but
cyanosis is severe
• Exception is Tet with pulm
atresia and multiple
aortopulmonary collateral
vessels→ prevent
cyanosis, continuous
murmur heard
throughout the back
VSD, pulm stenosis, overriding aorta, RVH
Cyanotic CHD
• Hypercyanotic spells (“tet spells”)
– Unusual in newborn period, but can happen any time
in an unrepaired tet
– Intense cyanosis develops rapidly
– Sudden decrease in loudness of murmur caused by ↓
systolic flow through the RV outflow tract
– Deep, rapid respiratory pattern
– Calming the infant (with or without sedation) may
resolve the spell
Cyanotic CHD
• Prognosis for TOF
– Once infant develops progressive cyanosis, surgical
correction is indicated
• Elective repair in first postnatal year
– Surgical survival of 95%
– However, 10% of neonates requiring bypass surgery
have some element of neurodevelopmental delay or
cognitive/school performance abnormality
– Speech and behavior disorders are common among
those who undergo neonatal heart surgery
Cyanotic CHD
• Polycythemia
– Desaturated arterial blood can cause increased
erythropoetin secretion
– Increased blood viscosity
– Risk for thrombosis to lungs, kidney, or brain
– Risk for cerebrovascular accident
• Anemia
– Chronic cyanotic heart disease pts. Are at risk for
cerebrovascular accident due to paradoxic emboli and a
relative anemia
– Iron deficiency in the presence of polycythemia poses a
greater risk for stroke
CHD with progressive heart failure
• Too much pulmonary blood flow or too little
systemic blood flow
• When pulm vascular resistance falls, signs and
symptoms start
– Tachypnea, sweating, difficulty feeding, FTT, gallop
rhythm, hepatomegaly
• Left-to-right shunt via VSD, atrioventricular septal
defect, or PDA causes pulm overcirculation
• Most diseases causing heart failure in infants can
be treated surgically as soon as signs develop
Question #4
• A 3-week-old infant presents to ER with
tachypnea, mottled gray skin, poor perfusion,
decreased peripheral and central pulses, a gallop
rhythm and hepatomegaly. CXR shows
cardiomegaly. You suspect left heart obstructive
disease and order prostaglandin.
• The MOST appropriate next step is:
A.
B.
C.
D.
E.
NS bolus 20ml/kg
Electrocardiogram
Start oxygen via nasal canula
Captopril 0.01mg/kg
Place patient in knee-to-chest position
CHD presenting as shock or
catastrophic heart failure
• Critical coarctation of the aorta, interrupted
aortic arch, critical aortic valve stenosis,
hypoplastic left heart syndrome
– Inadequate left heart development compromises
cardiac output
CHD presenting as shock or
catastrophic heart failure
• Potential for catastrophic deterioration due to
inadequate systemic flow is greater in these
lesions as the ductus undergoes spontaneous
closure
• Oxygenated blood from the lungs is diverted
across an atrial-level communication into right
ventricle
• Mixing in right atrium→ increased sats of right
heart blood→ minimizes the appearance of
cyanosis
CHD presenting as shock or
catastrophic heart failure
• In newborn nursery
– A single and loud S2
– Increase in RV activity on precordial palpation
– Minimally abnormal postductal pulse ox
– Decreased femoral pulses not present because
ductus is still large
CHD presenting as shock or
catastrophic heart failure
• Check pre- and post-ductal sats
– A postductal sat above 96-97% rule out a
completely ductal-dependent left heart
obstruction
– High sats can occur in the setting of coarctation of
the aorta
CHD presenting as shock or
catastrophic heart failure
• Often present after discharge due to ductal
patency
– As ductus closes, decreased systemic blood flow,
oliguria, acidosis, pulmonary edema, and heart
failure
– May mimic sepsis (tachypnea, mottled skin, poor
perfusion)
– Critical clues: a gallop rhythm and marked
hepatomegaly or cardiomegaly
CHD presenting as shock or
catastrophic heart failure
• If suspect critical coarc or HLH, prostaglandin
should be started immediately
• EKG and echo are part of evaluation for
patient with possible cardiogenic shock
• Fluid resuscitation as well as respiratory and
inotropic support are essential treatments
Follow-up for Coarc
• Recoarctation can occur as child grows
• Higher incidence of hypertension
– Frequent BP measurements by pediatrician
Question #5
• A 4 week old infant born at term without complications
presents with poor feeding. He ate well for the first 3
weeks after birth and gained weight appropriately. For the
past week, however, Mom reports that he appears hungry
but fatigues with feeding (now taking twice as long to
feed). He breathes fast during his feedings and stops
frequently to “catch his breath.” Of the following, what is
the most likely additional finding in this infant?
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A. Lobar consolidation on CXR
B. Lipid laden macrophages on BAL
C. Elevated BNP
D. Positive RSV
E. Posterior esophageal indentation on barium swallow
HEART FAILURE
Definition
• HF results when cardiac output is insufficient
to meet the metabolic demands of the body
• Triggers of HF in children:
– Excessive preload
– Excessive afterload
– Abnormal rhythm
– Decreased contractility
Pathophysiology
Clinical Manifestations
Infants
• Feeding difficulties
– Volume and duration
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Increased fatigability
Mild to severe retractions
Tachypnea/ dsypnea
Grunting
Tachycardia
Gallop rhythm (S3,S4)
Hepatomegaly
Older Children
• Exercise intolerance
• Somnolence
• Anorexia
• Cough/wheezing
• Crackles
• Gallop rhythm
• Hepatomegaly
• JVD
• Peripheral edema
Pulmonary Edema
Common Causes- Excessive Preload
• L R shunts at the ventricular level
– VSD, PDA
– Present at 2-3 mos: pulmonary vascular
resistance pulmonary blood flow
pulmonary venous return to the L atrium
(excessive preload) cardiac filling pressure
myofiber stretching and decreased contractility
(HF)
Common Causes- Excessive Preload
• AVM
– Divert blood from higher-resistance capillary beds
to low-resistance venous beds excessive venous
return increased ventricular filling pressure (HF)
• Valvular regurgitation lesions
– Most common mitral or aortic regurgitation
Common Causes- Excessive Preload
• R-sided volume loading can also HF
– Rarely causes HF early in life
• R ventricle highly compliant, so can accommodate more
volume without increasing filling pressures
– Examples:
• Large ASD
• TAPVR
• Pulmonary regurgitation
Common Causes- Excessive Afterload
• Patients present in first postnatal week:
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R
L
Normal Heart- Diastole
R
L
Heart with Excessive AfterloadDiastole
Increased filling pressures and decreased gradient b/t ventricle and aorta at
end- diastole inadequate coronary blood flow ischemia hypertrophy,
remodeling HF
Common Causes- Excessive Afterload
• Examples:
– Mitral stenosis
– Aortic stenosis
– Coarctation of the aorta
Common Causes-
Contractility
• Cardiomyopathy (HF presenting feature)
– Dilated
• Impaired systolic and diastolic function
• Causes:
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Idiopathic
Infection (myocarditis)
Operative injury
Chemo (anthracyclines)
Metabolic/ degenerative diseases
Common Causes-
Contractility
• Cardiomyopathy (con’t)
– Restrictive
• Abnormal diastolic function
• Causes:
– Idiopathic
– Infiltrative or storage diseases (hemochromatosis, Pompe dz)
– Hypertrophic
• Not usually associated with pediatric HF
Common Causes- Arrhythmias
• Tachycardia- related diseases (SVT)
– Decreased filling time Decreased CO HF
• Bradycardia- related diseases
– Left ventricle enlarges to accommodate larger
SV significant chamber dilation HF
Evaluation
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Pulse oximetry
12-lead EKG
CXR
Echocardiogram
HF biomarkers
– BNP
• Released in response to atrial stretching
• Sensitive marker of cardiac filling pressure/ diastolic
dysfunction
Evaluation
• HF Biomarkers
– BNP (con’t)
• Can distinguish b/t primary respiratory and cardiacinduced tachypnea
– CRP
– TNF-alpha
• Both correlate positively with worse outcome in HF
Question #6
• What is the role of ACE inhibitors in managing
HF?
– A. Preload reduction
– B. Afterload reduction
– C. Sympathetic inhibition
– D. Increased contractility
– E. Increased preload
Management
Prognosis
• Too little is known about HF risk assessment in
children to allow for confident statements
regarding response to treatment and
prognosis
• There is a need for studies of “standard” HF
treatments and surrogate end points
– Rate of weight pain
– Length of hospital stay
– Surgical morbidities
ARRHYTHMIAS
Basic Principles
• Abnormality in regular heart conduction and rate
• Spectrum of severity
– Benign
• PAC
• PVC
– Malignant
• Atrial
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SVT
Atrial ectopic tachycardia
A. flutter
A. fibrillation
• Ventricular
– V. tachycardia
– V. fibrillation
Clinical Manifestations
Infants
Children/ Adolescents
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• Palpatation
Pallor
Diaphoresis
Respiratory distress
Poor feeding
Diminished perfusion
CHF
Shock
– Rapid, strong or irregular
heart rate
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Shortness of breath
Dizziness
Light-headedness
Syncope
Premature Atrial Contractions
Premature Ventricular Contractions
•Wide QRS
•T wave in opposite direction to the QRS
•Dissociation from the P wave
•Full compensatory pause
Supraventricular Tachycardia
•2 peaks in presentation: 0-3 mos, 8-10 yo
•Narrow QRS tachycardia
•Usually without visible P waves
•Rate varies with age
•Infants: rate≥ 220 (270)
•Children: rate≥ 180 (210)
Treatment of SVT
• Acute management
– Vagal maneuvers
– Adenosine
• Transient complete AV block
– DC cardioversion
• Chronic management
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B-blocker (propranolol, atenolol)
Digoxin
Flecanide, sotalol, amiodarone
Radiofrequency catheter ablation
Wolff-Parkinson-White
•Short PR interval
•Delta wave
•Prolongation of the QRS
•Predisposes to SVT
Ventricular Tachycardia
•Wide complex tachycardia
•AV dissociation of P waves
•Associated with hemodynamic
compromise
Long QT Syndrome
•Must “correct” for patient’s HR: QTc=QT/Sq root
of RR
•QTc≥ 450 msec suggestive, QTc≥ 470 msec
abnormal
•Associated with development of torsades de
pointes
Torsades de Pointes
INFECTIVE ENDOCARDITIS
Definition and Epidemiology
• Definition: Inflammation of the valvular or mural
endocardium, caused by microorganisms
(bacteria or fungi), involving either the heart or
the great vessels
• Epidemiology:
– Rare diagnosis, but ?increasing
• Number of cases of ARF decreasing, but number of patients
living beyond infancy with CHD increasing
– 90% of cases occur in individuals with heart disease
• Increased use of invasive procedures in N/PICU are putting
structually normal hearts at risk
Pathogenesis
• Damage to endothelium (or foreign materal)
exposed fibronectin at the site of injury
activation of the clotting cascade and fibrin
deposition delivery of microbes to the clot by
blood stream original nidus grows into a
vegetation valve destruction/ HF/ embolization
• Gram positive cocci most likely pathogens
– Predilection for fibronectin
– S.viridans, S.aureus, S. epidermidis, B-hemolytic strep
Pathogenesis
• Gram negative organisms less common
– Inability to bind fibronectin
– “HACEK” organisms
• Fungi
– Candida
– Aspergillus
Clinical Manifestations
• Unexplained fever with
Known heart disease
• Myalgias/ arthralgias
• HA
• General malaise
• Anorexia/ wt. loss
• Changing/ new murmur
Clinical Manifestations
Janeway Lesions
Osler Nodes
Clinical Manifestations
Hemorrhagic
Lesions
Subungal splinter
hemorrhages
Diagnosis
• Clinical criteria
– 2 major
– 1 major, 3 minor
– 5 minor
Treatment
• Want to make sure BCxs have been obtained
appropriately before starting ABx!
• If empiric treatment necessary:
– Direct toward most common offenders
• Streptococci and Staphylococci
• IV Abx to attain high bactericidal concentrations
• Ampicillin (Vancomycin) + Gentamicin
• Treatment x4-6 weeks
– Longer with prosthetic valve
Complications
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Embolization!!
Abscess formation
Heart failure
Heart block
Mycotic aneurysms
Question #7
• You are referring one of your patients to have
some teeth extracted. Mom mentions that she
has a history of a “heart problem”. She asks if her
daughter will need antibiotics prior to her dental
procedure. Of the following, which cardiac lesion
would require endocarditis prophylaxis?
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A. Bicuspid aortic valve
B. Mitral valve prolapse
C. Hypertrophic cardiomyopathy
D. Pulmonary stenosis
E. Cardiac transplant with residual valvopathy
Endocarditis Prophylaxis: Who?
• 1. Prosthetic heart valves
• 2. Previous IE
• 3. Unrepaired cyanotic heart disease that includes
palliative shunts and conduits
• 4. Completely repaired congential heart disease with
prosthetic material or device during the first 6 months
following the procedure
• 5. Repaired congenitial heart disease with residual
defects at the site or next to the site of the prosthetic
device
• 6. Valvulopathy in a transplanted heart
Endocarditis Prophylaxis: When?
• Dental procedures
– Involve manipulation of gingiva, perforation of the
oral mucosa
• Tonsillectomy/ adenoidectomy
• Operations involving the respiratory mucosa
– Bronchoscopy with biopsy
• Surgical procedures on infected skin or
musculoskeleton
Endocarditis Prophylaxis: What?
Question #8
• A 12 yo female with right knee swelling, pain, and
erythema presents to clinic. She had similar
symptoms in left knee yesterday. She also complains
of fatigue and fever. On PE she has a macular rash on
trunk and arms and a 3/6 holosystolic murmur on
ausculatation that radiates to the axilla. You suspect
acute rheumatic fever, and are waiting on echo
results. Her rapid strep antigen test is negative.
• What is the next most appropriate test?
A.
B.
C.
D.
E.
AntiDNAase B
ESR
CBC
CRP
Throat culture
ACUTE RHEUMATIC FEVER
Epidemiology
• Prevalence is 0.05 cases per 1,000 in US
• Typically affects children 5 to 15 years old
Clinical Manifestations
• Delayed nonsuppurative complication of group A
streptococcal (GAS) pharyngitis
– A latent period of 2 to 4 weeks before symptoms
appear
• Typically see polyarthritis (migratory), carditis,
subcutaneous nodules, erythema marginatum, or
chorea
• Mitral regurgitation is the most common valvular
lesion
Laboratory Findings
• Must establish the presence of a
preceding GAS infection
– Rapid strep antigen (95% specificity, 80%
sensitivity)
– Throat culture
• Negative in 75% of patients by the time ARF manifests
– Antistreptococcal antibody titers (antistreptolysin
O, antiDNAse B, antihyaluronidase)
• Peak around onset of ARF and are most useful
• Elevated ESR and CRP indicate ongoing
inflammation
Carditis
• ARF can cause inflammation of pericardium,
myocardium, and endocardium
• Good cardiac exam and echo are a must!
– On exam most common murmurs:
• Apical, holosystolic murmur of mitral regurgitation
(radiates to left axilla)
• Early diastolic decrescendo murmur of aortic
regurgitation
• Cardiomegaly on CXR
• ECG may reveal varying degrees of heart block
Treatment
• Treatment of GAS pharyngitis must be started
within 9 days of onset to prevent ARF
– Penicillin is drug of choice
– Evaluate and treat all household contacts
• Long term prophylaxis to prevent additional GAS
infection, recurrent ARF, and increased risk of
developing rheumatic heart disease
• Short term high-dose Aspirin (100mg/kg/day) for
arthritis
• Treat heart failure
• Sedatives (haloperidol and pheonbarb) for chorea
Question #9
• A 14 yo M cross-country runner comes to your office with
c/o difficulty breathing with exercise. Three days prior to
his visit, he had been ill with fever, URI symptoms and sore
throat. His fever resolved yesterday, so he went outside for
a run, but couldn’t go more than ¼ mile due to SOB. In
your office, he appears in NAD. T 98.2, HR 110, RR 26, Pox
96% RA. He has a II/VI holosystolic murmur @ LSB and his
liver could be palpated ~2cm below the costal margin.
Which organism is the MOST likely cause of his symptoms?
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A. Adenovirus
B. Influenza A
C. S. aureus
D. Rhinovirus
E. Coronavirus
MYOCARDITIS
The Basics
• Inflammation of the cardiac myocytes
• Clinically evident myocarditis infrequent
• Follows a non-specific respiratory, flulike, or GI
illness with fever
– Most common causes: Viruses!!
• Adenovirus
• Enterovirus (coxsackie B)
Clinical Manifestations
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Atypical chest pain
Fatigue and exercise intolerance
Dyspnea
Tachycardia
Arrhythmias
– Heart block
– VT
– SVT
• CHF
• Cardiogenic shock
• Sudden death
Evaluation
• ECG
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Sinus tachycardia
Low-voltage QRS
T-wave inversion
ST-segment depression
Pathologic Q waves
• Echo
– LV size and function
• Labs
– Cardiac troponin levels
– CK-MB
Treatment
• Supportive
– Inotropes
– Afterload reduction
– Diuretics
– Oxygen
• IVIg
– Not proven to be of any benefit
Question #10
• A 14 yo female presents to ER with substernal chest
pain, that she states is worse when she tries to take a
breath. On PE, she looks toxic, she is leaning forward
seated on the exam table, and has a fever of 40°C. You
order a CXR, which reveals cardiomegaly and a right
lower lobe pneumonia.
• The most likely etiology is:
A.
B.
C.
D.
E.
HIV
Influenza
Mycobacterium tuberculosis
Adenovirus
Staphylococcus aureus
PERICARDITIS
Pericarditis
• Inflammatory condition that can arise from a wide
variety of causes:
•Infection
•Autoimmune
•Rheumatic fever
•Uremia
•Malignancy
•Reaction to a drug
•Post cardiac surgery
•Idiopathic (30%)
Viral infection
• Most common cause
• Prodrome of respiratory or GI illness
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Coxackievirus
Echovirus
Adenovirus
EBV
Influenza
HIV
• Presentation = fever, chest pain, friction rub
• Often accompanied by myocarditis
Bacterial pericarditis
• Less common, but higher mortality
– Staph aureus
– Haemophilus influenzae
• Presentation = toxic appearance, irritable,
chest pain, cardiomegaly
• May be post-op or from another site (PNA)
• TB pericarditis
– Spread from lymph nodes or blood borne
– Large effusions and cardiac tamponade common
Clinical Manifestations
• Chest pain tends to be substernal, sharp,
worse with inspiration and relieved by sitting
upright and leaning forward
– Radiates to scapular ridge
• Pericardial friction rub
– Scratchy, high-pitched to-and-fro sound
– Heard best in 2nd and 4th intercostal space at LSB
midclavicular line
Lab Eval
• Elevated WBC, ESR, and CRP
• Troponin may be increased
• Blood cx, viral cx, TB skin testing, gastric
cultures for Mycobacterium, RF, and ANA may
be helpful
• ECG most useful diagnostic test
Diffuse ST segment elevation and PR
segment depression; May be low voltage is
effusion; electrical alternans in tamponade
Effusion
“Water-bottle” heart
Management
• Treat the underlying cause
• NSAIDS = to alleviate chest pain
– If chest pain persists beyond 2 weeks, colchicine can
be added
• Steroids = reserved for those unresponsive to
NSAIDS and colchicine or with a rheumatologic
disease
• Pericardiocentesis = indicated with hemodynamic
compromise, cardiac tamponade, purulent
pericarditis, and suspected neoplastic pericarditis
– Resistant cases→ pericardial window or
pericardiectomy
KAWASAKI DISEASE
Cardiac complications
• 20-25% of untreated children develop coronary
artery aneurysms
• Other complications include:
– Myocarditis
– Pericarditis with effusion
– Valvulitis (mitral valve)
• Aneurysms resolve 1 to 2 years after onset in 50%
– Likelihood determined by size
– Can rupture within first few months
– Worst prognosis = giant aneurysms
• MI caused by thrombotic occlusion is cause of
death
– Occurs in first year
Echo
• Performed at diagnosis and 2 and 6 weeks
after disease onset
– Specifically look at all coronary artery segments
– If aneurysms not identified in first 1 to 2 months,
unlikely to develop
• Those with giant aneurysms need more
frequent imaging
Treatment
• Everyone gets IVIG and high-dose(80100mg/kg/d) Aspirin to start
– No coronary changes = Low-dose Aspirin (35mg/kg/d) x 6-8wks
– Transient coronary ectasia = Low-dose Aspirin x 68wks
– Small to medium aneurysm = Low-dose Aspirin until
regression documented
– >1 large or giant aneurysm (>8mm) = Low-dose
Aspirin + Warfarin or LMWH
– Coronary artery obstruction = Low-dose Aspirin +
Warfarin or LMWH
Other
• When refer to cardiology
– *FHx HOCM, Marfan,
muscular dystrophy
• Marfan Syndrome
– Due to risks of aortic root dilation and dissection,
NO participation in:
• Contact or competitive sports
• Isometric exercise
• Avoid activities that increased risk of joint injury/
pain
Other
• Cholesterol Screening
– Screen with fasting lipid panel:
• Children/ adolescents with positive FHx for
dyslipidemia or premature CVD
• Children/ adolescents with unknown FHx or with
additional risk factors
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Overweight/obese
HTN
Smoking
Diabetes