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Cardiology Board Review

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Presentation on theme: "Cardiology Board Review"— Presentation transcript:

1 Cardiology Board Review
August 30th, 2011

2 Test Question The Saints will win the Superbowl this year. True False

3 Cardiac history and Exam

4 Cardiac History Infants Children Gestation FHx Neonatal status
Growth and development Feeding patterns Children Presence of palpitations Chest pain Lightheadedness or syncope Activity level Any positive findings may increase your suspicion that a murmur might be pathologic

5 Cardiac Exam Observation Palpation Ausculatation Respiratory distress?
Central cyanosis? Clubbing? Syndromic appearance? Palpation Hyperdynamic precordium? Displaced PMI? HSM? Distal pulses equal? Bounding? Ausculatation

6 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 P2 is delayed due to reduced impedance in the pulmonary vascular bed

7 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 crescendo- decrescendo quality Diastolic murmurs Immediate Early or medium Late

8 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 A: PPS B: Venous hum C: Supraclavicular bruit D: Still murmur E: PDA

9 Innocent Murmurs Uniform characteristics Examples
Early systolic ejection Short duration Low intensity (grade 1&2) Vibrating or musical quality Examples Still murmur Venous hum Supraclavicular bruit PPS (peripheral pulmonary artery stenosis)

10 Pathologic Murmurs Longer and louder
All diastolic (except venous hum) and pansystolic murmurs are pathologic Systolic ejection murmur Ejection click? Is S2 widely split? Does the S2 split move? Normally? Hyperdynamic precordium? Distended neck veins? Peripheral pulses normal? Pansystolic murmurs occur when there is flow from a high pressure chamber into a low pressure chamber

11 Congenital Heart Disease in neonate and young infant

12 Clinical Presentations
Recognize dysmorphic features as increased risk for CHD 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%)

13 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

14 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

15 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

16 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)

17 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

18 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)

19 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: Start oxygen via nasal canula Prostaglandin infusion Atrial septostomy in cath lab Echocardiogram IV Furosemide

20 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

21 Cyanotic CHD Pulmonary valve atresia Ebstein malformation
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

22 TGA Ebstein’s Pulm atresia
Very young newborns with severe cyanosis are likely to have either transposition, pulm atresia, or Ebstein malformation. Evidence of normal or high pulmonary blood flow on chest radiograph (prominent pulmonary vascular markings) usually excludes the diagnosis of pulm atresia and Ebstein and points toward transposition. Pulm atresia

23 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”)

24 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

25 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

26 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

27 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

28 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

29 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

30 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

31 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

32 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

33 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

34 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

35 Cyanotic CHD Polycythemia Anemia
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

36 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

37 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: NS bolus 20ml/kg Electrocardiogram Start oxygen via nasal canula Captopril 0.01mg/kg Place patient in knee-to-chest position

38 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

39 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

40 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

41 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

42 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

43 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

44 Follow-up for Coarc Recoarctation can occur as child grows
Higher incidence of hypertension Frequent BP measurements by pediatrician

45 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? A. Lobar consolidation on CXR B. Lipid laden macrophages on BAL C. Elevated BNP D. Positive RSV E. Posterior esophageal indentation on barium swallow

46 Heart Failure

47 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

48 Pathophysiology Decreased CO increased metabolite production in downstream organ systems local vasodilation and decreased bp stimulation of angiotensin and mineralocortcoid release further fluid retaining mechanisms in kidney and increases in SVR AND stimulation of the sympathetic NS (and increased catecholamines) tachycardia, enhanced myocardial contractility and maladaptive forms of cardiomyopathy Longstanding increases in myocardial work and oxygen consumption worse HF Sx remodeling (increase in cardiac mass with more shperical shape to the heart, scar tissue poorly contractile and less compliant heart) Endogenous protective mechanisms that defend the heart from worsening HF: IGF-1, GH; ANP/BNP increase vasodilation and diuresis acutely and chronically prevent inflammation, cardiac fibrosis, and hypertrophy

49 Clinical Manifestations
Infants Older Children Feeding difficulties Volume and duration Increased fatigability Mild to severe retractions Tachypnea/ dsypnea Grunting Tachycardia Gallop rhythm (S3,S4) Hepatomegaly Exercise intolerance Somnolence Anorexia Cough/wheezing Crackles Gallop rhythm Hepatomegaly JVD Peripheral edema

50 Pulmonary Edema TAPVR- figure 8 or snowman appearance

51 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) Increased cardiac filling pressures also pulmonary edema

52 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

53 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 TAPVR: pulmonary vv (oxygenated blood) drain into RA or one of the vv draining into the R atrium

54 Common Causes- Excessive Afterload
Patients present in first postnatal week: R L R L Increased end diastolic filling pressure and decreased pressure gradiant b/t aorta and ventricle and end-diastole subendocardial ischemia due to inadequate coronary blood flow maladaptive cardiac hypertrophy, ventricular remodeling and HF Normal Heart- Diastole Heart with Excessive Afterload- Diastole Increased filling pressures and decreased gradient b/t ventricle and aorta at end- diastole inadequate coronary blood flow ischemia hypertrophy, remodeling HF

55 Common Causes- Excessive Afterload
Examples: Mitral stenosis Aortic stenosis Coarctation of the aorta

56 Common Causes- Contractility
Cardiomyopathy (HF presenting feature) Dilated Impaired systolic and diastolic function Causes: Idiopathic Infection (myocarditis) Operative injury Chemo (anthracyclines) Metabolic/ degenerative diseases

57 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

58 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

59 Evaluation Pulse oximetry 12-lead EKG CXR Echocardiogram HF biomarkers
BNP Released in response to atrial stretching Sensitive marker of cardiac filling pressure/ diastolic dysfunction Pulse ox: identifies cyanosis in an infant with LR shunt EKG: identifies arrhythmia-induced HF CXR: demonstrates cardiac enlargement (high specificity but low sensitivity), increased pulmonary blood flow, venous congestion, or pulmonary edema Echo: identify cause for HF (structural, ventricular dysfxn, chamber dimensions, effusions)

60 Evaluation HF Biomarkers BNP (con’t) CRP TNF-alpha
Can distinguish b/t primary respiratory and cardiac-induced tachypnea CRP TNF-alpha Both correlate positively with worse outcome in HF

61 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

Medical therapy for children largely guided by studies in adults; aims to maximize CO and tissue perfusion while minimizing stress (work) on the heart: 1. Reducing amount of force it takes for the heart to eject blood 2. Reducing overfilling of the heart

63 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

64 Arrhythmias

65 Basic Principles Abnormality in regular heart conduction and rate
Spectrum of severity Benign PAC PVC Malignant Atrial SVT Atrial ectopic tachycardia A. flutter A. fibrillation Ventricular V. tachycardia V. fibrillation * Benign as long as there is no underlying heart disease

66 Clinical Manifestations
Infants Children/ Adolescents Pallor Diaphoresis Respiratory distress Poor feeding Diminished perfusion CHF Shock Palpatation Rapid, strong or irregular heart rate Shortness of breath Dizziness Light-headedness Syncope **Sensations in younger infants/children usually do not become apparent until hemodynamics are affected Syncope with exercise, particularly concerning for AV block, LQTS, HOCM, WPWSVT; ALL OF THESE PATIENTS NEED CARDIOLOGY REFERRAL

67 Premature Atrial Contractions
Common during the newborn period Associated with abberant conduction and pauses due to failure of the premature atrial impulse to conduct to the ventricle

68 Premature Ventricular Contractions
Want to do an EKG during brief exercise to be sure that the ectopy doesn’t become more frequent Wide QRS T wave in opposite direction to the QRS Dissociation from the P wave Full compensatory pause

69 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) Usually due a re-entry of electrical activity of electrical activity passing from the atria to the ventricles over the AVN and then back to atria via accessory pathway

70 Treatment of SVT Acute management Chronic management Vagal maneuvers
Adenosine Transient complete AV block DC cardioversion Chronic management B-blocker (propranolol, atenolol) Digoxin Flecanide, sotalol, amiodarone Radiofrequency catheter ablation Digoxin not used as much b/c for it to be effective, serum concentrations have to be near toxic range

71 Wolff-Parkinson-White
Short PR interval Delta wave Prolongation of the QRS Predisposes to SVT

72 Ventricular Tachycardia
Wide complex tachycardia AV dissociation of P waves Associated with hemodynamic compromise

73 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 Can present with syncope, seizures, cardiac arrest; fainting spells while exercising; FHx of unexplained sudden death Ask about congenital deafness in the family associated with a particularly malignant form of LQTS

74 Torsades de Pointes

75 Infective endocarditis

76 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

77 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 Destruction regurgitation

78 Pathogenesis Gram negative organisms less common Fungi
Inability to bind fibronectin “HACEK” organisms Fungi Candida Aspergillus Haemophilus sp, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella, Kingella kingae

79 Clinical Manifestations
Unexplained fever with Known heart disease Myalgias/ arthralgias HA General malaise Anorexia/ wt. loss Changing/ new murmur More common findings in adults like Splinter hemorrhages, Roth spots, Oslers nodes, Janeway lesions less common in kids

80 Clinical Manifestations
Janeway Lesions Osler Nodes

81 Clinical Manifestations
Hemorrhagic Lesions Subungal splinter hemorrhages

82 Diagnosis Clinical criteria 2 major 1 major, 3 minor 5 minor
Blood culture most important test in dx of endocarditis Broad categories of minor criteria: Predisposition Fever Vascular phenomenon (arterial emboli, septic pulmonary infarctions, mycotic aneurysm, ICH, conjunctival hemorrhage, Janeway lesions Immunologic phenomenon (GN, Osler nodes, Roth spots, RF) Single positive BCx, or serologic evidence of infxn with an organism c/w IE

83 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 Need Abx to penetrate avascular valve leaflets and infected thrombi Surgery: continued bacteremia after 2 weeks of appropriate therapy, fungal vegetations, abscess formation, worsening heart failure, systemic emboli

84 Complications Embolization!! Abscess formation Heart failure
Heart block Mycotic aneurysms

85 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? A. Bicuspid aortic valve B. Mitral valve prolapse C. Hypertrophic cardiomyopathy D. Pulmonary stenosis E. Cardiac transplant with residual valvopathy

86 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 THOSE AT HIGHEST RISK FOR POOR OUTCOME FROM IE

87 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 Don’t forget that atopic dermatitis, acne and poor dental hygiene all increase the risk of IE in susceptible individuals

88 Endocarditis Prophylaxis: What?
Keep in mind prophylactic amoxil reduces incidence, nature, and duration of bacteremia, but no studies have shown that such a reduction decreases the risk/ prevents IE

89 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? AntiDNAase B ESR CBC CRP Throat culture

90 Acute rheumatic fever

91 Epidemiology Prevalence is 0.05 cases per 1,000 in US
Typically affects children 5 to 15 years old

92 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

93 Erythema marginatum = painless, non pruritic erythematous macule or papule that spreads in a circular pattern on the trunk and proximal extremities Subcutaneous nodules = round, firm, mobile, painless, most common over bony prominences Chorea = rapid irregular involuntary and uncoordinated movements

94 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

95 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

96 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

97 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 LSB and his liver could be palpated ~2cm below the costal margin. Which organism is the MOST likely cause of his symptoms? A. Adenovirus B. Influenza A C. S. aureus D. Rhinovirus E. Coronavirus

98 Myocarditis

99 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) Remember that any almost any virus, as well as other organisms, may cause myocarditis

100 Clinical Manifestations
Atypical chest pain Fatigue and exercise intolerance Dyspnea Tachycardia Arrhythmias Heart block VT SVT CHF Cardiogenic shock Sudden death Remember that in the vast majority of pts, chest pain is NOT cardiac in origin (more likely MS, RAD/Asthma, PNA, PTX, pleuritis, esophagitis/GER, anxiety) Cardiac causes of CP: Pericarditis Angina/MI (with h/o Kawasaki dz) Arrhythmia Aortic dissection HOCM/IHSS Obstruction (AS) Coronary a. dz (anomalous origin of the L coronary, Kawasaki-induced aneurysms and stenosis) **Worry about CP that is exertional, associated with syncope, dyspnea, exercise intolerance, oxygen desaturation or marked tachycardia; also CP that is extremely severe squeezing that radiates to the back or is associated with a sense of impending doom

101 Evaluation ECG Echo Labs 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 Troponin and CK-MB relatively specific for myocardial injury, may be helpful for serial F/U

102 Treatment Supportive IVIg Inotropes Afterload reduction Diuretics
Oxygen IVIg Not proven to be of any benefit

103 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: HIV Influenza Mycobacterium tuberculosis Adenovirus Staphylococcus aureus

104 Pericarditis

105 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%) 2 layers = a visceral layer and a fibrous parietal layer with ultrafiltrate of plasma in between Blood supply = internal mammary arteries Innervation = phrenic nerves

106 Viral infection Most common cause
Prodrome of respiratory or GI illness Coxackievirus Echovirus Adenovirus EBV Influenza HIV Presentation = fever, chest pain, friction rub Often accompanied by myocarditis

107 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

108 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

109 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

110 Effusion “Water-bottle” heart

111 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

112 Kawasaki Disease

113 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

114 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

115 Treatment Everyone gets IVIG and high-dose(80-100mg/kg/d) Aspirin to start No coronary changes = Low-dose Aspirin (3-5mg/kg/d) x 6-8wks Transient coronary ectasia = Low-dose Aspirin x 6-8wks 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 IVIG shown to prevent aneurysms, although 5% still develop some coronary artery dilation Attempt to treat within first 10 days of illness

116 Other Marfan Syndrome 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

117 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 Overweight/obese HTN Smoking Diabetes Premature: men<55, women<65

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