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CV Exam III > Pediatric Enhancement: Fundamentals of Pediatric Cardiology > Flashcards

Pediatric Enhancement: Fundamentals of Pediatric Cardiology Flashcards

1
Q

Tools for Evaluation of the Pediatric Cardiovascular System

A 
•History
•Physical
•Routine studies:
–EKG
–CXR
•Studies for the cardiac patient:
–cardiac cath
–echocardiogram
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2
Q

Perinatal infections account for 2% to 3%

A

of all congenital anomalies

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3
Q

TORCH:

A

–are some of the most common infections associated with congenital anomalies (a lot of eye and skin findings in common) including cardiac defects

–Most of the TORCH infections cause mild maternal morbidity, but have serious fetal consequences

–Toxoplasmosis
–Other (syphilis, varicella-zoster, parvovirus B19, HIV)
–Rubella(think “bluebella”)
»congenital rubella syndrome includes cardiacmanifestations: PDA, PS
–Cytomegalovirus(CMV)
–HSV
–Again, they can have really serious fetal consequences, or fetal loss

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4
Q

Coxsackievirus B, CMV, HSV

A

»In early pregnancy are teratogenic; later in pregnancy may cause myocarditis

»Active HSV lesions at time of delivery is an indication for cesarean section

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5
Q

PRENATAL exposures (cont’d)

Meds

A

•Amphetamines >VSD, PDA, ASD, TGA
•Anticonvulsants
–hydantoin: PS, AS, coarc, PDA
–trimethadione: TGA, TOF, hypoplasticleft heart
•Alcohol >FAS: in which VSD, PDA, ASD, and TOF are common

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6
Q

prenatal exposures

maternal condition

A

–Of course, maternal congenital heart disease: increases risk of CHD from 1% to 15%.

–Infant of diabetic mothers (IDM):
•cardiomyopathy, TGA, VSD, PDA
•Also hypoglycemia, hypocalcemia, polycythemia, LGA (large for gestational age)or SGA (small for gestational age)

–Maternallupus/mixed connective tissue disease: congenital heart block

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7
Q

POSTNATAL history

A 
(they may be presenting with these as chief complaints):
–Poor growth (aka FTT = failure to thrive)
–Poor feeding (secondary to fatigue and dyspnea)
–Tachypnea
–Cyanosis
–Dyspnea, puffy eyelids
–Frequent respinfections
–Exercise intolerance
–Murmur
–Chest pain
–Palpitations
–Joint symptoms
–Neuro symptoms
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8
Q

*Buzz words of presentation:

A

infant who presents with diaphoresis and tachypnea with feeding, cyanosis, FTT (feeding is all they do = exertional symptoms)

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9
Q

Family history

A

–Hereditary disease

–Congenital heart disease

–Rheumatic fever
*•Frequently occurs in more than one family member: higher incidence among relatives of rheumatic children, unknown genetic component
–Hypertension, atherosclerosis

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10
Q

Physical Exam

A

•General: well nourished, well developed “WN/WD”

–“Abnormal facies?” implies chromosomal syndrome

–Examples of syndromes with cardiac manifestations:
•Cornelia de Lange (thick eyebrows, distinct facial features): VSD, ASD
•CHARGE: Coloboma, Heart defects, choanal Atresia, growth/mental Retardation, GU anomalies and genital hypoplasia, Ear anomlies
–conotruncal anomalies (truncus, TOF)
–aortic arch anomalies

 •Holt Oram(cardiac-limb): defects or absence of thumb or radius
      –ASD 
      –VSD
  • Color (keep in mind the newborn always has acrocyanosis!)
    • Clubbing
    • Pectus excavatum: rarely causes cardiac disease
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11
Q

CHARGE

A

Coloboma, Heart defects, choanal Atresia, growth/mental Retardation, GU anomalies and genital hypoplasia, Ear anomlies
–conotruncal anomalies (truncus, TOF)
–aortic arch anomalies

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12
Q

Coloboma

A

normal tissue in or around the eye is missing from birth

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13
Q

Choanal atresia

A

blue but pink when cry, try to pass catheter

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14
Q

Cornelia de Lange

A

Cornelia de Lange (thick eyebrows, distinct facial features): VSD, ASD

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15
Q

Holt Oram

A

Holt Oram(cardiac-limb): defects or absence of thumb or radius
–ASD
–VSD

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16
Q

*BP norms are based

A

on age, gender, and height percentile

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17
Q

*wide and fixed split S2 is

A

abnormal

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18
Q

Murmurs

A

•Remember to think about murmurs in terms of:
–Timing (systolic or diastolic)
–Intensity (grade I-VI)
–Quality (musical, harsh, high or low pitched)

  • Not present in many severe forms of CHD, such as tricuspid atresia, coarctation of the aorta and transposition of the great vessels.
  • When a murmur is associated with a cardiac defect, the intensity of the murmur is unrelated to the severity of the abnormality.
  • However, murmur type, along with other heart sounds, is useful in differentiating mild defects from severe abnormalities
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19
Q

Innocent Murmurs

A
  • in children, physiologic murmurs are more common than in adults
  • •Low pitched (non-turbulent, not high velocity)
  • Still’s: low-pitched sounds heard at the lower left sternal area, “musical.” These most commonly occur between age 3 and adolescence. Low pitched -best heard with the bell of the stethoscope. Can change with position alteration and then can decrease or disappear with the Valsalva maneuver. No clicks are present.
  • venous hum: low-pitched continuous murmurs made by blood returning from the great veins to the heart -bell
  • pulmonary flow murmur:upper left sternal border. High pitched -best heard with the diaphragm. Also known as benign peripheral pulmonary stenosisof the newborn. Also seen in adolescents or in children with pectus excavatum. Prominent in high-flow situations, such as when a child has a fever or is anemic.
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20
Q

*suspicious murmurs

all of it was in red

A
  • high-pitched
  • harsh
  • S1 coincident (holosystolic)
  • diastolic murmurs
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21
Q

Still’s

A

low-pitched sounds heard at the lower left sternal area, “musical.” These most commonly occur between age 3 and adolescence. Low pitched -best heard with the bell of the stethoscope. Can change with position alteration and then can decrease or disappear with the Valsalva maneuver. No clicks are present.

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22
Q

Associated ejection clickalong with a high intensity murmur? 

A

stenotic valve

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23
Q

Transient systolic murmur in first hours after birth

A

Closing pda

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24
Q

The Seven S’s: Key Features of Innocent Murmurs

A
  • Sensitive (changes with child’s position or with respiration)
  • Short duration (not holosystolic)
  • Single (no associated clicks or gallops)
  • Small (murmur limited to a small area and nonradiating)
  • Soft (low amplitude)
  • Sweet (not harsh sounding)
  • Systolic (occurs during and is limited to systole)
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25
Q

Pulses

A

–Differences between upper and lower? coarctation of the aorta

–Differences between right upper and left upper? coarctation of the aorta proximal to or near the origin of left SC artery, or supravalvular AS

–Bounding? PDA, AR, AVF, rarely persistent truncus

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26
Q

EKG*

A

–Right ventricular dominancein newborns

–Manifested by right axis deviation

–Several interval lengths vary with age

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27
Q

CXR

A

–Large thymus! sail sign

–Film during expiration affects view of the heart shadow

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28
Q

Thymic Shadow

A

An important feature to recognize in the pediatric chest is the normal thymic tissue in the anterior mediastinum. Normal thymic tissue, as demonstrated on this image, should not be confused with a mediastinal or pulmonary mass. This is known as the “sail sign.”

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29
Q

Studies for the cardiac patient: echocardiogram

A

–Echocardiogram
•Basic principles:
–M mode technique uses one US beam passing through heart in a single axis to measure wall/chambers
–2D: transducer beam through a number of cross-sectional planes; four transducer locations

  • Transesophageal echocardiogram (TEE): great to visualize valves
  • Doppler flow:combines structure and blood flow
  • fetal echo
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30
Q

Perinatal and Neonatal Circulation

A 
•Four shunts in fetal circulation
–Placenta
–Ductus venosus
–Foramen ovale
–Ductus arteriosus
•Changes at birth
–Interruption of umbilical cord flow:
•Increased SVR with removal of the low resistance placenta.
•Closure of the ductus venosus because of lack of blood return from the placenta
–Lung expansion
•Decreased PVR, increased PBF, fall in PA pressure
•Functional closure of foramen ovale
•Closure of PDA
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31
Q

Cardiac defects in Genetic Disorders and Nonhereditary Syndromes

A 
–Down:endocardial cushion defect, VSD
–Turner:coarc, AS, ASD
–Noonan:PS, ASD, AVSD (partial), coarc, HCM
–Williams: SVAS
–Marfansyndrome
–FAS:VSD, PDA, ASD, TOF
–Rubella
–DiGeorge: interrupted aortic arch, truncus arteriosus, VSD, PDA, TOF
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32
Q

Down*

A

endocardial cushion defect, VSD

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33
Q

Turner*

A

coarc, AS, ASD

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34
Q

Noonan*

A

PS, ASD, AVSD (partial), coarc, HCM

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35
Q

FAS*

A

VSD, PDA, ASD, TOF

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36
Q

Congenital Heart Defects

A

•Present in nearly 1% of―or about 40,000―births per year
•VSD is the most common
•25% of babies with a CHD have a critical CHD. Infants with critical CHDs generally need surgery or other procedures in their first year of life.
•Infant deaths due to CHDs often occur when the baby is less than 28 days old(the neonatal period). In a study of neonatal deaths, 4.2% of all neonatal deaths were due to a CHD –one of leading causes of neonatal death secondary to birth defects.
•About 75% of babies born with a critical CHD are expected to survive to one year of age. About 69% of babies born with critical CHDs are expected to survive to 18 years of age
•Basic categories:
–Acyanotic (left to right)
–Cyanotic (the T’s)
–Malpositions
–Obstructive and valvular disease

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37
Q

Most common congenital heart defect*

A

VSD

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38
Q

Basic Categories of congenital heart defects*

A

–Acyanotic (left to right)
–Cyanotic (the T’s)
–Malpositions
–Obstructive and valvular disease

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39
Q

Left to Right Congenital Heart Diseaseaka acyanotic

A

ASD

VSD

PDA

endocardial cushion defects

Partial TAPVR

40
Q

ASD

A

–Often asymptomatic; 87% of secundumtypes close by age 4.
–Primary and sinus types require surgery.
–Late sequelae include mitral valve prolapse, atrial fibrillation or flutter, and pulmonary hypertension

41
Q

VSD

A

–Size of defect dictates hemodynamic presentation.
Cardiomegaly in moderate to large VSDs
–In 30 to 40% of cases, spontaneous closure occurs within the first 6 months
–Surgical repair required if infant exhibits failure to thrive, pulmonary hypertension, or right-to-left shunt > 2:1

42
Q

PDA

A

–In premature infants, spontaneous closure or indomethacin-induced closure may occur.
–In term infants, spontaneous closure is less likely, and indomethacin is not helpful.
•Surgical ligation usually required. No long-term sequelae if adequately treated

43
Q

Endocardial cushion defects

A

–Combination of the primum type of atrial septal defect, ventricular septal defect and common atrioventricular valve.
–Presentation similar to that of ventricular septal defect.
–Palliative pulmonary artery banding in refractory congestive heart failure.

44
Q

Cyanotic Congenital Heart Disease

*Presentation>is it always obvious cyanosis at birth?

whole slide*

A

–No; many will do fine and then develop s/sx of excessive pulmonary blood flow and heart failure after PVR decreases (after newborn period)

–Sometimes ductal patency may persist for weeks (even months) constriction and closure of ductus cause decreased systemic blood flow, oliguria, acidosis, pulmonary edema, and heart failure can lead to ischemia and ventricular dysfunction and death.

–Clinical presentation of left heart obstructive disease may mimic sepsis
•Tachypnea, mottled gray skin, poor perfusion, decreased pulses
•Clinical clues that are critical are gallop rhythm and hepatomegaly or cardiomegaly

45
Q

Cyanotic Congenital Heart Disease

A 
•5 T’s:
   –Tetralogy of Fallot: “Tet spells” in infancy
   –Transposition of the Great Arteries
   –TAPVR
   –Truncus arteriosus
   –Tricuspid Atresia
  • Hypoplastic Left Heart
  • Ebstein Anomaly (right sided heart abnormality)
  • Pulmonary Atresia
  • Single ventricle
  • Double Outlet Right Ventricle
46
Q

Transposition of Great Vessels*

A

**TGV is associated with severe cyanosis in the first hours after birth (in other words, TGV is the mostly likely diagnosis in a severely cyanotic neonate who is just a few hours old)

47
Q

Transposition of Great Vessels

A
  • Ductus-dependent lesion (no mixing!)
  • Consider palliative balloon atrial septostomy, but definitive surgical switch of aorta and pulmonary artery required as soon as possible.
  • Late complications include pulmonary stenosis, mitral regurgitation, aortic stenosis, coronary artery obstruction, ventricular dysfunction and arrhythmias.
48
Q

Tetralogy of Fallot

A

1.VSD
2. Overriding aorta
3. RV outflow obstruction
4. RV hypertrophy
•Think of it as an Aortic Takeover!
•Most common cyanotic CHD beyond infancy.
•Intermittent episodes of hyperpnea, irritability, cyanosis with decreased intensity of murmur
•Palliative shunting may be necessary
•Surgical repair required before age 4

49
Q

TOF xray

A

boot shaped heart (sometimes seen in tricuspid atresia –EKG will differentiate)

50
Q

Egg shaped heart (”egg on a string” = narrow mediastinum)

A

TGA

51
Q

snowman

A

tapvr

52
Q

coarctation of aorta

A

rib notching

53
Q

Malpositions

A
  • Situs Inversus
  • Vascular Rings and Slings
  • Anomalous Origin of Left Coronary Artery
54
Q

Pulmonic stenosis

A

–May be asymptomatic or may result in severe congestive heart failure. Prostaglandin E1 infusion at birth may be helpful. Valvular type may require balloon valvuloplasty.

55
Q

Obstructive and valvular disease

A

Pulmonic stenosis

Peripheral pulmonic branch stenosis

Aortic disease

Mitral valve stenosis, prolapse, and regurgitation

Mitral valve stenosis, prolapse, and regurgitation

Tricuspid Stenosis

56
Q

Aortic disease

A

–Stenosis (may be asymptomatic. Valve replacement and anticoagulation may be required)
–Aortic regurgitation
–Supravalvular aortic stenosis
–*Coarctation of the aorta
•98% of cases occur at origin of left subclavian artery.
•Blood pressure higher in arms than legs, bounding pulses in arms,
•Surgical repair usually required between 2 and 4 years of age.
–Hypoplasia

57
Q

Coarctation of the Aorta*

A
  • While the presentation in the first year of life can be rather dramatic (heart failure, circulatory collapse, death), later in life the presentation can be more insidious and can go overlooked or underappreciated. Late presentation (with HTN or murmur) is because of less obstruction and good collateral blood flow.
  • (1)Systolic murmur (often conducted to back)
  • (2)Weak or absent femoral pulses (radio-femoral delay in older patients)
  • (3)Upper limb hypertension
  • (4)Exercise intolerance
  • (5)Leg claudication
58
Q

Acquired heart disease

A
  • Disorders of Myocardium: cardiomyopathy, myocarditis
  • Kawasaki
  • Rheumatic Heart Disease
  • Endocarditis
  • Pericardial disease
59
Q

Myocarditis*

A

–Inflammation of myocardial tissue

–*Etiology: viral
•Coxsackievirus, echovirus, poliomyelitis, mumps, rubella, CMV, HIV, arbovirus, adenovirus, influenza

–Sxs: nonspecific and inconsistent, depends on severity of disease
     •Anorexia
     •Lethargy
     •Emesis
     •Lightheadedness
     •Cool extremities
     •SOB
60
Q

Myocarditis Diagnosis*

A

–EKG: low voltage throughout, *ST changes, prolonged QT, arrhythmias (premature contractions, AV block)

–CXR
•Variable cardiomegaly and pulmonary edema

–Echo findings
•Enlargement of heart chambers, impaired LV function

–Labwork:
* •PCR:used to find the viral genome in myocardial cells; it is rapid and sensitive, and it may become the test of choice for the diagnosis of viral myocarditis

–Treatment
•Bedrest, diuretics, inotropes. Digoxin, gamma globulin, ACEI, possible steroids, heart transplant.
*•IVIGhas been associated with improved left ventricular function and improved survival, though still controversial

61
Q

Cardiomyopathy dilated*

A

Dilated:
•20-50% familial
•Acquired: often viral illness triggers myocarditis that leads to dilated cardiomyopathy

62
Q

cardiomyopathy hypertrophic*

A

Hypertrophic (HCM)
•*Autosomal dominant genetic disorder that has a variable presentation and carries a high incidence of sudden death.
•myocardial hypertrophy that is inappropriate and often asymmetrical and that occurs in the absence of an obvious inciting hypertrophic stimulus

63
Q

Kawasaki diagnostic criteria*

A

–High fever for FIVEdays
PLUS*

–At least FOUR of the following (head to toe):

  • Bilateral bulbar *conjunctival injection, without exudate
  • Erythematous mouth and pharynx, *strawberry tongue, and/or red, cracked lips
  • *Cervical lymphadenopathy(> 1.5 cm in diameter), usually single and unilateral
  • Polymorphous exanthem(morbilliform, maculopapular, or scarlatiniform)
  • *Swelling of hands and feetwith erythema of palms and soles

–Infants can have atypical presentation

64
Q

Kawasaki other findings

A 
•Etiology unknown
•Other clinical findings
irritability, abdominal pain, V/D, anterior uveitis (80%), arthritis/arthralgias, aseptic meningitis, pericardial effusion or arrhythmias, gallbladder hydrops, carditis, perineal rash with desquamation
•Lab findings
–Leukocytosis with left shift
–Elevated CRP or ESR
–Thrombocytosis (after first week, peaking at 2 weeks)
–Normocytic/normochromic anemia
–Sterile pyuria (70%)
–Increased LFTs (40%)
65
Q

Kawasaki cont’d*

A

•Why are we talking about this in pediatric cardiology??

•CV complications!
–If untreated, *15-25% develop coronary artery aneurysmsand dilatation (peak prevalence 2-4 wks post onset of disease) and are at risk for coronary thrombosis acutely and coronary stenosis chronically
–Carditis, valvular regurgitation (AR, MR, and TR)

  • Management: IVIG and ASA
  • Follow up long term
66
Q

rule out kawasakis it is most likely

A

adenovirus

67
Q

Kawasaki is also known as

A

mucocutaneous lymph node syndrome

68
Q

Rheumatic Heart Disease

A
  • Up to 39% of patients with acute rheumatic fever may develop varying degrees of pancarditis with associated valve insufficiency, heart failure, pericarditis, and even death.
  • With chronic rheumatic heart disease, patients develop valve stenosis with varying degrees of regurgitation, atrial dilation, arrhythmias, and ventricular dysfunction.
  • Chronic rheumatic heart disease remains the leading cause of mitral valve stenosis and valve replacement in adults in the United States.
69
Q

Endocarditis

A
  • Sticky valves, wimpy bugs

* Smooth valves, sticky bugs

70
Q

Pericardial disease

A
  • Pericarditis
  • Pericardial effusion
  • Tamponade
  • Constrictive pericarditis
  • Postpericardiotomy
71
Q

Other cardiac issues in pediatrics

A
  • HTN
  • Arrhythmias (prolonged QT, SVT)
  • Pulmonary Hypertension
  • Syncope
  • Chest pain in children (cardiac vs noncardiac)
  • Sports PE screening
72
Q

Hypertension in pediatric patients*

A

•Obesity is a strong risk factor for developing childhood hypertension

•Before puberty –secondary cause of HTN
–**The younger the child and the higher the BP, the more likely it is a secondary to an identifiable cause (such as renal disease)

•After puberty –likely essential HTN (primary cause)

73
Q

Arrhythmias*

A

•*Less common in children than in adults

•Conduction abnormalities
–*prolonged QT: disorder of myocardial repolarization characterized by prolongation of QT interval on the electrocardiogram and an increased risk of sudden death (due to the potential to degenerate into polymorphic ventricular tachycardia)

74
Q

Sinus tachycardia

A

–Compatible history consistent with known cause
–P waves present and normal
–Variable R-R with constant PR
–Infants HR

75
Q

SVT

A 
–Compatible history
–(vague, nonspecific, h/o abrupt rate change)
–P waves absent or abnormal
–HR not variable with activity
–Infants HR >220
–Children HR >180
76
Q

Syncope

A 
•DDx
–Noncardiac
•Vasovagal (fear, anxiety, prolonged standing)
•Hypovolemia
–Cardiac
•Arrhythmia
•HCM
•Evaluation?
–History
–Orthostatic BP/P (“Tilt” test)
–EKG
77
Q

Chest pain in children

noncardiac problems*

A

*(much more common than cardiac etiology)!

–Musculoskeletal etiology very common
     •Costochondritis
     •Tietze syndrome (recent URI) –similar to costochondritis but often a single joint with associated warmth, swelling, tenderness
     •Nonspecific
     •Slipping rib syndrome
     •Trauma, strain
     •Precordial catch (Texidor twinge): posture or pinched nerve related
     •Xiphodynia (reproducible)

–GI (GERD)

–Psychogenic (anxiety)

–Zoster (superficial pain
–before lesions appear)

–Spinal cord/nerve root compression in conjunction with scoliosis

78
Q

pain out of porpotion is

A

zoster or necrotizing fasciitis

79
Q

Costochondritis

A

number 1 diff for kids with chest pain found on palpation

80
Q

Chest pain in children

Cardiac causes

A

Inflammatory

Increased myocardial demand or decreased supply
cardiomyopathy
LVOT
Arrhythmias

Coronary artery abnormalities

Miscellaneous
   Aortic dissection
   Rupture of aortic aneurysm
   Pulmonary HTN
   MVP
   Atrial myxomas
   Cardiac device/stent complications

Drugs
Cocaine
Overdose of sympathomimetics

81
Q

Chest Pain

•When to refer?*

A 
–Abnormal cardiac findings
–*Exertional chest pain
–*Exertional syncope
–Chest pain with palpitations
–EKG abnormalities
–*Significant family historyof arrhythmias, sudden death, or genetic disorders
–Heart transplant
–h/o Kawasaki
–First degree relative with familial hypercholesterolemia
82
Q

Sports PE screening

Refer for*:

A

•*Family h/o early sudden death
–Cardiac, seizure, one car accident, unknown (could be arythymia

  • *Murmurs (HCM)
  • *Marfan’s stigmata
  • Simultaneous palpation of radial and femoral pulses (undiagnosed coarc) reveals unequal pulses
  • *Other PE findings consistent with cardiac disease
83
Q

Palliative systemic to pulmonary artery shunts*

A

use of systemic arterial flow to increase pulmonary blood flow in cardiac lesions with impaired pulmonary perfusion (TOF, hypoplastic right heart, TA, PS)

84
Q

Blalock-Taussig shunt*

A

Palliative cava to pulmonary artery shunts: use of systemic venous flow to increase pulmonary blood flow, usually in older children with lower PVR, as an intermediate step to Fontan: Glen

85
Q

Fontan*

A

anastomosis of SVC to RPA (Glenn shunt), and anastomosis of RA and/or IVC to pulmonary arteries, separates systemic and pulmonary circulations when there is a functionally single ventricle

86
Q

norwood*

A

repair of hypoplastic left heart, also 2 stages

87
Q

Special Considerations: recent cath or cardiac surgery

A
  • Embolization or compression of adjacent structures
  • Can have MI
  • Fever and chest pain worse when supine: postpericardiotomy syndrome
88
Q

You are seeing a 3 day old infant in the emergency department.
CC: “She has not been feeding well since we took her home from the hospital, and I think she is breathing faster.”
Preliminary DDx?
Tip:
You can ask mom to feed the baby during encounter.

OB history
–33 year old G1P1001
–good PNC throughout pregnancy
–All prenatal labs unremarkable; GBS negative, no infections in pregnancy
–Induced vaginal delivery at 41 weeks
–APGARS 8/9
–Hep B received in NBN
Family hx: no congenital heart disease or early childhood deaths, no seizure disorders, no genetic syndromes
•Social hx:
–Diet as in HPI
–Sleep
–Who lives at home?
–Any pets or smokers?
–Any daycare?
•ROS
Family hx: no congenital heart disease or early childhood deaths, no seizure disorders, no genetic syndromes
•Social hx:
–Diet as in HPI
–Sleep
–Who lives at home?
–Any pets or smokers?
–Any daycare?
•ROS
A

•Coarctation of the aorta (corrected –previously an error here)
–Admit
–Consult pediatric cardiology, pediatric surgery
–Treatment of early presentation: surgery or balloon angioplasty

89
Q

mona

A

morhine oxygen nitroglycerin and aspirin for mi

90
Q

Causes of altered mental status in a neonate

A
  • T–Trauma (nonaccidental and accidental)
  • H–Heart disease andhypovolemia
  • E–Endocrine (eg, congenital adrenal hyperplasia and thyrotoxicosis)
  • M–Metabolic (electrolyte imbalance)
  • I–Inborn errors of metabolism
  • S–Sepsis (eg, meningitis, pneumonia, and urinary tract infection)
  • F–Formula mishaps (eg, under-or overdilution)
  • I–Intestinal catastrophes (eg, volvulus, intussusception, and
  • necrotizing enterocolitis)
  • T–Toxins and poisons
  • S–Seizures
91
Q

15 year old female athlete presents to you with syncope.
•Preliminary DDx?

  • She was out on the soccer field and fainted while playing. Team members helped her to the ground.
  • No known head injuries.
  • Quickly returned to consciousness.
  • She recalls sudden chest pain and dizziness before fainting.
  • PMH is unremarkable
  • General -WN/WD, healthy appearing teen in NAD
  • Skin -pink
  • HEENT -clear
  • Lungs -CTAB
  • Heart -ejection click with grade III/VI SEM at base of heart and RUSB, radiation to both carotid arteries.
  • Abdomen soft, no organomegaly
  • Extremities no c/c/e
  • Neuro –alert, CNs 2-12 intact, strength 5/5 in all major muscle groups, DTRs 2/4 in all extremities, sensation intact in all extremities, cerebellar function intact to RAM, Romberg neg (aka: normal)

•EKG:
–Left ventricular hypertrophy and ST segment depression in left precordial leads suggestive of strain pattern caused by transient left ventricular subendocardial ischemia
•Echocardiogram
–Bicuspid aortic valve with moderate to severe aortic stenosis and LVH

A
  • Adrenal Insufficiency and Adrenal Crisis
  • Aneurysm, Abdominal
  • Aortic Stenosis
  • Asystole
  • Atrial Fibrillation
  • Brugada Syndrome
  • Cardiomyopathy, Restrictive
  • Dissection, Aortic
  • Heart Block, Second Degree
  • Heart Block, Third Degree
  • Hypoglycemia
  • Hyponatremia
  • Long QT Syndrome
  • Mitral Stenosis
  • Multifocal Atrial Tachycardia
  • Myocardial Infarction
  • Pulmonary Embolism
  • Pulmonic Valvular Stenosis
  • Sinus Bradycardia
  • Subarachnoid HemorrhageTetralogy of Fallot
  • Torsade de Pointes
  • Toxicity, Amphetamine
  • Toxicity, Antidepressant
  • Toxicity, Antidysrhythmic
  • Toxicity, Beta-blocker
  • Toxicity, Calcium Channel Blocker
  • Toxicity, Cocaine
  • Toxicity, Cyclic Antidepressants
  • Wolff-Parkinson-White Syndrome

•EKG:
–Left ventricular hypertrophy and ST segment depression in left precordial leads suggestive of strain pattern caused by transient left ventricular subendocardial ischemia
•Echocardiogram
–Bicuspid aortic valve with moderate to severe aortic stenosis and LVH

92
Q

12 year old male child presents with intermittent chest pain.
Preliminary DDx?

•HPI
–LUSB
–sharp, stabbing
–No radiation
–5/10 severity
–Intermittent for 5 days
–Not worsening
–No clear alleviating factors
–Worse with deep inspiration

VSS
Pertinent PE
•Chest wall: pain upon palpation at LUSB, costochondral junction
•Heart* unremarkable exam

•Diagnosis based on physical exam finding: reproducible pain

A 
Cardiac
–Inflammatory
–Increased myocardial demand or decreased supply
cardiomyopathy
LVOT
Arrhythmias
Coronary artery abnormalities
Miscellaneous
Aortic dissection
Rupture of aortic aneurysm
Pulmonary HTN
MVP
Atrial myxomas
Cardiac device/stent complications
Drugs
Cocaine
Overdose of sympathomimetics
Noncardiac
–Musculoskeletal etiology very common
•Costochondritis
•Tietze syndrome
•Nonspecific
•Slipping rib syndrome
•Trauma, strain
•Precordial catch
•Xiphodynia
–GI
–Psychogenic
–Zoster
–Spinal cord/nerve root compression in conjunction with scoliosis
•Costochondritis
–Normal findings
–Well appearing child
–Reproducible tenderness
Treatment:
NSAIDs, warm compresses if needed
93
Q

Parents bring a 3 year old child to the clinic because of “lethargy” and fast breathing.
Preliminary DDx?

•Over the past week they’ve noticed that she has been fussy and less playful. She had a cold about a week and a half ago which seemed to have resolved.
•She has been lying around “lethargic” all day.
–Let’s take a moment to clarify lethargy!
•Decreased intake but normal urine output.
•No fevers

  • VS –HR 180, RR 44, T 99.0F, BP 110/76, O2 sat: 88% RA
  • General –tired appearing, tachypneic, WN/WD female
  • Skin –no apparent cyanosis
  • HEENT -clear
  • Lungs –faint crackles bilateral bases, tachypnea, no retractions
  • Heart -tachycardic, S1 and S2 present, S3 gallop noted, PMI displaced to anterior axillary line
  • Abdomen –hepatomegaly
  • GU –Tanner I
  • Extremities –no c/c/e
  • Neuro –alert and interactive
A 
•See Dyspnea
•Physiologic and mechanical
•Fever
–Feverincreases Respiratory Rateup to 10 breaths/min per degree Celsius
•Exertion
•Pain
•Abdominal distention
•Respiratory muscle paralysis
•Obesity
•Anxiety or Panic Disorder
•Hypoglycemia
•Cardiovascular (decreased perfusion or oxygen carrying capacity)
•Congestive Heart Failure
•Anemia
•Hyperthyroidism
•Pulmonary Embolism
•Respiratory
•Pneumonia(or Pediatric Pneumonia)
•Chronic Obstructive Pulmonary Disease
•Asthma
•Pneumothorax
•Hypoxemiaor Hypercapnia
•Interstitial Lung Disease
•Pulmonary edema
•Compensatory acid-base
•Metabolic Acidosis
•Sepsis(Lactic Acidosisas well as fever)
•Neurologic
•Brain mass
•Hepatic Encephalopathy
•Medications
•Salicylates
•Sympathomimetics (Amphetamines, Cocaine)
•Anticholinergics
•Cholinergics (variable effect)
•Hallucinogens (Ketamine, PCP)
•Cannabinoids (Marijuana,

Acquired dilated cardiomyopathy of viral etiology
Treatment
-O2, IV, monitor
-Same as for CHF: preload reduction, afterload reduction, diuresis, and airway support.

94
Q

Heart* -grade II/VI systolic ejection murmur best heard over interscapularregion; normal S1 and S2; femoral pulses weaker than brachial bilaterally
•Abdomen –slight hepatomegaly

A

Coarctation of the aorta (corrected –previously an error here)

95
Q

Heart* -ejection click with grade III/VI SEM at base of heart and RUSB, radiation to both carotid arteries.

A

Aortic stenosis with LVH

96
Q

Reproducible tenderness

A

costochondritis

97
Q

tachycardic, S1 and S2 present, S3 gallop noted, PMI displaced to anterior axillary line
•Abdomen –hepatomegaly

A

Acquired dilated cardiomyopathy of viral etiology

CV Exam III (17 decks)

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