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PANP802 > Exam 1 Cardiac > Flashcards

Exam 1 Cardiac Flashcards

1
Q

Functional closure of PDA at:

A

48-72 hours after birth

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2
Q

Complete anatomical closure of PDA at:

A

2-3 weeks

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3
Q

Medical closure of PDA with what drug?

A

Prostaglandin inhibitor, like indomethacin

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4
Q

What 2 conditions can be detected by blood pressure measurements in children?

A 
#Coarctation of the aorta
#Systemic hypertension
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5
Q

How long does it take for fingernail clubbing to begin?

A

At least 6 months of arterial O2 desaturation

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6
Q

What peripheral pulse finding is present with coarctation of the aorta?

A

Pulse is absent or weaker in lower extremities in comparison with upper ones

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7
Q

Hepatomegaly, when noted in conjunction with other heart findings, is a strong indicator of what condition?

A

Right heart failure

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8
Q

Heave

A

PMI is diffuse, rises slowly

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9
Q

Tap

A

PMI is well localized & sharp

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10
Q

What percentage of kids have an innocent murmur?

A

50%

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11
Q

Innocent murmurs: Still’s

A 
#Between LLSB & apex
#Grade 1-3 systolic ejection
#Most commonly 2-7 yrs old
#Disappears with Valsalva
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12
Q

Innocent murmurs: peripheral pulmonic

A 
#LUSB with radiation to back & axillae
#Grade 1-2 systolic ejection
#Premature or low birth weight infants. Document resolution by 4-5 months vs organic cause or valve involvement
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13
Q

Innocent murmurs: pulmonary ejection

A 
#Localized to LUSB
#Grade 1-2 systolic ejection
#Disappears with valsalva
#8-14 yrs old, mostly adolescents
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14
Q

Innocent murmurs: venous hum

A 
#Inferior to clavicles @ RUSB, LUSB
#Grade 1-3 continuous
#Obliterated by light jugular venous compression
#3-6 yrs old
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15
Q

Innocent murmurs: supraclavicular carotid bruit

A 
#Superior to clavicles, radiation to neck
#Grade 1-3 holosystolic
#Diminishes with shoulder hyperextension
#Common @ any age
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16
Q

Criteria for positive pulse ox screening

A 
#Any O2 sat < 90%
#Any O2 sat < 95% in both extremities on 3 measures taken 1 hour apart
#Any 3% absolute difference between readings in upper &amp; lower extremity on 3 measure taken 1 hour apart
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17
Q

What CXR finding indicates cardiomegaly?

A

A cardiothoraic (CT) ratio greater than 0.65

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18
Q

Usefulness of ECG in pediatric cardiology

A

To confirm rather than diagnose a structural heart defect, or to diagnose an arrhythmia

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19
Q

Usefulness of echocardiogram in pediatric cardiology

A

Basically the diagnostic tool for EVERYTHING structural

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20
Q

What percentage of pediatric chest pain is cardiac in origin?

A

4%

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21
Q

Questions to ask in pediatric chest pain

A 
#Recent fever or illness
#Related to activity, breathing, exercise, or rest
#Sports activities or injuries preceding
#Palpitations, dizziness, or fainting
#Aggravating/Alleviating
#Illicit drugs, caffeine supplements or energy drinks
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22
Q

Serious business chest pain

A

Associated with exertion, dizziness, fainting, palpitations or radiates to back, jaw, or left arm

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23
Q

Maternal infections that may cause cardiac anomalies in the infant:

A 
#Rubella
#Viruses: cytomegalovirus, herpesvirus, coxsackievirus B teratogenic in early pregnancy, myocarditis in late pregnancy
#HIV assoc with infant cardiomyopathy
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24
Q

Maternal medications that may cause fetal anomalies

A 
#Amphetamines
#Anticonvulsants
#ACE inhibitors and ARBs
#Lithium
#Retinoic acid
#Valproic acid
#Progesterone, estrogen
#Alcohol
#Cigarette smoking (intrauterine growth delay)
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25
Q

Maternal conditions associated with infant heart defects

A 
#Diabetes
#Lupus erythematosus and connective tissue disease
#Congenital heart defect history
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26
Q

Growth impairment patterns in patients with CHD:

A 
#Cyanotic: height and weight
#Acyanotic: weight problems more than height
#Acyanotic with pressure overload lesions without shunt show normal growth
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27
Q

Inspection points in pediatric CHD

A 
#General appearance &amp; nutritional state
#Obvious syndrome or chromosomal abnormalities
#Color
#Clubbing
#Respiratory rate &amp; effort
#Diaphoresis
#Chest inspection
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28
Q

CXR: Transposition of the great arteries

A

Egg on a string

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29
Q

CXR: Total anomalous pulmonary venous return (TAPVR)

A

Snowman

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30
Q

CXR: Partial anomalous pulmonary venous return

A

Scimitar

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31
Q

CXR: Endocardial cushion defects

A

Gooseneck

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32
Q

CXR: Tetralogy of Fallot

A

Boot (Dansko!) shaped heart

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33
Q

CXR: Coarctation of the aorta

A

Figure of 3 or reverse figure of 3

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34
Q

CXR: Ebstein anomaly

A

Box-shaped heart

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35
Q

Pathology of polycythemia in CHD

A

Low arterial O2 stimulates erythropoetin from kidneys, increases production of RBC in bone marrow. Increased O2 capacity is beneficial.

36
Q

What can go wrong with polycythemia in CHD?

A

When hematocrit reaches 65%, blood suddenly much more viscous. Increased workload for the heart, and oops! Congestive heart failure.

37
Q

Pathology of clubbing in CHD

A

Tissue growth under nail bed. We’re not sure why.

38
Q

Pathology of CNS complications in CHD

A 
#Maybe high hematocrit or iron-deficient RBCs mean cyanotic CHD @ high risk for brain abscess, vascular stroke. 
#Pulmonary capillary bed provides filtering, bypassed by some right to left shunts, possibly allowing more bacteria opportunity to get in dat brain
39
Q

Common bleeding disorders in CHD

A

Thrombocytopenia & defective platelet aggregation. May need to withdraw RBCs, given equal amount of plasma to lower viscosity

40
Q

Other comorbidities found in CHD

A 
#Hypoxic spells, squatting
#Scoliosis (especially girls &amp; TOF)
#Hyperuricemia &amp; gout
41
Q

Transposition of the Great Arteries

A 
#Aorta arises from the RV, pulmonary artery arises from LV, so aorta is now anterior to the PA. 
#Desaturated blood goes from RV to system
#Already saturated blood goes from LV back to lungs
#Two parallel circuits
#Incompatible with life unless something stays open for the circuits to communicate
42
Q

How does TGA present?

A

Severe hypoxia, acidosis, and left heart overload lead to CHF within the first week of life.

43
Q

Why is atrial septal defect beneficial in TGA?

A

Large ASD allows the otherwise separate circuits communication, meaning blood mixing is possible and O2 sats can be up to 80-90%

44
Q

How does a VSD affect TGA?

A

Won’t present with arterial desaturation immediately, cyanosis possible to miss & metabolic acidosis doesn’t develop. Left CHF will happen in few weeks as PBF increases with decreasing PVR.

45
Q

Persistent Truncus Arteriosus & Single Ventricle

A 
#A single blood vessel arising from the heart and a single large ventricular chamber from which arises a single artery (either PA or aorta). In either case, there's total mixing of systemic &amp; pulmonary venous blood &amp; the O2 sat is basically the same everywhere. 
#Level of O2 sat in systemic circulation is proportional to the magnitude of pulmonary blood flow
46
Q

Do patients with PTA & SV get CHF?

A

No, because while there’s some cyanosis there’s no volume overload. At least there’s one thing going for it!

47
Q

Tetralogy of Fallot

A

Most common cyanotic CHD, has 4 abnormalities:

1) VSD
2) Pulmonary stenosis (RVOT obstruction; infundibular or valvular or both)
3) Right ventricular hypertrophy
4) Overriding aorta

48
Q

How does right ventricular outflow obstruction change the clinical picture in TOF?

A 
#Mild stenosis: shunt goes L to R and the overall picture is  that of a VSD
#Severe stenosis: raises the RV pressure, shunting R to L and worsening cyanosis
49
Q

Will acyanotic TOF stay that way?

A

Nope, they’ll be cyanotic TOF by 1-2 yrs old with the dyspnea & the tet spells

50
Q

What does the severity of the pulmonic ejection murmur tell us about TOF?

A

The more blood moves through the area of stenosis, the louder the murmur. Severity of murmur is inversely proportionate to the severity of stenosis!

51
Q

What’s the most severe form of TOF?

A

With pulmonary atresia, in which all systemic venous return is shunted R to L and the only pulmonary blood flow is through collaterals or the PDA. Incompatible with life if the PDA closes & requires immediate prostaglandin!

52
Q

What’s the treatment for severe TOF with pulmonary atresia?

A

Prostaglandin E1: KEEP THAT PDA OPEN!

53
Q

What’s up with hypoxic, or tet, spells?

A

Sudden increase in R to L shunting

54
Q

Clinical features of hypoxic spells

A 
#Hyperpnea
#Worsening cyanosis
#Disappearance of the murmur
55
Q

Treatment of hypoxic spells

A 
#Hold infant in knee-to-chest, decreasing venous return and increasing systemic vascular resistance by reducing arterial flow to the legs
#Morphine to slow respiratory rate
#Bicarb to correct acidosis (which stimulates respiratory center)
#Oxygen
#Vasoconstrictors to raise systemic vascular resistance
#Ketamine to raise systemic vascular resistance and sedates patient
#Propanolol but we're not sure why
56
Q

Squatting in TOF

A 
#Happens when kids are playing
#Increases systemic arterial oxygen
#Reduction of venous return by trapping blood in the legs, reducing R to L shunt
#Reduced arterial flow to legs reduces venous washout from leg muscles
#Increase in systemic vascular resistance, which reduces R to L shunt
57
Q

Tricuspid atresia

A

Tricuspid valve & portion of the RV do not exist. Because there’s no way from the RA to the RV, systemic venous return to RA is shunted first to LA through the ASD or PFO.

58
Q

Pulmonary atresia

A

Direct communication between RV and the pulmonary artery does not exist. The patent ductus arteriosis becomes the main source of pulmonary blood flow.

59
Q

Clinical features of pulmonary atresia

A 
#Notable cyanosis
#S2 is single because there's only one semilunar valve
#Biatrial hypertrophy, LVH
#Closure of PDA means baby is gonna tank unless there's a bunch of collaterals, so get that prostaglandin ready again
60
Q

Total Anomalous Pulmonary Venous Return

A

Pulmonary veins drain abnormally to the RA, either directly or indirectly

61
Q

Types of TAPVR

A 
#Supracardiac: Common pulmonary vein drains to superior vena cava
#Cardiac: Pulmonary veins empty directly into RA through coronary sinus
#Infracardiac (subdiaphragmatic): Common pulmonary vein traverses diaphragm and drains into portal or hepatic vein or inferior vena cava
#Classified physiologically as obstructive (infracardiac) or non-obstructive (cardiac &amp; supracardiac)
62
Q

Obstructive TAPVR clinical picture

A 
#Like a large ASD
#Right atrial &amp; ventricular hypertrophy
#Pulmonary congestion due to R heart failure
#Quadruple rhythm: S1, widely split S2, and S3 or S4
63
Q

Atrial septal defect

A 
#Communication between L and R atria
#3 types: secundum, primum, and sinus venosus
64
Q

Secundum atrial septal defect

A 
#At the site of fossa ovalis
#LA to RA shunting
65
Q

Sinus venous ASD

A 
#Located at entry of SVC into RA, maybe at entry of IVC into RA
#Commonly associated with anomalous pulmonary drainage
66
Q

Rate of spontaneous ASD closure

A

As high as 87%

67
Q

ASD spontaneous closure tidbits

A 
#ASD > 8mm rarely closes spontaneously
#Spontaneous closure unlikely after 4 years old
68
Q

If a large ASD left untreated:

A 
#Maybe CHF in infancy
#CHF, pulmonary hypertension begin in 20s-30s, and becomes common after 40
#Atrial arrhythmias
69
Q

ASD Management

A 
#Medical management for CHF in infancy, d/t possibility of spontaneous closure
#Non-surgical closure with catheter delivered device
#Surgical closure if non-surgical device isn't indicated (mid-sternal incision on CP bypass)
70
Q

Ventricular septal defect

A 
#VSD
#Communication between LV and RV
#Can be in the membranous vs muscular part of septum
71
Q

VSD clinical history

A 
#If small, asymptomatic
#If moderate to large, delayed growth &amp; development, decreased activity level, pulmonary infections, and CHF
72
Q

VSD physical exam

A 
#Small VSD: well developed &amp; cyanotic
#Large VSD: poor weight gain, CHF, clubbing if there's pulmonary vascular obstruction
#Systolic thrill @ LLSB, precordial bulge and hyperactivity
73
Q

VSD spontaneous closure tidbits

A 
#Occurs more frequently with itty-bitty ones
#Most likely in first 6 months
#60% of small to moderate musculars close, but not after 8 yrs
#35% of small perimembranous close, but not after 5 yrs
74
Q

VSD Natural History

A 
#Might spontaneous close
#CHF in infants with big ones
#Pulmonary vascular obstructive disease early as 6 to 12 months in large VSD, but R to L shunt not until teen years
75
Q

VSD Management

A 
#Medical: treat CHF with diuretics, maybe digoxin, captopril to reduce afterload
#No exercise restriction in absence of pulmonary hypertension
#Nonsurgical device closure, sometimes "hybrid" with a left thoracotomy incision but no sternotomy
#Surgical: indicated with big VSD, CHF, and growth retardation not improved by medical treatment. Ideally at 3-4 months old, no later than 6 months
76
Q

Patent ductus arteriosis

A

The ductus connecting the pulmonary artery and the descending aorta stays open instead of closing

77
Q

PDA clinical manifestations

A 
#Usually asymptomatic when ductus is small
#Large shunt may cause pulmonary infections, atelectasis, CHF, tachypnea &amp; poor weight gain
#Exertional dyspnea
78
Q

PDA physical exam

A 
#Tachycardia, tachypnea with CHF
# Bounding peripheral pulses, wide pulse pressure (not with small shunt)
#Large shunt = hyperactive precordium, systolic thrill @ LUSB
#Grade 1-4 "machinery" murmur @ LUSB
#If pulmonary vascular obstruction develops, R to L ductal shunt causes lower extremity cyanosis
79
Q

PDA natural history

A 
#Spontaneous closure rare in full-term infants/kids, more likely in preemies (because in full-term, it's because of an abnormality in the muscle, not because of decreased responsiveness to oxygen)
#CHF or recurrent pneumonia develops if shunt is big
#Pulmonary vascular obstruction if big PDA with pulmonary HTN goes untreated
#Rarely, aneurysm of PDA may develop &amp; rupture as adult
80
Q

PDA management

A 
#In preemies, indomethacin. Not in full term infants because it won't work
#No exercise restriction unless pulmonary HTN
#Nonsurgical occlusion of PDA is standard
81
Q

PDA nonsurgical closure

A 
#Transcatheter device 95-100% success rate
#Definitely indicated with hemodynamic instability &amp; CHF
#Reasonable to close if murmur is audible
#Not much data on closing "silent ductus"
82
Q

Endocardial cushion defect: what is it?

A

Abnormalities in the structures derived from endocardial cushion tissue: mitral & tricuspid valves, portions of the atrial & ventricular septum

83
Q

ECD: clinical history

A 
#Failure to thrive
#Recurring pulmonary infections
#CHF
84
Q

ECD: physical exam

A 
#Undernourished
#Signs of CHF
#Common in Down syndrome
#Hyperactive precordium, systolic thrill @ LLSB
#S1 accentuated, S2 narrow split
#Grade 3-4 holosystolic murmur @ LLSB
85
Q

ECD: radiography

A 
#Cardiomegaly always present, all 4 chambers
#Increased pulmonary vascular markings
#Main PA segment is prominent
#Gooseneck sign
86
Q

ECD: natural history

A 
#CHF 1-2 months after birth if ECD complete
#Die by 2-3 years without surgical intervention
#Pulmonary vascular obstruction by 6-12 months
#Down syndrome develops pulmonary obstruction sooner
87
Q

ECD: management

A 
#Medical: CHF management with diuretics, ACEI
#Surgical: For complete defect, gonna need this
#Surgical repair 2-4 months

PANP802 (4 decks)

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