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CKPeds > Cardio > Flashcards

Cardio Flashcards

1
Q

First heart sound (S1)

• Closure of_____ and _____

A

mitral and tricuspid valves (MV, TV)

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2
Q

Usually no discernible splitting of S1 but in completely normal child, a split S1 represents _____

A

asynchronous closure of the 2 valves (20−30 msec difference);

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3
Q

Split S1 best heard at apex or right upper sternal border may be a click (opening of stenotic valve) may be heard in ________

A

aortic stenosis

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4
Q

Apical mid systolic click of _____

A

mitral valve prolapse

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5
Q

At upper left sternal border, a click may be heard from ________

A

pulmonic valve stenosis;

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6
Q

What pathology?

this changes with respiration (with inspiration, venous
return is increased, thus causing the abnormal pulmonary valve to float superiorly after which the click softens or disappears)

A

pulmonic valve stenosis;

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7
Q

______ (e.g., Ebstein anomaly) may cause billowing of the

leaflets and result in multiple clicks

A

Tricuspid valve abnormalities

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8
Q

S1 may be inaudible at the________ mostly due to sounds that obscure the closure of the MV and TV, e.g., in VSD, PDA, mitral or tricuspid regurgitation and
severe right ventricular outflow tract obstruction

A

lower left sternal border

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9
Q

if the first heart sound is not heard at the lower left sternal border, there is most likely a ________ and there will be other clinical and auscultatory findings

A

congenital heart

defect,

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10
Q

Wider splitting of S2 on inspiration is related not only to increased venous return but also to ______

A

pressures in the aorta and pulmonary artery (PA) (it is significantly higher in the Ao than in the PA, so Ao valve closes first)

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11
Q

Wider than normal splitting will occur with any lesion that _________

A

allows more blood to traverse the PV compared to normal

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12
Q

Increased splitting of S2 may be fixed with respect to respiration if there is __________otherwise, it will continue to vary with respiration; may also hear fixed splitting with a right bundle branch block

A

increased volume and hence pressure in the right atrium (e.g., ASD);

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13
Q

______: heard with PA hypertension (increased pressure closing the PV causes early closure of the anterior semilunar valve resulting in a loud single S2)

A

Loud single S2

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14
Q

Hear early in diastole; creates a gallop rhythm with S1 + S2; very low frequency and is best heard with bell of the stethoscope at cardiac apex; asking patient to lie on left side may increase intensity

A

S3

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15
Q

Occurs in late diastole, just prior to S1 (presystolic) and is produced by a decrease in compliance (increased stiffness) of the LV

A

Fourth heart sound (S4)

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16
Q

S4

never hear with atrial fibrillation because______

A

the contraction of the atria is ineffective

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17
Q

Summation gallop rhythm (S3 + S4) may be found with _______, _____ or ______

A

improving CHF, myocarditis,

or a cardiomyopathy

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18
Q

Generated by blood flowing into the lungs due to

(1) pulmonary arteries, which have limited blood flow in utero and are therefore small with significantly increased blood flow after birth (turbulence from RV blood flowing through these arteries), and
(2) increasing cardiac output associated with declining [Hgb] over the first weeks of life (physiologic anemia)

A

Peripheral pulmonic stenosis

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19
Q

Peripheral pulmonic stenosis

• Normal finding age ________

A

6 weeks to 1 year

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20
Q

Precordial activity is normal, as are S1 and S2; the murmur is typically low-pitched (bell of stethoscope), musical-quality and often radiates throughout the precordium.

A

Still’s murmur

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21
Q

Stills murmur is Murmur is loudest while supine (greater blood flow) and decreases sitting or standing—
opposite to the finding of _______

A

HOCM

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22
Q

Still’s murmur

• Commonly heard first at age ______

A

3−5 years

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23
Q
  • Most common congenital heart lesion

* Most are membranous

A

Ventricular Septal Defect (VSD)

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24
Q

VSD

Shunt determined by ratio of _______

A

PVR to SVR

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25
Q

VSD

When PVR>SVR, ______ (must not be allowed to happen)

A

Eisenmenger syndrome

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26
Q

VSD murmur findings

A

− Harsh holosystolic murmur over lower left sternal border ± thrill; S2 widely split
– With hemodynamically significant lesions, also a low-pitched diastolic rumble across the mitral valve heard best at the apex

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27
Q

Small muscular VSD more likely to close in first 1–2 years than _________

A

membranous

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28
Q

Indications for Sx of VSD

A

Failure to thrive or unable to be corrected medically
° Infants at 6–12 months with large defects and pulmonary artery hypertension
° More than 24 months of age with Qp:Qs >2:1 (shunt fraction)

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29
Q

Atrial Septal Defect (ASD)

• ________ most common (in region of fossa ovalis)

A

Ostium secundum defect

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30
Q

PE of ASD

A

− Wide fixed splitting of S2

− Systolic ejection murmur along left mid to upper sternal border (from increased pulmonary flow)

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31
Q

ECG of ASD

A

ECG—right-axis deviation and RVH

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32
Q

Sx for ASD

A

Surgery or transcatheter device closure for all symptomatic patients or 2:1 shunt

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33
Q

Cx of ASD

A

− Dysrhythmia

− Low-flow lesion; does not require endocarditis prophylaxis

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34
Q

− When both ASDs and VSDs occur, which are contiguous, and the atrioventricular valves are abnormal

A

Endocardial Cushion Defect

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35
Q

SSx of Endocardial Cushion defects

A

Left-to-right shunt at both atrial and ventricular levels; some right-to-left shunting with desaturation (mild, intermittent cyanosis)

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36
Q

PE of Endocardial Cushion defects

A

Pulmonary systolic ejection murmur, low-pitched diastolic rumble at left sternal border and apex; may also have mitral insufficiency (apical harsh holosystolic murmur
radiating to left axilla

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37
Q

CXR of Endocardial Cushion defects

A

significant cardiomegaly, increased pulmonary artery and pulmonary blood flow and edema

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38
Q

ECG of Endocardial Cushion defects

A

signs of biventricular hypertrophy, right atrial enlargement, superior QRS axis

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39
Q

Sx for Endocardial cushion defects

A

Treatment—surgery more difficult with heart failure and pulmonary hypertension (increased pulmonary artery pressure by 6−12 months of age); must be performed in
infancy

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40
Q

Results when the ductus arteriosus fails to close; this leads to blood flow from the aorta to the pulmonary artery

A

Patent Ductus Arteriosus (PDA)

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41
Q

RF for Patent Ductus Arteriosus (PDA)

A

− More common in girls by 2:1
− Associated with maternal rubella infection
− Common in premature infants (developmental, not heart disease

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42
Q

PE of PDA

A

If large—heart failure, a wide pulse pressure, bounding arterial pulses, characteristic
sound of “machinery,” decreased blood pressure (primarily diastolic)

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43
Q

CXR of PDA

A

increased pulmonary artery with increased pulmonary markings and edema; moderate-to-large heart size

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44
Q

2D echo of PDA

A

Echocardiogram—increased left atrium to aortic root; ductal flow, especially in diastole

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45
Q

Pathophysio of PS

A

Deformed cusps → opens incompletely during systole; obstruction to right ventricular outflow → increased systemic pressure and wall stress → right ventricular
hypertrophy (depends on severity of pulmonary stenosis

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46
Q

Neonate with severe pulmonary stenosis = critical pulmonary stenosis = R → L shunt via _____

A

foramen ovale

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47
Q

PE of PS

A

Pulmonary ejection click after S1 in left upper sternal border and normal S2 (in mild); relatively short, low-to-medium−pitched SEM over pulmonic area radiating
to both lung fields

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48
Q

ECG of PS

A

right ventricular hypertrophy in moderate to severe; tall, spiked P-waves; right atrial enlargement (RAE)

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49
Q

CXR of PS

A

poststenotic dilatation of pulmonary artery; normal-to-increased heart size (right ventricle) and decreasing pulmonary vascularity

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50
Q

Tx of PS

Treatment
− Moderate to severe—______ initially; may need surgery
− Neonate with critical pulmonary stenosis—______

A

balloon valvuloplasty

emergent surgery

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51
Q

AS

__________—sporadic, familial, or with Williams syndrome

A

Supravalvular stenosis (least common form)

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52
Q

What syndrome?

mental retardation, elfin facies, heart disease, idiopathic hypercalcemia; deletion of elastin gene 7q11.23

A

Williams syndrome

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53
Q

AS

If severe early in infancy = critical aortic stenosis =________

A

left ventricular failure and decreased cardiac output

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54
Q

Findings of severe AS

A

With increasing severity—decreased pulses, increased heart size, left ventricular apical thrust

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55
Q

Tx of AS

A

− Balloon valvuloplasty
− Surgery on valves
− Valve replacement

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56
Q

narrowing at any point from transverse arch to iliac bifurcation

A

Coarctation of the Aorta

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57
Q

Location of most COA

A

90% just below origin of left subclavian artery at origin of ductus arteriosus (juxtaductal coarctation)

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58
Q

What type of COA

Ascending aortic blood flows normally through narrowed segment to reach descending aorta, but there is left ventricular hypertrophy and hypertension

A

Discrete juxtaductal coarctation (adult type)

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59
Q

PE of Discrete juxtaductal coarctation (adult type)

A

Femoral and other lower pulses weak or absent; bounding in arms and carotids; also delay in femoral pulse compared to radial (femoral normally occurs slightly
before radial)

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60
Q

Normally, leg systolic pressure is 10–20 mm Hg higher than in arms; in coarctation, leg systolic pressure is _______

A

decreased (>5%)

61
Q

Severe narrowing starting at one of the head or neck vessels and extending to the ductus

A

Tubular hypoplasia (preductal, infantile type)

62
Q

Tubular hypoplasia (preductal, infantile type) SSx

A

Seen as differential cyanosis—upper body is pink, lower is cyanotic; prominent heart failure as ductus closes (if completely atretic = interrupted aortic arch)

63
Q

Xray findinfs of COA

 Increased size of subclavian artery-_______
 Notching of inferior border of ribs from______
_________n of ascending aorta

A

—prominent shadow in left superior mediastinum

passive erosion of increased collaterals in late childhood

 Poststenotic dilatatio

64
Q

COA Tx

A

− Neonate—PGE1 infusion to maintain patent, ductus, which establishes adequate
lower extremity blood flow; surgery after stabilization
− Surgery soon after diagnosis of any significant coarctation

65
Q

Cx of COA

A

− Associated cerebrovascular disease
− Systemic hypertension
− Endocarditis
− Aortic aneurysms

66
Q

Cyanotic Lesions Associated with Decreased Pulmonary

Blood Flow

A

Tetralogy of Fallot (TOF)
Tricuspid atresia
Ebstein anomaly

67
Q

Components of TOF

A

− Pulmonary stenosis and infundibular stenosis (obstruction to right ventricular outflow)
− VSD
− Overriding aorta (overrides the VSD)
− Right ventricular hypertrophy

68
Q

TOF

Pulmonary stenosis plus hypertrophy of subpulmonic muscle (crista supraventricularis)
→ varying degrees of ________

A

right ventricular outflow obstruction

69
Q

What are Paroxysmal hypercyanotic attacks (tet spells)

A

° Acute onset of hyperpnea and restlessness → increased cyanosis → gasping → syncope (increased infundibular obstruction with further right-to-left shunting

70
Q

Tx of Paroxysmal hypercyanotic attacks (tet spells)

A

place in lateral knee-chest position, give oxygen, inject subcutaneous morphine, give beta-blockers

71
Q

PE of TOF

A

substernal right ventricular impulse, systolic thrill along thirdto- fourth intercostal space on left sternal border, loud and harsh systolic ejection murmur (upper sternal border), may be preceded by a click; either a single S2 or soft
pulmonic component

72
Q

CXR of TOF

A

boot-shaped heart plus dark lung fields (decreased pulmonary blood flow)

73
Q

ECG of TOF

A

right axis deviation plus right ventricular hypertrophy

74
Q

Tx of TOF depends on?

A

Depends on degree of obstruction

75
Q

Medical Tx of TOF

A

PGE1 infusion—prevent ductal closure; given if cyanotic at birth

76
Q

Sx Tx of TOF

A

Augment pulmonary blood flow with palliative systemic to pulmonary shunt (modified Blalock-Taussig shunt)

77
Q

Sx Tx of TOF

A

Corrective surgery (electively at age 4–12 months)—remove obstructive muscle, valvulotomy, and patching of VSD

78
Q

What condition?

no outlet from the right atrium to the right ventricle; entire
venous (systemic) return enters the left atrium from a foramen ovale or ASD (there must be an atrial communication); left ventricular blood to right ventricle (atretic) via a VSD and is augmented by PDA;

A

Tricuspid atresia

79
Q

Tricuspid atresia dependes on?

A

pulmonary blood flow depends on presence

(and size) of VSD

80
Q

PE of TA

A

Increased left ventricular impulse (contrast to most others with right ventricular impulse), holosystolic murmurs along left sternal border (most have a VSD; though right ventricle is small, it is still a conduit for pulmonary blood flow)

81
Q

CXR of TA

A

Chest x-ray—pulmonary undercirculation

82
Q

ECG of TA

A

ECG—left axis deviation plus left ventricular hypertrophy (distinguishes from most other congenital heart disease)

83
Q

Tx of TA

A

− PGE1 until aortopulmonary shunt can be performed
− May need an atrial balloon septostomy (to make larger ASD)
− Later, staged surgical correction

84
Q

Downward displacement of abnormal tricuspid valve into right ventricle; the right ventricle gets divided into two parts: an atrialized portion, which is thin-walled, and
smaller normal ventricular myocardium

A

Ebstein anomaly

85
Q

Ebstein anomaly is associated with?

A

Development associated with periconceptional maternal lithium use in some cases

86
Q

Why is RV output decreased in Ebstein?

A

− Poorly functioning, small right ventricle
− Tricuspid regurgitation
− Variable right ventricular outflow obstruction

87
Q

Ebstein: Severity and presentation depend upon

A

degree of displacement of valve and degree

of right ventricular outflow obstruction

88
Q

PE of Ebstein

A

Holosystolic murmur of tricuspid insufficiency over most of anterior left chest (most characteristic finding)

89
Q

CXR of Ebstein

A

Chest x-ray—heart size varies from normal to massive (increased right atrium); if severe, decreased pulmonary blood flow

90
Q

ECG of Ebstein—

A

tall and broad P waves, right bundle branch block

91
Q

Tx of Ebstein

A

− PGE1
− Systemic-to-pulmonary shunt
− Then staged surgery

92
Q

Aorta arises from the right ventricle, and the pulmonary artery from the left ventricle; d = dextroposition of the aorta anterior and the right of the pulmonary artery
(normal is posterior and to the right of the pulmonary artery)

A

TGA

93
Q

In TGA, Series circuit changed to 2 parallel circuits; need _______ and _______ for some mixture of desaturated and oxygenated blood; better mixing in half of patients with a VSD

A

foramen ovale and PDA

94
Q

SSx of PDA

_________—as PDA starts to close, severe cyanosis and
tachypnea ensue

A

With intact septum (simple TGA)

95
Q

PE of TGA

A

S2 usually single and loud; murmurs absent, or a soft systolic ejection murmur at
midleft sternal border

96
Q

CXR of TGA

A

“Egg on a string” appearance—narrow heart base plus absence of main segment of the pulmonary artery

97
Q

ECG of TGA—

A

normal neonatal right-sided dominance

98
Q

What condition?

− Single arterial trunk arises from the heart and supplies all circulations.
− Truncus overlies a ventral septal defect (always present) and receives blood from both ventricles (total mixing).
− Both ventricles are at systemic pressure

A

Truncus Arteriosus

99
Q

Truncus arteriosis is one of the major conotruncal lesions

associated with the____________Also seen are transposition of the great arteries and aortic arch abnormalities.

A

CATCH-22 syndrome, i.e., DiGeorge.

100
Q

In Truncus,

With dropping pulmonary vascular resistance in first week of life, pulmonary blood flow is greatly increased and results in___________

A

heart failure.

101
Q

SSx of Truncus

A

Large volume of pulmonary blood flow with total mixing, so minimal cyanosis

102
Q

PE of Truncus

A

Single truncal valve, which may be incompetent (high-pitched, early diastolic decrescendo at mid-left sternal border)

103
Q

PE of Truncus

A

Initially, SEM with loud thrill, single S2, and minimal cyanosis

104
Q

CXR of Truncus

A

Chest x-ray—heart enlargement with increased pulmonary blood flow

105
Q

ECG of Truncus

A

ECG—biventricular hypertrophy

106
Q

What condition?

A

Complete anomalous drainage of the pulmonary veins into the systemic venous circulation; total mixing of systemic venous and pulmonary venous blood within the
heart produces cyanosis

107
Q

Blood flow in TAPVR

A

Right atrial blood → right ventricle and pulmonary artery or to left atrium via foramen ovale or ASD

108
Q

SSx of TAPVR with obstruction

A

Obstruction (of pulmonary veins, usually infracardiac):

° Severe pulmonary venous congestion and pulmonary hypertension with decreasing cardiac output and shock

109
Q

SSx of TAPVR without obstruction

A

total mixing with a large left-to-right shunt; mild cyanosis; less likely to be severely symptomatic early

110
Q

CXR ot TAPVR

A

large supracardiac shadow with an enlarged cardiac shadow forms a “snowman” appearance; pulmonary vascularity is increase

111
Q

ECG of TAPVR

A

− ECG—RVH and tall, spiked P waves (RAE)

112
Q

Atresia of mitral or aortic valves, left ventricle, and ascending aorta (or any combination

A

Hypoplastic Left Heart Syndrome

113
Q

In TAPVR

Right ventricle______ maintains both pulmonary and systemic circulation.

A

Right ventricle

114
Q

BF on Hypoplastic Left Heart Syndrome

A

Pulmonary venous blood passes through foramen ovale or ASD from left atrium → right atrium and mixes with systemic blood to produce total mixing

115
Q

IN HLHS,

________ supplies the descending aorta, ascending aorta and coronary arteries from retrograde flow

A

Ductus arteriosus

116
Q

In HLHS,

Systemic circulation cannot be maintained, and if there is a moderate-to-large ASD → ________

A

pulmonary overcirculation

117
Q

SSx of HLHS

A

− Cyanosis may not be evident with ductus open, but then gray-blue skin color (combination of hypoperfusion and cyanosis as ductus closes)
− Signs of heart failure, weak or absent pulses, and shock

118
Q

ECG of HLHS

A

right ventricular hypertrophy and right arial enlargement with decreased left-sided forces

119
Q

Best Tx for HLHS

A

The best treatment today is the three-stage Norwood procedure. (better results currently than cardiac transplantation

120
Q

Abnormal cusps—billowing of one or both leaflets into left atrium toward end of systole (congenital defect)

A

MVP

121
Q

Arrhythmias associated with MVP

A

especially uni- or multifocal premature ventricular contractions

122
Q

PE of MVP

A

Apical late systolic murmur, preceded by a click—in abrupt standing or Valsalva, click may appear earlier in systole and murmur may be more prominent

123
Q

MC organisms asstd with IE

A

Most are Streptococcus viridans (alpha hemolytic) and Staphylococcus aureus

124
Q

IE organisms associations

°_______—after dental procedures
° ______—large bowel or genitourinary manipulation
°_______—intravenous drug users
° _______—after open heart surgery
° ________—indwelling intravenous catheters

A

S. viridans

Group D streptococci

Pseudomonas aeruginosa and Serratia marcescens

Fungi

Coagulase-negative Staphylococcus

125
Q

Highest risk of IE with______ and _______

A

prosthetic valve and uncorrected cyanotic heart lesions

126
Q

IE

Most cases occur after _____ or _____

A

surgical or dental procedures (high risk with poor dental hygiene) are performed.

127
Q

IE

Splenomegaly, petechiae, embolic stroke, CNS abscess, CNS hemorrhage, mycotic aneurysm (all more with ____________

A

Staphylococcus

128
Q

IE

Skin findings—rare; late findings (uncommon in treated patients); represent _________

A

vasculitis from circulating Ag-Ab complexes;

129
Q

IE findings

° ______—tender, pea-sized, intradermal nodules on pads of fingers and toes
° ______—painless, small erythematous or hemorrhagic lesions on palms
and soles
° Splinter hemorrhage—linear lesions beneath nail beds
º Roth spots—
retinal exudate

A

Osler nodes

Janeway lesions

130
Q

Dx of IE

A

Duke criteria (2 major or 1 major + 3 minor or 5 minor)

131
Q

Major Duke Criteria

A

• Positive blood culture (two separate
for usual pathogens; at least two for less
common)

• Evidence on echocardiogram
(intracardiac or valve lesion, prosthetic
regurgitant flow, abscess, partial
dehiscence of prosthetic valve, new
valvular regurgitant flow)
132
Q

Minor Criteria Duke Criteria

A 
• Predisposing conditions
• Fever
• Emboli or vascular signs
• Immune complex disease (glomerulonephritis,
arthritis, positive rheumatoid
factor, Osler node, Roth spots [retinal
hemorrhages with white centers])
• Single positive blood culture
• Echocardiographic signs not meeting
criteria
133
Q

Tx of Duke

A

Organism specific for 4−6 weeks (S. viridans, Enterococci, S. aureus, MRSA,
S. epidermidis, HACEK)

134
Q

ARF related to what organism

A

Related to group A Streptococcus infection within several weeks

135
Q

Remains most common form of acquired heart disease worldwide (but Kawasaki in United States and Japan)

A

Acute Rheumatic Fever

136
Q

What is the Jones criteria

A

Absolute requirement: evidence of recent Streptococcus infection (microbiological or serology); then two major or one major and two minor criteria

137
Q

ARF Tx

__________ (if allergic) for 10 days will eradicate group A strep; then need long-term prophylaxis

A

Oral penicillin or erythromycin

138
Q

Anti-inflam meds for ARF

Hold if arthritis is only typical manifestation because?

A

(may interfere with characteristic migratory progression)

139
Q

If carditis with CHF, _____ for 2–3 weeks, then taper; start ______ for 6 weeks

A

prednisone

aspirin

140
Q

If chorea is only isolated finding, do not need aspirin; drug of choice is _______

A

phenobarbital

then haloperidol or chlorpromazine

141
Q

ARF prophylaxis

reatment of choice—

A

single intramuscular benzathine penicillin G every 4 weeks

142
Q

Pathophysiology

− Obstructive left-sided congenital heart disease

A

Hypertrophic Obstructive Cardiomyopathy (HOCM)

143
Q

SSx of Hypertrophic Obstructive Cardiomyopathy (HOCM)

A

Clinical presentation—weakness, fatigue, dyspnea on exertion, palpitations, angina, dizziness, syncope; risk of sudden death

144
Q

Problem with Hypertrophic Obstructive Cardiomyopathy (HOCM)

A

Decreased compliance, so increased resistance and decreased left ventricular filling, mitral insufficiency

145
Q

PE with Hypertrophic Obstructive Cardiomyopathy (HOCM)

A

left ventricular lift, no systolic ejection click (differentiates
from aortic stenosis), SEM at left sternal edge and apex (increased after exercise, during Valsalva, and standing)

146
Q

ECG with Hypertrophic Obstructive Cardiomyopathy (HOCM)

A

ECG—left ventricular hypertrophy ± ST depression and T-wave inversion; may have intracardiac conduction defect

147
Q

2D ECHO with Hypertrophic Obstructive Cardiomyopathy (HOCM)

A

Echocardiogram—left ventricular hypertrophy, mostly septal; Doppler—left ventricular outflow gradient usually mid-to-late systole (maximal muscular outflow
obstruction)

148
Q

Drugs contraindicated for HOCM

A

Digoxin and aggressive diuresis are contraindicated (and infusions of other inotropes)

149
Q

Drugs indicated for HOCM

A

Beta blockers (propranolol) and calcium channel blockers (verapamil

CKPeds (20 decks)

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