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Pediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Congenital disorders that can result in CHF

A
  • Increased pulmonary blood flow
  • Obstructive lesions
  • AV malformations
  • Mitral or tricuspid regurgitation
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2
Q

Acquired heart disorders that can result in CHF

A
  • Viral myocarditis
  • Endocarditis
  • Pericarditis
  • Metabolic disease (eg hypothyroidism)
  • Medications (eg doxorubicin)
  • Cardiomyopathies
  • Ischemic diseases
  • Dysrhythmias (tachycardia and bradycardia)
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3
Q

Miscellaneous causes of CHF

A
  • Severe anemia (high-output CHF)
  • Rapid infusion of IV fluids, esp in premature infants
  • Obstructive processes of the airways (enlarged tonsils or adenoids, laryngomalacia, CF - may cause CHF as a result of chronic hypoxemia that results in right sided heart failure)
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4
Q

Clinical features of CHF

A
  • Tachypnea
  • Cough
  • Wheezing
  • Rales
  • Pulmonary edema on CXR
  • Tachycardia
  • Sweating
  • Pale or ashen skin color
  • Diminished urine output
  • Enlarged cardiac silhouette
  • Hepatomegaly
  • Peripheral edema
  • Failure to thrive
  • POOR FEEDING (common in newborns)
  • Exercise intolerance
  • Cyanosis and shock (late manifestations)
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5
Q

Innocent cardiac murmurs

A
  • Result from turbulent blood flow and are NOT caused by structural heart disease and have no hemodynamic significance
  • Up to 50% of children
  • INCLUDE: Still’s murmur, pulmonic systolic murmur/ systolic ejection murmur, venous hum
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6
Q

Still’s murmur

A
  • Ages 2-7
  • Mid-left sternal border
  • Grade 1-3
  • Systolic
  • Vibratory, twanging, or buzzing
  • Loudest supine
  • Louder with exercise
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7
Q

Pulmonic systolic murmur/ systolic ejection murmur

A
  • Any age
  • Upper left sternal border
  • Grade 1-2
  • Peaks early in systole
  • Blowing, high-pitched
  • Loudest supine
  • Louder with exercise
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8
Q

Venous hum

A
  • Any age
  • Neck and below clavicles
  • Continuous murmur
  • Heard only sitting or standing
  • Disappears if supine; changes with compression of the jugular vein or with neck flexion or extension
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9
Q

Classifications of ASDs

A
  • Ostium primum
  • Ostium secundum
  • Sinus venosus
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10
Q

Ostium primum

A
  • Defect in the lower portion of the atrial septum
  • A cleft, or divison, in the anterior mitral valve leaflet may also be present and may cause mitral regurgitation
  • Common in Trisomy 21
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11
Q

Ostium secundum

A
  • Defect in middle portion of the atrial septum

- Most common type of ASD

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12
Q

Sinus venosus

A
  • Defect high in the septum near the junction of the right atrium and SVC
  • Right pulmonary veins usually drain anomalously into the right atrium or SVC instead of into the left atrium
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13
Q

Physical exam findings of ASD

A
  • Increased right ventricular impulse as a result of right ventricular overload
  • Systolic ejection murmur (from excessive pulmonary blood flow) best heard at mid and upper left sternal borders (a mid-diastolic filling rumble representing excessive blood flow through the tricuspid valve may also be heard)
  • Fixed split second heart sound because of the excessive pulmonary blood flow, the normal physiologic variation in timing of the aortic and pulmonic valve closure with respiration is absent
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14
Q

VSD classification

A

By location - inlet, trabecular (muscular), membranous, and outlet (supercristal)

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15
Q

Clinical features and course of small VSDs

A
  • Little to no shunt across the VSD
  • May close spontaneously
  • Thrill at the lower left sternal border and a grade 4 high pitched holosystolic murmur
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16
Q

Clinical features and course of moderate VSDs

A
  • May have a large shunt across the VSD that may result in signs and symptoms of CHF
  • Holosystolic murmur
  • If 2:1 pulmonary to systemic flow, then a diastolic murmur of mitral turbulence (mitral filling rumble representing the excess blood from the lungs now passing through the mitral valve) may be heard at apex
17
Q

Clinical features and course of large VSDs

A
  • Often cause signs and symptoms of CHF
  • Less turbulence across the VSD so systolic murmur is shorter and lower in pitch
  • Mitral filling rumble may be heard at the apex
18
Q

Large VSDs are associated with a high incidence of

A

Pulmonary infections from excessive blood flow

19
Q

Indications for surgical closure of VSDs

A
  • Heart failure refractory to medical management
  • Large VSDs with pulmonary hypertension are usually surgically closed at 3-6 mo of age
  • Small to moderate VSDs are usually surgically closed between 2 and 6 years of age
20
Q

Symptoms of small PDAs

A

Usually produce no symptoms

21
Q

Symptoms of moderate and large PDAs

A

Generally result in signs and symptoms of VHF due to increased pulmonary blood flow

22
Q

Clinical features of neonates or infants with severe coarctation

A
  • Depend on a right to left shunt through the PDA for perfusion of the lower thoracic and descending aorta
  • May be minimally symptomatic initially, but symptoms of CHF develop and progress as PDA closes
  • BP may be elevated in the upper extremities and low in the lower extremities before the onset of CHF
  • Once CHF develops, pulses in all 4 extremities are poor, any murmur is absent and hypotension may develop
23
Q

Clinical features of older children or adolescents with coarctation

A
  • May have no symptoms and may have only hypertension or a heart murmur
  • HTN is typically noted in the right arm and BP is reduced in the lower extremities
  • Femoral pulse, which normally precedes the radial pulse is dampened and delayed until after the radial pulse (radio-femoral delay)
  • BP and pulse findings may be less prominent if collateral vessels (intercostal arteries) develop that allow the ascending aortic pressure and flow to circumvent the coarctation
  • Bicuspid aortic valve or aortic stenosis is present in 50% of patients
  • Bruit of turbulence through the coarctation may be audible at the left upper back near the scapula
24
Q

Initial management of coarctation

A
  • Directed at improving circulation to the lower body
  • IV prostaglandin E (PGE) is given urgently to open the ductus arterioles
  • Inotropic medications are given to overcome myocardial depression and low dose dopamine is used to maximize renal perfusion and function
25
Q

In the neonate, severe aortic stenosis may be associated with

A

Hypoplasia of the left ventricle as a result of impaired fetal left ventricular development

26
Q

Clinical features of neonates with severe aortic stenosis

A
  • Critical aortic stenosis

- Normal at birth, but develop signs and symptoms of CHF at 12-24 hours of age

27
Q

Clinical features of older children with aortic stenosis

A
  • Generally, no symptoms

- Once severe, symptoms include exercise intolerance, chest pain, syncope, and even sudden death

28
Q

Peripheral cyanosis

A

Caused by vasomotor instability or vasoconstriction as a result of cold temperature

29
Q

Central cyanosis

A

Attributable in both cardiac and non cardiac causes, it is esp apparent in the tongue and inner mucous membranes:

  • Non-cardiac: pulmonary disease, sepsis, hypoglycemia, polycythemia, and neuromuscular diseases that impair chest wall movement
  • Cardiac: Tetralogy of Fallot, transposition of the great arteries, tricuspid atresia, truncus arterioles and total anomalous pulmonary venous connection
30
Q

Most common cause of central cyanosis presenting beyond the newborn period

A

Tetralogy of Fallot

31
Q

Physical exam findings of transposition of great vessels

A
  • Central cyanosis
  • Quiet precordium
  • Single S2 (because the aortic valve is anterior and the pulmonary valve is posterior in TGA, the closure of the pulmonary valve is difficult to hear)
  • No murmur
32
Q

What is always present in tricuspid atresia

A

An ASD or PFO

Pediatrics (11 decks)

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