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Pediatrics > Peds Cardio > Flashcards

Peds Cardio Flashcards

1
Q

At what day of gestation does the fetal heart begin pumping?

A

Day 22

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2
Q

In utero, why is blood shunted to bypass the lungs?

A

Fetal lungs are not yet functioning and have high resistance due to presence of fluid

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3
Q

Outline the steps to fetal circulation (poor oxygen blood to medium oxygen blood)

A

POB (poor oxygenated blood) Leaves via Umbilical Arteries (2) and goes to the placenta for oxygenation

HOB (high oxygenated blood) returns via Umbilical Vein - goes to fetal IVC and enters in the the Right Atrium.

Some of the HOB crosses to the LA via the Foramen Ovale.

The rest mixes with POB blood from the SVC = MOB (medium oxygen blood)

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4
Q

Outline the steps to fetal circulation (medium oxygen blood to placenta)

A

MOB blood enters the RV and exits via the Pulm trunk.

A portion of MOB bypasses the lungs –> Aorta via the Ductus Arteriosus

The remaining MOB is delivered to the lung and returns to the LA via the pulm veins. –> LV –> Aorta –> fetal tissue & back to placenta via umbilical arteries

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5
Q

Fetal vs. neonate structures: what does ductus arteriosus become after birth?

A

Ligamentum arteriosus

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6
Q

Fetal vs. neonate structures: what does foramen ovale become after birth?

A

Fossa ovalis

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7
Q

Fetal vs. neonate structures: what does umbilical vein become after birth?

A

Ligamentum teres

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8
Q

Fetal vs. neonate structures: what do umbilical arteries become after birth?

A

Medial umbilical ligaments

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9
Q

Newborn (and adult) blood circulation - right atrium to lungs

A
  • Right atrium receives deoxygenated blood from SVC, IVC, and coronary sinus.
  • Right atrium blood goes through tricuspid valve into right ventricle.
  • Right ventricle blood goes through pulmonary valve into pulmonary trunk and pulmonary arteries.
  • Blood in pulmonary capillaries loses CO2 and gains O2 (in the lungs).
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10
Q

Newborn (and adult) blood circulation - lungs to body

A
  • Oxygenated blood goes from lungs through pulmonary veins into left atrium.
  • Left atrium sends blood through bicuspid valve into left ventricle.
  • Left ventricle sends blood through aortic valve into aorta and systemic arteries.
  • In systemic capillaries, blood loses O2 and gains CO2 (in the body).
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11
Q

Heart murmurs in infants and children

A
  • common finding on routine exam

- 50% are innocent murmurs

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12
Q

Innocent murmurs are due to…

A

turbulent blood flow at the origin of the great vessels

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13
Q

Innocent murmurs are easier to hear on children than adults due to…

A
  1. Thin chest wall in children
  2. More angulated great vessels in children
  3. More dynamic circulation in children
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14
Q

List 6 features of pathologic murmurs

A
  1. All diastolic murmurs***
  2. All pansystolic murmurs
  3. Late systolic murmurs
  4. Loud murmurs > 3/6
  5. Continuous murmurs
  6. Associated cardiac abnormalities
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15
Q

Acyanotic vs. cyanotic defects

A

Acyanotic defects = left to right shunting

Cyanotic defects = right to left shunting

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16
Q

What are the 2 causes of acyanotic congenital heart diseases?

A
  1. abnormal connections

2. abnormal valves/vessels

17
Q

List acyanotic congenital heart diseases d/t abnormal connections (3)

A
  1. Ventricular septal defect (VSD)
  2. Atrial septal defect (ASD)
  3. Patent ductus arteriosus (PDA)
18
Q

List acyanotic congenital heart diseases d/t abnormal valves/vessels (5)

A
  1. Pulmonary stenosis (PS)
  2. Aortic stenosis (AS)
  3. Coarctation of aorta
  4. Mitral stenosis
  5. Ebstein’s anomaly
19
Q

What is the single MC congenital heart defect?

A

Ventricular septal defect (VSD)

20
Q

Where do VSD defects occur?

A

can occur in both the membranous portion of the septum (most common) and the muscular portion

21
Q

Pathophysiology of VSD

A
  • If the VSD is large enough, it can lead to symptoms.
  • This occurs since a large amount of blood goes from the LV to the RV, then back to the LV causing an abnormally large amount of blood to enter the LV.
  • Over a long period of time, the LV and RV hypertrophies and systolic dysfunction may occur when the heart can no longer compensate.
22
Q

Pathophysiology of atrial septal defect

A
  • Abnormal flowing of blood between the atrium, allowing blood to flow from the left atria into the right atrium
  • Results in RAE and RVE → CHF
  • Pulmonary vascular changes occur after decades of this defect
  • Blood vessels in the lungs become damaged by the extra pressure.
  • May have atrial dysrhythmias
23
Q

Pathophysiology of patent ductus arteriosus (left to right shunt)

A
  • With a drop in pulmonary arterial pressure or increased aortic pressure, blood will flow through PDA.
  • LEFT TO RIGHT SHUNT***
  • Increased pulmonary blood flow may lead to pulmonary edema.
  • Reduced blood flow to all postductal organs
  • At risk for endocarditis and pulmonary vascular disease in later life
24
Q

Pathophysiology of patent ductus arteriosus (right to left shunt)

A
  • If pulmonary artery pressure rises above aortic pressure, blood will move in the other direction.
  • RIGHT TO LEFT SHUNT***
25
Q

Pathophysiology of pulmonary stenosis

A
  • The pulmonary artery narrowing can cause the RV to pump harder and hypertrophy.
  • No symptoms in mild or moderately severe lesions.
  • Can lead to right ventricular failure.
26
Q

Pathophysiology of aortic stenosis

A

-Obstruction of outflow tract leading from the heart into the aorta
-The left ventricle must work harder and hypertrophy
More muscle requires more blood and O2
-This may lead to arrhythmias (atrial fibrillation), left ventricular failure, and sudden death.

27
Q

Pathophysiology of coarctation of the aorta

A
  • Constriction of the aorta of unknown cause*
  • Increased work on the heart leading to CHF and cardiovascular collapse.
  • Location of narrowing determines the clinical signs.
  • Severe cases rely on the PDA to supply the descending aorta and may present in collapsed state in neonatal period (when PDA closes).
28
Q

List the cyanotic congenital heart diseases

A
  1. Tricuspid atresia (TA)
  2. Pulmonary atresia (PA)
  3. Hypoplastic left heart
  4. Transposition great vessels (TGA)
  5. Tetralogy of Fallot
29
Q

Pathophysiology of tricuspid atresia

A
  • There is no forward flow through the tricuspid valve and blood shunts R-L across the foramen ovale/ASD.
  • A VSD is often present allowing blood to flow from LV to RV and then into the lungs.
30
Q

Pathophysiology of pulmonary atresia with intact septum

A
  • The atretic pulmonary valve prevents flow of blood into the lungs.
  • The pulmonary flow may be sustained by a PDA.
  • Without a VSD the RV is underdeveloped and blood flows to the L side at atrial level.
31
Q

Pathophysiology of pulmonary atresia with VSD

A
  • Blood is able to shunt R to L at both atrial and ventricular levels.
  • The RV is not underdeveloped***
  • Collateral vessels directly from the aorta (at systemic pressure) supply some parts of the lungs, resulting in patchy pulmonary congestion and hypertension.
32
Q

Pathophysiology of hypoplastic left heart

A
  • LV underdeveloped**
  • Right heart pumps blood to body through PDA.
  • Closure of PDA results in hypotension, shock, and death**
33
Q

What anomalies are associated with hypoplastic left heart?

A
  • Patent foramen ovale
  • Coarctation of the aorta
  • Patent ductus arteriosus (PDA)
  • Narrowed aorta
  • Hypoplastic left ventricle
  • Aortic atresia
34
Q

What is the 2nd MC cyanotic congenital heart defect?

A

Transposition of great arteries

35
Q

What is the MC cyanotic lesion?

A

Tetralogy of Fallot

36
Q

What are the 4 defects that make up tetralogy of fallot?

A
  1. Pulmonary artery stenosis (determinant factor for severity)
  2. VSD (usually large)
  3. Overriding Aorta
  4. RV hypertrophy
37
Q

Pathophysiology of Tet Spells

A

**Hypoxemic spells (“Tet spells”) are one of the hallmarks of severe tetralogy

MC start around 4 to 6 months of age:

  • Sudden onset or deepening of cyanosis
  • Sudden onset of dyspnea
  • Alterations of consciousness
  • Decrease in intensity of systolic murmur
  • Usually progressive
38
Q

Pathophysiology of the hypoxemia during Tet spells

A
  • Hypoxemia due to acute change in balance between PVR and SVR
  • Decreased SVR (crying, eating, fever, exercise)
  • Decreased SVR causes an increase in R –> L shunt, increasing cyanosis
  • Agitation –> dynamic subpulmonary obstruction

Life-threatening if untreated*

Pediatrics (9 decks)

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