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Anatomy 1 > Congenital Heart Disease > Flashcards

Congenital Heart Disease Flashcards

1
Q

Signs of ventricular failure

A
  • Exercise intolerance
  • Growth failure
  • Elevation of venous pressures (interstitial edema instead of alveolar in children)
  • Hepatomegaly

–>kids usually have biventricular failure even if vol load is only on 1 side

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2
Q

What is Eisenmenger’s disease?

A

Pulmonary vascular disease

-protects the lungs from increased pulmonary flow

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3
Q

What occurs in cyanosis?

A
  • Dec O2 delivery per RBC
  • Metabolic acidosis in severe cases (trying to get rid of CO2)
  • Polycythemia (make more RBCs)
  • ->leads to hyper viscosity and iron def anemia
  • Exercise intolerance (compensatory mech are used at rest)
  • Accelerated PV disease if high PBF
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4
Q

What drives flow in large VSDs?

A

Pressures of the two ventricles are essentially equal (unlike small VSDs), so flow is driven by vascular resistance

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5
Q

What determines pulmonary flow?

A

Ratio of pulmonary to systemic vascular resistance

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6
Q

What happens to pulmonary resistance after birth and why is this impt in VSD?

(i.e. explain when pul resistance<systemic)

A

After birth, get a gradual fall in pulmonary resistance so that it is lower than systemic resistance. With VSD, the blood has a choice to go through the systemic system or the vascular system from the LV. It chooses to go through the pulmonary system and the pul vessels see more volume and therefore more pressure.

–>note: systemic system always gets enough blood

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7
Q

What are the heart changes when pul resistance<systemic resistance in VSD?

A

RA: Fine/last to go
RV: equalizes with LV because of hole=pressure overload
LA: vol overload
LV: vol overload (it is the LV that is pumping the blood through both PA and aorta)

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8
Q

What happens if you have high pulmonary flow at high pressure for a while?

A

Get congestive heart failure

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9
Q

What kind of murmurs do you hear with pul resistance<systemic VSDs?

A

Systolic: holosystolic flow over VSD
Diastolic: inc flow of MV

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10
Q

What happens with pulmonary resistance>systemic resistance in VSD?

A

Later in life (2-20yrs), PVR increases to protect the lungs from the high pressure flow. This is the Eisenmenger reaction. Now deoxy blood flows from the RV to the LV through the VSD. This can lead to cyanosis.

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11
Q

What are the heart changes in pul resistance>systemic VSD?

A

RV: Volume overload, hypertrophy

LV: Shrinks to normal size, handling even less volume than normal LV

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12
Q

What murmurs do you hear with pul resistance>systemic VSDs?

A

Murmur goes away because flow is normal again

-Have pul HTN resulting in no S2 splitting on PE

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13
Q

What determines ASD shunting?

A

Ventricular compliance (don’t see vascular resistance)

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14
Q

What happens in ASD when RV compliance=LV compliance?

A

Newborn period, the compliances are equal, therefore there is not much shunting of blood

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15
Q

What happens in ASD when the child is a toddler?

A

The PVR falls normally and the atria thins and becomes more compliant. Because of this, RV compliance>LV compliance and blood comes back through atria to the RV

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16
Q

What changes in the chambers do we see due to toddler ASD?

A

RA and RV see extra volume load, so they enlarge

17
Q

What murmur do we hear in toddler ASD?

A

Systolic: pulmonary ejection murmur (lots more blood)
Diastolic: tricuspid valve murmur if flow is very increased (lots more blood)
-also have increased splitting because it takes longer for pul valve to close due to inc vol

18
Q

What kind of shunting occurs with a PDA?

A

DA goes from pul artery to the descending aorta. Thus, flow is determined by vascular resistance. Fall in PVR at birth leads to inc flow through the pulmonary system and L–>R shunting across the PDA

19
Q

When is there flow in a PDA?

A

Systole AND diastole because there is always a P difference between the aorta and the pul arteries.
-thus a small PDA can have as much flow as a large VSD

20
Q

What murmur do we hear with PDA?

A

Continuous holosystolic murmur that continues past S2

21
Q

What are the disease manifestations of L–>R shunts?

A
  • Volume overload
  • Inc in PA pressure
  • RV pressure overload–>RV hypertrophy
22
Q

Complications of L–>R shunts?

A
  • CHF secondary to P and V overload (ie VSD)
  • Pul vascular disease (occurs later in ASD than VSD and PDA)
  • Growth failure
  • Repeated pneumonias (edema stops you from clearing well and large pul arteries compress bronchioles)
  • Endocarditis
23
Q

List three LH obstructive lesions

A
  1. Aortic stenosis
  2. Coarctation of the aorta
  3. Hypoplastic left heart
24
Q

What is the isthmus of the aorta?

A

Part in fetal dev that doesn’t get much blood at the ductus

25
Q

What happens if there is an obstruction to aortic outflow during fetal life?

A
  • ex bicuspid aortic valve
  • Less blood flows through foramen ovale (R–>L) and more blood thus flows through the ductus art. Now the blood branches in two directions from the DA opening into the aorta: up toward the brain, and down towards the heart. This forms a little ridge of tissue directly opposite to DA in the aorta=discrete coarctation. After birth, ductus begins to close, the blood must come from the LV and go down to the descending aorta passed the coarctation/stenosis. Because this is a slow process, it is able to form collaterals to circumvent the partial blockage.
26
Q

What are the clinical consequences of fetal obstructed aortic outflow?

A
  • Collaterals mess with pulsatility of flow and the kidneys think there is low BP so they pump out renin causing HTN at an earlier age
  • LV is hypertrophied due to inc P from stenosis
27
Q

What is hypoplastic Left heart syndrome?

A

Entire left side not developed so there is a tiny LV and ascending aorta so all the blood comes from the PDA.
***started to run out of computer battery here

28
Q

What is tetrology of Fallot?

A

This is a pulmonary blood flow dependent cyanotic defect (i.e. cyanosis is inversely proportional to PBF because there is systemic/pul mixing)

  • Pulmonary stenosis
  • RVH (high P due to stenosis)
  • Overriding aorta
  • VSD
  • boot shaped heart on XRAY
29
Q

What is the treatment for TOF?

A

shunt placed from systemic artery into pul artery. More blood flow then flows to the lungs and bypasses small pul outflow tract

30
Q

What is an example of a PBF independent cyanotic defect?

A

Transposition of the great arteries (independent because there isn’t systemic/pul mixing). Usually have increased PBF and ventricular compliances and size of septal defect determine mixing across the foramen ovale (i.e. ASD).

31
Q

What are some clinical consequences of transposition?

A

-Compensatory polycythemia
-Cerebrovascular accident
-Brain abscess
-Growth failure
-Bilirubin gallstones due to inc RBC breakdown
-

Anatomy 1 (11 decks)

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