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Cardiovascular System > Congenital Heart Disease-Levitas > Flashcards

Congenital Heart Disease-Levitas Flashcards

1
Q

What percentage of births have Congenital Heart disease?

A

1%

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2
Q

Types of Left-Right shunt: pink babies?

A

ASD, VSD, AVSD, DORV (double outlet RV-can become blue if not early enough), PDA,

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3
Q

What are the causes of cyanotic heart disease/Blue baby?

A

TOF, D-TGA, TAPR (total anomalous pulmonary return), TA (tricuspid atresia)

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4
Q

Types of obstructive heart disease with no shunts

A

HRHS (hypoplastic), Ebstein’s (can also be pink baby), PS, CoA

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5
Q
A
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6
Q

Oxyhemoglobin Dissociation Curve

A

SaO2=%ge of hemoglobin molecules oxygenated in arterial blood

PaO2=mmHg of O2 PP in arterial blood

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7
Q

Why is the blue baby blue?

A

Discoloratino of skin and mucus membranes due to reduced hemoglobin by at least 5g/dL.

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8
Q

What is the O2 saturation of a blue baby?

A
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9
Q

What is the PaO2 of a blue baby?

A
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10
Q

What 4 physiological reasons would a blue baby be blue?

A

Disordered breathing, lungs, hemoglobin or heart

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11
Q

What is the appearance of a baby with disordered breathing

A

Seizures, apathy, hypotonia, abnormal breathing like Kussmaul (labored) breathing.

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12
Q

What is the appearance of a baby with disordered lungs?

A

Distressed and anxious. Health brain but working hard.

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13
Q

What is the appearance of a baby with disordered hemoglobin?

A

Normal disposition, normal breathing rate but purple or bluish. Could also have polycythemia.

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14
Q

What is the appearance of a patient with a disordered heart

A

Happy tachypneic, maybe in CHF or cardiac shock. Lungs delivering but heart not delivering to body. Pt may go into shock.

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15
Q

How to treat a patient with a disordered heart

A

Physical exam, 4 limb blood pressure (to check for coarctation), pre and post ductal saturations (for PDA), EKG, PaO2/hyperoxic test.

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16
Q

What is a hyperoxic test

A

Give 100% O2 for 5 minutes, check PaO2. If above 250mmHg: exclude CHD. 150-250mmHg: unlikely CHD but possible, below 150mmHg: likely CHD. Double check with an echo.

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17
Q

What to look for in a CXR for CHD

A

ABCDE: Airways and Air Filled Lungs – Bronchi (normal-asymmetrical) focal opacifications, or extra fluids?; Bones – rib number/abnormalities; Cardiac side (situs), size, siluhete, and Apex; Diaphragm and below, flattened (asthma) or not and where is the liver and the stomach.; Extra equipment

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18
Q

What could black lungs mean?

A

Not enough blood flow to lungs (undercirculation) from obstruction, small right heart, obstructed pulmonary outflow or pulmonic stenosis.

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19
Q

What does big heart/black lungs mean?

A

Obstruction problem (PS or Epsteins)

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20
Q

What does big heart/white lungs mean?

A

CHF (from large AVSD or VSD), HLHS, etc.

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21
Q

What does a boot shaped heart indicate?

A

Tetrology of Fallot, RV hypertrophy

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22
Q

What does “Eggs on a String” represent?

A

Aorta on RS and pulm on LS/D-TGA

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23
Q

What is the most common cause of cyanotic heart disease?

A

Tetrology of Fallot

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24
Q

What percentage of CHD patients have tetrology of Fallot?

A

8%

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25
Q

What are the 4 defects in Tetrology of Fallot?

A
  1. Pulmonary Stenosis, 2. Overriding aorta, 3. VSD, 4. Right ventricular hypertrophy
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26
Q

What is the responsibility of the neural crest cells?

A

Migrate and invade truncal ridges and bulbar ridges. Common truncus makes vessels, signals truncus to rotate and create septum. Signals creation of AV valves.

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27
Q

Embryologically: what creates the ventricular septum?

A

Ventricular ridges to truncoconal septum

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28
Q

What underlying conditions may you expect in Tetrology of Fallot?

A

Di George, Velocrardiofacial syndrome, Catch 22 and any other Chromosome 22q Deletions associated with conotruncal abnormalities and neural crest migration problems.

29
Q

Findings in physical exam in tetrology of Fallot

A

Cyanosis, clubbing (of fingers), normal pulses, normal BP. Normodynamic precordium with quiet apical impulse. Ejection systolic click (large aorta with big valve) and murmur. Normodynamic precordium.

30
Q

Clinical vascular variations of tetrology of Fallot

A

Mild stenosis – asymptomatic, acyanotic progress to cyanotic-may appear pink and move to blue. Severe stenosis – severe cyanosis, failure to thrive, squatting – in children. Risk for IE.

31
Q

Clinical musculoskeletal variations on TOF

A

Clubbing, scoliosis.

32
Q

Clinical hematological variations on TOF

A

Polycythemia, iron deficiency, bleeding disorders. A result of compensation for hypoxia.

33
Q

CNS variations on TOF

A

Thrombo-embolic event, brain abscess.

34
Q

EKG findings on tetrology of Fallot

A

Right axis deviation, RV hypertrophy.

35
Q

Hypercyanotic spells in tetrology of Fallot (Tet spells)

A

Occur in cyanotic or acyanotic patients, Common in the morning (low preload), Precipitated by activity, Presentation: intense cyanosis, abnormal respirations, often-altered level of consciousness.

36
Q

Why is there a murmur in tetrology of Fallot?

A

RVOT spasm, decreased SVR and increased venous return lead to increase in R-L shunt which decreases PO2, increased PCO2 and decreases pH, which causes hyperventilation, and increases venous return which continues the cycle with increased R-L shunt.

37
Q

What is the treatment for a Tet spell?

A

Oxygen to vasodilate BV in lungs. If dehydrated, rehydrate. Knee-chest position decreases Venous return which decreases venous return which decreases RL shunt. Morphine stops hyperventilation, decreases venous return, relieves spasm and averts arrest. If morphine doesn’t work, beta blockers decrease RVOT and RL shunt and BP in systemic side. Vasoconstriction increases SVR and decrease RL shunt. Chronic treatment is beta blockade, surgical treatment.

38
Q

Medical treatment for tetrology of Fallot

A

Iron supplements, prevent hypercyanotic spells, IV Prostaglandin E1

39
Q

Surgical treatments for TOF

A

Palliation: permanent PDA with a shunt, correction (make as normal as possible)

40
Q

When is palliation used?

A

While kids grow and wait for surgery. Can live with 75% O2. Body adjusts in kids but not adults.

41
Q

What are the types of palliative shunts for TOF?

A

BT (Blalock Taussing) shunt: From R subclavian artery to R pulmonary arteries. Central shunt, ascending aorta to pulmonary trunk. Waterson (Asc Aorta to RPA), Potts (Desc Aorta to LPA).

42
Q

Complications of shunting

A

Too large leads to CHF, Pulmonary vascular resistance increase, distortion of the PA

43
Q

What percentage of TOF patients have right sided aortic arch?

44
Q

What percentage of ToF patients have other important coronary anomalies? (LAD from RCA, large branches from RCA course across the subpulmonary infundibulum)

45
Q

Picture of TOF shunts

46
Q

What are the advantages of surgery for ToF in early infancy?

A

Early elimination of hypoxia, decrease RVH and RV fibrosis, reduction of late arrhythmias

48
Q

Disadvantages of early infancy tetrology of Fallot

A

Increase risk factors (surgeon dependent), increase use of transannular patch – increase PR

49
Q

What is done in a repair surgery for TOF?

A

Relieve RVOT obstruction, close VSD, PA repair, close shunt.

50
Q

What is the mortality rate for TOF repair?

51
Q

Complications of TOF repair surgery

A

Residual RVOT obstruction, pulmonic regurgitation that may lead to RV dysfunction, residual VSD, late arrhythmia, left BBB (depending on entry to VSD), late death.

52
Q

What is the most common cause of cyanosis in the first month of life?

A

DTGA (TOF usually appears later)

53
Q

Incidence of DTGA

54
Q

What conditions are associated with DTGA?

A

Not many, not as syndromic as TOF, but increased prevalence in infants of diabetic mothers.

55
Q

Pathology of DTGA

A

Malposition of the great arteries, the aorta arises from RV and PA arises from LV

56
Q

Picture of DTGA

58
Q

With a closed circuit to the lungs, how can a DTGA patient survive?

A

PDA, patent foramen ovale, or other mixing. Often VSD, 30% LVOT obstruction with VSD, 15% aortic coarctation/interruption.

59
Q

What would the PO2 of a DTGA patient be without any other defect?

60
Q

Embryology of DTGA

A

AP septum develops incorrectly as a result of failed neural crest cell migration (truncal part only).

61
Q

Clinical manifestations of DTGA

A

Prominent cyanosis. Neonate will appear healthy, well developed, no heart murmurs (except in small VSD or in PDA after a few days), normal pulses. With time – severe hypoxemia (no VSD). CHF (with large VSD despite 80%PO2 from good mixing).

62
Q

What is the prognosis of DTGA without treatment?

A

90% die in first year.

63
Q

EKG of DTGA

A

Right axis deviation, RVH and LVH develop later.

64
Q

Palliative treatment for DTGA

A

Don’t do it unless waiting for a surgery ASAP. IV prostaglandin E1, Rashkind balloon.

65
Q

What is a Rashkind balloon atrial septostomy?

A

If no mixing of blood and surgery can’t be performed immediately, need to open the foramen ovale. Can be done bedside by catheter through umbilical vein into RA through IVC. Balloon through hole to LA, inflate balloon and pull it back through puncturing a hole and improving circulation temporarily until surgery.

66
Q

What is an arterial switch surgery?

A

Great arteries transected and reanastamosed, coronary arteries reattached at base of aorta.

67
Q

What is the mortality in DTGA arterial switch surgery?

A

Early: anatomical/technical factors. Late: 1-2% from myocardial ischemia, pulmonary vascular disease, reoperation for supravalvular obstruction. Low incidence of arrhythmias (though a risk with any open heart surgery).

68
Q

What is the Rastelli arterial switch?

A

Create shunt from RV to pulmonary artery and connect aorta to left side.

69
Q

When is a Mustard Atrial switch done?

Cardiovascular System (28 decks)

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