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AS - N935 Advanced Patho II > Congenital Heart Defects > Flashcards

Congenital Heart Defects Flashcards

1
Q

Congenital

A

Existing at birth

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2
Q

Fetal Circulation

A 
Placenta → umbilical vein → liver → IVC → R atrium → R ventricle → lungs → L atrium → L ventricle → aorta → body (systemic circulation) → umbilical artery
OR
Placenta → IVC via ductus venosus
R atrium → L atrium via PFO
Pulmonary artery  → aorta via PDA
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3
Q

Fetal Circulation Characteristics

A

↑PVR 2° fluid filled lungs & hypoxic environment
↓SVR 2° large surface area & low resistance utero-placental bed
Hgb F P50 = 19mmHg ↑oxygen affinity
Most oxygenated blood from the umbilical vein perfuses the brain & heart by shunting across the liver via the ductus venosus & across the heart via PFO
Fetal pH 7.25-7.35

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4
Q

Circulation Transition AFTER Birth

A

Umbilical cord clamped ↑SVR
Lungs inflate w/ air ↑PaO2 ↓PVR ↑pulmonary blood flow & return to L atrium
↑L atrium pressure > R atrium → PFO functional closure

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5
Q

What factors contribute to the ductus arteriosus remaining patent in utero?

A

Hypoxia
Mild acidosis
Placental PGEs

Functional PDA close at birth when these factors are removed

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6
Q

What can cause the newborn to revert back to fetal circulation?

A

Physiologic stresses

Example: CDH

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7
Q

Obstructive Lesions

A

Prevent ventricular flow either R or L
↓CO
Coarctation or aortic stenosis

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8
Q

Mixing Lesions

A

Mixing venous & arterial blood
Single ventricle i.e. hypoplastic L heart syndrome
Cyanotic & dependent on PDA at birth

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9
Q

L → R shunts result in _____

A

Pulmonary over-circulation
↑R ventricle preload
L ventricle output bypasses the systemic circulation

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10
Q

R → L shunts result in _____

A

Blood bypasses the pulmonary system
Deoxygenated blood pumped out systemically
↓PaO2 ↓SpO2

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11
Q

Eisenmenger’s Syndrome

A

Uncorrected VSD L → R shunt
→ pulmonary HTN
Shunt reverse direction across the defect when ↑PVR
R → L shunt

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12
Q

Shunt Calculations

A

Qp = pulmonary blood flow
Qs = systemic blood flow
Normal 1:1 RV = LV output

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13
Q

Qp/Qs

A

(SaO2 - SvO2) / (SpvO2 - SpaO2)
Arterial (aorta) O2 saturation - venous (SVC) O2 saturation
Pulmonary vein O2 saturation - pulmonary artery O2 saturation

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14
Q

Qp/Qs Assumptions

A
  1. Patient breathing RA & pulmonary venous blood fully saturated
  2. O2 consumption normal resulting in SvO2 25-30% lower than SaO2
  3. Patient not severely anemia (normal SVC O2 saturation)
  4. Complete mixing results in aorta & pulmonary artery O2 saturations being equal

*Most cases the assumptions are valid & allow rapid determination Qp/Qs based on SpO2 alone

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15
Q

Qp/Qs = < 1

A

R → L shunt

Cyanosis

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16
Q

Qp/Qs = 1-2

A

Minimal L → R shunt

Asymptomatic

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17
Q

Qp/Qs = 2-3

A

Moderate L → R shunt

Mild CHF symptoms

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18
Q

Qp/Qs = > 3

A

Large L → R shunt

Severe CHF symptoms

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19
Q

What is the most common congenital defect in children?

A

Ventricular septal defect
20%

Pulmonary over-circulation L → R shunt

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20
Q

Restrictive VSD

A

Small size

Limited pulmonary over-circulation

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21
Q

Unrestrictive VSD

A

LARGE flow across the septum w/ balance b/w SVR & PVR

Regular serial echocardiograms to monitor

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22
Q

Indications to surgically repair VSD:

A

Poor feeding
Reduced weight gain
↑incidence respiratory infection

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23
Q

PDA

A

Patent ductus arteriosus connection b/w aorta & pulmonary artery
Significant diastolic run-off into the pulmonary circulation ↓systemic diastolic BP → compromising distal perfusion (mesenteric, renal, & coronary)

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24
Q

Complete AV Canal

A

Free communication b/w all four heart chamber
Located where the atrial septum joins the ventricular septum
Involves atria, ventricles, tricuspid, & mitral valves → single large valve

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25
Q

When should the AV canal surgical repair be performed?

A

< 6mos before pulmonary vascular changes develop

Residual septal defects including AV valve regurgitation, postop pulmonary reactivity, & conduction system damage

26
Q

How do critical coarctations present?

A

Circulatory collapse, shock, & acidosis d/t poor distal perfusion

PGEs to reopen the ductus
DUCTAL DEPENDENT

27
Q

Coarctation S/S

A

Upper extremity HTN
↓LE pulses
L ventricular hypertrophy

28
Q

Pulmonary Valve Stenosis

A

Narrowing ↑R ventricle workload
Symptoms dependent on obstruction severity
Often treated w/ balloon dilation

29
Q

Aortic Valve Stenosis

A

Narrowing ↑L ventricle workload
Severe aortic stenosis potential to impair LV development in utero
Balloon dilation
Valve replacements at young ages require multiple revisions over time

30
Q

Ross Procedure

A

Diseased aortic root resected & patient pulmonary valve root excised & implanted into the aortic position
Coronary arteries are then re-implanted into the “neo-aortic” root
R ventricle to pulmonary artery connection & valve obtained from cadaveric tissue or conduit (synthetic material)
Valve grows as patient grows
RV → PA connection potentially will require revisions over time, but better long-term solution to the aortic valve

31
Q

Blalock-Taussig-Thomas Shunt

A

Diverts systemic blood flow to pulmonary artery

32
Q

Classic BT Shunt

A

Subclavian artery divided & directly anastomosed to the ipsilateral pulmonary artery
Allows patient own subclavian artery to grow
↓pulses in ipsilateral arm or non-palpable

33
Q

Modified BT Shunt

A

SYNTHETIC shunt b/w subclavian artery & pulmonary artery
Ipsilateral arm reflects true pressures & available as A-line location
Artificial material does not grow w/ the patient
Hypotension → sluggish flow & possible thrombosis CRITICAL

34
Q

Tetralogy of Fallot

A

Ventricular septal defect
R ventricular outflow tract obstruction
Overriding aorta
R ventricular hypertrophy 2° pressure overload

Repair usually w/in 6mos
BT shunt palliation - neonates w/ hypercyanotic spells & too small for definitive repair (<5kg)

35
Q

What is the most common cyanotic cardiac lesion?

A

TOF 6-11% CHD

Impaired pulmonary blood flow R → L shunt
CXR boot-shaped heart d/t R ventricle hypertrophy

36
Q

Tet Spell Causes

A

Acute dynamic ↑pulmonary outflow tract obstruction (spasm) → cyanotic episode d/t R → L shunting
RVOTO + VSD

Crying, feeding, acidosis ↑PVR d/t HPV, catecholamines, surgical stimulation

37
Q

Tet Spell Treatment

A

↑SVR ↑afterload

Relax the spasm ↓PVR

38
Q

Tet Spell

Anesthetic Managment

A 
100% FiO2
Sedation
Fluid
Hyperventilation
β blocker ↓HR 
Esmolol 0.5mgkg or Propranolol 0.1-0.3mg/kg
α agonist ↑afterload/SVR ↓HR
Phenylephrine 1-10mcg/kg 
Knees to chest or squat ↑SVR
39
Q

Truncus Arteriosus*

A 
Failure truncus arteriosus to divide into the aorta & pulmonary artery
VSD present
R & L ventricle output into the truncus
Complete mixing at ventricle level
SpO2 75-80%
40
Q

Transposition of the Great Arteries*

A

Aorta & pulmonary are reverse
Aorta arises from R ventricle & pumps de-oxygenated blood to the body
Pulmonary artery arises from L ventricle & pumps oxygenated blood back to the lungs
PATIENT NEEDS MIXING TO SUSTAIN LIFE
ASD, VSD, or PDA
Emergency balloon atrial septostomy under echocardiogram at bedside or fluoroscopy in the cardiac cath lab

41
Q

Infective (Bacterial) Endocarditis

A

IE or subacute bacterial endocarditis (SBE)

Infection caused by bacteria that enter the bloodstream & settle in the heart lining, valve, or blood vessel

42
Q

What patient are at increased risk to develop SBE?

A

Uncorrected congenital heart defects

43
Q

How to prevent SBE?

A

Antibiotic prophylaxis especially in at risk patients (CHD)

44
Q

Acute bacterial endocarditis is most commonly caused by _____ _____

A

Staphylococcus aureus

45
Q

What patients require SBE prophylaxis?

A

Prosthetic cardiac valves
History infective endocarditis
Unrepaired or incomplete repair cyanotic heart disease (including shunts)
Complete repairs w/ prosthetic during 1st 6mos (d/t prosthetic material re-epithelization)
Cardiac transplant recipients w/ valve disease

46
Q

SBE Prophylaxis Antibiotics

A

Intraop:
- Cefazolin 50mg/kg IV
- Ampicillin 50mg/kg IV
(PCN allergy Clindamycin 20mg/kg IV)

Preop Amoxicillin 50mg/kg PO

47
Q

What dental procedures require SBE prophylaxis?

A

Gingival tissue manipulation
Periapical teeth region involvement
Oral mucosa perforation

*Patients w/ valvular heart disease, repair w/ prosthetic material, previous infective endocarditis, unrepaired cyanotic CHD, cardiac transplant, valve regurgitation

48
Q

What is considered more important to prevent VGS infective endocarditis for dental procedures?

A

VGS = viridins group streptococci

Good oral health maintenance & regular access to dental care&raquo_space;> antibiotic prophylaxis

49
Q

HLHS

A

Hypoplastic L heart syndrome
Single ventricle w/ complete mixing pulmonary & systemic circulation
SpO2 75-80%
Ductal dependent

50
Q

Stage I

Norwood

A

Connection from systemic → pulmonary circulation
1. Atrial septectomy & common atrium created
2. Reconstruct pulmonary artery to aortic arch
3. PDA ligation
4. Establish pathway for blood flow to lungs w/ shunt
SaO2 75-80%
R ventricle ejects blood into systemic circulation

51
Q

Blalock-Taussig Shunt

A

Connection from R subclavian to Pulmonary artery

52
Q

Sano Shunt

A

Gore-tex graft from R ventricle → pulmonary artery

Improves coronary perfusion

53
Q

Stage II

Bi-directional Glenn

A

Direct anastomosis b/w SVC & pulmonary artery branch
Blood flow to both R & L pulmonary arteries
Requires low PVR
Blood flow = passive
Maintain adequate volume/preload
PaO2 75-85%
IVC venous blood continues to flow into the heart → systemic circulation

54
Q

Stage III

Fontan Procedure

A

IVC connected to pulmonary vasculature
- Extra-cardiac
- Lateral tunnel
- Fenestrated
Allows passive blood flow from IVC directly to lungs (bypasses the heart)
Completes pulmonary & systemic circulation separation
PaO2 88-93%

55
Q

Anesthetic Considerations

BEFORE Stage I

A 
Maintain patent PDA w/ PGEs to allow systemic perfusion
Restrict excessive pulmonary blood flow
- Allow mild hypercarbia CO2 45-55mmHg
- Low oxygen concentrations
- PEEP
Inotropic support - Dopamine or Epi
Minimize myocardial depression
Prevent & treat pulmonary HTN crisis
56
Q

Chronic Fontan Complications

A

Dysrhythmias ↑atrial pressures on suture lines
Protein losing enteropathy - poorly understood hypoalbuminemia development despite normal renal & hepatic function
Thrombosis - dysrhythmias cause venous stasis or sluggish flow

57
Q

Pulmonary HTN

A 
Result from high blood flow & ↑PVR/pressure
PPHN common in un-repaired CHD
Acute ↑pulmonary artery pressure → shunt
- Desaturation
- Bradycardia
- Systemic hypotension
58
Q

Factors known to ↑PVR

A 
Hypoxemia
FiO2 <30%
Hypercarbia
Acidosis
Hypothermia
Atelectasis
\+pressure
PEEP
Stress or stimulation
Light anesthesia
59
Q

Factors known to ↓PVR

A

↑FiO2 100%
Hyperventilation
Inhalational agents ↓SVR
Nitric oxide iNO

60
Q

Nitric Oxide

A

Potent smooth muscle vasodilator
Short half-life
Stimulates guanylate cyclase → cyclic-GMP → activates protein kinase G → Ca2+ reuptake ↓calcium impairs MLCK cross-bridge formation → smooth muscle relaxation
Promotes capillary & pulmonary dilation
100ppm & 800ppm
Overdose → methemoglobin & pulmonary toxicity

AS - N935 Advanced Patho II (20 decks)

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