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

Congenital Heart Defects Flashcards

(60 cards)

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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
When should the AV canal surgical repair be performed?
< 6mos before pulmonary vascular changes develop Residual septal defects including AV valve regurgitation, postop pulmonary reactivity, & conduction system damage
26
How do critical coarctations present?
Circulatory collapse, shock, & acidosis d/t poor distal perfusion PGEs to reopen the ductus DUCTAL DEPENDENT
27
Coarctation S/S
Upper extremity HTN ↓LE pulses L ventricular hypertrophy
28
Pulmonary Valve Stenosis
Narrowing ↑R ventricle workload Symptoms dependent on obstruction severity Often treated w/ balloon dilation
29
Aortic Valve Stenosis
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
Ross Procedure
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
Blalock-Taussig-Thomas Shunt
Diverts systemic blood flow to pulmonary artery
32
Classic BT Shunt
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
Modified BT Shunt
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
Tetralogy of Fallot
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
What is the most common cyanotic cardiac lesion?
TOF 6-11% CHD Impaired pulmonary blood flow R → L shunt CXR boot-shaped heart d/t R ventricle hypertrophy
36
Tet Spell Causes
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
Tet Spell Treatment
↑SVR ↑afterload | Relax the spasm ↓PVR
38
Tet Spell | Anesthetic Managment
``` 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
Truncus Arteriosus*
``` 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
Transposition of the Great Arteries*
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
Infective (Bacterial) Endocarditis
IE or subacute bacterial endocarditis (SBE) | Infection caused by bacteria that enter the bloodstream & settle in the heart lining, valve, or blood vessel
42
What patient are at increased risk to develop SBE?
Uncorrected congenital heart defects
43
How to prevent SBE?
Antibiotic prophylaxis especially in at risk patients (CHD)
44
Acute bacterial endocarditis is most commonly caused by _____ _____
Staphylococcus aureus
45
What patients require SBE prophylaxis?
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
SBE Prophylaxis Antibiotics
Intraop: - Cefazolin 50mg/kg IV - Ampicillin 50mg/kg IV (PCN allergy Clindamycin 20mg/kg IV) Preop Amoxicillin 50mg/kg PO
47
What dental procedures require SBE prophylaxis?
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
What is considered more important to prevent VGS infective endocarditis for dental procedures?
VGS = viridins group streptococci | Good oral health maintenance & regular access to dental care >>> antibiotic prophylaxis
49
HLHS
Hypoplastic L heart syndrome Single ventricle w/ complete mixing pulmonary & systemic circulation SpO2 75-80% Ductal dependent
50
Stage I | Norwood
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
Blalock-Taussig Shunt
Connection from R subclavian to Pulmonary artery
52
Sano Shunt
Gore-tex graft from R ventricle → pulmonary artery | Improves coronary perfusion
53
Stage II | Bi-directional Glenn
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
Stage III | Fontan Procedure
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
Anesthetic Considerations | BEFORE Stage I
``` 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
Chronic Fontan Complications
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
Pulmonary HTN
``` Result from high blood flow & ↑PVR/pressure PPHN common in un-repaired CHD Acute ↑pulmonary artery pressure → shunt - Desaturation - Bradycardia - Systemic hypotension ```
58
Factors known to ↑PVR
``` Hypoxemia FiO2 <30% Hypercarbia Acidosis Hypothermia Atelectasis +pressure PEEP Stress or stimulation Light anesthesia ```
59
Factors known to ↓PVR
↑FiO2 100% Hyperventilation Inhalational agents ↓SVR Nitric oxide iNO
60
Nitric Oxide
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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