Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

10. Congenital Heart dz > TVD > Flashcards

TVD Flashcards

1
Q

Gross path lesions TV atresia

A
  • Absence of connection btw morphologic RA and RV

o Imperforated TV membrane in 5% of cases

  • Complete agenesis/absence of TV → no communication btw RA and RV
    o RV hypoplasia
    o Absent inlet portion of RV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pathophys TV atresia

A

systemic venous return → RA → ASD → LA → mixes w pulmonary venous return → single AV valve → LV → systemic and pulmonary circulations
o Functionally univentricular heart

  • Normal GA: blood flows from RA → ASD → LA
    o If VSD: will provide pulmonary blood flow (LV → VSD → RV → PA)
     Large VSD: pulmonary overcirculation and ↓ systemic blood flow
  • TGA: pulmonary overcirculation → L-CHF
  • No obstruction to pulmonary blood flow →larger volume of pulmonary venous return → high systemic O2
    o If RVOTO and ↓ pulmonary blood flow → systemic hypoxemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Anatomic features always present w/ TV atresia

A

 Absence of connection btw physiologic RA and RV
 Hypoplasia of morphologic RV
 Interatrial communication: PFO or ASD
 Morphologic LV w morphologic MV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Anatomic features sometimes present w/ TV atresia

A

 Transposition of GAs
 Pulmonary stenosis
 Size of coexisting VSD: need communication btw systemic and pulmonary circulation
* Occasionally PDA with pulmonary atresia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Goal of sx correction TV atresia

A

separation of systemic and pulmonary circuits
 Provide adequate pulmonary blood flow → ↓ hypoO2
 Prevent pulmonary overcirculation/PH → can lead to LV failure
 Preserve PA anatomy for later sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sx correction if no concurrent TGA TV atresia

A

 Systemic to pulmonary shunt performed at 6-8wks
 Primary bidirectional Glenn procedure in older children
* Classic Glenn’s shunt = CrVC → RPA
* No volume/pressure overload of single ventricle compared to systemic-PA shunting
* Provide venous flow to lungs for oxygenation and improve O2 saturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sx correction if concurrent TGA TV atresia

A

 Early palliation
* Pulmonary artery banding → ↓ pulmonary blood flow
* Norwood stage 1 procedure if severe stenosis and hypoplastic Ao
 Fontan procedure: only if good ventricular fct, unobstructed systemic blood flow and minimal AV valve regurgitation
* Diversion of systemic venous return → PA bypassing RV
* Definitive palliative sx tx if biventricular repair is not possible
* Ideally: younger, ↓PVR/PAP, adequate PA diameter, normal RA, systemic venous connections, sinus rhythm
o If ↑ venous or RAP → ↑ mean PAP → pleural effusion
o If ↑PVR/PAP → ↓ forward flow → ↓ L side filling → ↓ CO
 Fenestrations btw systemic venous atrium (RA) and pulmonary venous atrium (LA) = safety valve to ensure adequate LV filling
 Total cavopulmonary anastomosis
* Tunnel in RA directing caval blood → PA through anastomosis on underside RPA
* Eliminate diated systemic venous reservoir w ↑ RAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Histo TV atresia

A

o Fibrofatty tissue interposed btw muscular RA floor and parietal wall of ventricular mass in 95% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Size/development of trabecular portion of RV is variable in TV atresia and depend on

A

 Depend on presence/size of VSD → ↑ development if VSD present
 If no VSD: PDA provides pulmonary blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Survival in TV atresia depend on

A

ASD/PFO: allow blood flow from RA → LA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Types of TV atresia

A

o I – Normally related GA
 Ia: no VSD + PA atresia
 Ib: VSD + PS
 Ic: VSD + no PS
o II – D-TGA
o III – L-TGA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

TV atresia: Hemodynamics and c/s determined by presence/absence of

A

o PV atresia
o Severity of subpulmonary/PS
o Relationship of GA
o Subaortic obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

C/s TV atresia

A

o Cyanosis
o CHF signs
o ↓ growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

PE TV atresia

A

low frequency holosystolic murmur form VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ECG TV atresia

A

1st AVB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CTX TV atresia

A
  • Pulmonary overcirculation
  • Normal cardiac silhouette
17
Q

Echo TV atresia

A
  • Absent TV, no flow across RV inlet
    o Imperforated linear density at TV location
  • Discordant ventricular chamber sizes
    o Small/absent RV
    o RAE
  • ASD
  • +/- VSD
  • +/- LVE if pulmonary overcirculation
18
Q

TVD: gross exam

A
  • Abnormal TV
    o Malformation of TV leaflets, chordae tendinea and pap muscles
     Focal/diffuse thickening of valve leaflets
  • Irregular thickening w fenestrations
  • Septal leaflet directly adhered to wall
  • Direct papillary muscle attachment
  • Elongated leaflets
     Underdevelopment of chordae tendinea/pap muscles
  • Short/absent chordae
    o Incomplete separation of valve components from ventricular wall
    o Focal agenesis of valvular tissue
  • Fusion of papillary muscles
  • Fibrinous epicarditis around RA
  • PFO
19
Q

TVD: pathophys

A
  • TR → R sided volume overload
    o RAE and RVE
    o ↑ R sided pressures: potential for R → L shunt if concurrent shunting defects
20
Q

TVD: signalment

A

o Breeds: Labradors, English Sheepdogs, Great Danes, German Shepherds, Irish Setters
 Cats: Chartreux
o Usually young
o Common concurrent congenital defects: MVD, VSD, ASD, PS, AVSD

21
Q

TVD: c/s

A

most are asymptomatic until develop R CHF

22
Q

TVD PE

A

o Holosystolic R apical murmur
 Intensity does not correlate well with severity of TR
o R sided CHF: ascites

23
Q

ECG TVD

A
  • Ventricular pre-excitation: AP (WPW)
  • Splintered QRS
  • Atrial arrhythmias → Afib most common
  • R axis deviation from R sided enlargement
    o Deep S waves in lead I, II, III, aVF
  • Tall/peaked P waves
24
Q

CTX TVD

A
  • R sided cardiomegaly, RAE
  • Marked apex shifting to L
25
Q

2D Echo TVD

A

o Abnormal location, shape, attachment, motion of TV apparatus
 Adherence of septal leaflet to IVS
 Large mural leaflet
 ↓ valvular motion
 Thickened leaflets
o Large fused papillary muscles, malpositioning
o RAE/RVE
 RAE is marked vs RVE
o ↓ L sided parameters from reduced RV SV

26
Q

Doppler echo TVD

A

TR

27
Q

Contrast echo TVD

A

bubbles remain in R heart for prolonged period
o Can see bubbles in hepatic veins

28
Q

Cardiac KT angio TVD

A

o Dilated RV
o TR
o Dilated RA

29
Q

Physiology TVD

A

o Malformation of TV → TR → ↑ RA volume → RVEH → ↑ RV diastolic volume/dilation
o RVEH → annular diation → worsens TR
o ↑RAP → ↑ systemic venous P → ascites
o ↓ forward pulmonary flow → ↓ volume to L heart → ↓ systemic CO

30
Q

Natural history TVD

A
  • Can have multiple congenital defects: ASD, PS, ventricular pre excitation
  • Supportive treatment
  • Lesions usually tolerated for many years
    o Progressive valve dysfct
    o Cardiomegaly, arrhythmias
31
Q

Ebsteins etiology

A
  • From failure of delamination from ventricular myocardium = adherent
  • Rare in dogs, not reported in cats
32
Q

Gross exam Ebsteins

A
  • Basal attachment of TV displaced apically into RV
    o Normal mural leaflet or displaced
    o Septal leaflet apically displaced
     Arise from RV myocardium
  • Atrialized portion of RV
  • Poor motion of valve leaflet
33
Q

Pathiphys ebsteins

A
  • Severe TR, similar to severe TVD
  • RV dysfct: abn myocardial structure and fct
    o Atrialized RV is thin and dysfunctional
  • Smaller RV volume
34
Q

ECG ebsteins

A
  • RBBB frequent
  • ↑PR
  • Pre-excitation
35
Q

Cardiac KT dx ebstein

A
  • EGM (intracardiac ECG) = confirms from where the electrical activity comes from
  • RA pressures w/ simultaneous ventricular electropotentials on intracardiac ECG
    o When ECG close to TV = ventricular action potential.
    o When ECG more up in atrium = atrial action potential.
36
Q

Uhl anomaly

A
  • Absence of RVFW myocardial layer
  • Apoptosis/ no cell development of myocytes
  • Reported in DSH
37
Q

TVS: gross exam

A
  • Abnormal TV leaflets
    o Thickened leaflets
    o Commissural fusion
    o Short chordae
  • Annulus may be large
  • Hypoplastic/atretic RV
    o Unless associated VSD
38
Q

Pathophys TVS

A
  • ↑ resistance to blood flow from RA → RV
    o PG across TV leads to RAE
    o R-CHF

10. Congenital Heart dz (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions