Congenital Volume Overloads Flashcards

1
Q

What is a patent ductus arteriosus?

A
  • Persistent opening of the ductus arteriosus after birth
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2
Q

Who gets PDA?

A
  • Toy breeds

- Herding breeds (Sheltie, Collie, Shepherd, Corgi, etc.)

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3
Q

PDA sex predilection

A
  • Seen more commonly in female than male dogs
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4
Q

Pattern of inheritance for PDA

A
  • Inherited

- Polygenic trait

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5
Q

How common is PDA?

A
  • May be the most common dog defect
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6
Q

Ductus arteriosus function in utero

A
  • Umbilical vein from the mother and skips liver through ductus venosus
  • Comes into the caudal vena cava to right atrium
  • Preferentially shunted through foramen ovalis into left atrium and left ventricle through aorta into head and body
  • Deoxygenated blood from the head in the baby that mixes with oxygenated blood in the right atrium
  • SHunted through tricuspid through pulmonary artery and into ductus arteriosus
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7
Q

Where is the ductus arteriosus?

A
  • Junction of aortic arch and descending aorta and pulmonary artery
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8
Q

What is the point of the ductus arteriosus in the fetus?

A
  • Don’t want venous admixure to go to the brain
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9
Q

PDA murmur PMI, timing, and quality

A
  • PMI: Left heart base
  • Timing: continuous murmur
  • Quality: Continuous murmur
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10
Q

Femoral pulses of PDA

A
  • Normal to HYPERKINETIC*
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11
Q

Jugular distensions/pulses with PDA

A
  • None usually for distensions or pulses
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12
Q

Arrhythmias with PDA

A
  • Pulse deficits

- Possible

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13
Q

What can cause the hyperkinetic or bounding pulses with a PDA?

A
  • Pulse pressure = systolic - diastolic
  • Diastolic pressures are much lower because it’s leaking backwards during diastole
  • Normal is 120/80
  • During a PDA can be 110/50
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14
Q

Radiographic findings of PDA

A
  • Left atrial enlargement
  • left ventricular enlargement
  • Pulmonary arteries and veins will be enlarged
  • Aorta enlarged
  • MPA will be enlarged too
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15
Q

Why do the structures that get enlarged in a PDA get enlarged?

A
  • Going through multiple times

- Aorta –> MPA –> arterioles –> capillaries –> main pulmonary vein

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16
Q

What type of hypertrophy occurs with PDA?

A
  • Eccentric hypertrophy

- Volume overload

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17
Q

Echocardiogram with PDA

A
  • Right heart will look small compared to the left heart because the left heart is so big
  • Eccentric hypertrophy
  • Try to use Doppler
  • Continuous flow
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18
Q

What determines severity of PDA?

A
  • Depends on size of PDA

- Larger hole means larger volume overload and larger workload

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19
Q

Surgical treatment of PDA

A
  • Surgical ligation with thoracotomy

- Also invterventional closure with vascular access via the femoral artery

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20
Q

What other treatment may be necessary for PDA?

A
  • Treat left-sided CHF if present

- Furosemide + ACE inhibitors +/- Pimobendan

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21
Q

What’s the priority for PDA treatment: Treat CHF or treat the PDA?

A
  • Important to treat the left sided CHF FIRST

- No anesthesia, until the pulmonary edema is resolved

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22
Q

Description of interventional closure

A
  • Track up the femoral artery
  • Inject contrast to highlight the ductus
  • measure the size of the hole
  • Waist of the device expands the ductus
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23
Q

What is usually the smallest dog that can have an interventional closure?

A
  • 2kg
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24
Q

Mortality associated with interventional closure

A
  • Pretty significant mortality
  • Success rates are surgeon dependent
  • If they do a bad job, they could cause an embolism
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25
Q

Prognosis for PDA if they close the ductus

A
  • CURATIVE!!!!
  • Normal life expectancy
  • +/- cardiac meds (usually no meds)
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26
Q

Prognosis of PDA without closure

A
  • 50-60% develop CHF and die within 1 year

- 70-80% develop CHF and die within 2 years

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27
Q

VSD definition

A
  • Incomplete formation of the interventricular septum resulting in a communication between the left and right ventricles
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28
Q

Who gets VSD?

A
  • Most common congenital heart disease in all species except for the dog
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29
Q

Left ventricular pressure compared to right ventricular pressure

A
  • LV: 120/6

- RV: 20/5

30
Q

Mime the flow of blood from the left ventricle to the right ventricle with a VSD

A
  • Just do it
31
Q

VSD murmur PMI, timing, and quality

A
  • Hear it on the right side better (often basilar)
  • Systolic
  • Ejection quality
32
Q

What additional murmur can happen with a VSD?

A
  • Aortic regurgitation
33
Q

Aortic regurgitation murmur PMI, quality, and timing

A
  • PMI is left heart base
  • Quality is decrescendo
  • Timing is Diastolic
34
Q

Femoral pulse quality with VSD

A
  • Normal
35
Q

Jugular distensions or pulses with VSD

A
  • None
36
Q

Arrhythmias with VSD

A
  • Possible

- Pulse deficits

37
Q

Radiographic findings of VSD

A
  • Left atrial and left ventricular enlargement
  • Overcirculation of lungs
  • Should not see main pulmonary or aortic involvement with VSD
38
Q

What type of hypertrophy occurs with VSD?

A
  • Eccentric hypertrophy
39
Q

VSD echocardiogram findings

A
  • Aortic regurgitation can happen
40
Q

What determines severity of VSD?

A
  • Size

- Larger hole = more volume overload = larger workload

41
Q

For murmur with a VSD, will it be louder when it’s smaller or bigger?

A
  • Louder when it’s smaller

- Again, severity does not correlate very well with the loudness of the murmur

42
Q

Treatment and prognosis for a small VSD

A
  • No treatment needed

- Normal quantity and quality of life

43
Q

Treatment and prognosis for a large VSD

A
  • May develop Left sided CHF at some point

- If they develop left sided heart failure, furosemide + ACE-inhibitor +/- Pimobendan if CHF develops

44
Q

Surgical options for severe VSD

A
  • Pulmonary artery banding (palliative)
  • Open heart failure (people only)
  • Interventional closure
45
Q

What determines prognosis for VSD?

A
  • Size of the defect

- Development of CHF

46
Q

What is prognosis if an animal goes into stage C with VSD?

A
  • ~ 1 year
47
Q

Eisenmengers Physiology with VSD/PDA - initially

A
  • Pulmonary overcirculation, resulting in pulmonary vascular hypertrophy and fibrosis
  • Increased pulmonary pressures
  • As long as systemic pressures are higher than pulmonary pressures, blood will go to the lungs first
  • Make sure you can mime out where blood will go
48
Q

Physiology of no shunt with a PDA or VSD

A
  • Pulmonary pressures = systemic pressures
49
Q

Right to left shunting pathophysiology of VSD and PDA

A
  • Pulmonary overcirculation
  • Pulmonary vascular hypertrophy and fibrosis
  • Increased pulmonary pressures
  • Eventually, pulmonary pressures > systemic pressures
  • Right –> left shunting leading to deoxygenated blood in your body (AKA hypoxemia)
50
Q

What secondary condition can occur with hypoxemia?

A
  • Polycythemia
51
Q

Pathophysiology of polycythemia secondary to right to left shunting

A
  • Deoxygenated blood to systemic circulation
  • Hypoxia
  • Increased EPO secretion by the kidneys
  • Polycythemia
  • Hyperviscosity
52
Q

What causes R–> L PDA?

A
  • Reversal happens EARLY in life
  • 1st couple of months
  • Not a result of an uncorrected left to right PDA
  • If you have a left to right, it will often just go into CHF
53
Q

Findings for a R–> L shunt: murmur, jugular distension, and mucous membranes?

A
  • Murmur: usually none, as blood is too viscous
  • Jugular distension and pulsation: +/+
  • Mucous membranes cyanotic, especially with exercise
54
Q

On a PE, what would be different about the distribution of cyanosis for a R–>L PDA vs a R–>L VSD?

A
  • THINK ABOUT IT
55
Q

Treatment for right to left PDA

A
  • CLOSURE IS CONTRAINDICATED (right heart failure because it has to work against an increased pressure)
  • Treat polycythemia
56
Q

How to treat polycythemia

A
  • Phlebotomy (~20mL/kg q4-6 weeks)

- Medical treatment: sildenafil, hydroxyurea (bone marrow suppressor)

57
Q

Prognosis for R–> L VSD or PDA

A
  • Long term prognosis is guarded to poor
  • Better with control of polycythemia
  • Acceptable quality of life for ~5-10 years, but often quite high maintenance
58
Q

Breeds that get tricuspid dysplasia?

A
  • Lab!!!!!!**
  • Danes
  • Borzoi
  • German Shepherd Dog
  • Boxer
  • Shih Tzu
  • Mastiff
59
Q

Breeds that get mitral valve dysplasia?

A
  • Cats
  • Bull Terrier*
  • Labs
  • Danes
  • German SHepherd Dogs
60
Q

Murmur PMI, timing, and quality for tricuspid dysplasia?

A
  • Right apex
  • Systolic
  • Regurgitant
61
Q

Murmur PMI, timing, and quality for mitral valve dysplasia?

A
  • Left apex
  • Systolic
  • Regurgitant
62
Q

Femoral pulses, jugular distension/pulses, and arrhythmias for tricuspid dysplasia?

A
  • Femoral pulses: Normal
  • Jugular distension/pulses: +/+
  • Arrhythmias: pulse deficits
63
Q

Femoral pulses, jugular distension/pulses, and arrhythmias for mitral valve dysplasia?

A
  • Femoral pulses: Normal to weak
  • Jugular distension/pulses: -/-
  • Arrhythmias: pulse deficits
64
Q

Severity of AV Valve dysplasia

A
  • Varies greatly

- worse with larger regurgitant volume or of stenosis is also present

65
Q

Treatment of AV valve dysplasia

A
  • Treat CHF if present
  • Treat arrhythmias
  • Surgery not really an option for these guys
66
Q

How to treat CHF for AV valve dysplasia?

A
  • For either, furosemide + ACE inhibitors +/- Pimobendan

- For tricuspid valve dysplasia, abdominocentesis +/- thoracocentesis

67
Q

What is the common arrhythmia with AV valve dysplasia?

A
  • Atrial fibrillation
68
Q

How to treat atrial fibrillation?

A
  • Diltiazem (calcium channel blocker)

- +/- digoxin

69
Q

Prognosis for AV valve dysplasia if mild

A
  • Normal quantity/quality of life
70
Q

Relative prognosis for TVD vs MVD

A
  • TVD often fare better than MVD
71
Q

Prognosis once you hit CHF

A
  • ~ 1 year

- May be worse with atrial fibrillation