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Small Animal Medicine > Congenital Heart Disease > Flashcards

Congenital Heart Disease Flashcards

Exam IV

1
Q

What does stenosis do to blood flow?

A

Stenosis is a narrowing (for heart; valve)

Will increase pressure to go through the stenotic valve

Can cause secondary concentric hypertrophy

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2
Q

Examples of Pulmonic Stenosis

A

Dysplastic; fused valve with only a small hole available

Hypoplastic; valve grew too small (born this way)

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3
Q

What breeds are predisposed to pulmonic stenosis

A

Small breeds!

Terriers, brachiocephalic dogs

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4
Q

Pulmonic Stenosis

Murmur

A

PMI: left basilar
Timing: During systole, de-creshendo murmur
Quality: ejection murmur

Also can get a secondary murmur due to high right sided heart pressures: 
Tricuspid regurgitation 
PMI: right apex 
Timing: Systolic 
Quality: Regurgitant/plateau
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5
Q

Pulmonic Stenosis
Femoral Pulses
Jugular abnormalities
Arrhythmias

A

Femoral pulses:
Normal

Jugular vein:
May see both distension and pulses (b/c right heart disease) => could see ascities

Arrhythmias (usually not present)
Pulse deficits

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6
Q

What kind of hypertrophy and dysfunciton is Pulmonary Stenosis?

A

Concentric hypertrophy (can see an increase in size of papillary muscles)

Diastolic dysfunction

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7
Q

Pressure and Velocity Relationship

A

Modified Bernoulli Equation (can understand the pressure within the ventricle)

The higher the velocity the greater then pressure in the ventricle

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8
Q

Pulmonic Stenosis

Treatment of choice

A

Balloon valvuloplasty (70% success rate)

50-60% reduction in gradient

Not curative but palliative; only can decrease the stenosis so much (depends on initial severity)

Will be tearing valve – murmur will occur after

Cannot use for pulmonary annular hypoplasia (born that way)

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9
Q

Pulmonic Stenosis

Medical Management

A

Treat for diastolic dysfunction (Beta blockers)
Slow HR
Promotes RV filling and perfusion
Decrease contraction against obstruction

CHF?
Furosemide and ACE-inhibitors
+/- abdominocentesis (ascites)
DO NOT use Pimobendin because do NOT want to increase contractility

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10
Q

What is Anomalous L coronary artery?

A

Type of Pulmonic Stenosis

English Bulldogs, French Bulldogs, Boxers

Balloon valvuloplasty may rupture coronary artery!

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11
Q

Subaortic Stenosis

A

Development of a fibromuscular ridge in the left ventricular outflow tract proximal to the aortic valve

Valve is normal

Could see pulmonary edema

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12
Q

Subaortic Stenosis

Breeds

A

Large breeds!

Golden Retriever, Newfoundland, Rottweiler, Boxer, German Shepherd

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13
Q

Subaortic Stenosis

Murmur

A

PMI: left basilar (less cranial than pulmonic)

Timing: Systole

Quality: Ejection murmur, may also get aortic regurgitation

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14
Q

Subaortic Stenosis
Femoral Pulses
Jugular abnormalities

A

Femoral pulses:
Abnormal; weak and late

Jugular veins:
Normal

Arrhythmias:
Pulse deficits

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15
Q

Subaortic Stenosis

What hypertrophy and what dysfunction?

A

Concentric hypertrophy

Diastolic dysfunction

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16
Q

Subaortic Stenosis

Treatment

A

NO surgery available

Medical Management
Beta blockers (diastolic dysfunction)
Slow HR
Promote LV filling and perfusion
Decrease contraction against obstruction (NO Pimobenden)

Watch for Arrhythmias (can die due to sudden death!) - oxygen starved heart -> will see a significant ventricular tachycardia

Left sided CHF:
Furosemide and ACE-inhibitor

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17
Q

Subaortic Stenosis

Sequela

A

Increased risk for endocarditis
Must address infections as they arise

Due to blood speed and high velocity damage to the aortic valve (roughening of endothelium)

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18
Q

Patent Ductus Arteriosus (PDA)
What is it?
Etiology

A

Persistent opening of the ductus arteriosus after birth (blood skips lungs and enters descending aorta)

Etiology:
Toy breeds, herding breeds (Sheltie, Collie, Shepherd, Corgi)
Inherited
Female:Male (3:1)

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19
Q

Blood flow progression for PDA

A

Initially: blood flows from aorta to the MPA (from high to low pressure 120->20)

Pathology: blood will start flowing from MPA -> aorta (deoxygenated blood gets to tissues!)

Larger hole = larger volume overload = larger workload

20
Q

PDA

Murmur

A

PMI: left basilar (pulmonic and aortic)

Timing: Continuous murmur (constant swishing sound); can be louder in systole

21
Q

PDA
Femoral pulses
Jugular abnormalities
Arrhythmias

A

Femoral pulses:
Normal to hyperkinetic/bounding pulses

No jugular vein abnormalities

Arrhythmia not common

22
Q

Pathophysiology of hyperkinetic pulse

A

Systole: blood getting pushed forward through aorta (high velocity)

Diastole: blood is sitting for a moment and will leak into the MPA

Diastolic pressure much lower than normal animal -> get diastolic run off (blood leaking from aorta)

23
Q

Detailed blood flow for PDA

A

Vena cava -> RA -> RV -> MPA -> lungs -> pulmonary vein -> LA -> LV -> ascending aorta -> PDA -> MPA -> lungs -> etc.

24
Q

PDA Radiographic Changes

A

Enlargements:
LA, LV, aorta arch, ascending aorta, MPA, pulmonary artery and vein

(whatever the RBC goes through multiple times will be enlarged)

25
Q

PDA; what kind of hypertrophy and dysfunction?

A

Eccentric Hypertrophy (chamber is enlarged)

Systolic dysfunction
Volume overload

26
Q

PDA

Treatment

A

Close ductus! = currative
Surgical ligation; thoracotomy
Interventional closure; vascular access (put equipment into heart - approach via the femoral artery)
NO anesthesia until pulmonary edema is resolved

Left sided CHF if present
Furosemide
ACE-inhibitors
+/- pimobendan

Without closure most patients die within 1-2 years due to the development of CHF

27
Q

Ventricular Septal Defect
What is it?
Etiology
Types

A

Incomplete formation of the interventricular septum resulting in a communication between the LV and RV

Common in all species except the dog

High VSD: cats and horses
Low VSD: dogs

Larger the hole -> larger the volume overload -> larger the workload

28
Q

VSD
Murmur
Additional?

A

PMI: right sided (b/c left to right shunt)

Timing: Systolic

Quality: ejection murmur

Large defect = quiet murmur
Small defect = load murmur (velocity)

Additional murmur: Aortic Regurgitation
PMI: left base
Timing: Diastolic
Quality: decrescendo

29
Q

VSD
Femoral pulses
Jugular abnormalities
Arrhythmias

A

Femoral pulses normal
Jugular vein normal
Potential arrhythmias

30
Q

VSD

Radiographic abnormalities

A

None

31
Q

VSD

Treatment

A

Small VSD:
No treatment, monitor

Moderate to Severe VSD:
May develop Left sided CHF
Furosemide + ACE-Inhibitor
+/- pimobendan

32
Q

VSD

Treatment -Severe

A

Surgery options:
Pulmonary artery banding (increases pressure in pulmonic artery; artificial pulmonic stenosis; temporary fix, making RV and LV pressures equivalent)

Open heart surgery (Japan)

Interventional closure

33
Q

VSD and PDA
Shunt Reversal
PE findings

A

Pulmonary overcirculation
Pulmonary vascular hypertrophy and fibrosis -> increases pulmonary pressure (pulmonary hypertension)

Pressures can equalize and get no shunt/bidirectional

Advanced: Pulmonary pressure gets higher than systemic resulting in a right to left shunt

PE:
Occurs early in life 
No murmur detected
Jugular distension/pulsation
Cyanotic mucous membranes (especially with exercise)
34
Q

What occurs in R->L shunts

A 
Deoxygenated blood to systemic circulation 
Hypoxia
Increase EPO secretion by kidneys
Polycythemia
Hyperviscosity
35
Q

On PE what would be the difference about the distribution of cyanosis for R->L PDA vs. a R -> L VSD?

A

Reversed! So the Pulmonary system has higher pressure than the systemic blood supply
R-> L PDA: cyanosis in the extremities not mm. This is because the carotids come off before the PDA therefore oxygenated blood is getting to the mm.

R->L VSD: cyanosis in extremities and mm

36
Q

VSD and PDA
Shunt Reversal
Treatment

A

Closure of R-> L PDA is contraindicated; pulmonary pressures are too high will get acute right sided heart failure

Polycythemia
Phlebotomy (20 mL/kg q4-6 weeks)
Rx: Sildenafil, hydroxyurea

37
Q

VSD and PDA
Shunt Reversal
Prognosis

A

Long term: guarded to poor

Better with control of polycythemia; 5-10 years

38
Q

Mitral/Tricuspid Valve Dysplasia

A

Abnormal development of the valve often resulting in regurgitation (unable to close well) and occasionally resulting in stenosis (unable to open well)

Larger regurgitant volume the worse the dysplasia is

39
Q

Mitral Valve Dysplasia

Etiology

A 
CATS
Bull Terrier
Labrador
Danes
German Shepherd
40
Q

Tricuspid Dysplasia

Etiology

A 
LABRADOR
Danes
Borzoi
German Shepherd
Boxer
Shih Tzu
Mastiff
41
Q

Mitral Valve Dysplasia

Murmur

A

PMI: Left apex
Timing: Systolic
Quality: Regurgitation

42
Q

Tricuspid Dysplasia

Murmur

A

PMI: Right apex
Timing: Systolic
Quality: Regurgitation

43
Q

Mitral Valve Dysplasia
Femoral Pulses
Jugular Abnormalities
Arrhythmias

A

Femoral Pulses:
Normal to weak

No jugular pulse abnormalities

Arrhythmias: Pulse deficits

44
Q

Tricuspid Dysplasia
Femoral Pulses
Jugular Abnormalities
Arrhythmias

A

Femoral Pulses:
Normal

Jugular Distension
Jugular Pulses

Arrhythmias: Pulse deficits

45
Q

Mitral/Tricuspid Dysplasia

Treatment

A

Treat CHF if present
Furosemide
ACE-Inhibitor
+/- pimobendan

Tricuspid: +/- abdominocentesis

Atrial fibrillation is common:
Calcium channel blocker (diltiazem)
+/- Digoxin

Small Animal Medicine (8 decks)

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