Congenital Heart Disease Flashcards by Brittany Jermalovic

What does stenosis do to blood flow?

Stenosis is a narrowing (for heart; valve)

Will increase pressure to go through the stenotic valve

Can cause secondary concentric hypertrophy

How well did you know this?

Not at all

Perfectly

Examples of Pulmonic Stenosis

Dysplastic; fused valve with only a small hole available

Hypoplastic; valve grew too small (born this way)

How well did you know this?

Not at all

Perfectly

What breeds are predisposed to pulmonic stenosis

Small breeds!

Terriers, brachiocephalic dogs

How well did you know this?

Not at all

Perfectly

Pulmonic Stenosis

Murmur

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

How well did you know this?

Not at all

Perfectly

Pulmonic Stenosis
Femoral Pulses
Jugular abnormalities
Arrhythmias

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

How well did you know this?

Not at all

Perfectly

What kind of hypertrophy and dysfunciton is Pulmonary Stenosis?

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

Diastolic dysfunction

How well did you know this?

Not at all

Perfectly

Pressure and Velocity Relationship

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

The higher the velocity the greater then pressure in the ventricle

How well did you know this?

Not at all

Perfectly

Pulmonic Stenosis

Treatment of choice

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)

How well did you know this?

Not at all

Perfectly

Pulmonic Stenosis

Medical Management

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

How well did you know this?

Not at all

Perfectly

What is Anomalous L coronary artery?

Type of Pulmonic Stenosis

English Bulldogs, French Bulldogs, Boxers

Balloon valvuloplasty may rupture coronary artery!

How well did you know this?

Not at all

Perfectly

Subaortic Stenosis

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

Valve is normal

Could see pulmonary edema

How well did you know this?

Not at all

Perfectly

Subaortic Stenosis

Breeds

Large breeds!

Golden Retriever, Newfoundland, Rottweiler, Boxer, German Shepherd

How well did you know this?

Not at all

Perfectly

Subaortic Stenosis

Murmur

PMI: left basilar (less cranial than pulmonic)

Timing: Systole

Quality: Ejection murmur, may also get aortic regurgitation

How well did you know this?

Not at all

Perfectly

Subaortic Stenosis
Femoral Pulses
Jugular abnormalities

Femoral pulses:
Abnormal; weak and late

Jugular veins:
Normal

Arrhythmias:
Pulse deficits

How well did you know this?

Not at all

Perfectly

Subaortic Stenosis

What hypertrophy and what dysfunction?

Concentric hypertrophy

Diastolic dysfunction

How well did you know this?

Not at all

Perfectly

Subaortic Stenosis

Treatment

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

How well did you know this?

Not at all

Perfectly

Subaortic Stenosis

Sequela

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)

How well did you know this?

Not at all

Perfectly

Patent Ductus Arteriosus (PDA)
What is it?
Etiology

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)

How well did you know this?

Not at all

Perfectly

Blood flow progression for PDA

Study These Flashcards

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

PDA

Murmur

Study These Flashcards

PMI: left basilar (pulmonic and aortic)

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

PDA
Femoral pulses
Jugular abnormalities
Arrhythmias

Study These Flashcards

Femoral pulses:
Normal to hyperkinetic/bounding pulses

No jugular vein abnormalities

Arrhythmia not common

Pathophysiology of hyperkinetic pulse

Study These Flashcards

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)

Detailed blood flow for PDA

Study These Flashcards

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

PDA Radiographic Changes

Study These Flashcards

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

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

PDA; what kind of hypertrophy and dysfunction?

Eccentric Hypertrophy (chamber is enlarged) Systolic dysfunction Volume overload

PDA | Treatment

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

Ventricular Septal Defect What is it? Etiology Types

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

VSD Murmur Additional?

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

VSD Femoral pulses Jugular abnormalities Arrhythmias

Femoral pulses normal Jugular vein normal Potential arrhythmias

VSD | Radiographic abnormalities

None

VSD | Treatment

Small VSD: No treatment, monitor Moderate to Severe VSD: May develop Left sided CHF Furosemide + ACE-Inhibitor +/- pimobendan

VSD | Treatment -Severe

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

VSD and PDA Shunt Reversal PE findings

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) ```

What occurs in R->L shunts

``` Deoxygenated blood to systemic circulation Hypoxia Increase EPO secretion by kidneys Polycythemia Hyperviscosity ```

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

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

VSD and PDA Shunt Reversal Treatment

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

VSD and PDA Shunt Reversal Prognosis

Long term: guarded to poor Better with control of polycythemia; 5-10 years

Mitral/Tricuspid Valve Dysplasia

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

Mitral Valve Dysplasia | Etiology

``` CATS Bull Terrier Labrador Danes German Shepherd ```

Tricuspid Dysplasia | Etiology

``` LABRADOR Danes Borzoi German Shepherd Boxer Shih Tzu Mastiff ```

Mitral Valve Dysplasia | Murmur

PMI: Left apex Timing: Systolic Quality: Regurgitation

Tricuspid Dysplasia | Murmur

PMI: Right apex Timing: Systolic Quality: Regurgitation

Mitral Valve Dysplasia Femoral Pulses Jugular Abnormalities Arrhythmias

Femoral Pulses: Normal to weak No jugular pulse abnormalities Arrhythmias: Pulse deficits

Tricuspid Dysplasia Femoral Pulses Jugular Abnormalities Arrhythmias

Femoral Pulses: Normal Jugular Distension Jugular Pulses Arrhythmias: Pulse deficits

Mitral/Tricuspid Dysplasia | Treatment

Treat CHF if present Furosemide ACE-Inhibitor +/- pimobendan Tricuspid: +/- abdominocentesis Atrial fibrillation is common: Calcium channel blocker (diltiazem) +/- Digoxin

Congenital Heart Disease Flashcards

Exam IV (45 cards)