Congenital Heart Disease Flashcards
Exam IV
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
Examples of Pulmonic Stenosis
Dysplastic; fused valve with only a small hole available
Hypoplastic; valve grew too small (born this way)
What breeds are predisposed to pulmonic stenosis
Small breeds!
Terriers, brachiocephalic dogs
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
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
What kind of hypertrophy and dysfunciton is Pulmonary Stenosis?
Concentric hypertrophy (can see an increase in size of papillary muscles)
Diastolic dysfunction
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
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)
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
What is Anomalous L coronary artery?
Type of Pulmonic Stenosis
English Bulldogs, French Bulldogs, Boxers
Balloon valvuloplasty may rupture coronary artery!
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
Subaortic Stenosis
Breeds
Large breeds!
Golden Retriever, Newfoundland, Rottweiler, Boxer, German Shepherd
Subaortic Stenosis
Murmur
PMI: left basilar (less cranial than pulmonic)
Timing: Systole
Quality: Ejection murmur, may also get aortic regurgitation
Subaortic Stenosis
Femoral Pulses
Jugular abnormalities
Femoral pulses:
Abnormal; weak and late
Jugular veins:
Normal
Arrhythmias:
Pulse deficits
Subaortic Stenosis
What hypertrophy and what dysfunction?
Concentric hypertrophy
Diastolic dysfunction
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
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)
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)
Blood flow progression for PDA
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
PMI: left basilar (pulmonic and aortic)
Timing: Continuous murmur (constant swishing sound); can be louder in systole
PDA
Femoral pulses
Jugular abnormalities
Arrhythmias
Femoral pulses:
Normal to hyperkinetic/bounding pulses
No jugular vein abnormalities
Arrhythmia not common
Pathophysiology of hyperkinetic pulse
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
Vena cava -> RA -> RV -> MPA -> lungs -> pulmonary vein -> LA -> LV -> ascending aorta -> PDA -> MPA -> lungs -> etc.
PDA Radiographic Changes
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
