1. CONGENITAL
HEART DISEASES
Dr. Hadi ALİHOSSEİNİ, DVM, DVSc, PhD
Small Animal Internal Medicine & Cardiology
Terapist Veterinary Hospital
Istanbul / Turkey
Small Animal’s
2. Congenital heart diseases are the most common type of heart
disease in young dogs and cats, but are occasionally diagnosed
in adult animals.
Congenital Cardiopathy
3. The incidence of CHD in dogs:
6.8 to 8.0 / 1000
On average 1/ 15 litters
The actual incidence is likely higher, as some
defects result in neonatal death and are
unreported.
Congenital Cardiopathy
Incidence
Congenital heart disease is less common in
cats than in dogs.
The reported incidence is
0.2 to 1.0 / 1000
No consistent breed or gender predilections
have been adequately demonstrated.
(Hospital admissions Reports)
4. Classification of Congenital Heart Disease
CHD
Acyanotics
LR-Shunts
ASD
VSD
PDA
Obstructive Lesions
AS – PS
Ms - Ts
Cyanotics
Decreased Pulmonary
flow
TF
TD
PF
Increased Pulmonary
flow
Transposition of great
arteries
5. The most common congenital heart defects in dogs
Patent Ductus Arteriosus (PDA)
Pulmonic Stenosis (PS)
Aortic Stenosis
Ventricular Septal Defect (VSD)
Tetralogy of Fallot
Less common defects in dogs
Mitral Valve Dysplasia
Atrial Septal Defects
Tricuspid Valve Dysplasia
Cor Triatriatum Dexter
Mitral Stenosis
Rare defects
Persistent Truncus Arteriosus
Tricuspid Stenosis
Right Ventricular Hypoplasia
Double Outlet Right Ventricle
Transposition Of The Great Vessels
Congenital Cardiopathy - Dogs
6. The most common congenital heart defects in cats
Mitral Valve Dysplasia
Tricuspid Valve Dysplasia
PDA
VSD
Aortic Stenosis
Tetralogy Of Fallot
Persistent Common Atrioventricular Canal
Endocardial Fibroelastosis.
Less common defects in cats
Persistent Truncus Arteriosu
Ps
Atrial Septal Defect
Tricuspid Stenosis
Right Ventricular Hypoplasia
Congenital Cardiopathy - Cats
9. Congenital heart defects etilogies in young present
4 Common inherited CHD in dogs:
PDA ...................................Poodle
Subaortic stenosis ...........Newfoundland
Tetralogy of Fallot ...........Keeshond
PS ........................................Beagle
Hereditary Aspects
1.a heritable TRAIT
2.a defect that originated during GESTATION
3.A primary genetic mutation
4.A environmental influences
10. Generally, a congenital heart defect is suspected when a heart murmur is detected in a young
dog or cat.
Other supporting clinical features may include:
Failure to Thrive
Exercise Intolerance
Cyanosis
Collapse or Seizure
Jugular Venous Distention
Diagnosis
11. A complete cardiovascular physical examination,
Routine ECG
Radiography
Echocardiography
Cardiac catheterization
Tentative & Specific Diagnosis
Information obtained echocardiographically is also helpful
in determining the severity of the defect, especially if
Doppler techniques are used (measurement of blood
velocities within the heart).
12. General Treatment Considerations
Minimally Invasive
Interventions
Surgery
Intervention
Medical treatment
Balloon Valvuloplasty
Stenotic lesions
Surgical correction or
palliation is possible for
certain defects.
Primarily for the control or
prevention of
complications, such as
CONGESTIVE HEART
FAILURE,
ARRHYTHMIAS, and
ENDOCARDITIS rather
than for correction of the
defect.
13. Not all young dogs and cats with heart murmurs have congenital heart disease!
Innocent, or functional, murmurs
Mild turbulence within the heart and great vessels
Usually diminish in intensity or resolve by 4 to 5 months of age.
DDX - Characteristic of the innocent murmur
Early-Systolic in timing
Short duration (ejection-type).
Soft” (Grade III/VI or less in intensity) low-pitched, vibrating, or musical quality.
Loudest along the left sternal border and are poorly transmitted.
Their intensity may vary with changes in position, with the phase of respiration, with exercise, and
from day to day.
Absence of any other demonstrable evidence of cardiovascular disease (e.g., lack of clinical signs or
radiographic abnormalities).
Innocent (Functional) Murmurs
Loud systolic murmurs (grade
IV/VI or greater), precordial
thrills, and diastolic murmurs are
indicative of cardiac disease and
should prompt further
diagnostics.
15. In fetal circulation, the ductus arteriosus serves to shunt
maternally oxygenated blood into the aorta, thereby bypassing
the nonfunctional lungs.
Shortly after birth, several factors contribute to effect closure of
the ductus.
(dramatically) Pulmonary vascular resistance drops
vasodilatory prostaglandin levels Oxygen tension
(marked) in pulmonary blood flow and vasoconstriction of the
ductus.
Following closure by vasoconstriction the ductus is
permanently closed by fibrous contracture, which produces
the ligamentum arteriosum.
Failure of the ductus to close is termed
Patent ductus arteriosus (PDA)
Persistent ductus arteriosus
PDA - Anatomy
16. The consequences of a PDA depend primarily on
The diameter of the Ductus
Pulmonary Vascular Resistance
When pulmonary vascular resistance is normal, blood
continually shunts from the aorta (high resistance) into the
pulmonary circulation (low resistance).
Shunting in this fashion (systemic to pulmonary) is referred
to as left-to-right and represents the most common pattern
in PDA.
PDA - Pathophysiology
17. When pulmonary vascular resistance increases and exceeds systemic vascular resistance, blood
will shunt from the pulmonary artery into the aorta (so-called Right-to-Left or Reversed PDA).
PDA - Pathophysiology
18. Ductal diameter.
Small ductus
The volume of blood shunted is restricted and there may be no
hemodynamic effects!
Large ductus (significant shunting)
1. Left heart Volume overload LHF
2. In the largest of shunts The excessive pulmonary blood flow
dramatic increases in pulmonary vascular resistance
1) Pulmonary Hypertension
2) Shunt Reversal (Eisenmenger’s physiology)
PDA - Pathophysiology
19. Etiology
A higher frequency in the DOG.
a higher frequency in the FEMALE.
Breeds predisposed or at increased risk include
Bichon Frisé, Chihuahua, Cocker Spaniel, Collie, English Springer
Spaniel, German Shepherd, Keeshond, Labrador Retriever, Maltese,
Newfoundland, Poodle, Pomeranian, Shetland Sheepdog and
Yorkshire Terrier.
Inherited PDA Miniature Poodle (transmitted as a polygenic trait)
PDA -Breed Disposition
20. Palpation
Femoral pulse: Water-hammer / bounding (Left-to-right shunting PDA)
This type of pulse represents a widened pulse pressure secondary to the loss of diastolic
pressure through the ductus, and elevation of systolic blood pressure from the volume-
overloaded left ventricle.
PDA - Physical Examination
The larger Ductus The More Prominent Arterial Pulse.
L-R Shunting PDA R-L Shunting PDA
Precordial Thrill Over the cranial left-heart base No precordial thrill
Apical Impulse Left Side Right Side
21. Auscultation
A continuous-type machinery murmur is a hallmark
of left-to-right shunting PDA.
The systolic component of the murmur
PDA: is usually quite prominent at the cardiac apex
A systolic murmur secondary to mitral regurgitation because
of annular dilation (Left heart enlargement)
PDA - Physical Examination
Loudest in mid-to-late systole
Gradually decreases in intensity
through diastole
In some cases murmur is restricted to the
cranial left-heart base & may be missed if
auscultation is limited to the apex
22. PDA Diagnosis - ECG
Tall R waves present in leads II (greater than 3.0 mV), III, and aVF
Deep Q waves are often present in leads II, III, and aVF
The QRS complexes are increased in duration (greater than 80 ms)
The Mean Electrical Axis may be shifted to the left (less than 40 degrees)
P -mitrale (widened P wave) is often present
Atrial fibrillation and ventricular arrhythmias may occur in association with CHF
Deep S waves in leads I, II, III, and aVF
Right shift of the mean electrical axis (more than 100 degrees)
23. PDA Diagnosis - CXR
he radiographic signs of
PDA vary considerably
with
• the volume of blood being shunted
• the age of the animal
• the degree of cardiac decompensation.
DV the left cardiac
silhouette.
• The aneurysmal bulge of the aortic arch
• The enlarged pulmonary outflow tract
• The enlarged left atrial appendage
CHF • Mild to moderate left ventricular and left atrial enlargement are usually present.
• Overcirculation of the lung field can often be visualized.
• Severe cardiomegaly, pulmonary congestion, and pulmonary edema will be present when there is
RL Shuntinf of PDA • Right ventricular enlargement and prominent tortuous pulmonary arteries are seen in animals with severe
pulmonary hypertension
24. The volume overloaded state of the LEFT SIDE OF THE HEART
Left atrial dilation,
left ventricular dilation, and normal to excessive wall motion
(fractional shortening).
In some cases the ductus can be visualized.
In cases with Pulmonary Hypertension and RL shunting
Right ventricular hypertrophy
Enlargement of the main pulmonary artery
Pulmonic insufficiency.
PDA Diagnosis - Echo
CONTRAST
ECHOCARDIOGRAPHY
can be used to confirm the
presence of a right-to-left
shunting PDA.
In this technique, agitated saline
is injected into a peripheral vein
during echocardiographic
examination (first injection) and
abdominal aortic imaging (second
injection) to detect right-to-left
shunting of blood. The absence of
intracardiac shunting with the
presence of microbubbles within
the abdominal aorta is diagnostic
of reversed PDA.
25. Selective Angiocardiography
The diagnosis of a LEFT-TO-RIGHT PDA can be made by injecting contrast
media into the aortic arch.
The simultaneous filling of the main pulmonary artery and the aorta is diagnostic
for PDA.
A main pulmonary artery contrast injection can be used to confirm the
diagnosis of a RIGHT-TO-LEFT SHUNT (simultaneous filling of main
pulmonary artery and aorta).
Nonselective Angiocardiography
Nonselective angiocardiography is performed by injecting contrast material
through a large diameter venous catheter and taking radiographs in quick
succession.
Nonselective angiocardiography may be used to support the diagnosis of a
RIGHT-TO-LEFT SHUNTING PDA; however, this technique is of no value in the
diagnosis of left to- right shunts.
PDA Diagnosis – Cat Lab
26. • Aorticopulmonary window
Aorta and the main pulmonary artery close to their origin from the
heart base.
This rare defect usually results in severe pulmonary hypertension.
Concurrent Aortic Stenosis and Insufficiency
The systolic murmur of aortic stenosis and the diastolic murmur of
aortic insufficiency combine to mimic the machinery murmur of PDA.
Echocardiography easily differentiates between these differentials.
PDA - DDX
27. Surgical Intervention
In Asymptomatic animals with left-to-right shunting PDA, surgical
correction of the ductus should be performed as soon as possible.
Current surgical ligation success rates are 95%.
Recent studies have shown asymptomatic large dogs and older
dogs (more than 2 years) have no significant added risk.
Heart Failure
Mild to moderate LHF, resolution of pulmonary edema must
precede anesthesia and surgery.
Severe heart failure, patient stabilization should be attempted;
however, these patients are poor anesthetic risks.
PDA - Therapy and Prognosis
Presence of myocardial
failure and atrial fibrillation
are negative prognostic
indicators.
28. Transcatheter Occlusion
Shunting through the ductus may be stopped by a relatively
noninvasive method termed transcatheter occlusion.
Coils
This procedure employs delivery of a Gianturco coil, resulting in
embolization of the ductus.
Coils are composed of prothrombotic poly-Dacron fibers.
The size of the coil selected is based on the approximate size of the
ductus (as determinedby angiography or echocardiography).
Multiple coils may be needed for full occlusion of the ductus.
Amplatzer
The device is delivered from a catheter passed up the femoral artery and
into the ductus.
PDA - Therapy and Prognosis
33. Patent ductus arteriosus (dorsoventral projection)
in a 3-month-old poodle. There is generalized
heart enlargement, an aneurysm-like bulge of the
descending aorta (open arrow), a bulge of the main
pulmonary artery (curved arrow), and enlargement
of the left auricle (straight arrow). Alveolar infiltrate
due to pulmonary edema is present in the caudal
lung lobes.
38. Septal defects may occur in any area of the
septum, but are most commonly located in
the membranous portion.
VSDs may occur as isolated defects, may
coexist with concurrent defects
PDA
ASD
or may be a component of complex cardiac
anomalies.
VSD - Anatomy
VSD
- PM: Perimembranous VSD
- SC: Supracristal VSD
- IL: Inlet VSD
- MUS: IVS Muscular VSD
39. 2 major factors that determine the consequences of a VSD
the size of the defect
the relative pressures (or resistances) of the ventricles
Normal pressure VSD blood will shunt left to right (5-6
times).
Typical VSD (left-to-right shunting membranous defect)
shunt flow into
RV
Main pulmonary artery
Large volume overload to
Pulmonary circulation
LA & LA
VSD - Pathophysiology
40. VSD shunt diameter
Small defects
No hemodynamic significance.
May predispose to the development of Endocarditis.
In some cases, small defects close spontaneously.
Moderately sized defects
Significant shunting
Produce clinical signs.
Very large defects
Create a functional single ventricle LVP=RVP)
RV resistance increases (e.g., PS, pulmonary hypertension)
RVP shunt volume Shunt Resvering Right To Left VSD
signs of CYANOSIS may develop.
VSD - Pathophysiology
41. Breed studies in the keeshond have shown the defect to be polygenic.
The English bulldog appears to have a higher incidence than other breeds, but the defect is
seen in many purebred and mixed-breed dogs.
• Breed incidence in the cat has not been determined.
VSD – Breed Predispistion
42. Palpation
Precordial thrill
NORMAL
At the right-heart base (third to fourth intercostal spaces)
Volume overloading of the left ventricle often accentuates the left-sided impulse.
RL-Shunting (PAH)
Precordial thrills are unusual.
Right apical impulse is accentuated.
VSD -Examination
43. Auscultation
Typically, the murmur is
Harsh, holosystolic murmur
Heard best at the RIGHT STERNAL border
At the second through 4’ İNTERCOSTAL spaces.
A murmur of functional PS
Heard over the pulmonic valve area (PAM-T)
Due to the extra volume of blood passing through the
pulmonic valve.
Not related to a structural valve problem.
VSD -Examination
A Splitting S2
Due to slightly prolonged right ventricular ejection
time.
Advnced VSD
Diastolic murmur of AORTIC INSUFFICIENCY
(destabilaized aortic valve cusp)
In addition to the systolic murmur. (VSD murmur)
This combination is referred to as a TO-AND-FRO
MURMUR and is not a continuous murmur.
PAH
Absent murmur (elevations in right ventricular
resistance result in diminished shunting)
44. Normal for Small VSDs.
LV/RV or biventricular enlargement
Right bundle branch block (RBBB) may also be observed.
VSD Diagnosis - ECG
45. Small defects usually do not cause radiographic changes.
Larger defects
Left ventricular enlargement
Left atrial enlargement
Increased pulmonary artery prominence
PAH & RL Shunting VSD
Right ventricular enlargement
Prominent tortuous pulmonary arteries
VSD Diagnosis - CXR
46. The main Diagnosis.
Moderate to large shunt
LV & LA Dilation (Left Heart Enlargement)
A hole Interventricular septum (2D)
Contrast echocardiography will confirm .
Small shunting volume VSD
High-velocity flow (>4.5 m/s) across the VSD
Normal transpulmonic valvular velocities
Large shunting volume
Low-velocity flow (<4.5 m/s) across the VSD
Increased transpulmonic valvular velocities
VSD Diagnosis - Echo
Restrictive VSD
Unrestrictive VSD
Qp/Qs
50. Cardiac catheterization and angiography Confirm the diagnosis of VSD.
Determination of oxygen saturation of blood from each chamber may be used to confirm
shunting.
Left-to-right shunts produce a step-up in oxygen saturation in the right ventricle compared
with the right atrium.
VSD Diagnosis – Cat Lab
Qp/Qs
51. Surgery
Open heart techniques have been used with
reasonable success.
Cardiopulmonary bypass machine
Medical Management
In patients where surgical correction or
palliation is not an option, medical management
of CONGESTIVE HEART FAILURE may be
required.
VSD - Therapy and Prognosis
52. Excellent for
Small defects
Surgically corrected defects
Moderate to Large defects
Variable clinical course and prognosis,
depending on shunt volume.
VSD - Prognosis
54. The left ventricular outflow tract dimension narrowing at
Subvalvular (fibrous ring or muscular)
Valvular
Supravalvular level
The subvalvular form (subaortic stenosis) is the most common
form in the dog.
Fixed valvular and supravalvular stenosis have been reported
in the cat.
AS - Anatomy
55. Associated with
Systolic Anterior Motion Of The Anterior Mitral Valve Leaflet.
This condition has been described in patients with
Fixed aortic/ Subaortic Stenosis (SAS)
Hypertrophic cardiomyopathy
Mitral Valve Dysplasia
Other conditions aused hypertrophy of the interventricular septum.
Dynamic Aortic Stenosis
56. Some breeds (Boxers, Bull Terriers, Golden Retrievers) have mildly decreased left
ventricular outflow tract dimensions that result in mild elevations of transvalvular
blood velocity without other structural abnormalities.
AS – Breed Anatomy
57. LVOT Stenosis LV Pressure overload
Chronic pressure overload CONCENTRIC HYPERTROPHY
As blood is forced through the stenotic area
Velocity increases Turbulence
A systolic ejection murmur
A post-stenotic Dilation of the aorta.
Left ventricular hypertrophy the myocardial oxygen
demand.
Myocardial hypertrophy
Capillary density
wall tension all contribute to produce myocardial
hypoxia/ischemia.
Focal areas of myocardial infarction & Fibrosis
Papillary muscles
Subendocardium)
AS - Pathophysiology
These cases are prone to SUDDEN DEATH
FATAL VENTRICULAR ARRHYTHMIAS
induced by hypoxia.
Infrequently, LHF develops.
The presence of AS/SAS may risk of
INFECTIVE ENDOCARDİTİS.
58. A polygenic inheritance pattern Newfoundland
Other commonly affected breeds include
Bouvier de Flanders, boxer, English bulldog, German
Shepherd, German shorthair pointer, golden retriever, great
Dane, rottweiler, and samoyed.
Bull terriers are predisposed to valvular aortic stenosis
characterized by thickened aortic valve leaflets and a
hypoplastic annulus.
AS - Breed Predisposition
59. Palpation
Left ventricular impulses
Severe AS Precordial thrill over the aortic valve area.
Femoral pulses: Weak and Late rising (Pulsus Parvus Et Tardus).
Auscultation
Systolic ejection- type murmur heard best over the left 4’ ICS aortic valve area).
Carotid artery can be auscultated in the midcervical area.
Occasionally, the murmur may be loudest in the right 3or 4 ICS midway up the thorax.
Diastolic murmur of aortic insufficiency is present.
AS - Examination
60. The ECG may be normal.
Left ventricular hypertrophy
tall R waves in leads II [greater than 3.0 mV], III, and aVF).
Ventricular or supraventricular arrhythmias (occasionally)
AS - ECG
61. Enlargement
of the Aortic Arch (post-stenotic dilation)
Left Ventricle.
Left atrial enlargement (concurrent mitral insufficiency)
AS - CXR
62. The most sensitive noninvasive method to diagnose
and grading
Left ventricular hypertrophy.
Severe cases:
Hypertrophied Papillary muscles and
myocardium (bright) secondary to calcium
deposition, ischemia and/or fibrosis.
Doppler echocardiography
20-50 mmHg
50-80 mmHg
>80mmHg
AS - Echo
63. Used to confirm the diagnosis.,
Cardiac catheterization and angiography are occasionally used when
multiple cardiac defects are suspected.
A ngiography will illustrate the stenosis and poststenotic dilation.
Pressure measurements obtained during selective catheterization are
used to determine the gradient across the stenosis.
AS – Cat Lab
64. Surgery
There are several surgical techniques used to
relieve left ventricular obstruction.
There are only a limited number of
institutions currently performing these
techniques owing to their complexity, special
equipment requirements (cardiopulmonary
bypass), and expense.
AS - Therapy
65. Balloon Dilation
As in PS, balloon valvuloplasty may be effective in alleviating outflow
obstruction.
This technique has much less morbidity than corrective surgery because
it requires insertion of an arterial catheter rather than a thoracotomy.
Studies have documented significant reductions (50%) in pressure
gradients immediately following balloon dilation.
However, although short-term (2 to 3 months) effects are favorable,
there does not appear to be a long-term survival benefit.
AS - Therapy
66. Medical Management
Beta blockers (Atenolol) are used to reduce myocardial oxygen
demands.
Antibiotics should be administered when bacteremia is
suspected or likely (e.g., dental procedures) to reduce the chance
of endocarditis developing.
Treatment of CHF: Cardiac drugs, diuretics, low-salt diets, and
rest
AS - Therapy
68. PS is the THIRD MOST COMMONLY reported congenital
defect in the dog.
Obstruction to the ejection of blood from the right ventricle
may occur at the following levels.
The latter two types are uncommon.
Valvular (pulmonic valve dysplasia)
Subvalvular
Supravalvular
PS - Anatomy
69. Type A
A type valvular PS is characterized by an annulus of normal
dimensions and a lack of division of the two valvular leaflets.
The valve behaves as a diaphragm, adopting in systole a dome-
shaped appearance moving toward the main pulmonary artery.
Type B
B type Valvular PS is characterized by a hypoplastic pulmonic
valve annulus, thickening of valvular leaflets, which may not
necessarily be fused.
Valvular PS - Anatomy
70. PS RV Pressure overload RV hypertrophy
post-stenotic dilation
The valvular lesion may be characterized by
fusion of the valve leaflets
dysplasia of the valvular apparatus, or both.
Depending on the severity of the right ventricular
hypertrophy, some patients will have a dynamic,
infundibular stenosis in addition to the fixed
valvular stenosis.
PS - Pathophysiology
71. PS occurs in both the dog and cat (rare).
The defect is more common in the following breeds:
Airedale terrier, beagle, Boykin spaniel, boxer, Chihuahua,
cocker spaniel, English bulldog, bull mastiff, samoyed,
schnauzer, and West Highland white terrier.
A polygenic inheritance pattern has been identified in
the BEAGLE.
Some authors note that SUPRAVALVULAR STENOSIS
occurs with increased incidence in GIANT
SCHNAUZERS.
PS - Breed Disposition
72. Mild or moderate PS Asymptomatic
Symptomatic animals
Dyspnea
Fatigue secondary to low cardiac output.
Exercise-induced syncope
Approximately 35% of dogs with severe stenosis develop clinical signs.
Decompensation and signs of RHF may occur.
Cyanosis Concurrent right to left shunting patent foramen ovale
or coexisting atrial septal defect or VSD.
Similar to subaortic stenosis, severe hypertrophy can result in myocardial
hypoxia and ventricular arrhythmias.
PS - Clinical Signs
73. Palpation
Moderate to severe PS Right ventricular impulses.
A precordial thrill at the left lower 3,4 ICS
Jugular venous distention and pulsations
Present if tricuspid regurgitation and/or congestive
heart failure is present.
Auscultation
A systolic, crescendo-decrescendo murmur .
A S2 Splitting second heart sound due to delayed
closure of the pulmonic valve may also be present.
PS – Physical Examination
74. Right ventricular hypertrophy
There are deep S waves in leads I, II, and III
Right shift of MEA (more than 120 degrees).
Ventricular arrhythmias
Atrial fibrillation may be present in severe cases.
PS Diagnosis - ECG
75. Right ventricular enlargement
Right Atrial Enlargement
Enlargement of the main pulmonary segment
Decreased pulmonary vascularity
pulmonary arteries smaller than normal
PS Diagnosis - CXR
76. Echocardiography
Diagnosis
Grading
Right ventricular dilation
Hypertrophy of the right ventricular wall
Hypertrophy of interventricular septum.
Owing to increased pressures within the
right ventricle, the septum is typically
flattened.
PR
A Post-stenotic dilation
PS grading:
Mild (Less Than 50 mmHg)
Moderate (50 To 80 mmHg)
Severe (Greater Than 80 mmHg)
PS Diagnosis - Echo
77. Cardiac catheterization may be used to confirm
.
Cardiac catheterization and angiography are
performed routinely prior to an interventional
procedure such as balloon valvuloplasty.
Selective coronary angiography is required to
rule out the presence of an anomalous left main
coronary artery in English bulldogs and
Boxers if surgery or balloon valvuloplasty is
considered.
PS Diagnosis – Cat Lab
78. Atrial septal defect
The right ventricular volume overload associated with a left-to-
right shunting atrial septal defect may result in a systolic ejection
murmur over the pulmonic valve.
Such murmurs are usually softer than those associated with PS.
Innocent or physiologic murmurs
These murmurs are usually much softer than typical PS murmurs
and do not typically persist beyond 6 months of age.
PS – DDX
79. Surgery Intervention
Repair of valvular or discrete subvalvular PS can be
accomplished by pulmonary arteriotomy (using inflow
occlusion).
The patch graft technique is effective in young animals
with valvular PS.
The bistoury technique or the modified Brock procedure
has also been used effectively.
In general, surgical correction is not recommended
unless the surgeon is experienced with the procedure.
PS - Therapy and Prognosis
80. Balloon Valvuloplasty
In this procedure, a special cardiac catheter is guided through the stenotic valve, and a balloon situated at the end of the catheter is
inflated, effectively enlarging the valve diameter.
Balloon valvuloplasty is most effective when valves are thin and fused, and hypoplasia of the annulus is not present.
Generally, balloon valvuloplasty results in a significant (40% to 60%) decrease in the pressure gradient and is maintained in 60% to
70% of the patients; however, the long-term effects on survival improvement have not been definitely determined.
PS - Therapy and Prognosis
81. Medical Management
Signs of right-sided congestive heart failure
should be treated as described in Chapter
15.
Beta blocker therapy (atenolol 0.25 to 1.5
mg/kg po every 12 hours) is routinely
administered to patients with moderate to
severe right ventricular hypertrophy in an
effort to decrease myocardial oxygen
consumption and to suppress ventricular
arrhythmias.
PS - Therapy and Prognosis