Transcript diseases of the cardiovascular system

DON’T COMPARE
YOURSELF TO OTHERS
“Everyone
is a genius, but if you judge
a fish by its ability to climb a tree, it
will live its whole life believing its
stupid.”
-Albert Einstein
DISEASES OF THE
CARDIOVASCULAR
SYSTEM:
CARDIOMYOPATHIES
PATIENT PRESENTATION
http://www.youtube.com/watch?
v=X-wLIoYTpOU
http://www.youtube.com/watch?v=Zp7
CiC7SXjk
FELINE HYPERTROPHIC
CARDIOMYOPATHY
NEUTERED MALE CATS BETWEEN 1-16 YRS. OF AGE
THE MOST COMMON CARDIOMYOPATHY IN CATS!
FELINE HYPERTROPHIC
CARDIOMYOPATHY: CLINICAL SIGNS and
DIAGNOSIS
 Soft, sytolic murmur
 Gallop rhythms or other arrhythmias
 ECG: ↑ p wave duration, ↑ QRS width, sinus
tachycardia
 Echo: shows ↑ ventricular wall thickness, dilated
left atrium
 Acute onset of heart failure
 Acute onset of systemic thromboembolism
 Hindlimb paresis
 Cold rear legs
 Painful rear legs
FELINE HYPERTROPHIC
CARDIOMYOPATHY
 THE PREDOMINANT PATHOLOGY OF
THIS DISEASE IS LEFT VENTRICULAR
HYPERTROPHY
 CAUSE:
 Genetics
 Related to abnormal myocardial myosin or
calcium transport within the muscles of the
heart
FELINE HYPERTROPHIC
CARDIOMYOPATHY
FELINE HYPERTROPHIC
CARDIOMYOPATHY:
DIAGNOSIS
http://www.youtube.com/watch?v=yNj-lQaUBao
http://www.youtube.com/watch?v=KvUFb4qZwmw&feature=related
http://www.youtube.com/watch?v=xlsq5tJpj04&feature=related
FELINE HYPERTROPHIC
CARDIOMYOPATHY:
Pathophysiology
PROBLEM #1: The walls lose compliance and resist filling during
diastole! (diastolic failure)
FELINE HYPERTROPHIC
CARDIOMYOPATHY:
Pathophysiology
 PROBLEM #2: If the left ventricle cannot fill
adequately with blood, the blood backs up into
the left atrium (enlargement) → pulmonary
veins → pulmonary edema!
 PROBLEM #3: The left atrium becomes dilated
with blood → the blood becomes static →
blood stasis leads to clot formation → clot
becomes dislodged and trapped elsewhere in
the arterial system → thromboembolism!
***90% of thrombi become lodged in the aortic trifurcation
causing “saddle thrombus”***
FELINE HYPERTROPHIC
CARDIOMYOPATHY: SADDLE THROMBUS
ACUTE, PAINFUL CONDITION CAUSING
PARESIS, COLD REAR LEGS/FEET!
FELINE HYPERTROPHIC
CARDIOMYOPATHY: SADDLE THROMBUS
FELINE HYPERTROPHIC
CARDIOMYOPATHY: TREATMENT
FUROSEMIDE (DIURETIC)
ASPIRIN
ANTICOAGULANT
OR
PROPRANOLOL (B-BLOCKER)
DILTIAZEM (CALCIUM CHANNEL BLOCKER)
FELINE HYPERTROPHIC
CARDIOMYOPATHY: TREATEMENT
 LASIX (furosemide): a diuretic used to treat
pulmonary edema
 DILTIAZEM: a calcium channel blocker used to
inhibit cardiac and vascular smooth muscle
contractility; reduces blood pressure and cardiac
afterload; overall improvement in diastolic function
 Or Propranolol: a beta-blocker to decrease heart rate
and myocardial oxygen demand
 ASPIRIN: an anticoagulant used to thin blood and
help prevent clot formation in HCM
 TPA (Activase): serves as a fibrolysin resulting in
the breakdown of clots that have already formed
 Or Heparin, Warfarin: acts on the coagulation factors to
inhibit the formation of a stable clot
FELINE HYPERTROPHIC
CARDIOMYOPATHY: CLIENT INFO
 There is no cure!
 Cats with HCM may experience heart failure,
arterial embolism, or SUDDEN DEATH!
 Cats whose heart rates stay below 200
beats/min have a better prognosis than
those whose heart rate is >200 beats/min
CANINE HYPERTROPHIC
CARDIOMYOPATHY:
 An UNCOMMON canine disease, but the
cause appears to be heritable
 CLINICAL SIGNS:





Fatigue
Sudden death
Tachypnea
Syncope
Cough
 BREEDS: German Shepherds, Rottweilers,
Cocker Spaniels, and others
DISEASES OF THE
CARDIOVASCULAR
SYSTEM:
CONGENITAL DEFECTS
CONGENITAL DEFECTS:
PATENT DUCTUS ARTERIOSUS
CHIHUAHUAS, MALTESE, POODLE, POMERANIAN, SHELTIE
PUPPIES COMMONLY AFFECTED
CONGENITAL DEFECTS: PATENT DUCTUS
ARTERIOSUS
Normally, the ductus arteriosus carries blood from the pulmonary artery
to the aorta during fetal development. It bypasses the lungs of the fetus.
CONGENITAL DEFECTS: PATENT DUCTUS
ARTERIOSUS
The duct should close in the first
12-24 hours after birth. If it does
not, the blood begins to shunt
from the aorta into the pulmonary
artery and hyperperfuse the
lungs.
The left side of the heart will
have an increase in blood return
and become volume overloaded.
THIS IS CALLED A LEFT-TO-RIGHT SHUNT
LOL!
“People
who think they know
everything are a great annoyance
to those of us who do.”
-Isaac Asimov
CONGENITAL DEFECTS:
PATENT DUCTUS ARTERIOSUS
(PDA)
CONGENITAL DEFECTS: PATENT
DUCTUS ARTERIOSUS
 CLINICAL SIGNS:
 A loud murmur best heard over the left base
 Sometimes called a “machinery” murmur or a continuous
murmur
 If the shunt is small some animals may be asymptomatic
 In large shunts the animal will develop left-sided heart
failure





Pulmonary edema
Cough
Exercise intolerance
Tachypnea
Weight loss
 ECG: wide range of arrhythmias including APCs and
VPCs
 Echocardiography (ultrasound)
 Radiographs: left atrial and ventricular enlargement
PATENT DUCTUS ARTERIOSUS:
TREATMENT
EXCELLENT PROGNOSIS WITH SURGICAL CORRECTION: LIGATION OF
THE DUCTUS ARTERIOSUS
PATENT DUCTUS
ARTERIOSUS: TREATMENT
 CLIENT INFO:
 64% OF ANIMALS WILL DIE WITHIN 1
YEAR IF NOT TREATED SURGICALLY
 Dogs with this condition should not be used
for breeding
CONGENITAL DEFECTS: ATRIAL AND
VENTRICULAR SEPTAL DEFECTS
Atrial Septal Defect
During fetal life, the foramen ovale is an openingi n the interatrial septum, allowing
shunting of blood from the right atrium to the left atrium in order to bypass the
nonfunctioning fetal lungs. It should close at birth. If it doesn’t, after birth, the blood
will shunt from left to right resulting in overload of the right side of the heart.
CONGENITAL DEFECTS: ATRIAL AND
VENTRICULAR SEPTAL DEFECTS
 CLINICAL SIGNS: ATRIAL SEPTAL
DEFECTS
 Result in overload of the right side of the
heart → dilation and hypertrophy of the rightsided chambers
 Systolic murmur
 Right-sided heart failure
 Radiographs: right ventricular enlargement
 Echo: right ventricular dilatation
CONGENITAL DEFECTS: ATRIAL AND
VENTRICULAR SEPTAL DEFECTS
Blood is shunted from the oxygen-rich left ventricle into the right ventricle. The blood
goes through pulmonary circulation and right back into the left atrium and ventricle
resulting in volume overload of the left side of the heart. The right ventricle may dilate
as well.
CONGENITAL DEFECTS: ATRIAL AND
VENTRICULAR SEPTAL DEFECTS
 CLINICAL SIGNS: VENTRICULAR SEPTAL
DEFECTS:
 Animals with small defects may have minimal or no
signs
 Larger defects may result in acute left-sided heart
failure, usually by 8 weeks of age
 A harsh holosystolic murmur
 CLIENT INFO:
 Repair of these defects requires open-heart surgery or
cardiopulmonary bypass. These procedures are
uncommon in the dog and cat
 Most of these animals will eventually experience
development of congestive heart failure
CONGENITAL DEFECTS:
PULMONIC STENOSIS
Chihuahuas, English Bulldogs, are commonly affected. CAUSE: polygenic inheritance
PULMONIC STENOSIS
In pulmonic stenosis, the right ventricular outflow tract is narrowed,
either at the valve itself, just below it, or just after it.
PULMONIC STENOSIS
The most common form of pulmonic stenosis involves
a deformed pulmonary valve such that the valve leaflets
are too thick, the opening is too narrow, or the valve cusps
are fused.
The heart must pump extra hard to get blood through
This unusually narrow, stiff valve.
The right ventricle becomes thickened from all this extra work. The right atrium
May become dilated and hypertrophied.
CONGENITAL DEFECTS:
PULMONIC STENOSIS
NORMAL CANINE CHEST RADS
THIS DOG HAS PULMONIC STENOSIS –
THE HEART LOOKS “PREGNANT” IN THE
FRONT DUE TO RIGHT VENTRICULAR
ENLARGEMENT
CONGENITAL DEFECTS: PULMONIC
STENOSIS
 CLINICAL SIGNS:




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
Syncope
Tiring on exercise
Right-sided congested heart failure
Left basilar (base) murmur
Right ventricular enlargement
Radiographs: right ventricular enlargement, dilation
of the pulmonary artery, pulmonary underperfusion
 Echo: right ventricular hypertrophy and
enlargement, dilation of the main pulmonary artery
PULMONIC STENOSIS:
TREATMENT
A special balloon is inserted into the
valve where it is inflated and the
obstruction is broken down.
Unfortunately, medical management is not
very beneficial in these cases. Beta-blockers
may be used to relax the heart muscle and
possibly dilate the stenosis.
CONGENITAL DEFECTS:
SUBAORTIC STENOSIS
Newfoundland, Boxer, Golden Retriever, and Bull Terrier are most commonly affected
LESION DEVELOPS IN THE FIRST 4-8 WEEKS OF LIFE
CONGENITAL DEFECTS:
SUBAORTIC STENOSIS
 There is a scar-like
narrowing just below the
aortic valve. The heart
must pump extra hard to
get blood through the
narrowed area. The
blood is pushed through
in a turbulent fashion
creating a heart murmur.
CONGENITAL DEFECTS: SUBAORTIC
STENOSIS
THE HARD WORK RESULTS IN LEFT VENTRICULAR HYPERTROPHY, LEFT
ATRIAL ENLARGEMENT, AORTIC DILATION
CONGENITAL DEFECTS: SUBAORTIC
STENOSIS:
 CLINICAL SIGNS:





Fatigue
Exercise intolerance (low cardiac output)
Syncope
Systolic murmur at the left heart base
ECG: evidence of left ventricular
enlargement - ↑ QRS height
 Echo: left ventricular hypertrophy,
subvalvular fibrous ring, aortic dilation
ALWAYS FORGIVE
“The person with no forgiveness in his
heart, lives in even worse punishment than
death.”
- Mr. Miyagi, The Karate Kid 2
CONGENITIAL DEFECTS:
SUBAORTIC STENOSIS
 TREATMENT
 Balloon catheter dilation – has been done with
variable and temporary results
 Medical management: THE GOAL IS TO SLOW
THE HEART RATE AND DECREASE
CONTRACTILITY; PROPRANOLOL (BETABLOCKER WILL DO THIS)
CONGENITAL DEFECTS:
SUBAORTIC STENOSIS
 CLIENT INFO:
 Should not be used for breeding
 Acute, left-sided congestive heart failure is
possible
 Sudden death is not uncommon
DCM
HCM
PDA
Aortic
stenosis
Pulmonic
stenosis
•1 – dogs
•Enlarged Heart
bronchoconstric
tion
•Dilated Flappy
muscle
•Nutritional: no
taurin in cats
•1 – Cats
•Saddle
thrombus
•Rarely in dogs
(hereditary)
•Noncompliant
heart muscle
•Aorta –
pulmonary a –
lungs back L
side
•Stenotic aortic
valve causes
LV hypertrophy
•High pressure
in aortic valve
can lead to
aortic dilatation
•Stenotic
pulmonic valve
•Pregnant heart
•L sided heart
failure (HF)
•LV hypertrophy •RV
hypertrophy
•R sided HF
•Sudden death
if aorta ruptures
•Increased HR
•Cough
•Increased HR
•Weakness in
hindlimbs,
acute pain, rear
cold feet
•Pulmonary
edema
•Digoxin:
increased
contractibility
•Beta blocker:
Slow HR
•Diuretic
•Blood thinner
•Treat surgically •No breeding
or die
•Balloon
valvuloplasty
CONGENITAL DEFECTS:
TETRALOGY OF FALLOT
Keeshonds are the most commonly affected breed,
but bulldogs and cats have increased incidence as well.
Cause: polygenic inheritance
CONGENITAL DEFECTS:
TETRALOGY OF FALLOT
 THERE ARE 4 MAIN ANATOMICAL
ABNORMALITIES IN THIS DISEASE!




Pulmonic stenosis
Right ventricular hypertrophy
Ventricular septal defect
Overriding aorta
CONGENITAL DEFECTS:
TETRALOGY OF FALLOT
 CLINICAL SIGNS and DIAGNOSIS:






Affected puppies are smaller than littermates
Exercise intolerance
Dyspnea, tachypnea
Syncope
Cyanosis
Polycythemia: occurs as a response to the large
amount of deoxygenated blood going to the
systemic circulation
 Systolic murmur over the pulmonic area
 ECHO: right ventricular hypertrophy, subaortic
ventricular septal defect, right outflow tract
obstruction
CONGENITAL DEFECTS:
TETRALOGY OF FALLOT
 TREATMENT:
 Phlebotomy: to keep PCV below 65%
 Surgery:
 Create a left–to–right shunt by doing systemic
artery to pulmonary artery anastamosis
 Complete correction requires cardiopulmonary
bypass which is uncommon in animals
CONGENITAL DEFECTS:
TETRALOGY OF FALLOT
 CLIENT INFO:




These dogs should not be bred
Congestive heart failure rarely develops
Affected animals need regular phlebotomy
Limit stress and exercise
CONGENITAL DEFECTS:
PERSISTENT RIGHT 4TH AORTIC
ARCH
Great Danes, German Shepherds, Irish Setters
are most commonly affected
CONGENITAL DEFECTS:
PERSISTENT RIGHT 4TH AORTIC
ARCH
CONGENITAL DEFECTS:
PERSISTENT RIGHT 4TH AORTIC
ARCH
Clinical signs include regurgitation due to megaesophagus,
aspiration pneumonia, dyspnea, weight loss
CONGENITAL DEFECTS:
PERSISTENT RIGHT 4TH AORTIC
ARCH
 TREATMENT: Early surgical correction
 Prognosis is poor without surgery
 Even with surgery, some esophageal dilation
may persist
 CLIENT INFO:
 These dogs should not be used for breeding
DISEASES OF THE
CARDIOVASCULAR
SYSTEM
ACQUIRED VALVULAR
DISEASES
CHRONIC MITRAL VALVE
INSUFFECIENCY
SMALL BREED/TOY BREED DOGS, USUASLLY OLDER THAN 10 YEARS
THE PREVALENCE OF THIS DISEASE INCREASES WITH AGE, AND IS
PROGRESSIVE. IT ACCOUNTS FOR ~95% OF ALL HEART FAILURE CASES
CHRONIC MITRAL VALVE
INSUFFICIENCY
ONE OF THE MOST COMMON
CAUSES IS CHRONIC PERIODONTAL
DISEASE!
BACTERIA THAT LIVE IN TARTAR,
GET SHOWERED INTO THE BLOOD
STREAM AND COLONIZE IN THE
VALVE LEAFLETS.
CHRONIC MITRAL VALVE
INSUFFICIENCY
CHRONIC PERIODONTAL DISEASE CAN AFFECT SEVERAL ORGAN SYSTEMS
1.Lungs: Pulmonary fibrosis, bronchitis,
and chronic obstructive pulmonary
disease.
2.Heart: Endocarditis, mitral valve
regurgitation, and myocardial
degeneration.
3.Liver: Hepatic parenchymal
inflammation and hepatopathy.
4.Kidneys: Interstitial nephritis and
glomerulonephritis.
MITRAL VALVE
INSUFFICIENCY
THIS IS THE OPEN LEFT
VENTRICLE SHOWING THE
MITRAL VALVE LEAFLETS.
WHAT ARE THE STRING-LIKE
STRUCTURES THAT ATTACH
THE VALVES TO THE
PAPILLARY MUSCLES?
MITRAL VALVE
INSUFFICIENCY
CHORDAE TENDINEAE
MITRAL VALVE
INSUFFICIENCY
TOP LEAFLET IS NORMAL
BOTTOM LEAFLET IS
THICKENED AND NODULAR. THIS
IS DUE TO INCREASED
FIBROBLASTIC TISSUE WITHIN
THE VALVE LEAFLETS
CHRONIC MITRAL VALVE
INSUFFICIENCY
THE STIFF MALFORMED VALVE
FAILS TO CLOSE SUFFICIENTLY
DURING SYSTOLE.
DURING LEFT VENTRICULAR
CONTRACTION, BLOOD FLOWS
BACK INTO THE LEFT ATRIUM
MITRAL VALVE
INSUFFICIENCY
IF BLOOD CONTIUES THIS BACKWARD
FLOW, THE ANIMAL MAY EXPERIENCE
LEFT-SIDED HEART FAILURE
CHARACTERIZED BY PULMONARY
EDEMA
CHRONIC MITRAL VALVE
INSUFFICIENCY
 DIAGNOSIS:
 Radiographs
 Echo
 Systolic murmur at left apex; “whooping” quality
 There is no treatment to delay the onset of
clinical signs. Treatment is aimed at improving
symptoms of heart failure
 Diuretics (lasix)
 ACE inhibitor, vasodilator (Enalapril)
 Diet change: low sodium
TRICUSPID VALVE
INSUFFICIENCY
TRICUSPID VALVE
INSUFFICIENCY
TRICUSPID INSUFFICIENCY RESULTS
IN RIGHT-SIDED HEART FAILURE
CHARACTERIZED BY PLEURAL
EFFUSION
TRICUSPID VALVE
INSUFFICIENCY
RIGHT-SIDED HEART FAILURE ALSO
LEADS TO ASCITES
NOTE: THE LOSS OF ABDOMINAL
DETAIL
TRICUSPID VALVE
INSUFFICIENCY
 Treatment and client info are the same
as for mtiral insufficiency; repeated
abdominocentesis may be needed in
these cases.
LIVE LIFE TO THE FULLEST!
“You only live once, but if you
work it right, once is enough.”
-Joe E. Lewis, comedian
DISEASES OF THE
CARDIOVASCULAR
SYSTEM
HEARTWORM DISEASE
CANINE HEARTWORM DISEASE
 PARASITE CAUSING HEARTWORM
DISEASE: DIROFILARIA IMMITIS
MICROFILARIA OF D. IMMITIS
ADULT HEARTWORMS
CANINE HEARTWORM
DISEASE
ONLY FEMALE MOSQUITOES BITE
DISTRIBUTION OF CANINE
HEARTWORM DISEASE
CANINE HEARTWORM DISEASE
ADULT HEARTWORMS LIVE
IN THE PULMONARY
ARTERIES. THE HEART MUST
WORK EXTRA HARD TO PUMP
AGAINST THIS OBSTRUCTION.
CANINE HEARTWORM
DISEASE
ADULT HEARTWORMS IN
RIGHT VENTRICLE AND
PULMONARY ARTERY
CANINE HEARTWORM DISEASE
 PREDOMINANT PATHOLOGY: DAMAGE TO THE
PULMONARY ARTERY FROM ADULT HEARTWORMS
 Endothelial damage and sloughing
 Inflammation (leukocytes, platelets)
 Risk of thromboemboli
 Pulmonary hypertension
 Disruption of vascular integrity
 Thickened, fibrosed
 RIGHT VENTRICULAR HYPERTROPHY AND
RIGHT-SIDED HEART FAILURE
 The right ventricle compensates by dilating and
increasing muscle thickness
 Ultimately, there is decompensation and heart failure
CANINE HEARTWORM
DISEASE
 Severe infection can lead to CAVAL
SYNDROME
 Worms back up into the right atrium and
venae cavae
 Found in heavy worm burdens (>60)
 Associated with a poor prognosis
 Surgical treatment: pull worms from the right heart
and venae cavae via jugular venotomy
CANINE HEARTWORM DISEASE
CANINE HEARTWORM
DISEASE
IDEXX SNAP TEST
ADULT FEMALE ANTIGEN
CANINE HEARTWORM
DISEASE
CANINE HEARTWORM DISEASE
CANINE HEARTWORM DISEASE:
PREVENTION
 HEARTGARD/IVERHEART
 Ivermectin/pyrantel pamoate
 INTERCEPTOR/SENTINEL
 Milbemycin oxime/ milbemycin oxime+lufeneron
 REVOLUTION
 Selamectin
 ADVANTAGE MULTI/PROHEART 6
 Moxidectin
 Q 6 month injectable
 TRIFEXIS
 Milbemycin oxime + spinosad
CANINE HEARTWORM DISEASE:
TREATMENT
STANDARD PROTOCOL: 1 epaxial injection, followed
By a second injection on the opposite side 24 hours later
ALTERNATIVE PROTOCOL: 1 Injection given followed in
4-6 weeks by 2 injections given 24 hours apart
ONLY KILLS ADULT (L5) STAGE WORMS; DOXYCYCLINE IS REC. AS
COMPLIMENTARY TX