1. DISEASES OF THE CARDIOVASCULAR SYSTEM:
CONGENITAL DEFECTS

2. DUCTUS ARTERIOSUS
In the developing fetus, the ductus arteriosus carriers blood from the pulmonary artery to the aorta
This allows blood to flow directly from the right side of the heart to the aorta, without stopping for oxygen in the lungs
After birth, the ductus closes within hours of life
Ductus Arteriosus: connection between the Aorta (oxygenated blood to body) and Pulmonary artery (deoxygenated blood to the lungs).
In fetus, lungs are skipped because the fetus gets its oxygen from the mother's bloodstream and does not yet have to oxygenate its own blood.
It closes to stop blood flow between the pulmonary artery and the aorta.

3. CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS
This is what the fetal flow looks like. After birth this should close.

4. CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS
Mostly in small breed dogs. Show signs as puppies.
CHIHUAHUAS, MALTESE, POODLE, POMERANIAN, SHELTIE
PUPPIES COMMONLY AFFECTED

5. PATENT DUCTUS ARTERIOSUS
Failure of the ductus to close after birth
This results in blood shunting from the aorta to the pulmonary artery
This allows blood flow back into the lungs
The left side of the heart will have an increase in blood return and become volume overloaded
The problem: blood continues to flow from the aorta (through pulmonary artery) into the lungs. Blood that should have gone to the body is going back into the lungs due to the high pressure of the aorta.

6. CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS
The duct should close in the first 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.
Too much blood is going to the lungs. In this case blood shunts backwards into the pulmonary artery because pressure in L side of the heart is higher than R so pressure in aorta is higher and it backflows (it is already oxygenated).
THIS IS CALLED A LEFT-TO-RIGHT SHUNT

7. CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS (PDA)

8. PATENT DUCTUS ARTERIOSUS
2 minutes

9. 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
In large shunts the animal will develop left-sided heart failure
If the shunt is small some animals may be asymptomatic
Diagnose: Heart murmur that does not go away. Continues murmur, sounds choppy
Coughing
Exercise intolerance
Increased breathing rate

10. Congenital Defects: Patent Ductus Arteriosus
Diagnostics:
ECG: wide range of arrhythmias
Echocardiogram (ultrasound of heart)
Radiographs: left atrial and ventricular enlargement
Because more blood is going to the left side of the heart.

11. PATENT DUCTUS ARTERIOSUS: TREATMENT
Not open heart surgery because the shunt can be tied off outside the heart.
Needs to be done before 2 years old, they will die before that.
Can use suture to tie off the shunt. Complication rates are low.
EXCELLENT PROGNOSIS WITH SURGICAL CORRECTION: LIGATION OF
THE DUCTUS ARTERIOSUS
THIS IS NOT OPEN HEART SURGERY!

12. 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

14. CONGENITAL DEFECTS: ATRIAL SEPTAL DEFECTS
During fetal life, the foramen ovale is an opening in 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.

15. CONGENITAL DEFECTS: ATRIAL SEPTAL DEFECTS
Blood shunt from L to R. Overload to R side, R side heart failure. Flap closes and seals the hole.

16. CONGENITAL DEFECTS: ATRIAL SEPTAL DEFECTS
CLINICAL SIGNS: ATRIAL SEPTAL DEFECTS
Result in overload of the right side of the heart → dilation and hypertrophy of the right-sided chambers
Systolic murmur
Right-sided heart failure
Radiographs: right atrial enlargement
Echo: right atrial dilatation
Since blood is being shunted back into the right atrium, the right atrium will become enlarged. Will become dilated due to excess blood within right atrium.

17. CONGENITAL DEFECTS: ATRIAL SEPTAL DEFECTS

18. CONGENITAL DEFECTS: VENTRICULAR SEPTAL DEFECTS
Hole between ventricles. Not normal in the fetus. Backflow to RV and lungs, and back to the L side. Left sided heart failure. Defect, high pressure shunts blood in full circle(shunts from LV to RV, through lungs and right back into left side of heart).

19. CONGENITAL DEFECTS: 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
Left-sided heart failure
A harsh holosystolic murmur

20. VENTRICULAR SEPTAL DEFECTS
Holosystolic murmur
Holosystolic murmur: All the time during systole (the phase of the heartbeat when the heart muscle contracts and pumps blood from the chambers into the arteries) - a holosystolic murmur begins with or immediately after the S1 heart sound(lub) and extends up to the S2(dub) (hard to hear)

21. CLIENT INFO for both:
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
Cardiopulmonary bypass (CPB) is a technique that temporarily takes over the function of the heart and lungs during surgery, maintaining the circulation of blood and the oxygen content of the patient's body

23. CONGENITAL DEFECTS: PULMONIC STENOSIS
Valve is too narrow.
Polygenic inheritance occurs when one characteristic is controlled by two or more genes
Chihuahuas, English Bulldogs, are commonly affected. CAUSE: polygenic inheritance

24. PULMONIC STENOSIS
Pulmonary valve is smaller than normal. Just malformed.
(Pulmonary artery)
In pulmonic stenosis, the right ventricular outflow tract is narrowed,
either at the valve itself, just below it, or just after it.

25. 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.
Leaflets: Valve folds
valve cusps: where the parts of the valve meets (in this case they are fused together)
This causes the right ventricle to become thickened (hypertrophied) due to extra work and
Dilated (wider)

26. 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

27. CONGENITAL DEFECTS: PULMONIC STENOSIS
CLINICAL SIGNS:
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
Underperfusion: narrow.
left base indicates that turbulent blood flow is associated with either the pulmonic or aortic valves

28. PULMONIC STENOSIS: TREATMENT
Balloon Valvuloplasty:
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.
B blockers: Slow the heart. Relaxation it stretches the heart.
Don’t use for breeding. Mild to moderate: live normal lives, moderate to severe: sudden death can occur.

29. CONGENITAL DEFECTS: SUBAORTIC STENOSIS
Same as above but in the aortic valve.
Lesion consist of thickening of the endocardial tissue below the aortic valve.
Newfoundland, Boxer, Golden Retriever, and Bull Terrier are most commonly affected
LESION DEVELOPS IN THE FIRST 4-8 WEEKS OF LIFE

30. 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.
Turbulent: Not controlled
Sub: underneath

31. CONGENITAL DEFECTS: SUBAORTIC STENOSIS
L side heart failure. More blood sits in left atrium resulting in back flow to lungs.
THE HARD WORK RESULTS IN LEFT VENTRICULAR HYPERTROPHY, LEFT
ATRIAL ENLARGEMENT, AORTIC DILATION

32. 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
A murmur that occurs when the heart muscle relaxes between beats is called a diastolic murmur. A systolic murmur occurs when the heart muscle contracts
subvalvular fibrous ring: The part that narrowed under the aorta

33. 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 (BETA-BLOCKER WILL DO THIS)
Propanalol B blocker.

34. 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

35. CONGENITAL DEFECTS: TETRALOGY OF FALLOT
4 congenital defects in the heart with poor prognosis
polygenic inheritance: occurs when one characteristic is controlled by two or more genes
Keeshonds are the most commonly affected breed,
but bulldogs and cats have increased incidence as well.
Cause: polygenic inheritance

36. CONGENITAL DEFECTS: TETRALOGY OF FALLOT
THERE ARE 4 MAIN ANATOMICAL ABNORMALITIES IN THIS DISEASE!
Pulmonic stenosis
Right ventricular hypertrophy
Ventricular septal defect
Overriding aorta septal defect
Pulmonic stenosis (Valve is too narrow) results in RV hypertrophy
Ventricular septal defect: Abnormal connection between the ventricles.
Overriding aorta is a congenital heart defect where the aorta is positioned directly over a ventricular septal defect (VSD), instead of over the left ventricle.

37. Not open(Pulmonic stenosis)
Thickened R ventricular wall(RV hypertrophy)
Ventricular septum(Ventricular septal defect: Abnormal connection between the ventricles)
Opening of aorta points more to the right-Block flow=mixed blood

38. Overiding aorta: Blood from RV into aorta: mixed blood, not fully oxygenated blood. Body stimulates more RBC production to stimulate oxygen carrying capacity.

39. TETRALOGY OF FALLOT

40. 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
Polycythemia: RBC are increased. The body is making more RBC’s due to lack of oxygenated blood because of the overriding aorta.

41. 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 anastomosis
Complete correction requires cardiopulmonary bypass which is uncommon in animals
Remove blood. Take more samples to decrease RBC’s.
Systemic artery to pulmonary artery : This would help blood in circulation go to the Pulmonary artery and then to the lungs to get oxygen.
Cardiopulmonary bypass (CPB) is a technique in which a machine temporarily takes over the function of the heart and lungs during surgery, maintaining the circulation of blood and the oxygen content of the patient's body

42. 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
Some can live for years with the defect

43. CONGENITAL DEFECTS: PERSISTENT RIGHT 4TH AORTIC ARCH
This defect results in regurgitation of solid food in weanlings because of obstruction of the esophagus(due to the aortic arch).
Great Danes, German Shepherds, Irish Setters
are most commonly affected

44. CONGENITAL DEFECTS: PERSISTENT RIGHT 4TH AORTIC ARCH
Constrict the esophagus , food cannot get passed and megaesophagus will be formed.
During normal development, this arch should atrophy and go away, in this case it does not and causes constriction of the esophagus.

45. CONGENITAL DEFECTS: PERSISTENT RIGHT 4TH AORTIC ARCH
Food backs up because of stricture. Fibrous ring did not break down. Regurgitate food, weight loss, aspiration pneumonia. Tx: Surgery. Main cause of megaesophagus in puppies: dyspnea and weight loss.
Aspiration pneumonia is when you inhale food into lungs
Clinical signs include regurgitation due to megaesophagus,
aspiration pneumonia, dyspnea, weight loss

46. 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
Regurgitation than megaesophagus

48. DISEASES OF THE CARDIOVASCULAR SYSTEM
ACQUIRED VALVULAR DISEASES

49. CHRONIC MITRAL VALVE INSUFFICIENCY
Leaking mitral valve
characterized by degenerative valvular changes causing progressive thickening of mitral leaflets and incomplete closure of mitral valve
Results in the nodular thickening of the valve edges, which will then roll up when the heart contracts.

51. The stiff malformed leaflets do not close during systole, which results in regurgitation of blood back into the left atrium.

52. CHRONIC MITRAL VALVE INSUFFICIENCY
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

53. What can cause it?
Chronic periodontal disease can increase the progression
Bacteria living in tartar in periodontal pockets are showered into the bloodstream
75% of all dogs over the age of 16 years are affected by this disease
Dental : Gums are bleeding and gingival recession
Mostly gram-negative-causes the valve leaflet to become inflamed and thickened.

54. CHRONIC MITRAL VALVE INSUFFICIENCY
CHRONIC PERIODONTAL
DISEASE!
2nd picture can see root of tooth. Should only see the crown. Infected tooth.
BACTERIA THAT LIVE IN TARTAR,
GET SHOWERED INTO THE BLOOD
STREAM AND COLONIZE IN THE
VALVE LEAFLETS.

55. 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.
Pulmonary fibrosis is a lung disease that occurs when lung tissue becomes damaged and scarred
Hepatic parenchymal inflammation: Chronic liver disease
Chronic obstructive pulmonary: lung diseases that block airflow and make it difficult to breathe
Interstitial nephritis is a kidney condition characterized by swelling in between the kidney tubules
Glomerulonephritis: Acute inflammation of the kidneys

56. 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?

57. MITRAL VALVE INSUFFICIENCY
CHORDAE TENDINEAE
Heart strings: Functionally, the chordae tendineae play a vital role in holding the atrioventricular valves in place while the heart is pumping blood

58. MITRAL VALVE INSUFFICIENCY
TOP LEAFLET IS NORMAL
BOTTOM LEAFLET IS
THICKENED AND NODULAR. THIS
IS DUE TO INCREASED
FIBROBLASTIC TISSUE WITHIN
THE VALVE LEAFLETS
This condition is also referred to as
Myxomatous mitral valve disease
(MMVD)
Nodule, rough fibrous nodule. Valves don’t close as well and blood backflows through LA, mitral regurgitation. Murmur can be heard. L sided HF.
Myxomatous means weakening of connective tissue

59. 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

60. MITRAL VALVE INSUFFICIENCY
IF BLOOD CONTIUES THIS BACKWARD
FLOW, THE ANIMAL MAY EXPERIENCE
LEFT-SIDED HEART FAILURE
CHARACTERIZED BY PULMONARY
EDEMA
Pulmonary edema(A condition caused by excess fluid in the lungs) in LHF.

61. 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
ACE inhibitor(hypertension), vasodilator enalapril, avoids retention of fluid.
Dilate blood vessels, better flow, low sodium, less fluid build up in lungs.

62. TRICUSPID VALVE INSUFFICIENCY
Can also be caused by periodontal disease.
Same as Mitral valve insufficiency, but in the right side of the heart. Right sided heart failure.

63. TRICUSPID VALVE INSUFFICIENCY
TRICUSPID INSUFFICIENCY RESULTS
IN RIGHT-SIDED HEART FAILURE
CHARACTERIZED BY PLEURAL
EFFUSION
A buildup of fluid between the tissues that line the lungs and the chest

64. TRICUSPID VALVE INSUFFICIENCY
RIGHT-SIDED HEART FAILURE ALSO
LEADS TO ASCITES
Ribs with belly. Fluid belly. RHF: Ascites. Blood backs up in vena cava and this back up causes back overload, liver overloaded with fluids. Vascular permeability, leaky vessels.
RHF: Ascites(the accumulation of fluid in the peritoneal cavity, causing abdominal swelling), pleural effusion(fluid between chest and lungs)
Temporary problem: Abdominocentesis, ventral wall, comfort
Lasix: Diuretics
Enalapril: Reduces retention of disease
NOTE: THE LOSS OF ABDOMINAL
DETAIL

65. TRICUSPID VALVE INSUFFICIENCY
Treatment and client info are the same as for mtiral insufficiency; repeated abdominocentesis may be needed in these cases.
Aimed at treating the heart disease

66. DISEASES OF THE CARDIOVASCULAR SYSTEM
HEARTWORM DISEASE

67. CANINE HEARTWORM DISEASE
PARASITE CAUSING HEARTWORM DISEASE: DIROFILARIA IMMITIS
Mff: L1 and L5 adults. L3 infective stage what is spread by the mosquito
MICROFILARIA OF D. IMMITIS
ADULT HEARTWORMS

68. CANINE HEARTWORM DISEASE
The parasite requires the mosquito as an intermediate(development of nonreproductive stages) host before it can complete its life cycle in the dog.  
Mosquito transmits L3 stage.
L1 – L3 develops in the mosquito.
Dog L1 goes to mosquito.
Dog L3 – L5
ONLY FEMALE MOSQUITOES BITE

69. So what happens?
Mosquito bites dog and picks up L1. In the mosquito microfilariae develop from L1 – L3.
Mosquito bites healthy dog and transmits L3. The infective larvae enter the dog's body.
They migrate into the bloodstream and move to the heart and adjacent blood vessels, maturing to adults
Mating and reproducing microfilariae within month.
The microfilariae develop further for days in the mosquito's gut and then enter its mouth. At this stage, they are infective larvae(L3). They are then transferred to the dog.
By day 120 they have matured into adults and made their way to the heart and pulmonary artery.

70. CANINE HEARTWORM DISEASE
Dog L1 goes to mosquito
L1 – L3 develops in the mosquito
Mosquito transmits L3 stage.
Dog L3 – L5
After reproducing microfilariae, another mosquito can pick up L1 and start the process back over

71. DISTRIBUTION OF CANINE HEARTWORM DISEASE

72. CANINE HEARTWORM DISEASE
ADULT HEARTWORMS LIVE
IN THE PULMONARY
ARTERIES. THE HEART MUST
WORK EXTRA HARD TO PUMP
AGAINST THIS OBSTRUCTION.
RHF: Pleural effusion(A buildup of fluid between the tissues that line the lungs and the chest) and ascites. Backflow into R chambers, because of physical blockage.

73. CANINE HEARTWORM DISEASE
ADULT HEARTWORMS IN
RIGHT VENTRICLE AND
PULMONARY ARTERY

74. Heartworm video: https://www.youtube.com/watch?v=RPV3_sA5HJE
1 minute 22 seconds

75. 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
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
Vascular integrity: vascular homeostasis (keep happy medium)
RIGHT VENTRICULAR HYPERTROPHY: enlarged ventricle

76. Clinical signs: Mild persistent cough Reluctance to exercise
Fatigue after moderate activity, decreased appetite, and weight loss
As heartworm disease progresses, pets may develop heart failure and the appearance of a swollen belly due to excess fluid in the abdomen

77. 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 side of the heart and venae cavae via jugular venotomy
Go in through the right side and extract the worms.

78. CAVAL SYNDROME https://youtu.be/phCod-0tfkE
3 minutes 26 seconds
4 minutes 41 seconds

79. OH SNAP a DIAGNOSIS!
IDEXX SNAP TEST
ADULT FEMALE ANTIGEN
Heartworm Antigen Test as the primary method of testing for adult heartworm infection. This test is specific for the adult female worm. Antigen is detectable by 6½ - 7 months after infection and positive results are possible using some tests when there are as few as 1-3 adult females in the heart
You can get a negative if tested to early (<6 months of infection).
If positive: Chest rads and pre-diagnostic blood work prior to treatment

80. Treatment: Heartgard (Ivermectin/pyrantel pamoate)
Doxycycline – fights off Wolbachia
Give for 30 days prior to treatment
Immiticide:
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
Heartgard: helps fight off microfilariae
Doxycycline: To weaken the bacteria on the heartworm (Wolbachia)
Also can use these medications as a slow kill method
Standard: mild cases
Alternative: more sever cases, better results though

81. CANINE HEARTWORM DISEASE: TREATMENT
This goes into the epaxial muscles

82. New Brand of Melarsomine
DIROBAN – created by Zoetis (the veterinary side of Pfizer Pharmaceuticals)

83. CANINE HEARTWORM DISEASE
Interceptor does heartworms and other intestinal parasites

84. Tri-Heart Plus: Does heartworm and other internal parasites

85. CANINE HEARTWORM DISEASE: PREVENTION
HEARTGARD/IVERHEART
Ivermectin/pyrantel pamoate
SENTINEL
milbemycin oxime+lufeneron
REVOLUTION
Selamectin
ADVANTAGE MULTI/PROHEART 6
Moxidectin
ProHeart: Q 6 month injectable
TRIFEXIS
Milbemycin oxime + spinosad
Sentinel kills heartworm larvae(also helps with and flea eggs and larvae)
Revolution: kills fleas, flea larvae, flea eggs and other external parasites, does fight off heartworms
ADVANTAGE MULTI: flea control and prevention, killing adult fleas and larvae/prevents heartworm
PROHEART 6: Prevents heartworms for 6 months
Trifexis: Does heartworms and fleas. Milbemycin oxime is the heartworm control

86. DON’T BE CONFUSED…
Must differentiate Microfilaria from Dipetalonema reconditum
D. reconditum rarely causes disease
They look the same except D. reconditum travels on the blood smear while microfilaria stay in one spot on the field