DISEASES OF THE CARDIOVASCULAR SYSTEM: CONGENITAL DEFECTS

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 12-24 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.

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

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

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.

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. 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

CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS (PDA)

PATENT DUCTUS ARTERIOSUS https://www.youtube.com/watch?v=7DKaCqubuSg 2 minutes

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

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.

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!

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 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.

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.

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.

CONGENITAL DEFECTS: ATRIAL SEPTAL DEFECTS https://www.youtube.com/watch?v=e46jtin-H50

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).

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

VENTRICULAR SEPTAL DEFECTS https://www.youtube.com/watch?v=MzORJbyHTT0 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)

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

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

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.

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)

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: 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

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.

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

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

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

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

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.

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

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

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.

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

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

TETRALOGY OF FALLOT https://www.youtube.com/watch?v=NBbceSFRTRA

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.

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

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

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

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.

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

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

DISEASES OF THE CARDIOVASCULAR SYSTEM ACQUIRED VALVULAR DISEASES

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.

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

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

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.

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.

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

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 Heart strings: Functionally, the chordae tendineae play a vital role in holding the atrioventricular valves in place while the heart is pumping blood

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

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 Pulmonary edema(A condition caused by excess fluid in the lungs) in LHF.

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.

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.

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

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

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

DISEASES OF THE CARDIOVASCULAR SYSTEM HEARTWORM DISEASE

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

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

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 6 - 7 month. The microfilariae develop further for 10 - 30 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.

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

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. 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.

CANINE HEARTWORM DISEASE ADULT HEARTWORMS IN RIGHT VENTRICLE AND PULMONARY ARTERY

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

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

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

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.

CAVAL SYNDROME https://youtu.be/phCod-0tfkE https://youtu.be/HSE88BUb8VU 3 minutes 26 seconds 4 minutes 41 seconds

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). https://www.youtube.com/watch?v=FF4rkd9stMU If positive: Chest rads and pre-diagnostic blood work prior to treatment

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

CANINE HEARTWORM DISEASE: TREATMENT https://www.youtube.com/watch?v=1CUpfQ27fPQ https://www.youtube.com/watch?v=35MGazxK-aU This goes into the epaxial muscles

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

CANINE HEARTWORM DISEASE Interceptor does heartworms and other intestinal parasites

Tri-Heart Plus: Does heartworm and other internal parasites

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

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