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239 Cards in this Set
- Front
- Back
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what is the most common form of acquired heart disease in the cat?
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feline myocardial disease
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what is the definition of cardiomyopathy?
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a heart muscle disease with associated dysfunction
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in the feline, what are the five functional designations of cardiomyopathies?
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1. hypertrophic (HCM)
2. restrictive (RCM) 3. dilated (DCM) 4. arrhythmogenic right ventricular cardiomyopathy (ARVC) 5. unclassified |
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what are two feline secondary cardiomyopathies?
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1. thyrotoxic heart disease
2. hypertensive heart disease |
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define HCM
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hypertrophy of a nondilated ventricle in the absence of an outflow tract obstruction, SH, hyperthyroidism, etc.
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what is the general etiology of HCM in cats?
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genetic
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what is the pathophysiology of HCM in cats?
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- normal or hyperdynamic ventricular performance
- DIASTOLIC DYSFUNCTION |
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what is the definition of diastolic dysfunction?
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the inability of the ventricles to fill without an inordinate increase in pressure
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what are the two main determinants of adequate diastolic function?
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1. myocardial relaxation
2. compliance |
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what two problems of the heart may impair ventricular filling?
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1. relaxation is prolonged
2. compliance is reduced |
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what forces are exerted upon the atrium with a ventricle that has impaired filling?
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the atrium requires a higher pressure than normal to fill a smaller ventricular space (elevated P/V)
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how does diastolic dysfunction affect filling pressure and stroke volume, and what is a pathologic process associated with each of these parameters?
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- filling pressure is elevated → congestive signs
- stroke volume small → low CO |
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in HCM, what causes diastolic dysfunction?
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increased wall thickness → chamber stiffness (decreased compliance)
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on an echo, what disease process is indicative of an atrial dilation disproportionate to ventricular volume?
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diastolic dysfunction
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what is the most common pathogenesis of HCM in cats?
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- systolic anterior motion of the mitral valve (SAM)
- mitral valve leaflets move cranially during systole - obstruction of LV outflow tract, a sub-valvular pressure gradient, and potentially, a murmur - usually mitral valve regurgitation |
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what is the typical signalment of a cat with HCM?
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- male predisposition, average of 6 years
- but can be virtually any age, including kittens |
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what are four clinical signs that would suggest feline myocardial disease?
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1. (an incidental) murmur/gallop
2. CHF 3. systemic thromboembolism 4. sudden cardiac death |
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in cats with myocardial disease, what usually causes the murmur?
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mitral valve regurgitation / left ventricular outflow tract obstruction
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what is SAM?
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- systolic anterior motion
- An anomalous movement of the mitral valve's anterior leaflet, which appears to strike the interventricular septum in early diastole |
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comment on the heart rhythm and rate in cats with HCF
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- often, a gallop rhythm (S3 or S4) is heard
- tachycardia is not a consistent finding |
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how does feline HCM appear in thoracic radiography?
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- variable degrees of cardiomegaly ± pulmonary edema (especially with clinical signs)
- pleural effusion, IN THE ABSENCE OF ASCITES |
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how is feline myocardial disease definitively diagnosed non-invasively?
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echo
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what are three counterintuitive diagnostic findings and clinical signs of CHF in cats?
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1. cats with LV disease (HCM) may develop pleural effusion without ascites
2. they seldom cough 3. they are not tachycardic |
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what is the indicated therapy for CHF (HCM) in cats with pulmonary edema/pleural effusion?
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preload reduction
- diuresis (furosemide) - thoracocentesis if in respiratory distress |
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traditionally, therapeutic agents used to treat diastolic dysfunction do what two things?
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1. ↓HR
2. speed myocardial relaxation |
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what are two drugs used to reduce preload in cats with Chronic CHF - HCM?
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1. furosemide
2. enalapril |
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in cats with subclinical HCM with atrial dilation, what two drugs are commonly prescribed, and what do they do?
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1. enalapril - ACE inhibitor that ↓ preload
2. atenolol - β-blocker and "cardioprotectant" that slows HR - atenolol is controversial as to whether is it efficacious |
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what is RCM?
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cat myocardial disease: restrictive cardiomyopathy
- atrial dilation with normal or nearly normal ventricular dimensions and wall thicknesses - somewhat less common than HCM |
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what is ARVC?
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cat myocardial disease: arrhythmogenic right ventricular cardiomyopathy
- fatty or fibrofatty replacement of right (and occasionally left) ventricular myocardium - arrhythmias, sometimes marked RV dilation |
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comment on the effect of corticosteroid treatment in cats and the heart
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it is been associated with heart failure
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if a geriatric cat has a subclinical murmur, what is its probable diagnosis?
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thyrotoxicosis
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what hemodynamic disorder is associated with myocardial disease in cats?
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FATE - feline arterial thromboembolism
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what is FATE and what are clinical signs?
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feline arterial thromboembolism
- embolization and obstruction of the caudal aorta due to myocardial disease |
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what causes the obstruction in FATE?
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embolism of the caudal aorta and release of vasoactive mediators, from the clot, such as serotonin and prostaglandins
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what are three therapeutics that can be administered to treat FATE?
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1. analgesia
2. anticoagulants - heparin 3. vasodilators |
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what are four therapeutics that can be administered as prophylaxis of arterial thrombosis in cats?
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1. ASA (aspirin)?
2. LMWH (low MW heparin)? 3. coumadin? 4. clopidogrel (antiplatelet drug)? |
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clinical signs of feline cardiovascular disease are most often related to what two disease processes?
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1. CHF (HCM/RCM, etc.)
2. embolism |
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what is the definition of dilated cardiomyopathy?
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A syndrome of an "end-stage heart" resulting from pathologic insult from the myocardium and characterized by ventricular and atrial dilation resulting from hypokinesis
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where in the heart cycle does DCM disease manifest itself?
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systole
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where in the heart cycle does feline HCM manifest itself?
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diastole
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what are two major general pathogenic processes that cause systolic myocardial dysfunction?
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1. loss of cardiomyocytes due to necrosis
2. functional disorders that affect the contractile apparatus |
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what are five basic etiologies that cause an insult to the heart, which can lead to canine DCM?
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1. toxicosis
2. metabolic disturbances 3. immune-mediated 4. infective 5. nutritional |
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in which three breeds of dogs has DCM been shown to be an inherited, familial trait?
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1. Doberman Pinschers
2. Great Danes 3. Newfoundlands |
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what are four proteins that have been shown to be defective in dogs with inherited DCM?
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1. actin
2. dystrophin 3. desmin 4. troponin T |
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comment on the pathogenesis of the progression of canine DCM to a point that the animal will present for congestion/edema
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impaired systolic function → progressive ventricular dilation → increased ventricular filling pressure → elevated venous backpressure → congestion/edema
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name six dog breeds overrepresented for DCM
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1. Doberman Pinschers
2. Great Danes 3. Newfoundlands 4. Boxers 5. Irish Wolfhounds 6. Cocker Spaniels |
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what is the typical signalment of a dog with DCM?
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large- or giant-breed and middle-aged
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what are five clinical signs associated with canine DCM?
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1. DYSPNEA
2. COUGH 3. weight loss 4. syncope 5. abdominal distention due to ascites |
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comment on the onset of clinical signs of canine DCM
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- may develop quite suddenly (especially in Dobermans), although sub-clinical DCM is a progressive process
- In Boxers and Dobermans ventricular tachyarrhythmia may precede the development of overt CHF |
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what are four clinical signs of canine DCM that you would find on physical examination and auscultation?
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1. soft (Grade 1-2/6) systolic murmur and or gallop in some patients
2. crackles (pulmonary edema) 3. tachycardia (USUALLY accompanies CHF) 4. ascites |
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what are radiographic clinical signs of canine DCM?
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1. enlargement of cardiac silhouette
2. left atrial enlargement with pulmonary infiltrate indicates left sided CHF |
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what are four findings of canine DCM on EKG?
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1. ventricular arrhythmias
2. atrial fibrillation 3. chamber hypertrophy patterns 4. intraventricular conduction disturbances |
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what are two echo findings of canine DCM?
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1. increased end-systolic and end-diastolic volumes
2. mitral valve regurgitation |
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comment on some breed-specific features of DCM in Dobermans.
- arrhythmia - disease course - which ventricle? - radiographic findings |
- high incidence of ventricular arrhythmias and sudden cardiac death (sustained > 30 sec VT predicts SCD)
- heart failure is associated with a relatively brief and progressive course (↓ MST versus other breeds) - primarily the left ventricle - on radiograph: usually don't find cardiomegaly; there is usually a straightening of the caudal border of the silhouette and an increase in the dorsoventral dimension |
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what common clinical sign of canine DCM is usually NOT seen in Dobermans and why?
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effusion/ascites because DCM in Dobermans affects primarily the left ventricle
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comment on some breed-specific features of DCM in Boxers.
- what is the most common form of the disease? - disease pathogenesis |
- an arrhythmic form of CM is most common Boxers
- may or may not be associated with ARVC (arrhythmogenic right ventricular cardiomyopathy) |
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comment on some breed-specific features of DCM in giant breed dogs.
- why do they get it more often than smaller breeds? - most common clinical signs - heritability |
- they have larger hearts, so they are at a higher risk of DCM
- pleural effusion, ascites, and atrial fibrillation are common - DCM is heritable in Great Danes |
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comment on some breed-specific features of DCM in American Cocker Spaniels.
- comment on another common disease in relation to DCM in these patients that are predisposed - what is a unique diagnostic finding in the breed? |
- they have valvular disease more commonly than DCM
- low plasma taurine; the disease is responsive to taurine supplementation |
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what four drugs are used in conventional therapy of canine DCM?
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1. furosemide
2. ACE inhibitor (enalapril) 3. pimobendan 4. ± digoxin |
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in canine DCM, when is digoxin indicated and contraindicated?
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- indicated when there is concurrent atrial fibrillation
- contraindicated when there is sinus rhythm |
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pimobendan:
- mechanism of action - indications - used with what other drugs? - what breed of dog is particularly responsive? |
- calcium-sensitizing inodilator (inotrope + vasodilator)
- approved for canine heart failure due to DCM or valvular disease - used together with other agents, including furosemide and enalapril - strong evidence of efficacy in Dobermans |
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what are two "emerging therapies" for treatment of DCM?
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1. β-blockers
2. spironolactone - aldosterone receptor blocker (↑ norepinephrine uptake by the heart - less remodeling and better nerve activity) |
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what are two nutritional supplements that may be used as ancillary therapy in dogs with DCM?
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1. L-carnitine
2. taurine |
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in what breeds of dogs should taurine levels be measured when presenting for DCM?
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1. COCKER SPANIELS
2. Newfoundlands 3. Golden Retrievers 4. "atypical breeds" |
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what drugs may have a "cardioprotective" effect in patients with sub-clinical DCM?
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ACE inhibitors and β-blockers
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what is the only important cause of left-sided CHF in large breed dogs?
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dilated cardiomyopathy
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what is the basic theory of why certain drugs slow the progression of CHF in dogs with DCM?
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since CHF is a "NEUROENDOCRINE SYNDROME", effective therapies "spare" the heart through blunting of neurohumoral action
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what is Boxer Dog Cardiomyopathy?
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- ARVC (arrhythmogenic right ventricular cardiomyopathy)
- Boxers are predisposed to ventricular tachyarrhythmia - sudden death is high in affected dogs |
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what are the three categories of Boxer Dog cardiomyopathy?
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- Category I: ventricular arrhythmias occur in the absence of clinical signs (ID on routine vet visit)
- Category II: syncope, presumably related to ventricular tachycardia - Category III: CHF due to myocardial dysfunction (overt DCM) |
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comment on Boxer dog cardiomyopathy
- progression of the disease - its relationship to DCM - how is it acquired? |
- some patients progress from Class I to II or III, but not always
- this disease is not synonymous with DCM because it does not always occur with myocardial dysfunction - it is heritable |
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comment on HCM in dogs
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uncommon with an unknown cause, clinical presentation, or natural history
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what are the two basic types of canine valvular disease?
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1. degenerative
2. infective |
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what is the most common acquired cardiac disease in dogs?
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degenerative valvular disease
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describe the pathology of degenerative valvular disease
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- a STERILE degenerative process that affects the AV valves
- deposition of mucopolysaccharides in the spongiosa layer of the valve - myxomatous valvular degeneration - grossly, nodular thickening and distortion of the valve leaflets with lengthening, and occasionally rupture, of the chordae tendineae |
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describe what predisposes a dog to MVD (myxomatous valvular degeneration) and what endogenous compounds may be involved.
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- develops in breeds predisposed to other connective tissue abnormalities
- strong breed predispositions suggest a genetic basis - involves vasoactive mediators |
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what does MVD stand for?
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myxomatous valvular degeneration
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what is the pathophysiology of MVD in dogs?
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- distortion of the mitral valve leaflets and lengthening or rupture of the chordae tendineae result in valvular incompetence
- the regurgitant volume augments the pulmonary venous return - mitral valve regurgitation (MR) imposes a VOLUME LOAD on the LA AND LV - further distortion leads to activation of the RAAS and further volume load - CHF |
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what is the most common presenting clinical sign for MVD? What are three other common signs
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- COUGH
1. tachypnea 2. syncope 3. exercise intolerance |
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what three things cause coughing in dogs with MVD?
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1. pulmonary edema
2. compression of the mainstem bronchi (small dogs) 3. J-receptor mediated cough (J = juxtapulmonary; stimulated by ↑ pulmonary venous pressure) |
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why can dogs develop a cough with MVD before they develop CHF?
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because the cough is related to compression of the mainstem bronchi at this stage, rather than pulmonary edema
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characterize the murmurs associated with MVD.
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systolic, "plateau-shaped", and usually over the left apex
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how does the intensity of the murmur correlate with clinical signs and degree of disease with MVD.
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It does not correlate
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characterize a typical dog's body condition, HR, heart rhythm, and cardiac murmur for:
1. cardiac disease 2. respiratory disease |
1. cardiac disease: thin BCS, rapid HR, regular heart rhythm (unless pathologic arrhythmias are present), loud murmur
2. respiratory disease: obese BCS, normal or slow HR, exaggerated respiratory arrhythmia may be present, soft or no murmur |
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comment on the differences in disease presentation and prognosis of a small versus large dog with MVD.
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large breed dogs, more often than small dogs, present with severe MR and concurrent myocardial dysfunction. Therefore, larger dogs may have a worse prognosis.
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what is the most important test to diagnose MVD in dogs?
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radiography
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how does MVD present on echocardiography?
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- LA and LV dilation
- thick and or prolapsed mitral valve leaflets - ± compromised myocardial function |
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when a dog presents for MVD and evaluated for echocardiography, and it is found that mitral valve regurgitation is moderate or severe, comment on how you might determine if there is myocardial dysfunction
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if there is reduced %FS (fractional shortening = ejection fraction), this suggests that there is myocardial dysfunction
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for a dog presenting for possible MVD, what are five reasons that echocardiography would be indicated?
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1. the cause of the murmur is uncertain
2. it is difficult to discern from thoracic radiographs whether or not the left atrium is enlarged 3. sudden deterioration has occurred and rupture of the chordae tendineae (or left atrium) is suspected 4. when you need to evaluate systolic myocardial function 5. pulmonary hypertension is suspected |
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what are three arrhythmias associated with MVD in dogs?
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1. APC (SVPC)
2. SVT 3. AF |
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comment on the treatment of subclinical MVD with therapeutics?
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although research has been performed, there is not sufficient proof that drug therapy (i.e. ACE inhibitors) are efficacious.
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how is the cough associated with MVD treated with therapeutics?
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- vasodilation (ACE inhibitors) and antitussives
- vasodilation ↓ PVR, may ↓ regurgitant fraction, and may ↓ atrial pressure and size |
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what are four drugs used to treat heart failure in dogs with MVD?
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1. furosemide
2. enalapril 3. pimobendan 4. ± digoxin |
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comment on chordal rupture in canine MVD
- what happens when a primary chorda ruptures? - what happens when a minor chorda ruptures? - under what conditions is chordal rupture most likely to occur? |
- when a primary chorda ruptures, the corresponding leaflet becomes loose, flails, and fulminant MR and pulmonary edema ensue
- rupture of a minor chorda may result in less impressive clinical signs; if there is no MR, development of edema is unlikely - chordal rupture usually occurs in patients that have substantial, pre-existing MR |
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what is a rare, generally fatal complication of a severe mitral valve regurgitation?
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left atrial rupture
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what is the pathogenesis of infective endocarditis?
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1. endocardial damage
2. activation of clotting factors 3. bacteremia and colonization of a noninfective thrombus |
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what are three things that can predispose a dog to infective endocarditis?
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1. congenital cardiac malformation (SAS)
2. prostatitis 3. pyelonephritis |
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comment on degenerative valvular disease (e.g. MVD) with the development of infective endocarditis
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there is no known association between the two diseases
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what bacterial agents are associated with infective endocarditis?
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- Gram-positive bacteria such as strep and staph
- recent interest in fastidious, intracellular organisms, such as Bartonella |
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on which valves does infective endocarditis generally occur in small animals? Cattle?
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- small animals: left side
- large animals: mostly pulmonic, but also tricuspid |
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what are four pathologies that cause the clinical signs of infective endocarditis?
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1. sepsis
2. thromboembolism 3. cardiac dysfunction 4. episodic bacteremia |
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what are two sequelae to chronic infective endocarditis?
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1. polyarthritis
2. glomerulonephritis |
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comment on the effects on the heart of aortic valve infective endocarditis.
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- aortic incompetence
- aortic regurgitation → filling of LV during diastole - myocardial dysfunction due to volume overload (observed commonly and early) |
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what are four places in the body where embolization of fragments from infective endocarditis are typically found?
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1. spleen
2. kidney 3. brain 4. joints |
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what are five clinical signs in subacute infective endocarditis?
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1. lameness
2. inappetence 3. dyspnea 4. syncope 5. clinical signs of sepsis |
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what are some clinical signs on physical examination of a dog with left-sided infective endocarditis?
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- intermittent fever (not consistent)
- murmur - mitral valve regurgitation results in a systolic murmur |
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describe the murmur associated with aortic valve infective endocarditis when
1. mitral valve regurgitation is not present 2. mitral valve regurgitation is present |
1. when MR is not present, aortic valve IE results in a diastolic decrescendo murmur
2. when MR is present, a concurrent systolic murmur will be present, presenting with the diastolic aortic value murmur as a "bellows" or "to-and-fro" murmur |
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what diagnostics are used to evaluate infective endocarditis?
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1. radiography
2. EKG 3. echocardiography 4. laboratory data |
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what are two important laboratory findings that help to rule in infective endocarditis?
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1. leukocytosis
2. a positive blood culture (60-80% of patients) |
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comment on the therapy and prognosis of infective endocarditis?
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- parenteral antibiotics based on culture results and medical therapy of heart failure are indicated
- poor prognosis |
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what is an important cause of right-sided CHF in dogs?
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pericardial disease
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which part of the heart cycle is most affected by pericardial disease?
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diastole
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what are three congenital manifestations of pericardial disease?
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1. pericardial peritoneal diaphragmatic hernia
2. absence of a pericardium 3. intrapericardial cysts |
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what are two important forms of acquired pericardial disease?
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1. pericardial effusion
2. pericardial constriction |
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what is the major pathogenic cause of pericardial effusion in the dog?
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hemorrhage
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what are the two basic etiologies of hemorrhagic pericardial effusion in the dog?
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1. neoplasia (> 50%)
2. idiopathic (may be curable) |
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what are four neoplasias that can cause hemorrhagic pericardial effusion in the canine?
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1. hemangiosarcoma
2. chemodectoma (heart base tumor; tumor of the chemoreceptors of the proximal aorta) 3. mesothelioma 4. ectopic thyroid carcinoma |
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what are the two main determinants of the severity of the disease caused by pericardial effusion?
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1. volume of the effusate
2. compliance characteristics of the pericardium |
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at what point does ventricular filling become impaired due to pericardial effusion
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when the volume of effusate exceeds that of the "reserve volume", causing intrapericardial pressure to rise.
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a syndrome of impaired ventricular filling due to the presence of intrapericardial fluid
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tamponade
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what are the pathogenic factors that cause the clinical signs related to pericardial effusion?
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low cardiac output and elevated central venous pressure (due to impaired diastole)
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which side of the heart is affected by pericardial effusion first and why?
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The right side, because RV filling pressures are lower than LV filling pressures. Because of this, intrapericardial pressure resisting the opposing force of ventricular filling pressure will be affected on the RV first.
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why do clinical signs associated with pericardial effusion occur mostly on the systemic side, rather than on the pulmonary side?
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because the venous pressures required to produce ascites are lower than those required for pulmonary edema.
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what dog breeds are predisposed to pericardial effusion?
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1. German Shepherd Dog
2. retrievers 3. large breeds |
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what are five clinical signs associated with pericardial effusion in the dog?
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1. abdominal distension resulting from ascites
2. weakness / syncope 3. lethargy 4. inappetence 5. circulatory collapse (syncope) |
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what is pulsus paradoxus?
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arterial pulse that becomes weaker during inspiration, rather than expiration
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if a dog presents with a weak pulse that becomes weaker when the animal inhales, what might you put on your rule-out list?
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tamponade
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what are five findings of tamponade on physical examination and auscultation?
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1. tachycardia
2. quiet heart sounds 3. ascites / jugular distention 4. hypokinetic pulse 5. pulsus paradoxus |
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how is the degree of cardiac tamponade roughly evaluated without any diagnostic equipment?
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looking at the height of the jugular pulse
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what are some radiographic findings of pericardial effusion?
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- enlargement of the cardiac silhouette
- silhouette that lacks contour - small pulmonary vessels - note: pulmonary edema is uncommon |
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what is the most common finding on EKG, of tamponade?
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sinus tachycardia ± QRS alternans and small QRS complexes
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what is the most sensitive and specific non-invasive means to diagnose pericardial effusion?
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echo
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what is the appropriate initial therapy of pericardial effusion?
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pericardiocentesis
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which drugs should not be used to treat pericardial effusion and why?
|
diuretics, because they reduce venous pressure and may further compromise ventricular filling
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comment on what therapies would be used to treat and the affect of the treatment:
- idiopathic pericardial effusion - pericardial effusion associated with chemodectoma - pericardial effusion associated hemangiosarcoma |
- idiopathic: subtotal pericardectomy; curative
- chemodectoma: subtotal pericardectomy; palliative - HSA: chemotherapy; extends survival time |
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what pressure defines pulmonary hypertension?
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> 35 mmHg
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what are five pathogenic factors that can cause pulmonary hypertension?
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1. LA hypertension
2. left-to-right shunts 3. hypoxia 4. pulmonary vascular disease 5. pulmonary thrombosis |
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what are two common forms of pulmonary vascular disease / pulmonary thrombosis that cause pulmonary hypertension in dogs?
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1. Heartworm disease
2. Idiopathic pulmonary hypertension |
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what heart abnormality is most commonly seen in dogs with pulmonary hypertension?
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tricuspid valve regurgitation
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comment on the nuances of using vasodilators to treat pulmonary hypertension:
- effectiveness - monitoring - what could happen if the vasodilator fails to correct the problem? |
- no vasodilator is completely selective for pulmonary vessels and there is great variability between individuals in the response to vasodilator therapy for PH
- ideally, systemic blood pressure is monitored when vasodilators are administered - if the agent fails to reduce PVR, but causes systemic vasodilation, hypotension results |
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what are four oral vasodilators used to treat pulmonary hypertension in dogs?
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1. sildenafil
2. calcium channel antagonists 3. hydralazine 4. endothelin antagonists |
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what is the minimum temperature in which a heartworm microfilaria can mature to L3 in the mosquito?
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57 °F
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what is the pathogenesis of heartworm disease?
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- mature heartworms primary reside in the caudal pulmonary arteries
- in dogs, heartworms are fount in the RA and vena cava only when worm burden is high - damage to the pulmonary artery tunica intima results in myointimal proliferation - this leads to ↑ PVR → pressure overload on the RV |
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what are six clinical signs associated with heartworm disease?
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1. weight loss
2. cough 3. tachypnea 4. exercise intolerance 5. syncope 6. ascites |
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what is the most useful method for evaluating the severity of heartworm disease?
|
thoracic radiographs
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what are three diagnostic methods to evaluate patients with confirmed dirofilarial disease?
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1. thoracic radiographs (the most useful)
2. echocardiography 3. laboratory testing |
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what are four radiographic findings of heartworm disease in dogs?
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- distal attenuation of pulmonary arteries
- enlargement of proximal pulmonary arteries - pulmonary parenchymal abnormalities - cardiomegaly |
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define Class I heartworm disease
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minimally affected dogs with normal radiographs
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define Class II heartworm disease
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moderately affected dogs with occasional cough/tachypnea and distinct radiographic abnormalities
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define Class III heartworm disease
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severely affected dogs with marked radiographic abnormalities and systemic signs, including weight loss, exercise intolerance, and persistent cough or tachypnea
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define Class IV heartworm disease
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dogs affected by caval syndrome
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minimally affected dogs with normal radiographs have what class heartworm disease?
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Class I
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moderately affected dogs with occasional cough/tachypnea and distinct radiographic abnormalities have what class heartworm disease?
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Class II
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severely affected dogs with marked radiographic abnormalities and systemic signs, including weight loss, exercise intolerance, and persistent cough or tachypnea have what class heartworm disease?
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Class III
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dogs affected by caval syndrome have what class heartworm disease?
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Class IV
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what drug is used to kill adult heartworms?
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melarsomine (Immiticide™)
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comment on the occurrence of right-sided heart failure as a sequela to heartworm disease
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it is uncommon
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comment on the "alternative protocol" for administration of melarsomine to treat heartworm disease
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- recommended in all Classes of heartworm disease
- one injection, wait 4-6 weeks and then 2 injections 24 hours apart. |
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list four important aspects of treating heartworm disease
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1. exercise restriction / case rest
2. furosemide 3. abdominocentesis as required 4. adulticide using the alternative protocol |
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what is caval syndrome? How is it treated?
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- hemoglobinuria and potentially circulatory collapse due to central migration of adult heartworms.
- treated surgically using intravascular retrieval snares, after surgical isolation of the external jugular vein |
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what are five functions of Angiotensin II?
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1. vasoconstriction
2. modulates the ANS (↑ sympathetic tone) 3. dipsogen (↑ thirst) 4. stimulates aldosterone release 5. stimulates ADH release |
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what are the three primary compensatory mechanisms that are activated when cardiac performance declines?
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1. salt and water retention
2. vasoconstriction 3. increased strength and rate of cardiac contractions |
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comment on the compensatory mechanisms due to declining cardiac performance and their relationship to heart failure?
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- activation of compensatory mechanisms in the short term is favorable
- with chronicity, activation of the ANS and RAAS has detrimental effects - in most cases, CHF is characterized by inexorable progression |
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why is heart failure called a "neuroendocrine syndrome?"
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because activation of the adrenergic system and specific endocrine pathways is integral to its pathogenesis
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what finding on EKG is incompatible with a diagnosis of CHF?
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respiratory sinus arrhythmia
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What is Stage A heart failure?
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predisposed to the development of heart failure
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What is Stage B1 heart failure?
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subclinical heart disease without remodeling
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What is Stage B2 heart failure?
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subclinical heart disease with remodeling
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What is Stage C heart failure?
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- structural heart disease
- current or prior clinical signs |
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What is Stage D heart failure?
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refractory heart failure
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being predisposed to the development of heart failure is what stage of heart failure?
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Stage A
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subclinical heart disease without remodeling is what stage of heart failure?
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Stage B1
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subclinical heart disease with remodeling is what stage of heart failure?
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Stage B2
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structural heart disease with current or prior clinical signs is what stage of heart failure?
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Stage C
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refractory heart failure is what stage of heart failure?
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Stage D
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comment on the progression of heart failure if you can resolve congestion
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it is still progressive
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what are the two basic ways in which CHF is treated?
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1. manipulation of the four main determinants of cardiac output (preload, afterload, contractility, heart rate)
2. treatment of neuroendocrine abnormalities |
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what two types of drugs are used for preload reduction in acute decompensated CHF?
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1. diuretics (e.g. furosemide)
2. venodilators (e.g. nitroglycerin) |
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what class of drugs is the quickest to relieve pulmonary and peripheral edema in CHF?
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diuretics
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what type of drugs are used to reduce afterload in patients with CHF?
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vasodilators
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what are two classes of vasodilators commonly used to reduce afterload in patients with CHF?
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1. ACE inhibitors (enalapril, benazepril, captopril)
2. amlodipine (calcium channel blocker) |
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what is a potential complication of using diuretics with ACE inhibitors? How is this corrected?
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- azotemia
- corrected by reduction or discontinuation of diuretic - if this is refractory, discontinue ACE inhibitor and consider fluid therapy |
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what class of drugs is used to treat systolic failure in patients with CHF?
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positive inotropes
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what are five positive inotropes used to treat systolic failure in patients with CHF?
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1. pimobendan (an inodilator)
2. digoxin 3. dobutamine (β1 agonist), (and other catecholamines) 4. amrinone (inodilator) 5. milrinone (inodilator) |
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digoxin
- what affects does it have on the heart - how is it dosed? - what should be monitored? |
- SLOWS HR and ↑ force of contraction
- it has a low therapeutic index, so dose to body surface area - monitor K, RENAL FUNCTION, and blood concentration |
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pimobendan to treat CHF:
- mechanism of action - efficacy - what breed is especially responsive to this drug? - how does MST compare to ACE inhibition? |
- a calcium sensitizing "inodilator", which is a PDE inhibitor with favorable effects on myocardial energetics
- improves clinical status in dogs with DCM and MR - Doberman Pinschers - improves survival relative to ACE inhibition |
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pimobendan:
- what diseases in dog is it indicated for? - what sub-clinical diseases? - what two types of drugs is it used with? |
- indicated for dogs with radiographic edema resulting from valvular disease or DCM
- not indicated for sub-clinical disease - used with diuretics / ACE inhibitors |
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how is HR affected by control of congestion associated with systolic failure? What is an exception?
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- control of congestion usually results in ↓HR
- exception: pathologic tachyarrhythmia (AF in DCM, ventricular tachycardia) |
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what are four classes of drugs used to treat neurohumoral abnormalities in CHF?
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1. β-blockers
2. digitalis 3. ACE inhibitors 4. spironolactone (aldosterone antagonist) |
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β-blockade in treatment of CHF neurohumoral abnormalities:
- mechanism of action - in what situations is it used? - explain the very general dosage regimen - what are two examples of β-blockers used? |
- mechanism is unknown
- used in selected cases after resolution of clinical signs (or before these signs have developed) - the dose is cautiously titrated upwards over the course of weeks - carvedilol, metoprolol |
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use of digitalis in the treatment of CHF neurohumoral abnormalities:
- efficacy - mechanism |
- has a neutral effect on mortality, but may prevent clinical deterioration
- may normalize baroreceptor dysfunction - the autonomic effects of digitalis are probably favorable and more important than the inotropic effect |
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spironolactone in the treatment of CHF neurohumoral abnormalities:
- mechanism of action - efficacy - why is this drug thought to slow the development of CHF? |
- spironolactone is an aldosterone antagonist
- decreases mortality in people at a dose that doesn't affect hemodynamics, but efficacy is uncertain in dogs - extra-renal effects are likely important: aldosterone contributes to the development of myocardial fibrosis |
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what drugs are indicated in Stage A heart failure?
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(predisposed to development of HF)
- none |
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what drugs are indicated in Stage B heart failure?
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(subclinical structural heart disease)
- DCM: ACE inhibitors / β-blockers - MR: ACE inhibitors? |
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what drugs are indicated in Stage C heart failure?
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(structural heart disease with concurrent or prior clinical signs)
- furosemide - ACE inhibitors - pimobendan - ± digoxin - ± β-blockade - ± spironolactone |
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what drugs are indicated in Stage D heart failure?
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- triple diuretic Rx
- additional afterload reduction |
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What are the two main objectives in treating diastolic failure?
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1. improve ventricular filling
2. preload reduction |
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in diastolic failure, what are two ways to improve ventricular filling?
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1. slowing of HR when tachycardia contributes to diastolic dysfunction
2. improve myocardial relaxation |
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in diastolic failure, comment on the therapy to reduce preload?
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- diuretics indicated for left-sided CHF of any cause
- patients with diastolic dysfunction tolerate excess diuresis poorly |
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what is the standard therapy for systolic failure in CHF?
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- furosemide
- ACE inhibitor - pimobendan - ± digoxin |
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what are two emerging therapies in treating systolic failure in CHF?
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1. β-blockers
2. spironolactone |
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what is the standard therapy for diastolic failure in CHF?
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- furosemide
-?enalapril? |
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how is acute (decompensated) heart failure diagnosed and treated?
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- Dx: ideally, through examination of thoracic radiographs
- empirical therapy is appropriate, but note that the clinical signs of respiratory tract disease and heart disease are superficially similar - when treating empirically, assess response and modify accordingly |
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what is the theory of using BNP as a biomarker for diagnosis of heart failure?
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yet to have the actual clinical utility determined, BNP concentrations increase with increasing ventricular filling pressures.
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what are three appropriate measures to treat a patient with acute (decompensated) heart failure?
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1. supplemental O2
2. cage rest 3. morphine - reduces anxiety and decreases afterload |
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when is fluid therapy indicated for acute (decompensated) heart failure?
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- note that preload is already maximal when CHF is present
- fluids are used as a vehicle for drugs/electrolytes when recovery is slow and congestive signs have resolved |
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what effect on the heart does administration of diuretics have in a patient with CHF?
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diuretics reduce intravascular volume and therefore, preload; in general, this has a negative effect on stroke volume
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what is the mechanism of nitroglycerin? What effect does it have in the heart when administered to a patient with CHF?
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- venodilator
- reduces preload and stroke volume |
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comment on the use of nitroprusside in the treatment of CHF.
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- nitroprusside is a venodilator
- administered by CRI ideally with monitoring of BP - used when Dx of CHF due to systolic failure is certain |
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what are six things that should be monitored during the therapy of CHF?
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1. physical examination
2. HCT/TP 3. BUN 4. urine output 5. body weight 6. BP |
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comment on the effect of diuretic administration to treat cardiogenic pulmonary edema
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the response to diuresis is usually prompt and dramatic
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what question should you ask yourself before treating arrhythmias?
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"should it be treated?"
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what are two reasons to treat arrhythmias?
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1. arrhythmia is associated with clinical signs
2. the patient is at risk of SCD and treatment will reduce that risk |
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why could use of antiarrhythmic agents be bad?
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- they can worsen arrhythmias
- evidence is lacking in whether it actually decreases mortality |
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what are the mechanisms of the four classes of antiarrhythmic agents?
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- Class I: Na blockade
- Class II: β-blockade - Class III: K blockade - Class IV: Ca blockade |
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what is the mechanism of a Class I antiarrhythmic agent and what are six generic examples?
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(Na blockade)
'- Ia agents: procainamide, quinidine - Ib agents: lidocaine, mexiletine, tocainide - Ic agent: flecainide |
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what is the mechanism of a Class II antiarrhythmic agent and what is one generic example?
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(β blockade)
- atenolol |
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what is the mechanism of a Class III antiarrhythmic agent and what are two generic examples?
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(K blockade)
1. sotalol 2. amiodarone |
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what is the mechanism of a Class IV antiarrhythmic agent and what is one generic example?
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(Ca blockade)
- diltiazem |
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what are two "other" antiarrhythmic agents (other than Class I - IV)?
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1. digoxin
2. magnesium |
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what is the mechanism of digoxin when used as an antiarrhythmic and what arrhythmias does it treat?
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- it is a vagomimetic
- sometimes used in management of SVTA, especially AF |
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which antiarrhythmic agents are used for arrhythmias from ectopic myocardial sites, especially ventricular arrhythmias?
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Class I and Class III
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which antiarrhythmic agents are used to slow AV conduction?
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Class II, Class IV, and digoxin
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what are three drug classes (generic) used to treat SVT / SVPC arrhythmias?
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(agents that slow AV nodal conduction)
1. calcium channel blockers (diltiazem) 2. β-agonists 3. digoxin |
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what are two sites where stimulation of the vagus nerve can help to treat supraventricular tachycardia?
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1. ocular pressure
2. massage of the carotid sinuses |
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what is an expected response of a vagal maneuver (e.g. ocular pressure, massage of carotid sinuses) on
- sinus tachycardia? - junctional tachycardia? - atrial tachycardia? - ventricular tachycardia? |
- sinus tachycardia: GRADUAL slowing or no effect
- junctional tachycardia: ABRUPT termination or no effect - atrial tachycardia: AV BLOCK or no effect - ventricular tachycardia: no effect |
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what are four treatments for urgent management of SVT?
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1. vagal maneuvers
2. DILTIAZEM IV 3. esmolol 4. oral diltiazem if esmolol is not available |
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what are three drugs used to manage chronic SVT?
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1. digoxin
2. diltiazem 3. atenolol |
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what are two conditions in which treatment of atrial fibrillation will differ?
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1. when AF is a complication of DCM
2. when AF is idiopathic |
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what is the goal of therapy to treat AF when it is a complication of DCM?
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therapy is directed toward controlling ventricular response rate
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what three drugs are used to control AF with concurrent DCM?
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1. digoxin
2. ± diltiazem 3. ± β-blockers |
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what are four ways to treat idiopathic atrial fibrillation?
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1. conservative management (rate control, if necessary)
2. procainamide or quinidine (Class I) 3. Class III agents 4. DC cardioversion |
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when is treatment of ventricular tachyarrhythmia indicated?
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1. clinical signs present
2. at risk for SCD |
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what is proarrhythmia?
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when antiarrhythmic agents cause arrhythmias
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what are three common extracardiac factors that can cause ventricular tachyarrhythmia?
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1. electrolytes (K)
2. pain 3. hypoxia |
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when is antiarrhythmic therapy indicated for ventricular tachyarrhythmia associated with extracardiac disease.
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1. when the arrhythmia is associated with clinical signs
2. when the rate is rapid |
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what are six treatments for ventricular tachyarrhythmia in the order that you should use them?
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1. lidocaine
2. procainamide 3. β-blockade (esmolol) 4. Magnesium sulfate 5. bretylium or amiodarone 6. DC countershock |
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what are five drugs used to manage chronic ventricular tachyarrhythmias?
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1. procainamide
2. mexiletine 3. atenolol 4. sotalol 5. amiodarone |
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what is a common treatment for 2nd or 3rd degree AV blocks?
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cardiac pacing
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what are two ways to treat sick sinus syndrome?
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1. drugs such as propantheline and terbutaline (seldom efficacious in the long term)
2. cardiac pacing |
