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ACVIM Consensus StatementJ Vet Intern Med 2009;23:1142–1150 Consensus Statements of the American College of Veterinary Internal Medicine (ACVIM) provide theveterinary community with up-to-date information on the pathophysiology, diagnosis, and treatment ofclinically important animal diseases. The ACVIM Board of Regents oversees selection of relevant topics,identification of panel members with the expertise to draft the statements, and other aspects of assuring theintegrity of the process. The statements are derived from evidence-based medicine whenever possible and thepanel offers interpretive comments when such evidence is inadequate or contradictory. A draft is preparedby the panel, followed by solicitation of input by the ACVIM membership, which may be incorporated intothe statement. It is then submitted to the Journal of Veterinary Internal Medicine, where it is edited prior topublication. The authors are solely responsible for the content of the statements.
C. Atkins, J. Bonagura, S. Ettinger, P. Fox, S. Gordon, J. Haggstrom, R. Hamlin, B. Keene (Chair), V. Luis-Fuentes, and R. Stepien Key words: Cardiology; Cardiovascular; Heart failure; Therapy.
This is the report of the American College of Veteri- nary Internal Medicine (ACVIM) Specialty of Cardiology consensus panel convened to formulateguidelines for the diagnosis and treatment of chronic val- angiotensin converting enzyme inhibitors vular heart disease (CVHD, also known as endocardiosis American College of Veterinary Internal Medicine and myxomatous valve degeneration) in dogs. It is esti- constant rate infusion mated that approximately 10% of dogs presented to chronic valvular heart disease primary care veterinary practices have heart disease, and CVHD is the most common heart disease of dogs in many parts of the world, accounting for approximately mitral regurgitation 75% of canine cases of heart disease cases seen by veter-inary practices in North America.
CVHD most commonly affects the left atrioventricu- lar or mitral valve, although in approximately 30% of before the clinical onset of heart failure. When large cases the right atrioventricular (tricuspid) valve also is breed dogs are affected by CVHD, the progression of the involved. The disease is approximately 1.5 times more disease appears to be more rapid than that observed in common in males than in females. Its prevalence is also small breed dogs.2 Cavalier King Charles Spaniels are higher in smaller (o20 kg) dogs, although large breeds predisposed to developing CVHD at a relatively young occasionally are affected.1 In small breed dogs, the dis- age, but the time course of their disease progression to ease generally is slowly but somewhat unpredictably heart failure does not appear to be markedly different progressive, with most dogs experiencing the onset of a from that of other small breed dogs except for the early recognizable murmur of mitral valve regurgitation years The cause of CVHD is unknown, but the disease ap- pears to have an inherited component in some breeds From the Department of Clinical Sciences, North Carolina State studied.5,6 CVHD is characterized by changes in the cel- University, Raleigh, NC (Atkins, Keene); Department of Veterinary lular constituents as well as the intercellular matrix of the Clinical Sciences (Bonagura), Department of Veterinary Biosciences(Hamlin), The Ohio State University, Columbus, OH; California valve apparatus (including the valve leaflets and chordae Animal Hospital, Los Angeles, CA (Ettinger); Department of tendineae).7,8 These changes involve both the collagen Medicine, Animal Medical Center, New York, NY (Fox); Depart- content and the alignment of collagen fibrils within the ment of Small Animal Clinical Science, Texas A&M University, valve.9,10 Endothelial cell changes and subendothelial College Station, TX (Gordon); Department of Clinical Sciences, thickening also occur,11 although affected dogs do not University of Agricultural Sciences, University of Uppsala, Uppsala, appear to be at increased risk for arterial thromboembo- Sweden (Haggstrom); Royal Veterinary College, VCS, University ofLondon, London, UK (Luis-Fuentes); and Department of Medical lism or infective endocarditis. Mitral valve prolapse is a Sciences, University of Wisconsin-Madison, Madison, WI (Stepien).
common complication of myxomatous valve degenera- Corresponding author: Bruce Keene, Department of Clinical Sci- tion and represents a prominent feature of CVHD in ence, 4700 Hillsborough Street, North Carolina State University, some breeds.6,12 Progressive deformation of the valve Raleigh, NC 27606; e-mail: structure eventually prevents effective coaptation and Submitted June 12, 2009; Revised August 7, 2009; Accepted causes regurgitation (valve leakage). Progressive valvu- August 17, 2009.
lar regurgitation increases cardiac work, leading to Copyright r 2009 by the American College of Veterinary Internal ventricular remodeling (eccentric hypertrophy and inter- cellular matrix changes) and ventricular dysfunction.
Canine Chronic Valvular Heart Disease Abnormal numbers or types of mitogen receptors (eg, A newer classification system that might more objec- any of the subtypes of serotonin, endothelin, or angio- tively categorize patients in the course of their heart tensin receptors) on fibroblast cell membranes in the disease has been developed, and this scheme was used by valves of affected dogs may play a role in the pathophys- the panel for consensus recommendations. The goal was iology of the valvular lesions.13 Systemic or local to link severity of signs to appropriate treatments at each metabolic, neurohormonal or inflammatory mediators stage of illness. In formulating these guidelines, the con- (eg, endogenous catecholamines and inflammatory cyto- sensus panel adapted the 2001 American College of kines) also may influence progression of the valve lesion Cardiology/American Heart Association classification or the subsequent myocardial remodeling and ventricular system for the treatment of heart disease and failure in dysfunction that accompany long-standing, hemody- human patients to the management of canine CVHD.19 namically significant valvular regurgitation. However, In this approach, patients are expected to advance from 1 these factors are poorly understood at this time.14 stage to the next unless progression of the disease is al- The prevalence of CVHD increases markedly with age tered by treatment.
in small breed dogs (with up to 85% showing some evi- The classification system presented below and used in dence of the lesion at necropsy by 13 years of age), but these guidelines is meant to complement, not replace, the presence of the pathologic lesion does not necessarily functional classification systems. The new system de- indicate that a dog will develop clinical signs of heart scribes 4 basic stages of heart disease and failure: failure. Like the underlying cause of the disease, the fac-tors that determine the progression of the lesion remain  Stage A identifies patients at high risk for developing unknown, although age, left atrial size, and heart rate heart disease but that currently have no identifiable have been shown to predict outcomes.15,16 structural disorder of the heart (eg, every CavalierKing Charles Spaniel without a heart murmur).
 Stage B identifies patients with structural heart disease Classification of Heart Disease and Heart Failure (eg, the typical murmur of mitral valve regurgitation ispresent), but that have never developed clinical signs Heart failure is a general term that describes a clinical caused by heart failure. Because of important clinical syndrome that can be caused by a variety of specific heart implications for prognosis and treatment, the panel diseases, including CVHD. Heart failure from any cause is further subdivided Stage B into Stage B1 and B2.
characterized by cardiac, hemodynamic, renal, neurohor-  Stage B1 refers to asymptomatic patients that have monal, and cytokine abnormalities. The classification no radiographic or echocardiographic evidence of systems for heart failure most familiar to veterinarians are cardiac remodeling in response to CVHD.
the modified New York Heart Association (NYHA)17 and  Stage B2 refers to asymptomatic patients that have International Small Animal Cardiac Health Council18 hemodynamically significant valve regurgitation, functional classification systems, both of which were de- as evidenced by radiographic or echocardiograph- signed to provide a framework for discussing and ic findings of left-sided heart enlargement.
comparing the clinical signs of patients in heart failure.
 Stage C denotes patients with past or current clinical These functional classification systems vary in their signs of heart failure associated with structural heart details, but both serve as semiquantitative schemes for disease. Because of important treatment differences be- judging the severity of a patient's clinical signs. Such cat- tween dogs with acute heart failure requiring hospital egorization aids in teaching therapeutic protocols and care and those with heart failure that can be treated on constitutes a basis for stratification of subjects in clinical an outpatient basis, these issues have been addressed trials. The modified NYHA functional classification of separately by the panel. Some animals presenting with heart failure can be summarized as follows: heart failure for the 1st time may have severe clinicalsigns requiring aggressive therapy (eg, with additional  Class I describes patients with asymptomatic heart afterload reducers or temporary ventilatory assistance) disease (eg, CVHD is present, but no clinical signs are that more typically would be reserved for those with re- evident even with exercise).
fractory disease (see Stage D).
 Class II describes patients with heart disease that  Stage D refers to patients with end-stage disease with causes clinical signs only during strenuous exercise.
clinical signs of heart failure caused by CVHD that are  Class III describes patients with heart disease that refractory to ‘‘standard therapy'' (defined later in this causes clinical signs with routine daily activities or document). Such patients require advanced or special- mild exercise.
ized treatment strategies in order to remain clinically  Class IV describes patients with heart disease that comfortable with their disease. As with Stage C, the causes severe clinical signs even at rest.
panel has distinguished between animals in Stage Dthat require acute, hospital-based therapy and those Functional classification systems share a common that can be managed as outpatients.
problem in that they are based on relatively subjectiveassessments of clinical signs that can change frequently This classification system emphasizes that there are and dramatically over short periods of time. Further- risk factors and structural prerequisites for the develop- more, treatments may not differ substantially across the ment of heart failure in CVHD. The use of this functional classes.
classification system is meant to encourage veterinary cli- nicians to think about heart disease in a way analogous Diagnosis for Stage A to the current clinical approach to cancer. This classifi- cation system is designed to aid in:  Small breed dogs, including breeds with known  Developing screening programs for the presence of predisposition to develop CVHD (eg, Cavalier CVHD in dogs known to be at risk.
King Charles Spaniels, Dachshunds, Miniature  Identifying interventions that may (now or in the fu- and Toy Poodles) should undergo regular evalua- ture) decrease the risk of disease development.
tions (yearly auscultation by the family veter-  Identifying asymptomatic dogs with CVHD early in the inarian) as part of routine health care.
course of their disease, comparable to ‘‘in situ'' cancer,  Owners of breeding dogs or those at especially so that they can perhaps be treated more effectively.
high risk, such as Cavalier King Charles Spaniels,  Identifying symptomatic dogs with CVHD so that may choose to participate in yearly screening these patients can be treated medically and either po- events at dog shows or other events sponsored by tentially cured (interventionally or surgically) or their breed association or kennel club and con- managed with their chronic disease.
ducted by board-certified cardiologists partici-  Identify symptomatic dogs with advanced heart failure pating in an ACVIM-approved disease registry.
from CVHD and refractory to conventional therapy—these patients require aggressive or new treatment strat-egies or potentially hospice-type end-of-life care.
Therapy for Stage A Evaluating the Evidence for Efficacy and Safety  No drug therapy is recommended for any patient.
In classifying dogs with CVHD according to their dis-  No dietary therapy is recommended for any pa- ease stage and clinical status and matching them with diagnostic, pharmacologic, and dietary treatment recom-  Potential breeding stock should no longer be bred mendations, the consensus panel considered both the if mitral regurgitation (MR) is identified early, quantity and quality of evidence available to inform the during their normal breeding age of o6–8 years.
diagnostic and therapeutic decisions made in these pa-tients. The heading ‘‘Consensus recommendation''  Stage B—These patients have a structural abnormality preceding a diagnostic, therapeutic, or dietary recom- indicating the presence of CVHD, but have never had mendation indicates that the panelists were unanimous in clinical signs of heart failure. These patients are gener- their opinion that the combination of available clinical ally recognized during a screening or routine health trial evidence, other published experimental or anecdotal examination with a heart murmur typical of mitral evidence, clinical experience, and expert opinion indicate that the potential benefit of the approach under discus-sion clearly outweighs the potential risks to the patient Diagnosis for Stage B and minimizes financial impact on the client.
In situations in which the available evidence regarding the efficacy of a diagnostic or therapeutic maneuver was  Thoracic radiography is recommended in all pa- conflicting, weak, or absent and no consensus on a rec- tients to assess the hemodynamic significance of the ommended course of action could be reached by the murmur and also to obtain baseline thoracic radio- panelists based on the available evidence and their col- graphs at a time when the patient is asymptomatic lective clinical experience, the panel's opinions and reasoning on clinically important issues are briefly sum-  Blood pressure measurement is recommended for all patients.
grouped together and summarized under the heading  In small breed dogs with typical murmurs, echo- ‘‘No consensus.'' cardiography is recommended to answer specific The panel recognized that there is considerable varia- questions regarding either cardiac chamber en- tion in the scientific quality of the evidence available to largement or the cause of the murmur if those support clinical decision making, and sought to include topically relevant references. Whereas the status of a par- auscultation and thoracic radiography.
ticular recommendation (consensus versus no consensus)  Echocardiography generally is indicated in larger reflects the collective judgment of the panel on each ques- breed dogs because the murmur of MR is more tion addressed, no attempt was made to assign a specific likely to be related to other causes (eg, dilated scientific grade or value to each included citation.
 Basic laboratory work (a minimum of hematocrit, Guidelines for Diagnosis and Treatment of CVHD total protein concentration, serum creatinine concen-tration, and urinalysis) is indicated in all patients.
 Stage A—Dogs at high risk for development of heart failure, but without apparent structural abnormality Because their prognosis and therapy may differ sub- (no heart murmur is heard) at the time of examination.
stantially, asymptomatic patients with murmurs of Canine Chronic Valvular Heart Disease mitral valve insufficiency are further subcategorized into of b blockers for the treatment of dogs in Stage B2 2 groups based on the results of the above evaluation: are in progress.
 No other pharmacologic treatments were recom-  Stage B1: Hemodynamically insignificant MR (defined mended in Stage B2 by a majority of panelists. A as radiographically or echocardiographically normal or few panelists considered the use of the following equivocally enlarged LA, LV, or both, with normal LV medications for patients in Stage B2 under specific systolic function; normal vertebral heart score on radi- circumstances: pimobendan, digoxin, amlodipine, ography; normotensive, normal laboratory results).
and spironolactone. The panel felt in general thatthese treatment strategies needed additional inves- Therapy for Stage B1 (both pharmacologic and di- tigation into their efficacy and safety in this patient etary) is identical for both small and large breed dogs.
population before a consensus recommendationcould be made.
 Dietary treatment was recommended by a major- ity of panelists in Stage B2, a minority of the panel Small and large breed dogs: recommended no dietary changes. Principles guid-ing dietary treatment at this stage include mild  No drug or dietary therapy is recommended.
dietary sodium restriction and provision of a  Re-evaluation is suggested by either radiography highly palatable diet with adequate protein and or echocardiography with Doppler studies in ap- calories for maintaining optimal body condition.
proximately 12 months (some panelists rec-ommend more frequent follow-up in large dogs).
Larger breed dogs:  Stage B2: Hemodynamically significant MR with car-  Generally, panelists who recommended treatment diac remodeling (defined as clearly enlarged LA, LV, in smaller breed dogs strengthened their recom- or both); normotensive.
mendations promoting the use of both ACEI and bblockers in larger breed dogs in Stage B2.
Therapy for Stage B2 (both pharmacologic and di-  Dietary treatment recommendations for larger breed etary) is controversial, and no consensus could be dogs were the same as those for small breeds, empha- reached with currently available evidence.
sizing mild sodium restriction and adequate proteinand caloric intake if changes were recommended.
 Stage C—Patients have a structural abnormality and current or previous clinical signs of heart failure caused Small breed dogs: by CVHD. Stage C includes all patients that have had  Angiogensin converting enzyme inhibitor (ACEI): an episode of clinical heart failure. Such patients stay For patients with clinically relevant left atrial en- in this stage despite improvement of their clinical largement on either initial examination, or those signs with standard therapy (even if their clinical signs in which the left atrium has increased in size dra- resolve completely). Guidelines for standard pharma- matically on successive monitoring examinations, a cotherapy are provided for both in-hospital (acute) majority of the panel members recommend initia- management of heart failure and for home care tion of therapy with an ACEI. Clinical trials (chronic) management of heart failure, as well as rec- addressing the efficacy of ACEI for the treatment ommendations for chronic dietary therapy. Some of dogs in Stage B2 have had mixed results—either patients that present in Stage C may have life-threat- no effect or a small positive effect delaying the on- ening clinical signs, and require more extensive acute set of congestive heart failure.20–22 A minority of therapy than is considered standard therapy. These the panel members recommend no therapy for acute care patients may share some medical manage- asymptomatic animals pending further clinical tri- ment strategies with dogs that have progressed to als to examine the efficacy of therapy in this setting.
Stage D (refractory heart failure, see below). In Stage  b blockers: For patients with clinically relevant left C, heart failure secondary to CVHD, the panel did not atrial enlargement on either initial examination, or make clinically relevant therapeutic distinctions be- when the left atrium has increased in size dramat- tween small and larger breed dogs for either acute or ically on successive monitoring examinations, a chronic medical management.
minority of the panel members recommend initia-tion of therapy with a low dosage of a b blocker, For both Stages C and D (CVHD patients with symp- titrating to the highest tolerated dose over a period tomatic heart failure), the acute care of heart failure is of approximately 1–2 months depending on the focused on regulating the patient's hemodynamic status specific medication recommended. A majority of by monitoring (as well as possible under clinical circum- the panel members recommend no b-blocker ther- stances) and pharmacologically optimizing preload, apy for asymptomatic animals pending further afterload, heart rate, and contractility to improve car- clinical trials to examine the efficacy of therapy in diac output, decrease the extent of mitral valve this setting. Clinical trials addressing the efficacy regurgitation if possible, and relieve clinical signs associ- ated with either low cardiac output or excessively in-  For life-threatening pulmonary edema (expectora- creased venous pressures (preload). The broad goals of tion of froth associated with severe dyspnea; diffuse chronic (home care) management are focused on main- pulmonary opacity on thoracic radiographs; poor taining these hemodynamic improvements to the extent initial response to furosemide bolus with failure of possible, while providing additional treatments aimed at dyspnea and respiratory rate to improve over 2 slowing progression, prolonging survival, decreasing hours), furosemide is administered as a constant clinical signs of congestive heart failure, enhancing exer- rate infusion (CRI) at a dose of 1 mg/kg/h after the cise capacity, and otherwise improving quality life.
 Allow patient free access to water once diuresis has Diagnosis for Stage C  Pimobendan, 0.25–0.3 mg/kg PO q12h—Although the clinical trial evidence supporting the chronicuse of pimobendan in the management of Stage C  Because of the relatively high prevalence of heart failure from CVHD is stronger than for the chronic tracheobronchial disease in the same pop- acute situation, the recommendation to use pimo- ulation at risk for CVHD, the presence of a typical bendan in acute heart failure therapy is strongly left apical regurgitant murmur in a coughing dog supported by hemodynamic and experimental ev- does not necessarily mean that the clinical signs are idence24–27 as well as the anecdotal experience of the result of CVHD.
the panelists.
 A clinical database (including chest radiographs  Oxygen supplementation, if needed, can be admin- and preferably an echocardiogram and basic labo- istered via a humidity and temperature-controlled ratory tests) must be obtained and examined oxygen cage or incubator or via a nasal oxygen carefully to accurately determine the cause of clin- ical signs in animals with CVHD.
 Mechanical treatments (eg, abdominal paracente-  Serum N-terminal pro-B-type naturetic peptide sis and thoracocentesis) are recommended to (BNP) concentrations should become increasingly remove effusions judged sufficient to impair venti- useful in determining the cause of clinical signs in lation or cause respiratory distress.
dogs with CVHD. Although there is no doubt that,  Provide optimal nursing care, including mainte- as a group, dogs with clinical signs caused by heart nance of an appropriate environmental tempera- failure have higher serum BNP concentrations ture and humidity, increase in the head on pillows, than those with clinical signs caused by primary and placement of sedated patients in sternal posture.
pulmonary disease, the positive predictive value of  Sedation—Anxiety associated with dyspnea should any single BNP concentration, obtained by a com- be treated. Narcotics, or a narcotic combined with mercially available test, has not been adequately an anxiolytic agent, are most often used by panelists.
characterized at the time of this writing (August Butorphanol (0.2–0.25 mg/kg) administered IM or 2009) to make a consensus recommendation with IV was the narcotic most often utilized for this pur- regard to BNP testing.
pose; combinations of buprenorphine (0.0075–  The signalment and physical examination can be 0.01 mg/kg) and acepromazine (0.01–0.03 mg/kg helpful in determining the pretest probability of IV, IM, or SQ) as well as other narcotics, including heart failure as a cause of clinical signs in patients morphine and hydrocodone, also have been utilized.
with CVHD. For example, obese dogs with no his-  CRI of sodium nitroprusside for up to 48 hours is tory of weight loss are less likely to be in heart often useful for life-threatening, poorly responsive failure secondary to CVHD; dogs with marked si- pulmonary edema (refer to Class D below for spe- nus arrhythmia and relatively slow heart rates also cific dosing recommendations).
are less likely to have clinical signs attributable toCVHD.
 Most of these dogs are middle-aged or older, and it No consensus was reached on the following acute care is always prudent to complete the database with a CBC, serum biochemical profile, and urinalysis,  Care must be taken to monitor the blood pressure especially if therapy for CHF is anticipated.
and respiratory response to narcotics and tranquil-ilzers in the setting of acute heart failure. No Acute (Hospital-Based) Therapy of Stage C specific treatment or dosage regimen was used by all panelists.
 ACEI (eg, enalapril 0.5 mg/kg PO q12h). Although  Furosemide—The specific dosing of furosemide in treatment with ACEI is a consensus recommenda- a dog with CHF should be related to the severity of tion for chronic Stage C heart failure and a majority clinical signs and the response to initial therapy.
of panelists also treat acute heart failure with ACEI, Lower or higher doses (eg, 1–4 mg/kg) may be ap- the evidence supporting ACEI efficacy and safety in propriate in specific cases. Repeated IV boluses or acute therapy when combined with furosemide and a constant rate IV infusion may be indicated for pimobendan is less clear. There is, however, clear ev- poorly responsive dogs.
idence that the acute administration of enalapril plus Canine Chronic Valvular Heart Disease furosemide in acute heart failure results in substantial mended the addition of digoxin in cases compli- improvement in pulmonary capillary wedge pressure cated by persistent atrial fibrillation to slow the when compared with the administration of furose- ventricular response rate. Some panelists also pre- scribe digoxin at this dosage for patients in Stage C  Nitroglycerin 2% ointment, approximately 1/2'' heart failure in the absence of sustained supraven- paste per 10 kg body weight for 24–36 hours. Some tricular tachyarrhythmia, as long as no contra- panelists recommend administering the ointment indication to digoxin is evident (eg, increased in intervals (eg, 12 hours on, 12 hours off). Other serum creatinine concentration, ventricular ec- panelists do not use nitroglycerin in this setting.
topy, concerns over owner compliance, chronicGI disease resulting in frequent or unpredictable Home-Based (Chronic) Therapy for Stage C bouts of vomiting or diarrhea).
 Once heart failure signs have resolved, a stable medication regimen has been instituted, and the  Continue PO furosemide administration to effect, patient is eating and apparently feeling well, a mi- commonly at a dosage of 2 mg/kg q12h. The daily nority of panelists recommend attempting a low furosemide dosage for dogs with CHF is wide and dose, slow up-titration regimen of a b blocker.
can be as low as 1–2 mg/kg PO q12h to 4–6 mg/kg There is no clinical trial evidence in dogs to sup- PO q8h. The dosage must be titrated to maintain port this recommendation. If prescribed, there is patient comfort and with attention to effects on no consensus regarding which specific b blocker to renal function and electrolyte status.
use (carvedilol, atenolol, or metoprolol is the most  Chronic oral furosemide (doses 6 mg/kg q12h) frequently prescribed). The purpose of b blockade needed to maintain patient comfort in the face of in this setting is related to potential long-term pro- appropriate adjunct therapy indicates disease pro- gression to Stage D.
remodeling. These effects have been demonstrated  Continue or start ACEI (eg, enalapril 0.5 mg/kg, in some experimental animal models31 and in hu- PO q12h) or equivalent dose of another ACEI mans with heart failure, but not in clinical trials.
if approved for use. The labeled dosage range of  The presence of atrial fibrillation strengthens the enalapril is 0.25–0.5 mg/kg PO q12h; most panel- indication for b blockade (to slow the ventricular ists treat at the upper end of this range. Measure- response to atrial fibrillation) for those panelists ment of serum creatinine and electrolyte concen- who recommended a b blocker.
trations 3–7 days after beginning an ACEI is rec-  In patients taking a b blocker before the onset of ommended for animals with Stage C heart failure.
Stage C heart failure, the majority of panelists (0.25–0.3 mg/kg continue b blockade; some panelists would con- sider dosage reduction if needed clinically because  Panelists recommend against starting a b blocker in of clinical signs of low cardiac output, hypo- the face of active clinical signs of heart failure (eg, thermia, or bradycardia.
cardiogenic pulmonary edema) caused by CVHD.
 Some panelists prefer administration of oral diltia-  None of the panelists routinely use nitroglycerin in zem (several formulations are available, some the chronic treatment of Stage C heart failure.
sustained release) for chronic heart rate control in  Participation in a structured, home-based ex- tended care program to facilitate body weight,  Some panelists find cough suppressants useful in appetite, respiratory, and heart rate monitoring occasional patients in Stage C heart failure from while providing client support to enhance medica- tion compliance and dosage adjustments in  Some panelists find bronchodilators useful in oc- patients with heart failure is encouraged.
casional patients in Stage C heart failure fromCVHD.
No consensus was reached regarding the following home-based (chronic) treatment strategies in Stage C: Dietary Therapy for Stage C  Spironolactone (0.25–2.0 mg/kg PO q12–24h) was Cardiac cachexia is defined as the unintentional loss recommended by a majority of panelists as an ad- of 47.5% of the patient's normal, predisease weight, not junct for the chronic therapy of dogs in Stage C including weight loss associated with the resolution of heart failure. The primary purpose of spironolac- edema or the removal of body cavity effusions. Cachexia tone in this situation is thought to be aldosterone has substantial negative prognostic implications, and is antagonism. No clinically relevant diuretic effect much easier to prevent that to treat.32 should be anticipated. This treatment now is ap-proved in Europe at a dosage of 2 mg/kg/d.
 Digoxin (0.0025–0.005 mg/kg PO q12h) with tar- get plasma concentration 8 hours postpill of 0.8–  Maintain adequate calorie intake (maintenance 1.5 ng/mL. For the chronic management of Stage calorie intake in Stage C should provide approxi- C heart failure, a majority of panelists recom- mately 60 kcal/kg body weight) to minimize weight loss (specifically muscle mass loss) that often oc- gies for Stage D patients proved difficult. As with Stage curs in CHF.
C, guidelines for drug treatment are provided for both in-  Specifically address and inquire about the occurrence hospital (acute) and for home care (chronic) manage- of anorexia, and make efforts to treat any drug- ment of heart failure, and recommendations for chronic induced or other identifiable causes of anorexia that dietary therapy are also given.
 Record the accurate weight of the patient at every Diagnosis for Stage D clinic visit, and investigate the cause of weight gain orloss.
 Because Stage D heart failure patients are, by defi-  Ensure adequate protein intake and avoid low-pro- nition, refractory to the treatments for Stage C tein diets designed to treat chronic kidney disease, patients, defining refractory congestive heart fail- unless severe concurrent renal failure is present.
ure involves the same diagnostic steps outlined for  Modestly restrict sodium intake, taking into con- Stage C plus the finding of failure to respond to treatments outlined in the Stage C guidelines.
(including dog food, treats, table food, and foodsused to administer medications) and avoid any Acute (Hospital-Based) Therapy for Stage D processed or other salted foods.
(Refractory Heart Failure)  Monitor serum potassium concentrations and sup- plement the diet with potassium from eithernatural or commercial sources if hypokalemia is  In the absence of severe renal insufficiency (ie, identified. Hyperkalemia is relatively rare in pa- serum creatinine concentrations 4 3 mg/dL), ad- tients treated for heart failure with diuretics, even ditional furosemide is administered IV as a bolus in those concurrently receiving an ACEI in combi- at a dosage of 2 mg/kg followed by either addi- nation with spironolactone.33 Diets and foods with tional bolus doses, or a furosemide CRI at a high potassium content should be avoided when dosage of 1 mg/kg/h until respiratory distress (rate hyperkalemia has been identified.
and effort) has decreased, or for a maximum of4 hours. As indicated above, the dosage or furose- No consensus was reached on the following dietary ther- mide is a range and higher or lower doses may be appropriate for a given case.
 Continue to allow patient free access to water once  Consider monitoring serum magnesium concentra- diuresis has begun.
tions, especially as CHF progresses and in animals  Fluid removal (eg, abdominal paracentesis, thor- with arrhythmias. Supplement with magnesium in acocentesis) as needed to relieve respiratory cases in which hypomagnesemia is identified.
distress or discomfort.
 Consider supplementing with n-3 fatty acids, espe-  In addition to oxygen supplementation as in Stage cially in dogs with decreased appetite, muscle mass C (above), mechanical ventilatory assistance may loss, or arrhythmia.34 be useful to make the patient more comfortable, toallow time for medications35 to have an effect; and  Stage D—Patients have clinical signs of failure refrac- to provide time for left atrial dilatation to accom- tory to standard treatment for Stage C heart failure from CVHD, as outlined above. Stage D heart failure regurgitant volume in patients with acute exacer- patients therefore should be receiving the maximal bation of CVHD (eg, ruptured chordae tendinae recommended (or tolerated) dosage of furosemide, an with severe cardiogenic pulmonary edema) and ACEI, and pimobendan, as outlined in the Stage C impending respiratory failure.
guidelines above. Any indicated and tolerated antiar-  More vigorous afterload reduction in patients rhythmic medication, needed to maintain sinus that can tolerate arterial vasodilation. Drugs po- rhythm (if possible) or regulate the ventricular re- tentially beneficial include sodium nitroprusside sponse to atrial fibrillation in a heart rate range of (starting at 0.5–1 mg/kg/min), hydralazine (0.5– 80–160/min, also should be used before a patient is 2.0 mg/kg PO), or amlodipine (0.05–0.1 mg/kg considered refractory to standard therapy.
PO). Direct vasodilators should be started at alow dosage and up-titrated hourly until adequate Not surprisingly, there have been very few clinical tri- clinical improvement accompanied by a decrease als addressing drug efficacy and safety in this patient of approximately 5–10% in systolic blood pressure population. This leaves cardiologists treating patients is observed. These drugs are recommended in ad- with heart failure refractory to conventional medical dition to an ACEI and pimobendan. The clinician therapy with a perplexing variety of treatment options.
should be mindful that any decline in blood pres- Because of the relative lack of clinical trial evidence and sure will also depend on specific vasodilator drug.
the diverse clinical presentations of patients with end- For example, vasodilation effects are rapid onset stage heart failure, development of meaningful consensus with nitroprusside, but slower with amlodipine.
guidelines regarding the timing and implementation of Caution is warranted to avoid serious, prolonged individual pharmacologic and dietary treatment strate- hypotension (ie, monitor blood pressure and main- Canine Chronic Valvular Heart Disease tain systolic arterial blood pressure 4 85 mmHg or weight or girth measurements) varied widely mean arterial blood pressure 4 60 mmHg. Serum among the panelists.
creatinine concentration should be measured be-  Spironolactone, if not already started in Stage C, fore and 24–72 hours after administration of these is indicated for chronic treatment of Stage D drugs. Patients in Stage D have life-threatening heart failure, and a trial of additional afterload re-  b blockade generally should not be initiated at this duction is warranted. The panel emphasized that stage unless clinical signs of heart failure can be because afterload reduction may increase cardiac controlled, as outlined in Stage C.
output substantially in the setting of severe MRand heart failure, administration of an arterial di- No consensus was reached regarding the following lator in this setting does not necessarily decrease chronic Stage D therapeutic recommendations: blood pressure.
 Hydrochlorthiazide was recommended by several panelists as adjunctive therapy with furosemide, No consensus was reached regarding the following acute utilizing various dosing schedules (including only care Stage D recommendations: intermittent use every 2nd–4th day). Some panel- ists warned of the risk of acute renal failure and Pimobendan dosage may be increased (off-label) marked electrolyte disturbances, based on per- to include a 3rd 0.3 mg/kg daily dose. Some panel- sonal experience.
ists administer an additional dose of pimobendanon admission of Stage D patients with acute  Pimobendan dosage is increased by some panelists to include a 3rd 0.3 mg/kg daily dose (off-label use, pulmonary edema. Because this dosage recom- explanations and cautions apply as listed for in- mendation is outside of the FDA-approved label- hospital care, above).
ing for pimobendan, this use of the drug should beexplained to and approved by the client.
 Digoxin, at the same (relatively low) dosages rec- ommended by some panelists for Stage C heart In animals judged to be too sick to wait for the failure, was recommended for treatment of atrial effects of oral afterload reduction or inotropic sup- fibrillation for patients in Stage D, with the same port (eg, pimobendan with or without hydralazine cautions listed in Stage C above.
or amlodipine), nitroprusside (for afterload reduc-tion in life threatening pulmonary edema) or  Digoxin, at the same (relatively low) dosages rec- ommended by some panelists for Stage C heart dobutamine (for inotropic support of the hypo- failure, also was recommended by a minority of tensive patient) must be administered by CRI.
panelists for all patients in Stage D in sinus rhythm, Both drugs can be administered at dosages of 0.5– assuming no clear contraindication was present.
1.0 mg/kg/min and up-titrated every 15–30 minutesto a maximum of approximately 10 mg/kg/min.
 Sildenafil (1–2 mg/kg PO q12h) is used by some panelists to treat Stage D heart failure caused by These drugs, either separately or in combination, CVHD or to treat advanced CVHD complicated can be used for 12–48 hours to improve hemody- by pulmonary hypertension.
namic status and control refractory cardiogenic  The majority of panelists felt that b blockade ini- pulmonary edema. Continuous electrocardiograph- tiated at an earlier stage of heart failure in CVHD ic and blood pressure monitoring is recommended should not be discontinued, but that dose reduc- to minimize the potential risks of this therapy.
tion may be needed if shortness of breath could Sildenafil (1–2 mg/kg PO q12h) is used by a minor- not be controlled by the addition of other medica- ity of panelists to treat acute exacerbations of tions or if bradycardia, hypotension, or both were Stage D heart failure caused by CVHD, even in the absence of diagnosed pulmonary hypertension.
 Bronchodilators are recommended as an adjunct  b blockade still may be useful to decrease the ven- tricular response rate in atrial fibrillation after therapy in treating cardiogenic pulmonary edema stabilization and digitalization.
in hospitalized patients by a minority of panelists.
 Cough suppressants are recommended by a minor- ity of panelists to treat chronic, intractable cough Home-Based (Chronic) Stage D Therapy in Stage D patients receiving home care.
 Bronchodilators are recommended by a minority of panelists to treat chronic, intractable coughing  Furosemide dosage should be increased as needed in Stage D patients receiving home careanelists.
to decrease pulmonary edema or body cavity effu-sions, if use is not limited by renal dysfunction Home-Based (Chronic) Dietary Therapy for Stage D (which generally should be monitored 12–48 hours after dosage increases). The specific strategy andmagnitude of dosage increase (eg, same dose in-  All of the dietary considerations for Stage C creased to 3 times per day versus 2 higher doses, (above) apply.
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