Download Treating Congestive Heart Failure in 2007

CONGESTIVE HEART FAILURE
Etienne Côté DVM, DACVIM (Cardiology, Small Animal Internal Medicine)
Atlantic Veterinary College, University of PEI, 550 University Avenue, Charlottetown, PE, Canada
Heart disease is widespread in dogs and cats, but only a fraction of these situations are serious
enough to cause the animal problems.
Whether a cardiac abnormality causes clinical signs depends on the severity of the problem, and
how the body compensates.
In the struggle between deteriorating heart lesion on one hand, and endogenous compensatory
mechanisms on the other hand, patients may either be without clinical signs (compensatory
mechanisms predominate) or showing signs of decompensation (heart disease has surpassed
the maximal function of the compensatory mechanisms).
The most common form of decompensation in dogs and cats is called congestive heart failure.
Because it is so common, and potentially life threatening, congestive heart failure is a critical
aspect of veterinary medicine.
Heart failure, or Congestive heart failure (synonyms): The retention of fluid in tissues or body
cavities, and/or decreased perfusion caused by progressive, deteriorating cardiac function.
In layman’s terms, heart failure is a situation in which the heart is still doing something, just not
enough. Most patients with heart failure will respond well to medication and regain their
asymptomatic state when treated. Heart failure is *not* cardiac arrest, even though clients, from
watching television, may think so. Therefore, this term should not be used as a first-line
description for most clients because of the high risk of miscommunication.
Myocardial failure: Loss of the normal function of the myocardial tissue, either from
cardiomyopathy, or as a process of end-stage myocardial “exhaustion” in chronic heart diseases
of various types.
Left heart failure: Clinical signs caused by circulation problems originating from disease of the
aortic valve, left ventricle, mitral valve, or left atrium.
Right heart failure: Clinical signs caused by circulation problems originating from disease of the
pulmonary arteries, pulmonic valve, right ventricle, tricuspid valve, or right atrium.
Forward failure: Clinical signs caused by inadequate cardiac function resulting in organ
underperfusion. Classic manifestation of forward failure: syncope (underperfusion of the brain).
Syncope is a sign of forward, left-sided heart failure.
Backward failure: Clinical signs caused by the heart’s inability to accept the blood returning to it
from the venous system. This is a failure of the heart to “keep up” with the amount of blood
presented to it for recirculation. The result is an increase in the pressure of venous blood
returning to the heart. In turn, if this pressure increases excessively, the fluid part of blood
(plasma) seeps through the blood vessel wall, causing third-space accumulation of fluid, namely
effusions and edema. Classic example of left-sided, backward heart failure: pulmonary edema.
Right-sided, backward failure: typical signs are hepatomegaly, ascites, pleural effusion,
pericardial effusion, and jugular venous distension.
Systolic dysfunction: Poor contractile function of the ventricles. If severe enough, causes
forward failure. Example: dilated cardiomyopathy.
Diastolic dysfunction: Poor ability of the ventricles to accept incoming blood into their
chambers. Examples: hypertrophic cardiomyopathy, cardiac tamponade.
Preload: condition and pressure under which the ventricles fill. Too little preload (e.g.
voluminous hemorrhage, so too little blood enters ventricles) is detrimental because cardiac
output falls. Increasing preload is a good idea (e.g. as occurs naturally during exercise, when
splenic contraction increases volume of blood arriving at the heart), but to a certain limit. The
more blood enters the ventricles, causing a mild distension, the more strongly the ventricle can
contract. This is the Frank-Starling mechanism. However, excessive preload can occur if the
ventricles have not emptied adequately due to cardiac disease, resulting in fluid weeping into
surrounding tissues. Therefore, the Frank-Starling mechanism has its limits, and with heart
disease these limits may be exceeded, leading to congestive heart failure.
Afterload: condition and pressure against which the ventricles must work. This amounts to the
vascular resistance “downstream” and other factors such as obstruction (e.g. pulmonic or
subaortic stenosis), and viscosity of the blood. Less afterload means less work for the heart,
which is a good thing but to a point. Too little afterload can mean hypotension.
Inotropy: force of systolic function; contractile strength of the heart
Chronotropy: rate of cardiac depolarizations; heart rate
1. Why does congestive heart failure matter?
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Clinical signs. Onset of congestive heart failure= end of the asymptomatic state. A
patient with congestive heart failure has clinical signs that are directly caused by the
heart problem.
Treatment. Before congestive heart failure: medications are not essential.
With congestive heart failure: medications are usually indispensable for life.
Outcome. Patients who respond well to medications also regain a stable
(“asymptomatic”) state and can live a good quality of life with treatment.
Long-term prognosis. A patient with compensated (“asymptomatic”) heart disease may
continue to remain that way indefinitely; once a patient has developed congestive heart
failure, death is more likely to be from heart disease than anything else.
Error in diagnosis. Inaccurate diagnosis of congestive heart failure, which can occur
because many other processes produce similar clinical signs, can lead to long courses of
wrong medications with potentially detrimental side-effects.
Anesthetic risk. Congestive heart failure is a moderate to severe anesthetic risk factor
and must be managed prior to general anesthesia.
2. When to suspect congestive heart failure: common clinical signs
Dogs:
-increased respiratory effort, labored breathing
-restlessness, inability to become comfortable
-wheezing respirations
-ascites, abdominal distension
-exercise intolerance
-cyanosis
-other forms of cardiac decompensation (e.g. syncope)
Cats:
-increased respiratory effort, labored breathing
-ascites (uncommon)
-other forms of cardiac decompensation (e.g. syncope, aortic thromboembolism)
Notes:
-cough has long been associated with pulmonary edema/CHF in dogs, but an important caveat is
often overlooked: cough associated with CHF is almost always accompanied by varying
degrees of dyspnea. The dog that coughs but otherwise feels very well and is breathing
normally VERY uncommonly has pulmonary edema. In cats, cough is almost never
related to heart disease; coughing cats almost always have primary respiratory disease,
not heart failure. Cough is a nonspecific sign, and a common pitfall is to assume that a
dog with cough and a heart murmur must have congestive heart failure. Rather,
compensated (asymptomatic) heart disease plus coexisting primary respiratory disease
(collapsing trachea, chronic sterile bronchial disease, other) is a common impostor for
heart failure; thoracic radiographs help confirm.
-ascites is very uncommon as a predominant manifestation of congestive heart failure
in cats, in contrast to dogs.
-pleural effusion can be a manifestation of either left- or right-sided heart failure.
3. Causes of congestive heart failure (CHF):
Virtually any heart problem, if severe enough, can progress to congestive heart failure.
Dogs:
-Chronic valvular heart disease (myxomatous mitral and/or tricuspid valve endocardiosis)
-Dilated cardiomyopathy
-Congenital heart disease (patent ductus arteriosus [PDA], subaortic stenosis,
pulmonic stenosis, ventricular septal defect, other)
-Pericardial disease (tamponade from pericardial effusion or constrictive pericarditis)
-Heartworm disease
-Bacterial endocarditis (uncommon)
-Arteriovenous fistula (uncommon)
Cats:
-Hypertrophic cardiomyopathy
-Restrictive cardiomyopathy or unclassified cardiomyopathy
-Dilated cardiomyopathy
-Congenital heart disease
4. Differential diagnoses of selected clinical signs:
Dyspnea, cough, cyanosis
On physical exam of patients with heart failure, a murmur often is present, unless
respirations are too loud or pleural effusion muffles the heart sounds. Radiographically,
congestive heart failure patients will show pulmonary edema, pleural effusion, or both, as
a cause of the respiratory problem; atrial enlargement is common.
Ddx for dyspnea, cough, cyanosis:
-lung disease
 physical examination (respiratory sinus arrhythmia makes congestive heart
failure less likely; heart murmur, arrhythmia make congestive heart failure more
likely)
 thoracic radiographs (edema vs. pneumonia/hemorrhage/fibrosis/etc.)
-malignancy
 thoracic radiographs (pleural effusion plus lung metastases or mediastinal
mass make malignancy more likely; pleural effusion plus cardiomegaly
[especially with atrial enlargement] makes heart failure more likely)
 cytology of pleural effusion from thoracentesis (exudates, pure transudates,
and malignant cells are not consistent with congestive heart failure;
modified transudate is consistent with heart failure and other diseases)
 echocardiography (absence of structural heart disease makes cardiac cause
of pleural effusion very unlikely)
-upper airway problems
 thoracic, lateral cervical radiographs (collapsing trachea? foreign body?)
-intoxication, e.g. with zinc, onions (dogs), acetaminophen (cats)
 history of ingestion of toxic product
 complete blood count (methemoglobinemia, hemolytic anemia)
Ascites
Congestive heart failure patients have either a murmur, or muffled heart sounds often
with rapid heart rate (tachycardia); thoracic radiographs show a distended caudal vena
cava, often pleural effusion; and abdominal ultrasound detects distended hepatic veins in
addition to the ascites.
Ddx for ascites:
-portal hypertension, usually from chronic liver disease
 abdominal ultrasound
 post-prandial bile acids
-hypoalbuminemia
 low serum albumin
 abdominocentesis shows pure transudate
-hemoabdomen (trauma, or ruptured abdominal mass)
 history of trauma?
 abdominal ultrasound for mass
 abdominocentesis (= blood)
-purulent exudates
 penetrating wound?
 abdominal radiographs (free gas in peritoneal cavity?)
 abdominocentesis, cytology, and culture (purulent exudate)
5. Compensatory mechanisms
RENIN ANGIOTENSIN ALDOSTERONE SYSTEM (RAAS) and AUTONOMIC (SYMPATHETIC)
NERVOUS SYSTEM
Goal of RAAS (“why Mother Nature invented it”): to preserve circulation when a subacute drop in
arterial blood pressure occurs (e.g. very mild but long-term decrease in cardiac output as with the
early stages of many heart diseases).
Overall effect on the body: excellent preservation of adequate circulation, keeps clinical signs in
check. However, long-term activation of the RAAS increases the workload on the heart. Overall
effect: short-term and medium-term benefit, but long-term detriment.
Decrease in cardiac output (e.g. degenerative mitral valve first begins to “leak”)
Arterial baroreceptors sense
increased secretion of renin from kidney
Feedback to brain (medulla)
Renin converts circulating angiotensinogen
(made in liver) to angiotensin I
Increase sympathetic discharge
Direct
arterial
constriction
Increase renal
secretion of
renin
Angiotensin I converted to angiotensin II
in pulmonary vessels by the angiotensin
converting enzyme (ACE)
Angiotensin II is a
powerful arterial
vasoconstrictor
Angiotensin II elicits
aldosterone release
from adrenals (= Na
retention)
End results of RAAS and autonomic nervous system activation:
-arterial vasoconstriction
-sodium retention
-cardiac hypertrophy and fibrosis caused by angiotensin II
-beta-receptor downregulation (“dulling”) by chronic increase in sympathetic discharge
-vagal tone is overpowered by sympathetic drive
6. Evolution of congestive heart failure (CHF): origin and outcome
The usual sequence of events in a patient with heart disease is as follows:
1. Heart lesion first begins; compensatory mechanisms are activated, so no clinical signs
are apparent externally.
2. Heart lesion progresses (gets worse), but compensatory mechanisms respond by
activating even more, so there are still no clinical signs.
3. Heart lesion continues to progress until finally the compensatory mechanisms are unable
to keep up. The resultant disturbance in circulation is congestive heart failure.
Example (using degenerative/myxomatous mitral valve disease to illustrate)
1. Mitral valve first begins to leak. Murmur is present, but dog is fully active and
asymptomatic. (ACVIM stage B1)
2. Mitral valve regurgitation/insufficiency increases, but because compensatory
mechanisms like RAAS are further activated, dog is still fully asymptomatic despite
murmur. (ACVIM stage B2)
3. Mitral regurgitation worsens beyond ability to compensate. Pulmonary edema develops,
rapidly causes dyspnea, cough, and even cyanosis. (ACVIM stage C)
7. Diagnostic tests to strengthen suspicion of, or confirm, congestive heart failure
●History
-murmur ausculted previously during adulthood
-recent onset lethargy, exercise intolerance, loss of appetite
-recent onset appearance of discomfort, restlessness, inability to lie down and
“get comfortable”
-recent onset labored breathing (dyspnea), sometimes cough
-family history of congenital heart disease
● Physical examination
-habitus
-presence or absence of cough
-arrhythmia
-abdominal distension
-jugular vein distension
-subcutaneous edema (very rarely)
-respiratory effort
-heart murmur
-gallop sound
-muffled heart and/or lung sounds
-hepatomegaly
● Thoracic radiographs
-test of choice for ruling in or ruling out pulmonary edema, pleural effusion
● Echocardiography
-very poor sensitivity to detect congestive heart failure—b lines in TFAST scan are an
exception. Echocardiography pinpoints the cardiac lesion very well, but
congestive heart failure is a phenomenon of the whole body “paying the price” for
the heart’s problem. Therefore, must examine “weakest” points in circulation—
lungs (circulation leading to left heart) or pleura, abdomen, and neck (circulation
leading to right heart). Can be useful for finding pleural effusion.
● Electrocardiography (ECG)
-very poor sensitivity for detecting congestive heart failure. ECG remains
the best test for assessing arrhythmias, but does not reflect whether or not
congestive heart failure is present (one exception: the presence of respiratory
sinus arrhythmia is a good sign and usually indicates that congestive heart failure
is unlikely).
● Central venous pressure (CVP). Easy to measure using a jugular catheter. Diagnostic test of
choice to confirm diagnosis of right-sided congestive heart failure. Yields no information
on presence or absence of left-sided congestive heart failure, however.
8. Treatment of congestive heart failure (CHF)
ACUTE
-e.g. respiratory distress from severe pleural effusion or pulmonary edema
-treatment= lifesaving measure
-goal is to eliminate fluid from chest to prevent deterioration +/- suffocation
a. Avoid stress
-least amount of restraint as necessary
-plenty of soothing and calming language (verbal and body language)
-tranquilize if fractious (e.g. with butorphanol 0.1 mg/kg IV). Remember to monitor
respiratory effort because “fractiousness” in an animal in respiratory
distress may simply be a sense of suffocation, warranting immediate
termination of the echocardiogram, radiographs, or other procdure.
-as quiet, calm an environment as possible
b. Confirm diagnosis
-thoracic radiographs
-thoracentesis if pleural effusion (diagnostic centesis = few ml; also therapeutic centesis
(60-120 ml per 24 hours, no more) if large volume of chylous effusion with
evidence of chronicity (rounding of lung lobe margins on radiographs
-echocardiogram if thoracic radiographs show equivocal or uncertain lung
pattern (absence of structural heart disease on echo makes congestive heart
failure highly unlikely)
c. Emergency treatment—first 24 to 48 hours
-diuretic if dyspneic from pleural effusion or pulmonary edema (see thor XR)
FUROSEMIDE 2-6 mg/kg IV if possible, otherwise IM (much better IV, if cat
tolerates restraint). Repeat based on initial severity of dyspnea and response
to 1st doses. Can give every 1-12 hrs initially.
-tranquilizer/anxiolytic if showing signs of stress (common with severe cases)
and if quiet environment (e.g. cage) does not abolish signs of stress.
BUTORPHANOL 0.2 mg/kg IM is an excellent choice. BUPRENORPHINE 0.010.02 mg/kg IV or IM is a good alternative.
-THORACOCENTESIS if voluminous pleural effusion. Sedation is often necessary in
cats. Ultrasound can be very helpful to find “pocket” of pleural fluid for centesis
-OXYGEN THERAPY, as long as oxygen cage is not too warm (very
common problem, especially with large dogs), being in cage does not reduce
accessibility for treatments, and stress of placing nasal oxygen tube is not
excessive for unstable patient.
-DOBUTAMINE 2-15 μg/kg/minute CRI. Positive inotrope (increases myocardial
contractility). Begin at low dosage and titrate up over several minutes; decrease if
tachycardia or ventricular arrhythmia on ECG. Drawbacks: constant rate infusion
(CRI) only (need IV pump, and ECG monitor); may be arrhythmogenic; shortterm benefit does not clearly translate into better outcome—patient may feel
better but die sooner. Rarely used unless as a “bridge” to specific short-term goal
(e.g., last visit from owner, or myocardial failure preceding cardiac surgery).
-DOPAMINE 0.5-10 μg/kg/minute CRI. Peripheral vasoconstrictor; indicated
for use in critical hypotension. Little substance to support claims of renal vascular
preference, so uncommonly used for acute renal failure nowadays. Drawbacks:
may cause nausea; constant rate infusion (CRI), so IV pump necessary; may
increase workload on heart (afterload) excessively, so constant blood pressure
monitoring is essential.
-NITROGLYCERIN transcutaneous ointment (0.5 to 2 cm strip, applied to
pinna or to inguinal side of thigh, t.i.d. for 48 hours). Venodilator; reduces
preload. Probably minimally effective (questionable absorption through skin), but
not harmful.
-The animal’s usual DIET or “junk” diet if needed to preserve appetite
-IV FLUIDS: almost never indicated when initiating diuretics. Patient with congestive
has too much intravascular fluid volume, so giving further volume is
contraindicated. Giving diuretics and IV fluids simultaneously equals both
eliminating and replacing sodium, chloride, water, etc—makes no sense.
Rare exceptions: 1) severe hypokalemia (IV CRI is vehicle for K
supplementation), 2) concurrent congestive heart failure and renal failure when
renal failure is the chief complaint (vomiting, anorexia, etc.) rather than incidental,
mild to moderate azotemia that virtually always occurs with diuretics.
Acute right-sided congestive heart failure (e.g. acute ascites) almost never
occurs. Dyspnea can be caused by massive (“tense”) ascites, advancing the
diaphragm and compressing the lungs. Treatment, once problem is confirmed to be
cardiogenic: abdominal drainage or centesis.
CHRONIC
-e.g. routine recheck of a patient that at one time had acute congestive heart failure
(above); or, discharge of stabilized acute CHF patient; or, incidental discovery of
congestive heart failure in minimally symptomatic/asymptomatic animal
(uncommon)
-goal: to keep clinical signs away using the lowest effective medication doses
-chronic medications are “cruise control” drugs— administered when the situation is
stable and patient is comfortable, breathing well, and eating
a. Confirmation of diagnosis if unclear (should have been done during acute phase)
b. Elimination of cause when possible (e.g. PDA surgical ligation. Pulmonic stenosis 
valvuloplasty. Dilated cardiomyopathy in any cat or in any dog other than Doberman,
Boxer, and Great Dane taurine supplementation if deficient (500-1000 mg PO b.i.d.)
c. Medication
Standard long-term treatment consists of diuretic, an ACE inhibitor, a mildly to
moderately salt-restricted diet if the patient enjoys it, and pimobendan in many instances.
Additional treatments may be added if warranted based on recurrent CHF, concurrent
arrhythmia, etc.
-diuretics
Delay recurrence of fluid accumulation. Most patients depend on this above
all to remain free of clinical signs and out of trouble.
Caution: diuretics that have been given for months or years should never be
stopped acutely without supervision; a “rebound effect” of intense sodium resorption and
water retention risks recurrent CHF and is expected when diuretics have been given for
2-4 weeks or longer.
FUROSEMIDE 0.5 to 3 mg/kg PO every other day to three times daily.
Usually begin with 1-2 mg/kg PO b.i.d. Can adjust downward if patient is free of
edema/effusion and eating a diet that is moderate to low in salt. May eventually (usually
weeks to months) need to adjust upwards if CHF recurs.
SPIRONOLACTONE 0.5 to 2 mg/kg PO b.i.d. Usually added as a second
diuretic if furosemide alone fails to control signs of CHF, in cases with concurrent
hypokalemia notably. Chronically, using 2 diuretics is better than just high doses of a
single one because they work on different parts of the nephron.
-ACE inhibitors
Mild arterial dilators and mild sodium resorption inhibitors
ENALAPRIL and BENAZEPRIL 0.5 mg/kg PO s.i.d. to b.i.d. Can begin s.i.d. for 1-2
weeks and increase to b.i.d. if marked azotemia has not occurred (i.e. if
creatinine is less than two-fold elevated).
-pimobendan
Positive inotrope, vasodilator
VETMEDIN 0.3 mg/kg or less PO b.i.d. Drug of choice for CHF associated with dilated
Cardiomyopathy in Dobermans (absence of benefit in DCM in Cocker spaniels; unknown
in other breeds) and degenerative/myxomatous mitral valve disease. Optimal time for
start of administration has not been investigated, nor has patient profiling bee doe to
identify whether certain subgroups (notably of dogs with degenerative/myxomatous mitral
valve disease) benefit more than others. Note: this excellent and powerful drug has
profound beneficial effects, including improvement of appetite and demeanor, that are
useful in patients with end-stage heart disease. A stereotypical example is a Doberman
dog that presents for the first time with severe dyspnea and cyanosis that physical exam,
thoracic radiographs, and echocardiography prove is caused by dilated cardiomyopathy
causing severe pulmonary edema. Another classic example is a Cavalier King Charles
Spaniel that has had a murmur due to mitral valve regurgitation for the last 3 years and
who experienced dyspnea, coughing, and restlessness due to cardiogenic pulmonary
edema 1 year ago. Successful treatment with furosemide and an ACE inhibitor at that
time brought a normal quality of life, but relapse with pulmonary edema 4 months ago,
and again this week, this time with a loss of appetite and greater lethargy than ever
before. These 2 patients are emblematic of dogs that respond extremely well to the
addition of pimobendan therapy; many owners describe renewed vigor and stamina in
their dogs not seen for months or years, but others fail to improve meaningfully and some
deteriorate rapidly despite therapy. It is important when considering this drug to realize
this heterogeneity of response, especially when an owner cannot afford pimobendan and
is considering euthanasia on financial grounds (of a patient that could otherwise do
extremely well on furosemide and an ACE inhibitor alone).
-digoxin
Positive inotrope, negative chronotrope, autonomic and neurohormonal modifier
LANOXIN or CARDOXIN 0.003 mg/kg PO b.i.d.; s.i.d. if pre-existing mild
chronic renal failure or if signs of intolerance. Most effective with
supraventricular arrhythmias like atrial fibrillation—delays conduction through the AV
node, making the AV node more of a “barrier” and preventing excessively rapid
ventricular rates. Positive inotropic effect is mild. The 4 cardinal signs of digoxin toxicity:
vomiting, diarrhea, lethargy, loss of appetite. ALL clients whose pets are taking this drug
must be told to watch for these signs. If any of these signs occurs, the digoxin needs to
be stopped for 48 hours and restarted at half the dose; the risk of ongoing treatment in
the face of toxicity is much, much greater than the risk of stopping the drug for a few
days. The benefits of digoxin therapy are usually subtle; IV administration is therefore not
warranted.
-beta-blockers
Negative chronotrope; negative inotrope at higher doses
If CHF has been present, these drugs must be used with extreme caution (add
at the very, very lowest doses written below, and titrate up slowly over several weeks
while being very vigilant for recurrence of CHF). The minor decrease in contractility from
beta-blockers can be enough to push these patients back into CHF. However, if welltolerated, beta-blockers may increase survival in heart failure patients.
In contrast, if CHF has never been present and these drugs are being used for their
antiarrhythmic properties, then the usual published doses are appropriate.
Negative side-effects (signs of intolerance or excessive dose): lethargy, inappetence,
recurrent CHF.
ATENOLOL 0.25 to 1 mg/kg PO s.i.d. to b.i.d. (based on heart rate
monitoring at home and at rechecks)
CARVEDILOL 0.1 mg/kg PO b.i.d. Older: PROPRANOLOL.
-calcium-channel blockers
Negative chronotrope and negative inotrope; some reported positive lusitropy
(increases the myocardium’s relaxation [diastolic] properties)
Calcium channel blockers have similar indications and precautions for usage
as do the beta-blockers. In addition, their purported ability to increase myocardial
relaxation has led to their widespread use in patients with diseases where this is the
central problem (e.g. hypertrophic cardiomyopathy of cats).
Most common side-effect = vomiting.
DILTIAZEM 1.5 mg/kg PO t.i.d., or if sustained-release formulation (e.g. Cardizem CD),
5-10 mg/kg PO s.i.d.
-pure arterial dilator
Usually added later, if recurrent CHF despite high-dose diuretics
HYDRALAZINE 1 mg/kg PO b.i.d.
-low-salt diet
Perhaps one of the most misused forms of therapy in congestive heart failure.
1. Never introduced during the acute CHF episode; animal needs to eat what is familiar.
Always introduced only if the animal is eating well.
2. Sole purpose is to reduce need for diuretic. Less sodium in means less sodium out.
Therefore, also of no use (and possibly detrimental) prior to CHF. No such thing
as “prophylactic” low-sodium diet.
3. Always weaned onto, unless patient loves it immediately. Owner must be instructed to
change gradually over several days.
4. Many premium geriatric, renal, and high-fiber foods are quite salt-restricted (at levels
appropriate for CHF patients) but can be calorie-restricted, which risks worsening
cardiac cachexia. Therefore, caloric intake and lean body weight must be
monitored.
5. Treats can be a massive source of sodium (dog biscuits, chew treats, and the like);
dry rice cakes, baby carrots, and bits of roasted chicken or beef without salt are
good alternatives. Excellent resource: Tufts University nutrition service: Google
Tufts + veterinary + HeartSmart
6. Above all, and most importantly: it doesn’t matter how beneficial the diet is
if it sits on the shelf. Patients may need to be coaxed to eat what’s good for
them, but if that does not work, then the appetite must not be sacrificed.
-exercise restriction
Patients who have had acute CHF and are controlled chronically rarely benefit
from excessive exercise, which may precipitate an acute crisis. However, mild regular
physical activity can help these often older patients who may be obese or arthritic.
Some rules of thumb regarding exercise restriction:
1. Clients may think that more exercise is better for the heart, because of what we are told
about our own cardiac fitness. Clients must be told that when CHF occurs, an analogy
can be made to a person who has recovered from a heart attack: mild exercise is good,
but vigorous activity may put dangerous strain on the heart.
2. Leash walks (for dogs) and regular activity (for cats) is acceptable; encouraging the animal
to do more (throwing a ball over and over for a dog, or playing with toys to get a cat
excited) should probably be reduced, again to minimize risk. This does not mean the
extreme of total confinement. Rather, a bit less activity than before, and if the owner
notes sluggishness, dyspnea, or a long time to recover from the activity, then they must
understand that the animal has exceeded its capacity and should not be pushed to the
same extent again.
3. Ultimately it is an individual approach that is highly dependent on owner-pet interaction.
Excessive restriction is unnecessary, but owners must be aware that the joy of intense
activity comes at the cost of increased risk of problems.
d. Monitoring of complications: for most heart diseases of dogs and cats, the first recheck will be
7-14 days after the acute crisis (history to evaluate appetite and energy level; physical exam;
urea, creatinine, and electrolyte levels; thoracic radiographs if question about resolution of edema
or effusion). Then, subsequent rechecks dictated by patient’s stability; in general, re-evaluate
every 3-6 months, more often if complications. At each recheck, in addition to complete history
and examination, special attention should be paid to the following points for heart failure patients:
-habitus
-appetite
-electrolytes
-renal function
-cardiac rhythm
-recurrence of congestive heart failure? Or signs masquerading as CHF?
Going from acute, life-saving emergency treatment to long-term, chronic treatment
Acute= animal is in sufficient distress, usually respiratory, that you feel continuous
monitoring is necessary (hospitalization)
Chronic= animal seems sufficiently stable that oral, outpatient treatment is acceptable
Transition is often from injectable to oral forms of drugs (specifically, furosemide), so this takes
place when the acute phase has been controlled and, typically, once the patient is breathing
better. Ideally the patient should also have a return of appetite, but this can be difficult in the
hospital setting, especially with cats ( have owners hand-feed when visiting).
Typical sequence (usually during 2-4 days): Acute CHF crisis  acute treatment  good
response  switch to oral treatment when eating  stable, alert  home with oral medication
Diuretics summary
Class
Example
Loop
Furosemide,
torsemide
Thiazide
Hydrochlorothiazide
K-sparing
Spironolactone
Site of action
Mode of action
ascending loop of blocks Na
Henle
resorption
distal convol. Tubu decreases Na
permeability
distal tubule
blocks aldosterone receptors
Ions lost
Na, K, Cl, HCO3,
Ca
Na, K, Cl
Na, Cl
Notes:
● Note the critical distinction between acute and chronic treatments. Introducing low-salt food for
the first time during the acute phase is totally inappropriate, for example—the patient needs to
eat. Conversely, giving high-dose furosemide for a long time also is inappropriate—the kidneys
and electrolytes will be affected needlessly. Therefore, it is essential to treat according to acute or
chronic stages of heart failure.
● Note the permanence of the underlying heart problem but not of clinical signs—heart disease
stays, even though signs of heart failure have resolved. But animal was uncomfortable because
of heart failure, not underlying cause. Therefore, goal of treatment is good quality of life (which is
usually attainable), not cure (which often is not).
9. Prognosis, outcome in congestive heart failure
The prognosis for heart failure is usually fair to guarded. Most often, the underlying cause
(cardiac lesion) is irreversible and progressive. However, patients who respond well to medication
can expect a good quality of life.
Lifespan is highly variable, and based on the underlying cause. Patients with chronic mitral valve
endocardiosis as the cause for their CHF will live hours to many years, depending on severity at
time of presentation, response to treatment, complications, and owner diligence.
Dogs with dilated cardiomyopathy (DCM), unless it is taurine-responsive, will generally fall into
one of 3 groups: one third of dogs with DCM and CHF will die in the hospital during treatment for
the acute crisis; one third will live for days to weeks but show signs of recurrent CHF or
intolerance to medications, and either die or be euthanized within a few weeks; and one third will
do well and live for months to a year or more. Dobermans tend, in general, to not fare as well as
the average.
10. Follow-up
Routine follow-up typically includes physical exam, renal/electrolyte blood profile, and if
respiratory effort is unclear, thoracic radiographs, at 10-14 days after acute CHF, then periodically
every 2-6 months based on adequacy of response to treatment and owner financial and logistical
concerns. This needs to be clear to owners at the time of admission.