Aminophylline for Dogs

Aminophylline is a methylxanthine drug, a soluble salt of theophylline, theophylline ethylenediamine.

It has 79 percent of theophylline's potency on a mg-for-mg basis (100 mg aminophylline equivalent to
79 mg theophylline). The principal use of aminophylline is as a bronchodilator to provide symptomatic
relief from reversible obstructive airway disease (like asthma in people and in cats, bronchitis in dogs).
The pharmacodynamic effects of aminophylline are to relax smooth muscle of the airways and
pulmonary vasculature, stimulate the CNS, induce diuresis, increase gastric acid secretion, reduce
lower esophageal sphincter pressure, and inhibit uterine contractions. Its mechanism of action was
formerly thought to be due to phosphodiesterase inhibition, increasing cAMP; however, it is now
thought to work by either inhibiting intracellular adenosine, stimulation of endogenous catecholamine
release, antagonism of prostaglandins, mobilization of intracellular Ca++, or through a -adrenergic
agonist mechanism. It is readily absorbed from the gastrointestinal tract after ingestion and distributes
principally into non-fatty tissues. Aminophylline is 85 to 90 percent metabolized by the liver and is
excreted via the kidneys.
In the United States, aminophylline is a prescription drug.
This drug has not been specifically approved and labeled for use in animals by the Food and Drug
Administration. It can be prescribed legally by veterinarians as an extra-label drug.
BRAND NAMES AND OTHER NAMES
This drug is registered for use in humans only.
Human formulations: Various generic preparations exist. Manufacturers include Abbott, Balan, Bioline,
Roxane, Searle and URL.
Veterinary formulations: None
USES OF AMINOPHYLLINE
Aminophylline is used for bronchodilation in the treatment of bronchitis and asthma (cats). It is also
used in the symptomatic relief of pulmonary edema. Aminophylline has been used as a CNS stimulant
(analeptic function) such as in the treatment of apnea in neonates and as a cardiac stimulant in heart
failure.
PRECAUTIONS AND SIDE EFFECTS
Aminophylline should not be used in animals with known hypersensitivity or allergy to the drug. Liver
disease will reduce clearance and prolong effects so aminophylline should be used with caution in
animals with hepatic dysfunction. Aminophylline should be used with caution when cardiac disease or
cardiac arrhythmias are present, though dogs do not seem to be susceptible to aminophylline's
arrhythmogenic effects.
High doses of aminophylline may cause toxicity. Toxic signs include ventricular dysrhythmias,
restlessness and convulsions.
DRUG INTERACTIONS
Injectable aminophylline is compatible with all IV solutions except those containing 10 percent
fructose or invert sugar solutions.
Ketoconazole, rifampin, and loop diuretics are some drugs that may reduce the plasma level of

aminophylline. Calcium channel blockers, cimetidine, corticosteroids, and ephedrine are some drugs
that may increase plasma aminophylline levels.
The CNS effects of benzodiazepines and aminophylline oppose each other. Because of this,
aminophylline can be used to reverse excessive sedation resulting from benzodiazepines.
B-adrenergic agents are synergistic with aminophylline and aminophylline may augment the
arrhythmogenicity of certain anesthetic agents, like halothane. Coadministration of aminophylline and
ketamine potentiates ketamine's seizurogenic effects.
Aminophylline will, to some extent, antagonize the anesthetic effects of propofol.
HOW AMINOPHYLLINE IS SUPPLIED
Aminophylline is available in 100 mg and 200 mg immediate release tablets and a 105 mg/5 ml oral
liquid. Injectable aminophylline is available in a 250 mg/10 ml concentration. In addition,
aminophylline is available as 250 mg and 500 mg suppositories.
DOSING INFORMATION
In dogs, aminophylline is dosed at 6 to 11 mg/kg PO, IM, or IV every 8 hours. Be aware that the IM
injection is painful.
In cats, aminophylline is dosed at 5 mg/kg PO every 8 to 12 hours.
REFERENCES
Drug Facts and Comparisons, 57th Edition. 2003, pp 734-8
Boothe DM. Anticonvulsants drugs and analeptic agents. In Adams HR (editor), Veterinary
Pharmacology and Therapeutics, 8th Edition. 2001, pp 376-7
Hamlin RL, Sally JL: Lack of arrhythmogenicity of aminophylline in dogs. J Vet Pharmacol Therap.
1993, 16:15-22
Plumb, DC. Veterinary Drug Handbook, 4th Edition. Pharma Vet Publishing, White Bear Lake, MN.
1995.
Veterinarians frequently prescribe aminophylline for dogs suffering from asthma or bronchitis even
though it is not currently approved by the FDA for use in animals. Aminophylline belongs to a class of
drugs called bronchodilators, used to relax the smooth muscle wall in the airway and allowing
unrestricted air passage.
Dosage for Dogs
Aminophylline is available by prescription for dogs. It is available in tablets, oral liquid, injection and
suppository form. Typical dosage is 3 to 5 mg per pound every 8 hours.
Side Effects of Aminophylline for Dogs
A dog on aminophylline can experience side effects such as vomiting, diarrhea, anxiety or nervousness,
insomnia, or increased hunger, thirst and urination. Side effects may subside with continued therapy or
may require dosage adjustments.

Precautions:
Caution should be used when giving aminophylline to dogs with seizure disorders. Medications used
to treat seizures can lessen the effectiveness of this drug.
Animals with hypothyroidism, liver or kidney disease or congestive heart failure should use
aminophylline with caution as it can cause problems with these conditions.
Aminophylline should not be given to dogs that are pregnant or nursing or to dogs who are allergic to
this class of medication.
Although not approved by the FDA for use in dogs, aminophylline can be used with care in the
treatment of canine asthma and bronchitis. As with other prescription medications, dosing instructions
should be followed carefully.
Treating Congestive Heart Failure in Dogs With Vetmedin
Read more: Treating Congestive Heart Failure in Dogs With Vetmedin
Despite a diagnosis of congestive heart failure, dogs can live long happy lives. Today's medications aid
heart health for years. With dietary changes and prescription medications like Vetmedin, your dog can
remain energetic and comfortable.
Understanding Congestive Heart Failure
With congestive heart failure, dogs' lungs and chest cavity retain fluids because the heart is not
pumping as effectively. Congestive heart failure is common in large breeds like Great Danes and
Mastiffs, but all breeds can be susceptible to this disease. In most cases of congestive heart failure,
dogs usually have an underlying disease or genetic predisposition.
Keep Watch for Common Symptoms
In cases of congestive heart failure, dogs show clear symptoms. These common signs include:
Coughing
Difficulty breathing
Dizzy spells
Sudden fatigue
Weight loss
Some congestive heart failure dogs will be actively playing and suddenly drop to the ground wheezing
and unable to catch his/her breath. If this happens, seek veterinary care immediately.
Vetmedin for Congestive Heart Failure
When treating congestive heart failure, dogs respond well to the cost-effective heart medication known
as Vetmedin. Vetmedin works to expand the heart's blood vessels allowing blood to travel properly
throughout the body.
Once your pet is taking Vetmedin, you should see improvements in seven days.
Read more: Treating Congestive Heart Failure in Dogs With Vetmedin
Dog Congestive Heart Failure Prognosis
Dog congestive heart failure occurs when fluid builds up in your dog's chest cavity and compresses his
heart. It usually happens as a result of structural abnormalities in the heart muscle. Here's what you

should know about canine congestive heart failure.

Causes of Congestive Heart Failure in Dogs
There are a number of factors that can contribute to congestive heart failure in dogs. If your dog is born
with congenital heart defects, that can contribute to congestive heart failure. Heartworm infestation can
contribute to congestive heart failure, as can arrhythmia. Other causes of canine congestive heart failure
include:
Cardiomyopathy
Degeneration of the valves of the heart
Pericardium diseases affecting the membrane around the heart
Dogs of any age, breed or gender can develop congestive heart failure. However, the large and giant
breeds, which are also prone to dilated cardiomyopathy, are especially prone to congestive heart failure
as a result of their condition.
Congestive heart failure usually occurs in older dogs, over the age of eight years. Younger dogs may
develop this condition, though it's usually a result of birth defects in these animals.
Symptoms of Congestive Heart Failure in Dogs
Congestive heart failure causes your dog to experience chronic fatigue, since it reduces the amount of
blood being pumped through his body. He may accumulate fluid in his lungs, chest cavity and
abdomen. Symptoms of congestive heart failure include labored breathing, coughing, shortness of
breath, fatigue and weight loss.
Diagnosing Congestive Heart Failure in Dogs
Your vet will perform a complete physical exam and take your dog's medical history, if he doesn't
already have it. He may need to take X-rays, EKGs and ultrasounds to determine the extent of the
damage to your dog's organs. Blood pressure measurements will give your vet an idea of how well your
dog's heart is functioning at the time of the exam.
Treating Canine Congestive Heart Failure
Your dog may require hospitalization, especially if his heart failure is advanced. Your vet will
administer diuretic drugs to help your dog excrete any accumulated fluid from his chest, lungs or
abdomen. Nitroglycerin and enzyme inhibitors can help improve your dog's heart function.
Your dog will need to go on a new, low sodium diet. Your vet may recommend dietary supplements.
Your dog will also need to restrict himself to gentle exercise, since congestive heart failure can make
him get tired very easily. Follow your vet's instructions and administer all medications as directed.
Congestive Heart Failure Prognosis for Dogs
Your dog won't show many symptoms until his congestive heart failure becomes advanced. By this
time, it's generally too late for treatment to make any significant impact on your dog's health. While
beta blockers and other drugs can help to slow the progression of many canine heart conditions, by the
time your dog starts showing symptoms, his heart may be too damaged and drugs may not extend his
life. Most dogs with congestive heart failure die within six months to a year of diagnosis.
Read more: Dog Congestive Heart Failure Prognosis
ACE Inhibitors for Congestive Heart Failure Treatment in Dogs

Read more: ACE Inhibitors for Congestive Heart Failure Treatment in Dogs
The medications used in canine congestive heart failure treatment are ACE inhibitors, diuretics and
drugs such as digitalis. Supplements such as vitamin-B, taurine and coenzyme Q are also found to be
beneficial.
Congestive Heart Failure
As a dog ages, the muscles of the heart weaken and his heart fails to pump efficiently. There is an
insufficient amount of blood pumped through the dogs body. To compensate for the insufficient blood
supply, the heart beats faster resulting in more damage. This slowing of the heart leads to a condition
known as congestive heart failure or CHF. The condition can also strike younger dogs and may be
hereditary. CHF is fatal as there is still no known cure.
Symptoms of Congestive Heart Failure
Symptoms of congestive heart failure in dogs include:
Fatigue
Fainting after mild exercise
Discoloration of the gums and tongues of a bluish color
Pale colored gums
Decrease in physical activity
Coughing
Loss of appetite
Rapid breathing
Abdominal swelling
Loss of weight
Impaired function of the liver, lungs and kidneys
Labored breathing
Treatment of Congestive Heart Failure in Dogs
You should feed your pet a low salt diet if he has been diagnosed with congestive heart failure. You will
have to administer medications that improve heart function and reduce fluid accumulation in the lungs.
Angiotensin Converting Enzyme (ACE) inhibitors inhibit the action of the enzyme Angiotensin. This
enzyme causes the constriction of blood vessels and increases the pressure on the heart.
ACE inhibitors inhibit this action and allow the blood vessels to dilate allowing blood to flow easily
through them and reducing the amount of work the heart has to do. These medications thus help reduce
blood pressure and volume, ease the stress on the heart, and halt its deterioration.
ACE Inhibitors
ACE inhibitors such as enalapril maleate, lisinopril and benazepril are sold under the brand name of
Enacard, Prinivil and Fortekor respectively. ACE inhibitors have improved the clinical signs of canine
congestive heart failure and increased the life expectancy of affected dogs. These drugs can be given on
an empty stomach or with food.
Side Effects of ACE Inhibitors

Side effects of ACE inhibitors include:

Vomiting
Diarrhea
Impaired kidney function
Increase in potassium levels in the blood
Hypotension
Abnormalities in blood and urine tests
Usual Dosage of ACE Inhibitors
If you have to administer enalapril to your pet, the usual dosage is 0.5 mg for every kilogram of body
weight twice a day. Benazepril should be given only once daily and the recommended dosage is 0.25 to
0.5 mg for every kilogram of body weight. Dogs medicated with ACE inhibitors show decreased
pulmonary edema (fluid in the lungs) and a lower class of heart failure.
It is possible for your pet to live a full life for many years even after being diagnosed with congestive
heart failure if you administer the proper medications, monitor his diet, ensure he has no salt in his food
and restrict his exercise to gentle exercise only. You should also ensure that he is regularly checked by
the vet as a pet with CHF should be monitored regularly.
Read more: ACE Inhibitors for Congestive Heart Failure Treatment in Dogs
Systemic Therapy of Airway Disease
-Adrenergic Agonists
The -adrenergic agonists have beneficial effects in the treatment of bronchoconstrictive respiratory
tract diseases (see -Adrenergic Receptor Agonist DrugsTables). Bronchial smooth muscle is
innervated by 2-adrenergic receptors. Stimulation of these receptors leads to increased activity of the
enzyme adenylate cyclase, increased cAMP, and relaxation of bronchial smooth muscle. Stimulation of
receptors on mast cells decreases the release of inflammatory mediators from mast cells, but other
inflammatory cells are not suppressed. There is some evidence that -adrenergic receptor agonists
increase mucociliary clearance in the respiratory tract.
-Adrenergic Receptor Agonist Drugs
Drug
Dosage
Epinephrine
Dogs: 0.050.5 mg, intratracheally or IV

Cats: 0.1 mg, IV or IM

Large animals: 0.1 mg/kg, IV, SC, or IM

Isoproterenol
Dogs: 0.10.2 mg, IM or SC, qid

Cats: 46 g, IM, every 30 min as needed

Horses: 0.4 g/kg, IV (diluted)

Terbutaline
Dogs, cats: 0.1 mg/kg, SC, every 4 hr, or 0.03 mg/kg, PO, tid

Horses: 0.0033 mg/kg, IV, or 0.20.6 mg/kg, PO, bid

Albuterol
Dogs: 0.05 mg/kg, PO, tid

Horses: 8 g/kg, PO, bid

Clenbuterol
Horses: 0.83.2 g/kg, PO, bid
Epinephrine (adrenaline) stimulates and receptors, resulting in pronounced vasopressive and
cardiac effects in addition to bronchodilation. Epinephrine is reserved for emergency treatment of lifethreatening bronchoconstriction (eg, anaphylaxis). The nonspecific stimulation of other receptors and
its short duration of action make it unsuitable for longterm use. Epinephrine is available as a 1 mg/mL
solution. Its onset of action is immediate, and the duration of effect is 13 hr.
Isoproterenol is a potent -receptor agonist. It is selective for receptors, but cardiac (1) effects make
it unsuitable for longterm use. It is administered by inhalation or injection and has a short duration of
action (<1 hr). For emergency relief of bronchoconstriction in horses, it is given by slow IV solution at

a dilution of 0.2 mg/50 mL of saline. Administration is discontinued when the heart rate doubles.
Terbutaline is a 2-receptor agonist similar to isoproterenol but longer acting (68 hr). For cats with
feline asthma that experience frequent, severe bronchoconstrictive episodes while on chronic
glucocorticoid therapy, injectable terbutaline can be dispensed to clients with instructions to administer
0.01 mg/kg, SC, to abort episodes at home within 15 min. An increase in the cat's heart rate to 240
bpm and a 50% decrease in respiratory rate indicates a positive effect. Terbutaline also can be given as
chronic oral therapy at 0.625 mg/cat, bid ( of a 2.5 mg tablet). It should not be used in cats with
hypertrophic cardiomyopathy or glaucoma, in which 2-receptor stimulation would be detrimental. It
may be used concurrently with methylxanthine bronchodilators.
Albuterol (salbutamol) is similar to terbutaline and is used systemically in dogs and horses.
Clenbuterol is used in the treatment of recurrent airway obstruction in horses. Results of efficacy
studies for bronchoconstriction have been conflicting, but clenbuterol appears to significantly increase
mucociliary transport in horses with the disorder. The dosage is increased gradually until a satisfactory
clinical response is seen. If there is no response at the highest recommended dose, the horse is
considered to have irreversible bronchospasm. The most common adverse effects are tachycardia and
muscle tremors. Clenbuterol inhibits uterine contractions, so it should be used during late pregnancy
only if this effect is desired for obstetric manipulations. Clenbuterol is also a repartitioning agent; it
directs nutrients away from adipose tissue and toward muscle. The result is increased carcass weight,
increased ratio of muscle to fat, and increased feed efficiency. Because there is a significant human
health risk from clenbuterol residues, it is banned in food animals and should not be used in horses that
may be sent to slaughter.
Methylxanthines
The methylxanthines, particularly theophylline, are bronchodilators (see Methylxanthine
BronchodilatorsTables). Once the mainstay of human asthma therapy, theophylline has a high incidence
of adverse effects, and its use has diminished with the development of local drug delivery by metered
dose or disk inhalers. The methylxanthines have a variety of pharmacologic effects on various organ
systems, including bronchial smooth muscle relaxation, CNS stimulation, mild diuresis, and mild
cardiac stimulation.
Table 3
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Methylxanthine Bronchodilators
Drug
Dosage
Theophylline (parenteral)
Dogs: 10 mg/kg, IV (slow) or IM

Horses: 15 mg/kg, IV (slow)

Theophylline (oral)
Dogs: 57 mg/kg, PO, tid

Cats: 3 mg/kg, PO, bid

Horses: 1015 mg/kg, PO, bid

Theophylline (extended-release tablets)
Dogs: 20 mg/kg, PO, sid

Cats: 25 mg/kg, PO, sid

Horses: 15 mg/kg, PO, sid

Aminophylline (parenteral)
Dogs: 10 mg/kg, IV (slow)

Cats, horses: 5 mg/kg, IV (slow)

Aminophylline (oral)
Dogs: 10 mg/kg, PO, tid

Cats: 5 mg/kg, PO, bid

Horses: 15 mg/kg, PO, bid

The respiratory effects of methylxanthines are due to several cellular mechanisms. Antagonism of
adenosine is currently thought to be the most important action. Adenosine induces bronchoconstriction
in asthmatic animals and antagonizes adenylate cyclase. Adenylate cyclase is responsible for the
synthesis of cAMP, which controls bronchial smooth muscle relaxation and inhibits the release of
inflammatory mediators from mast cells. Methylxanthines also inhibit phosphodiesterase, which further
increases intracellular cAMP. They also inhibit calcium mobilization in smooth muscle, inhibit
prostaglandin production, augment the release of catecholamines from storage granules, and increase
the availability of calcium to contractile proteins of the heart and diaphragm. In addition to promoting
bronchial smooth muscle relaxation, methylxanthines decrease the release of inflammatory mediators
from mast cells and increase mucociliary transport.
Theophylline is available in several formulations including injectable, aqueous solutions, elixirs,
tablets, and capsules. Theophylline base is poorly soluble in water and often results in GI irritation
when administered PO. Aminophylline is a theophylline salt that is 7886% theophylline. It is more
water soluble and results in less GI irritation. Other theophylline salts, such as oxytriphylline (a choline
salt), are available, and their theophylline content must be considered when developing a drug dosage
regimen.
Several sustained-release formulations of theophylline are suitable for use in dogs and cats and may be
administered less frequently than the regular formulations. After oral administration, theophylline is
rapidly and completely absorbed. Therapeutic plasma concentrations, extrapolated from people, are 5
20 g/mL. Animals are sensitive to high concentrations of theophylline, especially after rapid IV
administration, and toxicity may be seen with concentrations <20 g/mL. Theophylline tablets may
become trapped in bezoars (such as hairballs in cats), and continued absorption can result in toxicity.
Cardiac arrhythmias, CNS excitement, tremors, convulsions, and GI irritation may be seen.
Theophylline undergoes enterohepatic recirculation, so activated charcoal is recommended if clinical
signs are present, no matter how long after the drug was administered. Theophylline metabolism is
inhibited by erythromycin, cimetidine, propranolol, enrofloxacin, and marbofloxacin; concomitant
therapy can result in theophylline toxicity. Theophylline metabolism is induced by rifampin and
phenobarbital, which may necessitate increasing the dose of theophylline.
Theophylline is used for the treatment of both cardiac and respiratory diseases in dogs and cats.
Theophylline is also used in the management of intrathoracic collapsing trachea and various forms of
canine bronchitis, but it is less effective than glucocorticoids such as prednisone. Theophylline or
aminophylline was used in horses in the management of recurrent airway obstruction, but efficacy was
often poor and their use has been replaced by -agonist bronchodilators. There is little clinical
experience with the use of theophylline in cattle; experimental evidence suggests that it is a poor
bronchodilator in this species.
Anticholinergic Drugs
The anticholinergic (parasympatholytic) drugs are effective bronchodilators that act by reducing the
sensitivity of irritant receptors and by inhibiting vagally mediated cholinergic smooth muscle tone in
the respiratory tract. Cholinergic stimulation causes bronchoconstriction; asthmatic individuals appear
to have excessive stimulation of cholinergic receptors.
Atropine is primarily used as a preanesthetic, to prevent bradycardia and reduce airway secretions, and
as emergency therapy of dyspneic animals with organophosphate intoxication. Atropine is also used for

acute bronchodilation in horses, in which a low IV dosage (0.014 mg/kg) is more effective and less
toxic than IV theophylline. A test dose of 0.022 mg/kg may also be used to determine prognosis in
horses with recurrent airway obstruction; if pulmonary function does not improve with a test dose of
atropine, successful management with bronchodilators is unlikely. Atropine should be used with
caution, as even low doses may cause tachycardia, ileus, neurologic derangement, and blurred vision in
horses.
Glycopyrrolate is twice as potent as atropine in people and does not cross the blood-brain barrier. Its
onset of action is slower than atropine, but its duration of effect is longer. Information about use in
horses is sparse, but doses of 23 mg can be given IM, bid-tid.
Glucocorticoids
The glucocorticoids inhibit the release of inflammatory mediators from macrophages and eosinophils
but do not inhibit the release of granules from mast cells. Glucocorticoids decrease synthesis of
prostaglandins, leukotrienes, and platelet-activating factor, which play important roles in the
pathophysiology of respiratory tract diseases. Studies suggest glucocorticoids enhance the action of
adrenergic agonists on 2-receptors in the bronchial smooth muscle. Because of immunosuppressive
effects, glucocorticoids are generally avoided in infectious respiratory diseases.
For severe attacks of canine bronchitis, feline asthma, or recurrent airway obstruction, parenteral
injection of glucocorticoids usually provides rapid relief. For chronic therapy in dogs, oral prednisone
is usually the drug of choice. Prednisone is a prodrug, as it is hepatically metabolized to the active drug
prednisolone. Pharmacokinetic studies have shown that cats and horses poorly metabolize prednisone
to prednisolone. In dogs, a typical anti-inflammatory dosage is 0.51.0 mg/kg, with chronic therapy on
an every-other-day basis. A similar dose of prednisolone can be used in cats; if prednisone is used,
higher doses may be necessary. Cats are somewhat resistant to the effects of glucocorticoids, and
dosages of prednisone of 1.0 mg/kg/day may be necessary for chronic therapy of feline asthma.
Alternatively, 20 mg of methylprednisolone acetate can be administered IM to asthmatic cats every 3
wk. For emergency treatment of dyspneic cats, a shock dose of an IV glucocorticoid (prednisone
sodium succinate, 510 mg/kg; or dexamethasone sodium phosphate, 12 mg/kg) should be used.
While prednisolone can be administered to horses, the small tablet sizes available make it inconvenient,
so equine formulations of oral dexamethasone (10 mg/450 kg) are recommended. The injectable
formulation of dexamethasone can be given IV to horses with acute bronchoconstriction and dyspnea.
Cyproheptadine
Because of serotonin's role in allergen-induced bronchoconstriction in cats, the serotonin antagonist
cyproheptadine (2 mg, PO, sid-bid) may be used as an adjunct to glucocorticoids and bronchodilators
to block bronchoconstriction in chronically asthmatic cats. Because of its long elimination half-life (12
hr), it requires several days to reach steady-state concentrations and may take 47 days to be clinically
effective. Cyproheptadine's serotonin antagonism in the appetite center stimulates appetite, so weight
gain may be a problem. Lethargy, depression, and increased appetite may occur within 24 hr of
initiating therapy.
Antimicrobial Therapy
Antimicrobial therapy may or may not be necessary in the treatment of airway inflammatory diseases.
Antimicrobial therapy should be started for cats with tracheo-bronchial cultures suggestive of a true
bacterial infection or those positive for Mycoplasma. Mycoplasma spp can be isolated from normal
dogs but are not found in normal cats. Doxycycline, azithromycin, and fluoroquinolones are effective
for treating Mycoplasma infections. Secondary bacterial infection from Streptococcus zooepidemicus

may exacerbate inflammatory airway disease in horses and can easily be treated with penicillin,
ceftiofur, or a trimethoprim/sulfonamide.
Antitussive Drugs
The afferent arc of the cough reflex receives input from sensory nerves in the bronchial and tracheal
airways. Airway irritation and inflammation stimulate the afferent nerves, which in turn activate the
cough center located in the medulla oblongata. Most of the antitussive drugs are opiates or opioids that
directly suppress the cough center in the medulla oblongata (see Antitussive DrugsTables). The
antitussive effect does not appear to be related to the binding of traditional opiate receptors.
Table 1
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Antitussive Drugs
Drug
Dosage
Morphine
Dogs: 0.1 mg/kg, IM, tid-qid
Codeine
Dogs: 12 mg/kg, PO, bid-qid
Hydrocodone
Dogs: 0.25 mg/kg, PO, bid-qid
Butorphanol
Dogs: 0.0550.11 mg/kg, SC, bid-qid or 0.0551.1 mg/kg, PO, bid-qid
Morphine is an effective antitussive at doses lower than the doses that produce analgesia and sedation.
It is not commonly used for antitussive activity due to adverse effects and the potential for abuse and
addiction. Morphine has poor oral bioavailability due to a significant first-pass effect by the liver.
Codeine is methylmorphine; methylation of morphine significantly improves the oral bioavailability by
reducing the first-pass effect. Codeine phosphate and codeine sulfate are found in many preparations,
including tablets, liquids, and syrups. Codeine has analgesic effects that are about one-tenth that of
morphine, but its antitussive potency is about equal to that of morphine. The adverse effects of codeine
are significantly less than those seen with morphine at antitussive doses. Toxicity (especially in cats) is
exhibited as excitement, muscular spasms, convulsions, respiratory depression, sedation, and

constipation. Codeine should not be used after GI tract surgery. The potential for addiction and abuse of
codeine is considerably lower than that for morphine.
Hydrocodone is chemically and pharmacologically similar to codeine but more potent. It is combined
with an anticholinergic drug (homatropine) to discourage abuse by people. It can be prescribed for
small animals but should be used with caution in cats.
Dextromethorphan is technically not considered an opiate because it does not bind to traditional opiate
receptors and is not addictive or analgesic. It is the d-isomer of levorphanol. The l-isomer of
levorphanol has addictive and analgesic properties. While recommended anecdotally for the treatment
of cough, a pharmacokinetic study in dogs demonstrated a short elimination half-life, rapid clearance,
and poor oral bioavailability, making its use as an orally administered cough suppressant in dogs
questionable.
Butorphanol, an opioid agonist-antagonist, is used as an analgesic and antitussive in dogs. It is more
potent than morphine as an analgesic and more potent than codeine as an antitussive. It may produce
considerable sedation. Because butorphanol has poor bioavailability, the oral dose in dogs is 10 times
the SC dose. Its use in cats is controversial.
Expectorants and Mucolytic Drugs
Expectorants and mucolytic drugs are used to increase the output of bronchial secretions, enhance the
clearance of bronchial exudate, and promote a productive cough. Saline expectorants are promoted to
stimulate bronchial mucous secretions via a vagally mediated reflex action on the gastric mucosa.
However, there are no well-designed studies that support these claims. Examples of these drugs include
ammonium chloride, ammonium carbonate, potassium iodide, calcium iodide, and ethylenediamine
dihydroiodide. Iodine-containing products should not be administered to pregnant, hyperthyroid, or
milk-producing animals.
Direct stimulants of respiratory secretions include the volatile oils, such as eucalyptus oil and oil of
lemon. They are believed to directly increase respiratory tract secretions. Their efficacy in animals is
unknown.
Guaifenesin (glyceryl guaiacolate) is a centrally acting muscle relaxant that may also have an
expectorant effect. It may stimulate bronchial secretions via vagal pathways. The volume and viscosity
of bronchial secretions does not change, but particle clearance from the airways may accelerate. It is a
common component of human cold remedies in combination with dextromethorphan.
N-acetylcysteine is available as a 10% solution that can be nebulized. Its mucolytic effect is due to the
exposed sulfhydryl groups on the compound, which interact with disulfide bonds on mucoprotein.
Acetylcysteine helps to break down respiratory mucus and enhance clearance. It may also increase the
levels of glutathione, which is a scavenger of oxygen free radicals. Aerosolization of acetylcysteine can
cause reflex bronchoconstriction due to irritant receptor stimulation, so its use should be preceded by
bronchodilator therapy.
Dembrexine is a phenolic benzylamine available in some countries for respiratory disease in horses.
The proposed effect is through an alteration of the constituents and viscosity of abnormal respiratory
mucus and an improved efficiency of respiratory clearance mechanisms. It also has an antitussive
action and enhances concentrations of antibiotics in lung secretions. It is supplied as a powder that is
sprinkled on the feed at a dosage of 0.33 mg/kg, bid.
Decongestants

Decongestants are commonly used in people for allergic rhinitis, but they are rarely used for this
purpose in animals. The -adrenergic agonist drugs cause local vasoconstriction in mucous membranes,
which reduces swelling and edema. They are used topically as nasal decongestants in allergic and viral
rhinitis, or systemically in combination with antihistamines as respiratory tract decongestants.
Antihistamines are effective for treatment of allergic rhinitis in people when combined with the adrenergic agonist drugs, but their effectiveness in animals has not been demonstrated. The topical adrenergic agonist drugs act within minutes with few adverse effects, but extended use may cause
rebound hyperemia and mucosal damage. Systemic administration can result in hypertension, cardiac
stimulation, urinary retention, CNS stimulation, and mydriasis. Systemic administration of
antihistamines often causes sedation.
Respiratory Stimulants
Doxapram stimulates the medullary respiratory center and the chemoreceptors of the carotid artery and
aorta to increase tidal volume. Other portions of the CNS are stimulated only when high doses are
administered. Doxapram is used primarily in emergency situations during anesthesia or to decrease the
respiratory depressant effects of opiates and barbiturates. Recommended dosages are 15 mg/kg, IV, in
dogs and cats, or 12 drops under the tongue of apneic neonates. In adult horses, the dosage is 0.51.0
mg/kg, IV, while foals are dosed carefully at 0.020.05 mg/kg/min, IV.
NEBULIZED BROCHODILATORS FOR DOGS AND CATS
Medication
Dosage
Reference
Isoetharine
0.5 - 1.0 ml of 1:3 saline dilution TID
Booth DM. Drugs affecting the respiratory system, in
Isoproterenol
0.5 ml of 1:200 dilution
King LG (ed): Textbook of Respiratory Disease in
Aminophylline
100 mg
Dogs and Cats, p. 229, 2004.
NEBULIZED ANTIBIOTICS FOR DOGS
Medication
Dosage
Reference
Gentamicin
50 mg / 3 ml
Bemis DA. Bordetella and Mycoplasma respiratory infections in dogs and
Gentamicin
4 - 6 mg / # / 3 - 4 ml NaCl
cats, Vet Clin North AM Small Anim Pract 22 (5), p. 1173, 1992 (all 4)
Kanamycin
250 mg / 3 ml
Sherding RG. Canine infectious tracheobronchitis, in Brichard SJ, Sherding
Polymyxin B
166,666 IU / 3 ml
RG (eds): Saunders Manual of Small Animal Practice, p.103, 2000.
Colistin
30 mg / 3 ml

McKiernan BC. Tracheobronchitis aerosol therapy (PT-59), Western

Veterinary Conference Notes, 2003. (gentamicin 4-6 mg/#)
NEBULIZED DRUGS FOR DOGS AND CATS
Medication
Dosage
Reference
Methylprednisolone sodium succinate (anti-inflammatory)
Ford RB. Infectious tracheobronchitis, in King LG (ed): Textbook
Saline
6 - 10 ml for 15-20 min SID-QID
of Respiratory Disease in Dogs and Cats, p. 364, 2004.
ANTIBIOTICS FOR AVIAN NEBULIZATION
Medication
Dosage (in 10 ml saline)
Reference
Amikacin Sulfate
50 mg for 15 min BID
Rupley AE, Manual of Avian Practice, p. 336, 1997
Carbenicillin
200 mg for 15 min BID
Cefotaxime
100 mg for 10-30 min BID-QID
Erythromycin
100 mg for 15 min TID
Gentamicin
50 mg for 15 min TID
Piperacillin
100 mg for 10-30 min BID-QID
Tylosin
100 mg for 10-60 min BID
ANTIFUNGALS FOR AVIAN NEBULIZATION
Medication
Dosage
Reference
Amphotericin B
1 mg/ml saline for 15 min SID-BID for 5-7 days
Rupley AE, Manual of Avian Practice, p. 505, 1997.
Clotrimazole
1% solution for 30-45 min SID for 3 days, off 2 days
Miconazole
Dilute in saline for 15-20 min BID
DRUGS IN METERED DOSE INHALERS
Medication
Dosage
Reference
BRONCHODILATORS - Beta2 Agonists
Dowling PM. Using metered dose inhalers in veterinary patients (PT-65),
Albuterol
180-360 ug every 20 min

Proc. Western Vet Conf, 2004. (albuterol 180-360 ug, salmeterol)

Albuterol
90 ug as needed up to QID
Padrid P. Feline Asthma: Diagnosis and Treatment, Vet clin North Am Small
Salmeterol
21 ug BID
Anim Pract 30(6), p. 1279, 2000. (albuterol 90 ug, fluticasone 220 ug BID
STEROIDS
Boothe DM. Drugs affecting the respiratory system, in King LG (ed): Textbk
Beclomethasone
200 ug TID-QID
of Respiratory Disease in Dogs and Cats, p. 229, 2004. (beclemethasone)
Fluticasone
110-220 ug BID
Johnson L. Prespectives and controversies in feline bronchial disease. Proc.
ANTICHOLINERGIC AGENTS
Atlantic Coast Vet Conf, 2003. (fluticasone 110 ug BID)
Ipratropium bromide
Dowling PM. Treatment options for feline asthma and canine bronchitis
MAST CELL STABILIZERS
(VET-321), Proc. Western Vet Conf, 2004.
Cromolyn Sodium
Nedrocromil
IVAX GENERIC DRUGS
Medication
Dosage
Albuterol sulfate inhalation solution
2.5 mg/3 ml - oral inhalation only
25 x 3 ml unit dose vials / box
Cromolyn sodium inhalation solution
20 mg/2 ml - aqueous solutoin for nebulization
30 x 2 ml unit dose vials / box
Ipratropium bromide inhalation solution
0.5 mg/ 2.5 ml unit dose vials / box
25 x 2.5 mlo unit dose vials / box
VALVULOPATIA MITRAL LA CINE
Noiuni generale
Valvulopatia mitral degenerativ (VMD) este una dintre cele mai frecvente cauze ale Insuficienei
cardiace la cine.
Afeciunea este frecvent diagnosticat la cine, cal, porc i excepional la pisic (Wendy Ware, 2009).
VMD se manifest la animalele de vrst adult i naintat, afectnd mult mai frecvent masculii (de
1,5 2 ori mai mult dect femelele).
Afeciunea afecteaz n special cinii din rasele de talie mic (sub 20 kg) i mai rar cinii de talie
medie.
Rasele frecvent afectate sunt: Pekinez, Teckel, Caniche pitic i mediu, Chihuahua, Pinscher, Fox terier,

Cocker spaniel i mai rar Dalmaian.

Valvulopatia mitral degenerativ poate evolua ca afeciune unic sau asociat cu valvulopatia
tricuspidian (30% din cazuri)(Ettinger S.J., 2010), valvulopatia tricuspidian izolat fiind o raritate
(Wendy Ware 2007).
Terminologia: degenerescen mitral mixomatoas, transformare mixomatoas, distrofie mucoid,
endocardioz, boal valvular cronic, valvulopatie mitral degenerativ. Toi aceti termeni se refer
la aceeai afeciune Valvulopatia mitral degenerativ.
Etiopatogeneza
Cauzele VMD sunt necunoscute fiind incriminai factori genetici.
Faptul c afeciunea afecteaz n mod special cinii din rasele de talie mic s-ar datora anatomiei
diferite fa de cinii din rasele de talie mare.
n cazul cinilor de talie mic, mitrala are form de semilun fa de cinii de talie mare la care
mitrala are aspect circular (Michele Borgarelli, 2011).
Morfopatologic se constat o distrofie de tip mixomatos care afecteaz n mod special valvulele i mai
puin aparatul tendinos sau inelul mitral.
Distrofia determin o ngroare progresiv a valvulelor i modificarea geometriei cu distrugerea n timp
a acestora.
Patogenetic, modificarea valvulelor determin o nchidere incomplet a valvei mitrale cu regurgitarea
sngelui n atriul stng pe timpul sistolei ventriculare.
Evoluia procesului distrofic afecteaz n timp i aparatul tendinos cu ruperea cordajelor i prolapsul
mitralei (n atriul stng).
Procesul patologic va determina o mrire a atriului stng i ulterior al ventriculului stng.
Regurgitarea sanguin determin o suprancrcare atrial stng cu creterea presiunii sanguine n
circulaia pulmonar.
Evoluia este cronic de luni sau chiar ani de zile, pacientul suportnd destul de bine modificrile
valvei mitrale mai ales dac volumul sanguin regurgitat nu este foarte mare.
Regurgitarea sngelui ctre atriul stng va determina o reducere a volumului sanguin ctre aort
tensiunea sanguin este n limite normal sau chiar redus.
Reducerea volumului sanguin prin aort declaneaz procese de adaptare prin:

Stimularea sistemului simpatic;

Atenuarea tonusului vagal;
Activarea sistemului Renin Angiotensin Aldosteron;
Activarea acestor sisteme duce la:
Tahicardie
Vasoconstricie

Retenie hidric.
Creterea presiunii la nivelul atriului stng determin o cretere a hormonilor natriuretici atriali
(element de diagnostic).
Toate acestea agraveaz boala primar i duc la decompensarea cordului cu apariia Insuficienei
cardiace.
Evoluia i Complicaii
Cei mai muli cini suport foarte bine afeciunea pn n fazele avansate cnd se declaneaz brusc
insuficiena cardiac congestiv.
Una dintre cele mai grave complicaii ale VMD este Hipertensiunea pulmonar.

Alte complicaii:
Tahiaritmiile pot determina o decompensare rapid a inimii cu apariia edemului pulmonar acut.
Sincopa; apare frecvent n evoluia VMD.
Aritmiile ventriculare sunt rar diagnosticate n cazul VMD. Apariia Fibrilaiei atriale =
prognostic grav.
Rupturile tendinoase agraveaz afeciunea i reprezint una dintre cauzele frecvente ale
decompensrilor cardiace.
Mrirea excesiv a atriului stng duce la compresiunea bronhiei stngi cu apariia tusei chiar n
absena insuficienei cardiace (Wendy Ware, 2009).
Dilataia excesiv a atriului stng poate duce la rupturi cu apariia tamponadei cardiace (urgen
medical).
Tabloul Clinic
VDM poate evolua asimptomatic foarte muli ani, fiind semnalate i cazuri asimptomatice toat viaa.
Diagnosticul VDM se stabilete n 3 situaii:

ntmpltor la un examen de rutin (forma asimptomatic);

Consecutiv apariiei simptomatologiei Insuficienei cardiace congestive (forma cronic);

n urgen Edemul pulmonar acut.

n prima situaie diagnosticul se stabilete pe baza decelrii suflului valvular pe zona de ascultaie a
mitralei.
n cele mai multe cazuri pacientul este adus la consultaie pentru simptomele insuficienei cardiace
stngi:
Dispnee
Oboseal limitarea capacitii de efort
Tuse
Rar: lipotimii, sincope, oc tamponada cardiac.
Dispneea se manifest prin tahipnee de intensitate variabil.
Tusea este scurt de tip avortat, de multe ori proprietarul aducnd cinele la medic deoarece acesta
are ceva n gt.
Tusea acut n lipsa simptomelor insuficienei cardiace stngi apare tardiv n evoluia bolii hipertrofia
atrial stng.
Tusea impune diagnosticul diferenial fa de:

Bronita cronic (emfizemul pulmonar cronic)

Neoplazii pulmonare

Hernia diafragmatic
O situaie aparte o reprezint tusea secundar:
Administrrii de inhibitori ai enzimei de conversie ai angiotensinei (Captopril, Enalapril,
Benazepril .a.);

Neoplasmelor (pacieni cu VMD care nu rspund la terapia specific, inclusiv la administrarea de

Pimobendan);
Alte cauze ale tusei: dirofilarioza, bronitele infecioase (de regul animalele sunt febrile),
bronitele alergice, eozinofilice .a.
Simptomatologia valvei mitrale ecraneaz simptomatologia valvei tricuspide (n situaia evoluiei
concomitente), aceasta din urm complicndu-se i cu apariia ascitei.
Examenul fizic

Diagnosticul valvulopatiei mitrale degenerative se stabilete pe baza ascultaiei decelarea suflului pe

zona de ascultaie a mitralei.
Zona de ascultaie a mitralei = zona de percepere a ocului apexian la nivelul hemitoracelui stng
(spaiile intercostale IV VI).
VMD evolueaz cu suflu holosistolic pe aria de ascultaie a mitralei.
Suflu holosistolic = suflu de intensitate egal pe toat perioada sistolei ventriculare (pauza mic).
Atenie ! De cele mai multe ori pacientul este examinat n criz de decompensare cardiac acut.
Aceasta se manifest cu tahicardie, frecvena cardiac putnd ajunge pn la 200 250 contracii/min.
Ori n cazul unei frecvene cardiace de 200 250 contracii/min 400 500 zgomote cardiace/min (1
contracie cardiac =
2 zgomote cardiace). n aceast situaie nu se poate stabili localizarea
suflului cardiac sistolic sau diastolic, la ascultaie percepndu-se doar un suflu continuu.
Ulterior, dup stabilizarea pacientului i reducerea frecvenei cardiace se poate stabili caracterul
suflului valvular.
Suflul ia natere la nivelul mitralei i se percepe la nivelul apexului cardiac dar el radiaz n toate
direciile fapt ce-l face decelabil pe toat suprafaa toracelui (stnga i dreapta).
Cu toate acestea, intensitatea este mult mai mare la nivelul focarului mitralei, loc n care se poate
decela i freamtul cardiac la palpaie.
ANTERIOR
DREAPTA
Dispoziia anatomic a valvelor la cine

Focarele de ascultaie valvular la cine

M mitrala; P sigmoida pulmonarei;
Ao. sigmoida aortei; T - tricuspida

Diagnosticul suflurilor cardiace

(Wendy Ware, 2007)
Diagnosticul diferenial al suflurilor
localizare i aspect
DSV defect septal ventricular; SsAo stenoz subaortic;
SAo stenoz aortic, PCA persistena canalului arterial;
IM, IT insuficien mitral, tricuspidian (Wendy Ware, 1992)
Valvulopatia tricuspidian se diagnostic pe prezena suflului holosistolic la acelai nivel, dar la nivelul
hemitoracelui drept.

Diagnosticul diferenial fa de suflul radiat de la nivelul mitralei se face prin prezena Pulsaiilor
jugulare i a freamtului valvular pe partea dreapt (n cazul afectrii tricuspidiene).
La ascultaia pulmonului se pot percepe fie zgomote pulmonare normale (murmur vezicular) fie raluri
(staz pulmonar edem pulmonar) sau raluri crepitante la sfritul inspiraiei n special la nivelul
zonei pulmonare ventrale.
Prezena revrsatelor pulmonare atenueaz att zgomotele pulmonare ct i suflurile valvulare.
Alte simptome:
Prezena freamtului precardiac apare n cazul suflurilor valvulare de gradul 5 6/6.
Prezena pulsaiilor jugulare sincrone cu sistola ventricular = valvulopatie tricuspidian.
Pulsaiile sunt mai evidente n cazul efortului, post excitaii sau a presiunii hepatice (reflux
hepato-jugular pozitiv).
Ascita.
Diagnosticul paraclinic
Examenul radiografic
Radiografia cardio-toracic clasic relev mrirea atrial i ventricular stng.
Modificrile sunt progresive n evoluia valvulopatiei.
Atriul stng se poate mri pn la depirea dorsal a nivelului traheii.
Alte semne: congestie sau edem pulmonar: edem la nivel ilar dorsal i bilateral (excepii edem cu
localizare doar la nivelul unei bronhii).
Afectarea i a tricuspidei determin:
-

Revrsate pleurale sau ascita (decompensare cardiac dreapt)

Hepatomegalie
Distensia venei cave caudale

Examenul Rx. important n diagnosticul afeciunilor asociate: neoplazii, bronite, hernie

diafragmatic .a.

Examenul electrocardiografic
ECG nu ofer informaii importante pentru diagnostic.
Examenul ECG: mrirea atrial stng sau biatrial, mrirea ventriculului stng.
ECG este util n diagnosticul aritmiilor cardiace asociate insuficienei cardiace: tahicardii
supraventriculare, extrasistole supraventriculare, mai rar fibrilaie atrial sau extrasistole ventriculare.
P mitral mrire atrial stng
Mrire biatrial

Examenul ecocardiografic
Ecocardiografia este metoda care confirm diagnosticul valvulopatiei i care stabilete gravitatea
procesului patologic.
Examenul ecocardiografic:
modul bidimensional
modul M
ecografia Doppler
Semnele ecografice:
v Mitrala ngroat i modificat (n special valva septal);
v Turbulene la nivelul orificiului mitralei (nuane de galben i verde alturi de culorile standard: rou i
albastru);
v Mrirea atriului stng: creterea diametrului peste 4 cm = patologic;
v Mrirea ventriculului stng;

Dinamica ventricular este normal Fracia de scurtare n limite normale;

- Scderea forei de contracie apare n insuficiena cardiac decompensat (stadii terminale);
- Creterea presiunii pulmonare determin echilibrarea presiunilor dintre cele 2 ventricule cu
aplatizarea septului interventricular (seciune transversal).
Prolaps de mitral
Valva trece spre atriul stng,
dincolo de dreapta imaginara
ce unete originea celor 2 valve
Funcia sistolic este normal
Creterea presiunii pulmonare determin echilibrarea presiunilor dintre cele 2 ventricule cu
aplatizarea septului interventricular (seciune transversal).
-

Ecocardiografia permite i diagnosticul revrsatelor pleurale.

n cazul revrsatelor reduse Eco n modul M este foarte util.

Aplatizarea septului interventricular consecutiv hipertensiunii pulmonare

Pleurezie redus
Turbulene orificiale
Distrugerea valvei septale
Prolapsul valvei mitrale

DIAGNOSTICUL DE LABORATOR
Diagnosticul de laborator este util pentru monitorizarea pacientului i pentru diagnosticul afeciunilor
asociate.
TRATAMENTUL
Tratamentul valvulopatiilor mitrale este complex, stadial i individual.
Exist mai multe scheme de tratament n materialul de fa prezentndu-se ghidul propus de Wendy
Ware, 2007.
Ghidul terapeutic n valvulopatiile cronice
GHIDUL pentru Diagnosticul i Tratamentul valvulopatiilor cronice la cine (engl. pdf.)
Ghidul se adreseaz la 4 grupe de pacieni:
Pacieni asimptomatici
Semne uoare spre moderate de Insuficien cardiac (I.C.)
I.C. sever
Strategia n forma cronic recurent sau I.C. refractar.
Dozele se vor prezenta la sfritul capitolului.
1. Pacienii asimptomatici
a)
b)

c)

Instruirea proprietarilor asupra bolii i a depistrii precoce a simptomatologiei I.C.

Prevenirea crizelor de decompensare
Pstrarea greutii corporale n limite normale
Exerciii fizice uoare moderate
Evitarea activitilor extenuante
Diagnosticul i profilaxia dirofilariozei
Managementul altor afeciuni medicale

d)

Evitarea excesului de sare restricie moderat de sare.

2. Semne uoare moderate de I.C.

a)
b)
c)
d)
e)
f)
g)
h)
i)

Cele expuse mai sus plus:

Administrarea de IEC (sau Pimobendan)
Furosemid la nevoie
+/ Digoxin
+/ alte diuretice (Spironolacton, hidroclortiazid)
f) Terapia antiaritmic specific (cnd este cazul)
g) Restricia total a efortului fizic
h) Restricie moderat a restriciei de sare
i) Repaus cu monitorizarea la domiciliu a frecvenei respiratorii i cardiace.

Nitroprusiat i.v. sau hidralazin p.o. sau amlopidin, +/ nitroglicerin.

3. Semne acute severe de I.C.

a)
b)
c)
d)
e)

Administrarea de oxigen (2 - 4 mg/kg n primele 1 - 4 ore)

Introducerea n corturile de oxigen
Reducerea micrilor excesive ale pacientului
Doze mari parenteral de Furosemid (i.v.)
Administrarea de vasodilatatoare
Nitroprusiat i.v. sau hidralazin p.o. sau amlopidin, +/ nitroglicerin.
f)
+/ Butorphanol sau morfin
g) Terapia antiaritmic dac este necesar
h)
+/ adm. de inotropice pozitive
Insuficien miocardic dovedit inotropice pozitive i.v. (dobutamin, amrinon, milrinon,
digoxin)
Dup stabilizarea pacientului se ncepe tratamentul oral cu pimobendan +/ digoxin
i)
+/ bronhodilatatoare (ex. teofilin)
j)
Toracocentez n cazul revrsatelor pleurale masive.
4. Valvulopatii cronice recurente sau I.C. refractar
a)
dozei i ratei de adm. a Furosemidului (doza se poate reduce la cteva zile de la stabilizarea
pacientului);
b)
Repaus absolut pn la dispariia simptomelor;
c) Adugarea Pimobendanului (dac nu s-a adm. n prealabil)
d)
dozei i ratei de administrare (de la 24 la 12 ore) a IEC (inhibitori enzimei de conversie ai
angiotensinei)
e) Adm. Digoxinului (dac nu s-a adm. n prealabil) cu monitorizarea nivelului plasmatic. Se poate
crete doza numai dup determinarea nivelului seric.
f)
Restricia total de sare i verificarea apei de but (fr sodiu);
g) Adm. (sau dozelor) diureticelor secundare (ex. Spironolactona 1 - 2 mg/kg p.o. la 12 - 24 ore;
Spironolactona cu Hidroclortiazida - Nefrix)
h) Adugarea IEC secundar (ex. Amlopidin 0,05 0,2 mg/kg p.o. la 24 ore sau Hidralazin (0,25
0,5 mg/kg p.o. la 12 ore). Se monitorizeaz presiunea arterial.

i)
j)

Terapia antiaritmic (cnd este cazul)

Punciile evacuatoare (n pleurezii sau ascit) la nevoie.

FUROSEMID
n formele acute
2 - 5 (pn la 8) mg/kg i.v. sau i.m. n primele 1 - 4 ore pn cnd frecvena respiratorie se
normalizeaz, apoi 1 - 4 mg/kg la 6 - 12 ore sau 0,6-1,0 mg/kg/or n perfuzie lent.
n formele cronice
1 - 3 mg/kg la 8 -24 ore p.o. (se utilizeaz dozele minime necesare).
Spironolactona
n formele cronice
0,5 1,0 mg/kg p.o. la (12 ) 24 ore.
n formele acute se poate adm. ca terapie secundar (v.a.)
Hidroclortiazida (Nefrix)
n formele cronice
2 4 mg/kg p.o. la 12 ore.
Inhibitorii Enzimei de conversie ai Angiotensinei (IEC)
ENALAPRILUL
n formele acute
0,5 mg/kg p.o. la 12 - 24 ore
n formele cronice
0,5 mg/kg p.o. la 24 (-12) ore
n formele cronice
Benazepril
(Cibacen, Fortekor)
0,25 0,5 mg/kg p.o. la (12-) 24 ore
Captopril
0,5 2,0 mg/kg p.o. la 8-12 ore (iniial se adm. doze reduse)
Fusinopril
0,25 0,5 mg/kg p.o. la (12-) 24 ore

Ramipril
0,125 0,25 mg/kg p.o. la 24 ore
Imidapril
0,25 mg/kg p.o. la 24 ore.
Nitroprusiat de sodiu
n urgene 0,5 - 1,0 mcg/kg/min (iniial) doza titrndu-se (n sol. de glucoz 5%) n funcie de presiunea
arterial pn la doza de 5-15 mcg/kg/min.
Tensiunea arterial sistolic nu trebuie s scad sub 90 110 mm Hg.
Nu se adm. mai mult de 48 ore pericol de intoxicaie.
Nu se amestec n soluie cu alte medicamente i se ferete de lumin.
(exist i form cutanat)
Hidralazina (Hidrazinoftalazine)
n formele acute
Iniial 0,5 1,0 mg/kg p.o. se repet la 2 3 ore (pn cnd tensiunea sistolic ajunge
la 90 110 mm Hg) apoi se adm. la 12 ore (se evit nitroprusiatul).
Se poate asocia cu nitroglicerina ca alternativ la adm. de nitroprusiat de sodiu.
n formele cronice
0,5 2,0 mg/kg p.o. la 12 ore (se ncepe cu 0,5 1 mg/kg)
Amlopidina
Vasodilatator pt. adm. cronic
0,05 (iniial) la 0,3 (- 0,5) mg/kg p.o. la (12 -) 24 ore.
Prazosin
Cini de:
- talie medie 1 mg p.o. la 8 - 12 ore
- talie mare 2 mg p.o. la 8 ore.
Nitroglicerina
(sol. 2% uleioas)
la 1 inch per cutanat la 4 - 6 ore.
Isosorbid dinitrat
0,5 2,0 mg/kg p.o. la (8 -) 12 ore
Isosorbit mononitrat
0,25 2,0 mg/kg p.o. la 12 ore

IONOTROPICE POZITIVE
DIGOXIN
Cine sub 22 kg 0,005 0,008 mg/kg la 12 ore.
peste 22 kg 0,22 mg/m sau 0,003 0,005 mg/kg la 12 ore. Doza maxim = 0,5
mg/zi sau 0,375 mg/zi la Doberman.
DIGITOXIN
0,02 0,03 mg/kg p.o. la 8 ore (cini talie mic) pn la 12 ore (la cinii de talie mare)
PIMOBENDAN (VETMEDIN)
0,1 0,3 mg/kg p.o. la 12 ore (pe stomacul gol); se ncepe cu doze mici
AMINOFILINA
n formele acute reduce bronhoconstricia
4 - 8 mg/kg lent i.v., i.m., s.c. sau p.o. la 6 - 8 ore.
Sedare pt. anxietii
n f. acute:
Butorphanol: 0,2 0,3 mg/kg i.m.
Morfin: 0,025 0,1 mg/kg i.v. Timp de 2 - 3 minute pn la obinerea efectului sau 0,1 0,5 mg/kg
inj. i.m. sau s.c.
[Morfina se adm. numai la cine !]
Alte manopere n
edemul pulmonar acut
Oxigen 6 - 10 litri/min. Se poate adm. iniial 50 100% oxigen; se reduce la 40% pt. a se evita
toxicitatea.
Pe masc sau tub nazal se recomand 50
100 ml/kg/min.
Flebotomia (6 10 ml/kg) pt. redistribuirea volumului circulant.