May 2003


Matthew W. Miller, DVM, MS
Diplomate ACVIM (Cardiology)

Charter Fellow-Michael E. DeBakey Institute
Associate Professor of Cardiology
Dept. of Small Animal Medicine and Surgery
College of Veterinary Medicine
Texas A&M University

Diagnosis and Management of Common Arrhythmias

Benefits and limitations: The electrocardiogram (ECG or EKG) provides a graphic representation of the electrical depolarization and repolarization processes of the cardiac muscle as "viewed" from the body surface. The amplitude of these electrical potential differences between various points on the body are measured in millivolts (mV) and their duration in seconds. The ECG can provide information on heart rate, rhythm, and intracardiac conduction; it may also reveal evidence of specific chamber enlargement, myocardial disease or ischemia, pericardial disease, certain electrolyte imbalances, and some drug toxicities. But note that although the ECG is a valuable part of the cardiac evaluation, it cannot determine if congestive heart failure is present, or (in itself) predict whether an animal will survive procedures requiring anesthesia, nor can it provide much information on the strength (or even presence) of cardiac contractions.

The normal cardiac rhythm originates in the sinoatrial node and is conducted through the atria, A-V node, His bundle, Purkinje fibers, and into the ventricular muscle.

ECG waveforms are generated as the heart muscle is depolarized, then repolarized:

P waveActivation of atrial muscle. Normally positive in leads II and aVF
P-Q intervalTime from onset of atrial muscle activation, through conduction over the A-V node, His bundle and purkinje fibers. Also called P-R interval
QRS complexActivation of ventricular muscle. By definition, Q is the first negative deflection, R the first positive, and S the second negative
S-T segmentRepresents the period of phase 2 of the action potential
T waveVentricular muscle repolarization
Q-T intervalTotal time of ventricular depolarization and repolarization

Sinus rhythm is the normal cardiac rhythm, described above. The P waves are positive in the caudal leads (II and aVF), the P-Q intervals are consistent and the R-R intervals occur regularly, with less than 10% variation in timing. Normally, the QRS complexes are narrow and upright in leads II and aVF; however, if an intraventricular conduction disturbance or ventricular enlargement pattern is present they may be wide and abnormally shaped.

Sinus bradycardia is a rhythm which originates in the sinus node and is conducted normally but has too slow a rate, while sinus tachycardia also originates and is conducted normally but is too rapid.

Sinus arrhythmia is characterized by a cyclical slowing and speeding of the sinus rate most commonly associated with respiration. The rate tends to increase on inspiration and decrease with expiration because of changes in vagal tone. Often there is an accompanying change in P wave configuration (wandering pacemaker), with the P waves becoming taller and spiked during inspiration and flatter in expiration. Marked sinus arrhythmia occurs in some animals with chronic pulmonary disease. Sinus arrhythmia is a normal rhythm variation. It is commonly seen in dogs, but not often in the clinical setting in normal cats. However, cats frequently have sinus arrhythmia when relaxed or sleeping.

Sinus arrest is a cessation of sinus node activity lasting at least twice as long as the patient's longest expected R-R interval. The resulting pause in heart rate is interrupted by either an escape beat or resumption of sinus activity. Fainting or weakness may result during these pauses.

Various "leads" are used to evaluate the cardiac activation process. The orientation of a lead with respect to the heart is called the lead axis. Each lead has direction and polarity. A lead records the components of the depolarization and repolarization process which are aligned with it. If the myocardial activation wave travels parallel to the lead, a large deflection will be recorded. As the angle between the lead axis orientation and the path of the wave comes closer to 90?, the inscribed ECG deflection for that lead becomes smaller and smaller.

Each lead has a positive and a negative pole or direction. If the wave of depolarization (cardiac activation) travels toward the positive pole (electrode) of the lead, a positive deflection will be recorded in that lead. If the wave of depolarization travels away from the positive pole, a negative deflection will be recorded on the ECG. Electrocardiographic leads are either bipolar or unipolar. The standard bipolar leads have two electrodes on the body surface. The lead axis is formed by connecting these two points. The augmented unipolar leads have one body surface electrode (positive) with the other (negative) electrode formed by the center of the heart.

Small Animal ECG Lead Systems
Standard bipolar limb leads:
I RA (-) compared with LA (+)
II RA (-) compared with LL (+)
III LA (-) compared with LL (+)
Augmented unipolar limb leads:
aVR RA (+) compared with average of LA and LL (-)
aVL LA (+) compared with average of RA and LL (-)
aVF LL (+) compared with average of RA and LA (-)
Unipolar chest leads:
CV6LL (V2-3) Sixth left ICS near sternum
CV6LU (V4-6) Sixth left ICS near costochondral junction
V10 Over dorsal spinous process of 7th thoracic vertebra
CV5RL (rV2) Fifth right ICS near sternum
RA= right arm, LA= left arm, LL= left leg, ICS= intercostal space

The standard lead system evaluates the heart's activation in the frontal plane. This is analogous to looking at a ventrodorsal x-ray; left-right and cranial-caudal currents are represented.

Shaded areas represent normal range for MEA. Left: dog; Right: cat.

The mean electrical axis (MEA) describes the "average" orientation of the ventricular depolarization wave. This is helpful for identifying major intraventricular conduction disturbances and/or ventricular enlargement patterns. The MEA is usually determined in the frontal plane; thus, only the six frontal leads are used.

The MEA can be estimated by either:
  1. Finding the lead with the largest R wave deflection. The positive electrode of this lead points to the approximate MEA.
  2. Finding the lead with the most isoelectric QRS, then identifying the lead perpendicular to this in the frontal plane. If the QRS in this perpendicular lead is mostly positive, the MEA is toward the positive pole of this lead. If the QRS in the perpendicular lead is mostly negative, the MEA is in the direction of the negative pole.
Atrial enlargement patterns: Left atrial enlargement (p mitrale): widening of the P wave; sometimes the P wave is notched as well as wide. Right atrial enlargement (p pulmonale): tall, spiked P wave

Ventricular enlargement patterns: Because activation of the left ventricle is normally so dominant, right ventricular enlargement (due to dilation or hypertrophy) generally must be marked to be evident on ECG. A right axis deviation and S wave in lead I are strong criteria for right sided enlargement (or right bundle branch block). Left ventricular dilation (eccentric hypertrophy) is usually manifested by greater than normal R wave voltages in the caudal leads. Left ventricular concentric hypertrophy may cause a left axis deviation, but this is not consistent.

Conduction blocks in the major ventricular conduction system also disturb the normal activation process and result in altered QRS configurations. The portion of the ventricles served by the diseased bundle branch is activated late and slowly, resulting in widening of the QRS with the terminal forces oriented toward the area of delayed activation.

Rhythm disturbances: Impulses originating from outside the sinus node are abnormal and create an arrhythmia (dysrhythmia). Abnormal or ectopic impulses are described based on their site of origin (atrial, junctional, supraventricular, ventricular). They are also characterized by timing, that is, whether they occur earlier than the next expected sinus impulse (premature) or whether they occur late (escape), as a rescue mechanism. Abnormal premature impulses (complexes) may occur singly or in multiples. Groups of three or more comprise an episode of tachycardia; bouts of tachycardia may be brief (paroxysmal tachycardia) or quite prolonged (sustained tachycardia). A bigeminal pattern occurs when each normal QRS is followed by a premature complex; the origin of the premature complexes determines whether the rhythm is atrial or ventricular bigeminy.

Supraventricular (atrial, junctional) premature complexes originate above the AV node, in either the atrium or the AV junctional (near the AV node) area; however, since they are conducted through the ventricles in the normal manner their QRS configuration is normal (unless an intraventricular conduction disturbance is also present). Atrial premature complexes are preceded by an abnormal P wave (either positive, negative or biphasic).

Ventricular premature complexes (VPCs or PVCs) originate below the AV node and do not activate the ventricles by the normal pathway; therefore, they have an abnormal ECG configuration. Ventricular ectopic complexes are also wider than the normal QRS complexes because of their slower conduction through ventricular muscle. When the configuration of ventricular premature complexes or tachycardia in a patient is consistent, the complexes are described as being uniform or unifocal. When the VPCs occurring in an individual have differing configurations, they are said to be multiform. Increased electrical instability of the heart is thought to accompany multiform ventricular premature complexes or tachycardia. Ventricular tachycardia defines a rapid series of VPCs (greater than 100 beats/minute in the dog, for example). The R-R interval is usually regular, although some variation is not uncommon. Sinus P waves may be seen superimposed on or between the ventricular complexes; they are unrelated to the VPCs because the AV node and/or ventricles are in the refractory period (physiologic AV dissociation).

Atrial fibrillation ("delirium cordis") is a common arrhythmia characterized by rapid, chaotic electrical activation of the atria. There are no P waves on the ECG; rather, the baseline usually shows irregular undulations (fibrillation waves). Since there is no organized electrical activity, meaningful atrial contraction is absent. The AV node, being constantly bombarded with these disorganized electrical impulses, conducts as many as possible to the ventricles. The (ventricular) heart rate is, therefore, determined by how many impulses the AV node can conduct. Atrial fibrillation results in an irregular heart rhythm which is usually quite rapid. Most often the QRS complexes appear normal in configuration, since the normal intraventricular conduction pathway is used. Atrial fibrillation tends to be a consequence of significant atrial disease and enlargement in small animals.

Ventricular fibrillation is a lethal rhythm characterized by chaotic electrical activity in the ventricles. The ECG consists of an irregularly undulating baseline. Like the atria during atrial fibrillation, the ventricles have no coordinated mechanical activity in the presence of disorganized electrical activation and cannot function as a pump. Ventricular flutter, appearing as rapid sine wave activity on the ECG, may precede fibrillation. Ventricular fibrillation may be "coarse", with larger ECG oscillations, or "fine". Ventricular asystole is the absence of ventricular electrical (and mechanical) activity.

Atrio-ventricular (AV) conduction blocks may result from therapy with certain drugs, high vagal tone, and organic disease of the AV node and/or ventricular conduction system. AV blocks are also called "Heart Blocks".

First degree (1o) AV block: conduction of an impulse from the atria into the ventricles is prolonged, although all impulses are conducted.

Second degree (2o) AV block: intermittent AV conduction; some P waves are not followed by a QRS complex. When many P waves are not conducted, the patient has "high-grade" 2o heart block. There are two subtypes of 2o block. Mobitz type I (Wenckebach) is characterized by progressive prolongation of the P-R interval until a nonconducted P wave occurs; it is frequently associated with disorders within the AV node itself and/or high vagal tone. Mobitz type II 2o block is characterized by uniform P-R intervals preceding the blocked impulse, and is thought to be more frequently associated with disease lower in the AV conduction system (e.g. His bundle or major bundle branches).

Third degree (3o) or complete AV block: no sinus (or supraventricular) impulses are conducted into the ventricles. Often there is a regular sinus rhythm or sinus arrhythmia evident; however, the P waves are not related to the QRS complexes which result from a (usually) regular ventricular escape rhythm.


Numbers to remember:

At paper speed 25 mm/sec each small box = 0.04 sec; there are 3 sec between vertical hash-marks at the top of the paper.

At paper speed 50 mm/sec each small box = 0.02 sec; there are 1.5 sec between vertical hash-marks at the top of the paper.

Standard is 1 cm = 1 mV
1/2 standard is 0.5 cm = 1 mV
2 x standard is 2 cm = 1 mV

Normal Values: Approximate normal range of ECG intervals in seconds.

  PPQ (R)QRSQT aHeart rate/min
Dogto 0.04 b0.06-0.13 bto 0.05-0.06 c0.15-0.2860-160 d
Catto 0.0350.05-0.09to 0.04 0.12-0.20140-240 e
Horseto 0.16to 0.38 eto 0.14to 0.5828-40 e,f

a QT is inversely related to heart rate
b May be longer in giant breeds (P = .05, PR = .14)
c Small breeds .05, large breeds .06
d Up to 220/min for puppies
e Varies according to study

Normal upper limit of wave height in mV:

Cat0.20.9 g

g The total QRS amplitude (Q + R + S) is usually less than 1.2 mV in Lead II

Approach to the ECG

  1. Record quality?
  2. Paper speed? (Know time/box; time marks)
  3. Calibration?
  4. Note artifacts
  5. Note lead markings
Determine heart rate:
  1. Count complexes in 3 or 6 sec. X 20 or 10, or
  2. Instantaneous HR = 60/R-R in sec
  3. At 50 mm/sec, count # of small boxes in R-R interval
    HR = 3000/# of boxes
Determine Rhythm:
  1. Scan whole strip
  2. Is rate too fast or too slow?
  3. Are R-R intervals regular? Any pattern?
  4. Are P-P intervals regular? Any pattern?
  5. Is there a P for each QRS-T?
  6. Is there a QRS-T for each P? Are they related?
  7. Do all P waves and QRS-Ts look similar?
Determine Mean Electrical Axis (MEA) in the frontal plane:
  1. Lead with tallest R wave.
  2. Pick isoelectric lead (if there is one), locate lead perpendicular to this and determine if QRS is mostly positive (MEA toward the positive pole of this lead) or negative (MEA away from this lead's positive pole).
Measure Complexes
  1. Lead II is used by convention.
  2. Only include 1 pen-line thickness in the measurements.
  3. Measure height (mV) of P wave, R wave (know recording calibration).
  4. Measure duration (sec) of P wave, P-R interval, QRS complex, Q-T interval (know paper speed).
  5. Note any J point/S-T segment deviation and T wave or other abnormalities.
Therapeutic Considerations: Occasional premature beats generally do not require therapy. Treatment for other arrhythmias may also not be necessary unless the rhythm disturbance causes a sustained very rapid or slow heart rate, or occurs in a context that has been associated with sudden arrhythmic. If the arrhythmia is likely to cause hemodynamic impairment and/or clinical signs, therapy is advised.

Supraventricular tachyarrhythmias: For acute therapy of rapid supraventricular tachycardias, a vagal manuever is attempted first. Since often unsuccessful, IV administration of a Ca++ entry blocker (diltiazem or verapamil) or beta blocker (propranolol, esmolol) is given. Carotid sinus massage is repeated after each drug bolus. IV fluids to support blood pressure is another way to increase vagal tone. Additional strategies for refractory SVT include edrophonium Cl, phenylephrine, IV digoxin, adenosine.

Chronic oral therapy for frequent atrial premature contractions or paroxysmal atrial tachycardia in dogs with heart failure (and cats with dilated cardiomyopathy) usually starts with digoxin. If digoxin alone does not correct the arrhythmia a beta blocker or diltiazem is added. Cats with hypertrophic cardiomyopathy or hyperthyroidism are given a beta blocker first.

Since atrial fibrillation tends to be a consequence of significant atrial disease in most small animals, a rapid ventricular response rate (high SNS tone) are common. Treatment is aimed at slowing the ventricular response rate by slowing A-V conduction. Digoxin is used initially PO except in cats with hypertrophic cardiomyopathy. A beta blocker or diltiazem is added to further slow the heart rate as needed. Acute IV therapy with diltiazem or esmolol could be tried. "Lone" atrial fibrillation sometimes develops in the absence of significant cardiac disease in giant breeds of dogs. This may convert to sinus rhythm either spontaneously or with drug therapy (quinidine has been used in the past; diltiazem and newer agents such as class Ic drugs or amiodarone may prove useful).

Ventricular tachyarrhythmias: have been associated with many disorders that directly affect cardiac tissue or indirectly induce arrhythmias by their neurohumoral effects. Correcting hypoxia, electrolyte (especially K+) or acid/base imbalances, abnormal hormone levels (e.g. thyroid), or discontinuing certain drugs may abolish the arrhythmia. Ventricular tachyarrhythmias thought to be electrically unstable or that promote hemodynamic instability are treated. Examples include frequent, multiform (polymorphic) premature beats; ventricular prematures with short coupling intervals (R-on-T); and rapid ventricular tachycardia. IV lidocaine is usually the first-choice agent for in dogs because it has minimal adverse hemodynamic effects. Second line choices include procainamide (or quinidine), and IV propranolol or esmolol with either lidocaine or procainamide. Newer drugs that might be useful include amiodarone, sotolol, others.

If chronic oral therapy for ventricular tachyarrhythmias is warrented, procainamide, mexiletine, a beta blocker (e.g. atenolol) - usually combined with the Class I drug, are commonly used. Sotolol and amiodarone are also promising agents, but veterinary experience is quite limited.

Symptomatic bradyarrhythmias - if not responsive to anticholinergic therapy, pacing is indicated.



Cordarone 200 mg tablets
Dog - 10-20 mg/kg PO SID X 7-10 days :loading dose, then3-15 mg/kg PO SID
I Refractory ventricular and suprventricular arrhythmias; T hepatotoxicity, anorexia, AV block

Tenormin: 25, 50, 100 mg tablets
DOG - 0.25-1 mg/kg q12h; CAT - 6.25-12.5 mg SID-BID
I Ventricular and supraventricular tachycardia; T bradycardia AV block, depression, hypotension

Brevabloc 10 mg/ml, 250 mg/ml
50-500 (usually 50-100) ug/kg IV bolus every 5 min (up to 500 ug/kg max) 50-200 ug/kg/min CRI
I Suprventricular tachyarrhhytmias, ventricular tachyarrhytmia; T AV block, bradycardia, hypotension, negative inotropism

Lanoxin, Cardoxin, Digoxin USP: 0.125, 0.25, 0.5 mg tablets; 0.05 mg/ml and 0.15 mg/ml elixirs; 0.25 mg/ml Lanoxin for injection
DOG - 0.0055 to 0.011 mg/kg q12h; or 0.22 mg/meter sq body surface area q12h. CAT - 0.0035 to 0.0055 mg/kg once or twice daily; Tablet (0.125 mg)-1/4 tablet daily or bid.
I Supraventricular tachyarrhymia; T anorexia, vomiting, AV block, VPC. Toxicity exacerbated by hyponatremia , hypercalcemia, hypokalemia , hypothyroidism and renal dysfunction


Cardizem: 30, 60, 90, 120 mg tablets
Cardizem CD 120, 180 and 300 mg capsules
25mg/ml injection
DOG - 0.5 to 1.3 mg/kg orally q8h; CAT - 0.5 to 2.0 mg/kg q8-12h, CD product 10 mg/kg PO SID
0.1-0.25 mg/kg SLOW IV bolus follwed by 2-6 ug/kg/min CRI
I supraventrciular tachycardia; T AV block, depression, anorexia and lethargy


Xylocaine, Lidocaine USP: 2% (20 mg/ml) for injection (without epinephrine)
DOG - 2 mg/kg [IV] up to 8 mg/kg over a 10-minute period; 25 to 75 mcg (occasionally up to 100) micrograms/kg/min constant rate IV infusion; CAT - 0.25 to 0.75 mg/kg [IV] over a 3-5-minute period.
I Ventricular arrhythmias; T Seizures, tremors, CNS and respiratory depression, vomiting


Mexitil: 150, 200, 250 mg capsules
DOG - 5-8 mg/kg orally q8-12h (?)
I Ventricular arrhythmias; T Seizures, tremors, CNS and respiratory depression, vomiting


Pronestyl (-SR), Procan SR: capsules & tablets (SR): 250, 375, 500 mg, 100mg/ml, 10 ml vials 500mg/ml, 2 ml vials
DOG - 5-15 mg/kg (IV) up to a maximum total dose of 20 mg/kg over a 30-minute period; 25-40 mcg/kg/min IV infusion; 8 to 20 mg/kg, IM q4-6h or orally q6-8 hours. CAT - 2-5 mg/kg, IM or orally q 6-8 h; 2 mg/kg (IV) up to a maximum total dose of 20 mg/kg over a 30-minute
I Supraventricular (A. fib) and ventricular arrhythmias; T Seizures, tremors, CNS and respiratory depression, vomiting, anorexia proarrhythmia, QT prolongation negative inotrope

Inderal (-LA), USP: 1 mg ampule for injection; 10, 20, 40, 60, 80 mg tablets; Inderal
DOG - 0.2 to 1.0 mg/kg orally q8h; CAT - 2.5 to 5.0 mg orally tid; IV dose: 20-60 mcg/kg over 5 to 10 min
I Ventricular and supraventricular tachycardia; T bradycardia AV block, depression, hypotension

Betapace 40mg, 60mg, 80 mg, 160 and 240 mg tablets
DOG - 1-3 mg/kg orally q12h
I Ventricular and supraventricular tachycardia; T bradycardia AV block, depression, hypotension, QT prolongation, negative inotropism


Tonocard: 400, 600 mg tablets
DOG - 10-20 mg/kg q8h
I Ventricular arrhythmias; T Seizures, tremors, CNS and respiratory depression, vomiting

** It is important to realize that all antiarrhythmic drugs (some more that others) may worsen the severity of the arrhythmia (proarrhythmia).

Valvular Heart Disease


Chronic valve disease (CVD) is the most frequent cause of congestive heart failure in dogs. This condition has also been termed chronic degenerative valvular disease, myxomatous atrioventricular valvular degeneration, chronic valvular fibrosis and endocardiosis. The incidence is reported as being between 11% (clinical determination) and 42% (necropsy determination) depending on the method of examination. The incidence of CVD is increased further, to above 60%, in aged dogs. The mitral valve alone is affected in 60% of dogs with CVD, with the mitral and tricuspid valves both affected in 30% of cases and the tricuspid valve alone in 10% of dogs. The aortic and pulmonic valves may be affected but clinically important disease is uncommon. Signs of mitral valve disease and left-sided cardiac dysfunction predominate in most cases.

The disease is most common in small to medium sized breeds of dogs. Cavalier King Charles Spaniels and Dachshunds are over-represented. CVD also occurs in large breed dogs (i.e., German Shepherd dog, Doberman pinscher), but dilated cardiomyopathy is much more common in these breeds than CVD. The incidence of CVD is increased in male dogs relative to females (1.5 to 1.0). This is a slowly progressive disease in which lesions may begin in the first half of life (e.g., 2 to 3 years), but clinical disease isunlikely before middle age. In the early stages, the only clinical sign may be a cardiac murmur detected on routine examination. Cardiac decompensation and congestive heart failure (CHF) typically occurs in later life (e.g., 6 to 10 years of age or older).

Valve leaflets may be grossly thickened and shortened with curled, nodular margins. There is fibrosis of the valves with an accumulation of acid mucopolysaccharide ground substance. Valvular hemorrhage and calcification may be seen. Chordae tendineae are thickened and may rupture. The disease is primarily a non-inflammatory, myxomatous degeneration of the A-V valve that is commonly referred to as endocardiosis. Many dogs with chronic mitral regurgitation have histologic evidence of small foci of myocardial fibrosis and necrosis, as well as intramural coronary arteriosclerosis (referred to as microscopic intramural myocardial infarction or MIMI). The left ventricle is dilated and hypertrophied if there has been significant volume overload. The left atrium is dilated and, in severe cases, the endocardium may split and rupture creating cardiac tamponade. The onset of congestive heart failure is associated with chronic passive congestion of the lungs (left-sided CHF) or abdominal viscera (right-sided CHF).

Valvular regurgitation results in a volume overload of the associated ventricle. Classic compensatory mechanisms (sympathetic nervous system, renin-angiotensin system, etc.) are activated to restore blood pressure and tissue perfusion towards normal. In compensated mitral regurgitation, cardiac remodeling occurs with ventricular dilatation and left ventricular (LV) wall hypertrophy. The left atrium (LA) is dilated and, as long as the atrium remains compliant enough to accept the regurgitated blood, CHF does not develop. Eventually LA pressure rises and pulmonary edema develops.

In the early to middle stages of the disease the LV wall thickness in increased and LV end- diastolic volume is greater than normal, yet the LV contracts down to a normal end-systolic volume (resulting in an increase in fractional shortening). Chronic mitral regurgitation eventually leads to myocardial dysfunction and myocardial failure, which can be manifest by increasing LV end systolic volume or decreasing fractional shortening. Chronic left heart failure leads to pulmonary hypertension, posing added strain to the right heart and contributing to signs of right-sided CHF in dogs with concurrent CVD of the tricuspid valve. There is reasonably good experimental evidence to indicate that dogs with significant mitral regurgitation have more compromise to myocardial systolic function than is evident from the "apparently" good systolic function seen on echocardiography. The leaking mitral valve allows a low pressure "pop-off" which permits a large volume of blood to be pumped into a low pressure chamber, allowing for a high fractional shortening on the echocardiogram despite significant myocardial dysfunction.

Clinical Syndromes
A wide range of clinical presentations are possible, depending on the degree and duration of valvular dysfunction. Many older dogs presented for routine examination or for other medical problems are identified to have the typical murmur of mitral (MR) or tricuspid (TR) regurgitation. Baseline testing (e.g., radiographs, echocardiography) is often helpful for comparison at subsequent examinations. In many dogs CHF is the cause for initial evaluation with cough, nocturnal dyspnea, altered sleep habits, abdominal distention or exercise intolerance as the presenting complaints. Congestive heart failure may be manifest as pulmonary edema, pleural effusion, or ascites. Acute, fulminant CHF result from rupture of a chorda tendineae or exacerbation of chronic CHF following a stressful or decompensating event (i.e., anesthesia/surgery, high sodium treats/diet, onset of rapid tachyarrhythmia, etc.). In dogs with advanced CVD and mitral regurgitation the LA may become large enough to put pressure on the large airways creating cough due to large airway compression. Tracheal and large airway collapse, concurrent bronchitis, and other respiratory diseases are common in small breed dogs and can contribute to cough, leading to confusion as to the most important cause of cough. Syncope can occur due to significant arrhythmias, cardiac output, or following a coughing spell (e.g., tussive syncope). In the author's experience, syncope occurring at the time of the initial presentation for heart failure usually resolves following resolution of pulmonary edema. Finally, endocardial splitting with left atrial rupture can result in acute collapse due to cardiac tamponade. In these cases, signs of reduced forward blood flow predominate; the lungs can be free of pulmonary edema.

Cough is the most common presenting complaint in dogs with clinical signs resulting from CVD. The cough is often described as a deep, resonant cough or a hacking cough. The cough may occur after exercise or excitement, or it may be more prominent at night. Additional historical complaints can include dyspnea, orthopnea, respiratory distress, reduced exercise tolerance, weight loss (cardiac cachexia), progressive abdominal distention due to right-sided CHF, and syncope.

Physical Examination
The classic auscultation finding is a systolic cardiac murmur in the typical mitral or tricuspid valve location. An extra systolic sound known as a mid-systolic "click" has been associated with early CVD and mitral valve prolapse. A mid-systolic click is likely the earliest auscultatory finding for CVD, but it can be easily missed or mistaken for a cardiac gallop. There is a tendency for the intensity of the murmur to be roughly correlated with the severity of cardiac dysfunction. The initial murmur of mitral regurgitation may not persist for the entire duration of systole and is localized to the 5th intercostal space at left apex. With increasing disease severity, the murmur becomes holosystolic and more intense, radiating cranially, dorsally, and to the right. When sufficiently intense, the murmur can radiate to the right midthorax, making it difficult to discern the presence of a second murmur due to tricuspid regurgitation. The murmur of tricuspid regurgitation is located on the right hemithorax, roughly midway between the cardiac apex and base. An S3 gallop is commonly heard in dogs with CHF or myocardial failure.

Dogs with CHF may have tachypnea, hyperpnea, dyspnea, or orthopnea, and anxiety with a reluctance to lie down. A cough may be elicited by gentle tracheal palpation or may occur unprovoked. Paroxysms of cough may end in swallowing or the production of a white foam; in advanced cases, a blood tinged froth is produced. Mucous membranes are pink in early stages, but may progress to a muddy to somewhat cyanotic color with decompensation and severe left-sided CHF. Pulmonary auscultation may also reveal increased respiratory sounds which progress to crackles with the onset of alveolar edema. The latter may be particularly prominent over the hilar or caudal lung fields on inspiration. Hepatomegaly and ascites may be evident in dogs with right-sided CHF from advanced disease, and in these cases the jugular veins are typically distended and/or exhibit a prominent systolic "V" wave due to the ejection of blood into the RA. The femoral pulses are often easily palpated and prominent, but may exhibit a jerky "collapsing" character due to the abbreviation of LV ejection. Arterial pulses often become weak in animals with advanced CHF or myocardial failure. There may also be irregularities in pulse rate and strength resulting from cardiac arrhythmia. In animals with CHF, the heart rate is usually elevated or in the upper normal range and sinus arrhythmia is typically absent. The ventricular apex beat is hyperdynamic and is progressively shifted caudally from the 5th intercostal space with increasing disease severity. When present, a precordial thrill is also palpated in this region.

Thoracic Radiology
The earliest finding on thoracic radiographs is left atrial enlargement. On the lateral projection, the left atrium is visualized at the caudodorsal aspect of the cardiac silhouette. The left atrium enlarges progressively with advancing disease. Left atrial and left ventricular enlargement result in elevation of the trachea and carina, with a decrease in the angle made between the trachea and the thoracic spine. The left mainstem bronchus may become elevated (compressed) in cases of marked left atrial enlargement. There is straightening of the caudal cardiac border and loss of the caudal cardiac waist. Pulmonary venous dilation occurs and is often evaluated in the cranial lung fields in this view. Early pulmonary edema is seen as a diffuse increase in interstitial density in the hilar or caudal lung fields, progressing to fluffy densities and air bronchograms with the onset of alveolar edema. With tricuspid regurgitation and right-sided or biventricular CHF, the cranial aspect of the trachea may be elevated and the caudal vena cava will increase in size. Hepatomegaly and splenomegaly may be present. On the DV or VD radiographic projection, the earliest findings in CVD is enlargement of the left atrial appendage, located at the 2 to 3 o'clock position (using the clockface analogy). Left ventricular enlargement leads to rounding of the LV apex, which may be displaced to the left. With progressive enlargement of the left atrium there is an increase in the angle formed by the right and left main stem bronchi (resulting in the bow-legged cowboy sign). Right atrial and ventricular enlargement leads to rounding of the cardiac silhouette from the 6:00 to 11:00 position. Pulmonary veins (and arteries in severe cases) are distended in the caudal lung fields and the previously noted pulmonary parenchymal changes are evident when left-sided CHF develops.

ECG findings include evidence of left ventricular hypertrophy, left atrial enlargement (P mitrale; P > 0.04 sec), and infrequently P pulmonale (P > 0.4 mv). ST segment slurring is seen in some dogs with left ventricular hypertrophy, and ST depression may result from hypoxemia. Sinus rhythm or sinus tachycardia with a normal mean electrical axis are typical. Supraventricular arrhythmias occur commonly. Atrial fibrillation develops in some dogs with marked atrial enlargement, and ventricular arrhythmias are uncommon in dogs with compensated disease.

Valvular thickening may be readily appreciated in most dogs with CVD. This valvular thickening and irregularity is most easily appreciated in the anterior mitral leaflet. With severe disease or with rupture of the chordae tendinae the valve motion takes on a vigorous, chaotic quality. The mitral valve leaflet can be noted to prolapse into the LA during systole. Left ventricular dilation is present to a variable degree depending upon disease severity. Progressive left atrial dilation occurs in most cases. Fractional shortening is increased with increasing regurgitant fraction, however fractional shortening can return toward "normal" or become diminished with disease progression and myocardial failure. End-systolic dimension or end-systolic volume index may be a better indication of myocardial function as these dimensions tend to increase with impending myocardial failure. As a crude indication of disease severity, the location and extent of the regurgitant jet can be estimated using color flow (CFD) Doppler echocardiography. While the degree of mitral or tricuspid regurgitation on color-flow Doppler may provide some qualitative information, the degree of disease progression is probably better characterized by left atrial size and measures of left ventricular function.

Cavalier King Charles Spaniels are known to get CVD early in life. Absence of a cardiac murmur before 5 years of age in male dogs and before 6 years of age in female dogs has been proposed as a criterion for recommendations of populations for breeding. Most dogs will live three to four years after development of a cardiac murmur. Necropsy results of a small percentage of those CKCS examined revealed that mitral valve prolapse and ruptured chordae tendineae are major findings with CVD in this breed. More specifically, those tendineae associated with the medial aspect of the anterior mitral valve leaflet are most commonly ruptured, often in the absence of significant thickening due to endocardiosis. A study of enalapril use in this breed to prevent progression of the disease or delay the onset of CHF failed to identify a significant clinical benefit in asymptomatic dogs.

The optimal treatment of dogs with CVD remains a topic of some discussion and debate. A variety of drugs and diets have been develop to manage the disease, however little research has been done to identify the cause of the valvular degeneration. If the cause of endocardiosis can be identified and treated then the disease could be slowed or reversed. Until that time, management of congestive heart failure (CHF) remains the cornerstone of therapy for CVD. Clinical trials of human heart failure patients have documented that use of certain therapies (e.g., Angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, spironolactone) leads to improved survival. The ACE inhibitors have been studied in dogs with CVD, however there is little information available regarding use of beta-blockers or spironolactone.

Angiotensin-converting enzyme (ACE) inhibitors are commonly used in the management of CVD. One published study and data from another recently presented study failed to identify a clear benefit from early use of ACE inhibitors in dogs with CVD that have not yet developed clinical signs. However, once clinical evidence of heart failure is present, use of ACE inhibitors is appropriate and is also typically safe in the absence of significant pre-existing renal disease or excessive concurrent diuretic use. In general, ACE inhibitors should be used in all dogs with CVD that have developed CHF, assuming drug therapy is well tolerated.

Diuretic therapy is indicated in any dog with evidence of congestion (e.g., pulmonary edema, pleural effusion, or ascites of cardiogenic origin). It can be quite difficult to define the exact dose of diuretic required by any individual dog. The dose required to clear significant edema accumulations and cause the animal to be minimally symptomatic (the desired dose) is often close to a dose that might result in electrolyte disturbance, dehydration and the development of pre-renal azotemia. The combined use of ACE inhibitors and diuretics compromises one of the kidneys' normal compensatory mechanisms (vasoconstriction of the efferent arteriole) and can lead to elevation of BUN and creatinine if an excessive diuretic dose is initiated. Diuretic dose should be reduced in dogs that are weak, lethargic, anorexic, or depressed, especially if congestive signs are well controlled. In most instances of mild CHF in dogs a furosemide dose of 2 mg/kg q 12-24 hours will control edema formation. When the furosemide dose of 2.2 mg/kg twice a day is exceeded during chronic therapy, diuretic resistance has been likely occurred and the author recommends addition of diuretics with differing mechanisms of action. Spironolactone has been documented to result in improved survival in a human CHF study, however information on the optimal dose and time of initiation of this drug is veterinary medicine is largely anecdotal. In cases of refractory CHF, a combination of hydrochlorothiazide with spironolactone is recommended. Serial electrolyte monitoring is advisable as spironolactone use can lead to mild hyperkalemia, and hydrochlorothiazide can result in hyponatremia and hypochloremia. Digitalis glycosides are also useful to control advanced CHF. The author most commonly uses digoxin as an add-on therapy to ACE inhibitors and diuretics for refractory CHF or in dogs with significant supraventricular arrhythmias.

Beta blockade has gained favor recently as a therapeutic modality for treatment of CHF. Several studies on the use of beta-blockers have documented benefits that accrue from chronic treatment, although these effects are often not seen for several months. Reported benefits include up regulation of previously down regulated beta-receptors, improved cardiac performance (improved stroke volume), and improved survival. These clinical benefits appear to have sound theoretical basis, and are currently being evaluated in dogs with naturally occurring CHF. It is true that beta-blockers are negative inotropes, and this may be the most demonstrable effect when these drugs are used in animals with active CHF. The negative inotropic and negative chronotropic effects of the drugs will likely contribute to worsening of CHF in animals with active failure or those that are on the edge of compensation. Beta-blockers are best employed in animals that are minimally symptomatic with early/mild heart failure, or in animals in later stages of CHF that are already well controlled on a stable cardiac drug regimen.

Sodium restricted diets and exercise restriction have long been a useful additions to the management of CHF in dogs. The optimal time to initiate a cardiac diet and the ideal sodium level relative to the severity of clinical disease are areas for debate and further research. A diet designed for early use in dogs with CVD has been recently developed (Waltham Early Cardiac Support Diet) and studies of this diet are ongoing. Exercise restriction with severe congestive heart failure is essential, however limited exercise in dogs with stable chronic heart failure is often well tolerated. Repetitive or strenuous activities like ball chasing and running should be restricted.

Surgical procedures are being developed to repair or replace the mitral valve in dogs with CVD. Cardiopulmonary bypass is required for these surgeries, and successful cardiopulmonary bypass requires a dedicated team of surgeons, perfusionist, anesthesiologist, cardiologist, intensive care specialist, and strong veterinary technician support. The cost associated with surgery can be prohibitive, however cardiopulmonary bypass and mitral valve surgery have become routine in the human field. Once these techniques are mastered and refined for veterinary medicine it seems probable that surgery will become the preferred therapy for those that can afford the procedure.

Re-evaluation with a physical examination and chemistry profile to check renal function and electrolytes 7 to 10 days after initiation or alteration of cardiac medications is prudent. Serum digoxin levels should be obtained if this drug is used, ideally 8 hours post-pill. Additional tests that might be appropriate at the time of the initial recheck examination include packed cell volume and total proteins to help assess hydration, blood pressure, follow-up thoracic radiographs in dogs with CHF, and follow-up electrocardiography in animals with arrhythmia. The next visit should be scheduled for 2 to 3 months and at that time a physical examination with chemistry profile should be performed.

Table 1

Category Clinical
(Category 1a)
No clinical signs systolic murmur; PMI left apex (mitral valve area) Normal Cardiac size; no evidence of CHF Normal Thickened MV; normal LA, LV size and LV function None Indicated
(Category 1b)
No clinical signs systolic murmur;PMI left apex (mitral valve area) Mild to moderate cardiac enlargement especially LA and LV enlargement Normal; may show evidence of LA or LV enlargement Thickened MV Mild LA and LV enlargement, Normal LV systolic function Monotherapy might include ACE inhibitors or a ?-blocker. There is little objective data to support intervention of any kind at this point in the disease
Mild Symptoms
(Category 2)
Occasional cough systolic murmur;PMI left apex (mitral valve area), may detect pulmonary crackles demonstrable left atrial and ventricular enlargement Normal; may show evidence of LA or LV enlargement ? APC=s Thickened MV, Mild to moderate LA and LV enlargement, normal systolic function ACE inhibitors. Moderate dietary sodium restriction, diuretics (furosemide/ spironolactone) to control edema if present, ? digitalis
Moderate to Severe
(Category 3)
Persistent cough with exercise intolerance systolic murmur; PMI left apex (mitral valve area) pulmonary crackles common; tachycardia, possibly with a demonstrable arrhythmia(pulse deficits) left atrial and ventricular enlargement; diffuse or perihilar pulmonary infiltrates, pulmonary venous enlargement Normal; may show evidence of LA or LV enlargement arrhythmia,s including APC=s and fibrillation are common, V tach much less common Thickened MV, Marked left atrial and left ventricular enlargement, LV systolic function may be normal or impaired ACE inhibitors. Moderate dietary sodium restriction , diuretics (furosemide/ spironolactone) to control edema, digitalis; antiarrhythmics as indicated cough suppresents and/or bronchodilators may be indicated
Severe, Recurrent
Heart Failure
(class 4)
1) unable to stabilize with routine therapy
(see Category 3)

2) previously controlled signs with acute exacerbation
systolic murmur; PMI left apex (mitral valve area); focal or diffuse pulmonary crackles Marked left atrial and left ventricular enlargement, or generalized cardiomegaly pulmonary venous distension, diffuse or perihilar pulmonary parenchymal infiltrates Normal; may show evidence of LA or LV enlargement; arrhythmias including APC=s and fibrillation are common, V tach much less common but may be seen Thickened MV, Marked left atrial and left ventricular enlargement, LV systolic function commonly impaired, ruptured chordae tendinea or LA rupture w/ pericardial effusion may be noted Therapy is typically in addition to the therapy used in category III. Control of heart failure may require additional diuretics (thiazide/ spironolactone) and/or vasodilators (hydralazine), ? blockers or calcium channel blockers may be needed to control arrhythmias.


ATENOLOL Tenormin: 25, 50, 100 mg tablets DOG - 6.25-12.5 mg q12h;
CAT - 6.25-12.5 mg daily
I: diastolic dysfunction
CARVEDILOL Coreg: 3.125, 6.25, 12.5, 25 and 50 mg tablet Dog 0.3 - 1.5 mg / kg
PO BID requires very gradual titration
I: compensated valvular disease or myocardial disease
Beware of acute decompensation
DIGOXIN Lanoxin, Cardoxin, Digoxin USP: 0.125, .25, .5 mg tablets; 0.05 mg/ml and 0.15 mg/ml elixirs; 0.25 mg/ml Lanoxin for injection DOG - 0.0055 to 0.011 mg/kg q12h; or 0.22 mg/meter sq body surface area q12h.
CAT - 0.0035 to 0.0055 mg/kg once or twice daily; Tablet (0.125 mg)-1/4 tablet daily or bid.
I: heart failure,supraventricular
tachyarrhythmias, (SVT)
T: GI, arrhythmias
G: renal excretion
DILTIAZEM Cardizem: 30, 60, 90, 120 mg tablets DOG - 0.5 to 1.3 mg/kg orally q8h
CAT - 0.5 to 2.0 mg/kg q8-12h
I:diastolic dysfunction (HCM), SVT
T: bradycardia
DILTIAZEM Dilacor: 240 mg capsules Cat: ½ of a 60mg tablet orally q12h I:diastolic dysfunction (HCM), SVT
T: bradycardia
DOBUTAMINE Dobutrex: 250 mg (20 ml) vial for injection DOG - 2.5 to 20 micrograms/kg/min, constant rate IV infusion.
CAT - 2.5 to 10 mcg/kg/min CRI
I: severe systolic dysfunction
T: tachyarryhtmias
ENALAPRIL Enacard: 1, 2.5, 5, 10 mg tablets DOG, CAT - 0.25-0.5 mg/kg orally once or twice daily I: CHF (MR, DCM), systemic
T: Beware azotemia
FUROSEMIDE Lasix: 12.5 [Vet] mg, 20, 40, 50 [Vet], 80 mg tablets; 1% syrup (10 mg/ml) DOG - 2-6 mg/kg repeated q8-12h as needed (IV, IM, SQ, oral).
CAT and HORSE - 1-4 mg/kg repeated q12h as needed (IV, IM, SQ, oral)
I: CHF (edema)
T: hypotension, dehydration,
hypokalemia, met. Alkalosis
HYDRALAZINE Apresoline: 10, 25, 50 mg tablets DOG - 1-3 mg/kg orally q12h (initial dose 0.5 mg/kg, titrate to effect or to at least 1 mg/kg q12h) I: CHF
T: hypotension, GI
HYDROCHLORTHIAZIDE SPIRONOLACTONE Hydrodiuril, USP: 25, 50 mg tablets; Aldactazide: 25 mg HCT combined with 25 mg spironolactone DOG, CAT - 2-4 mg/kg once or twice daily (of either HCT or combined product) I: CHF (edema)
T: hypotension, dehydration, hyperkalemia
LISINOPRIL Zestril, Prinavil Dog - 0.5mg/kg orally q24h I: CHF (MR, DCM), systemic
T: Beware azotemia I
NITROGLYCERINE Nitrol, Nitro-bid, Nitrostat: one inch = 15 mg NTG; Minitran transderm patches 2.5, 5, 10, 15 mg/24 hrs DOG - 4-12 mg (up to 15 mg) topically q12h;
CAT - 2-4 mg topically q12h (doses approximate)
I: CHF (severe pulm. edema)

Feline Cardiomyopathy: Diagnosis and Management

General Information

Diseases of the myocardium (cardiomyopathies, myocardiopathies) may be classified as primary or secondary. Primary or idiopathic cardiomyopathies are muscle disorders that are common in veterinary medicine. Examples include the cardiomyopathies of the cat, giant breed dogs, and the Boxer.

Secondary myocardiopathies also are encountered. These include bacterial myocarditis secondary to other primary infections (endocarditis), myocardial necrosis secondary to coronary insufficiency or ischemia (gastric torsion; microscopic intramural myocardial infarction of chronic endocardiosis), myocardial inflammation, viral infection, trypanasomiasis (Chagas' disaese) toxic injury, and nutritional myodegeneration.

The cardiomyopathies have been further classified as they comprise a spectrum of heart diseases of considerable clinical importance.

Dilated or congestive cardiomyopathy - is characterized by left and right-sided dilatation, normal coronary arteries, normal (or minimally-diseased) atrioventricular valves, significantly decreased inotropic state, and dysfunction occurring primarily during systole, if conventional methods (e.g. ejection fraction) are used for evaluation.

Hypertrophic cardiomyopathy - is characterized by left ventricular and septal concentric hypertrophy with decreased ventricular compliance and dysfunction primarily during diastole; ejection fraction is normal. Systolic dysfunction also can develop when secondary mitral regurgiation (MR) develops.

Obstructive cardiomyopathy - is characterized by myocardial hypertrophy with obstruction to left ventricular outflow, causing a subvalvular stenosis. This is related to ventricular septal hypertrophy.

Restrictive cardiomyopathy - which is increasingly being diagnosed in cats, causes markedly decreased ventricular compliance caused by myocardial fibrosis.


Hypertrophic CM: Fibrosis, concentric hypertrophy and possibly subendocardial myocardial ischemia result in loss of normal ventricular compliance Therefore, higher end-diastolic pressures (EDP) are needed to fill the ventricle. Tachycardia further decreases filling time, worsens ischemia, and impairs relaxation. Thus, left ventricular diastolic function is impaired, and is characterized by disturbed filling, increased end diastolic pressure (EDP), atrial dilatation, and pulmonary venous hypertension. Systolic pumping function is normal or increased (high ejection fraction); however, there may be mitral regurgitation which limits forward output. Interventricular septal hypertrophy may cause obstruction to left ventricular outflow, so-called HOCM (hypertrophic obstructive CM). Papillary muscle dysfunction due to hypertrophy and systolic anterior motion of the septal mitral valve leaflet, produces mitral regurgitation. Eventually signs of left-sided heart failure are recognized - often associated with the stress (tachycardia) of an acute aortic thrombus.

Thromboemboli: The etiology is not definitely known; however, left atrial dilation is the probable site of stagnant blood which comes in contact with exposed collagen (due to concurrent endomyocarditis) and begins to coagulate. LA thrombi are often noted at necropsy. These may break off and enter the systemic arterial circulation. Thrombi are reported in all forms of cardiomyopathy.

Clinical Findings of Feline Cardiomyopathy

Signalment: Average age, 6-9 years, with a wide range of 6 months to 13 years. Males are affected more commonly with HCM. Cats with restrictive cardiomyopathy tend to be older with an average age at diagnosis of approximately 9-12 years.

History: The cat may be asymptomatic or ill. Nonspecific signs of disease: Depression, reluctant to move. Anorexia, Relentless crying (secondary to pain from embolism). Dyspnea or tachypnea. Cough is somewhat unusual in cats with CM. Some cats vomit or retch. Thromboemboli inducing paralysis (usually to the rear limbs),vague neurologic signs, nondescript panful events (abdominal discomfort, muscle pain). Most owners do not notice significant premonitory signs of CHF owing to the fastidious nature of the cat. History of one diet (e.g. "off-brand")? taurine deficiency ? DCM.

Physical examination: Mucous membrane (MM) color and capillary refill time (CRT) are typically normal but marked disease especially complicated by pleural effusion, pulmonary edema and marked reductions in cardiac output may lead to abnormalities (cyanotic or pale MM, prolonged CRT). Jugular venous evaluation is commonly overlooked but abnormalities of the jugular veins (distension and/or pulsation provide strong evidence of signifcant cardiovascular disease. Abnormalities of precordial palpation may vary from a markedly increased precordial impulse associated with HCM to a diminshed apical impulse commonnly associated with DCM or pleural/pericardial effusion. It has been suggested that auscultatory abnormalities are present in greater than 80% of cats with clinically significant myocardial disease. Depending on the severity of disease the femoral pulses may range from normal to completely absent ( aortic thrombosis). The detection of pulse deficits suggests the presence of a hemodynamically significant arrhythmia and should prompt the clinician to perform an electrocardiogram.

Radiography: There is some overlap between forms of CM, thus a definitive anatomic diagnosis cannot always be made from survey thoracic radiographs. With hypertrophic CM the heart is typically "valentine" in shape with shifting of the apex to the midline, widening across the left atrium, maintenance of the apex "point", and possible evidence of left heart failure (pulmonary venous dilation, pulmonary edema, small pleural effusion. ( Note:cats have a tendency towards more diffuse cardiogenic edema).

Echocardiographic examination: Can usually determine the type of cardiomyopathy and give assessment of LA size and LV diameter, wall thickness and systolic and diastolic function (see text box).

Electrocardiography: Abnormalities of rate, rhythm,and conduction may be seen but the ECG is commonly normal.

Clinical Pathology: CBC, biochemical profile, urinalysis, pleural effusion analysis

Differential Diagnosis: Rule out other causes of dyspnea; paresis, or other causes of cardiac signs (murmur, cardiomegaly, abnormal ECG). Dyspnea/Tachypnea - a common sign of feline CM may be caused by other common disorders: Airway obstruction - foreign body, neoplasm, laryngeal paresis/paralysis, upper respiratory infection (URI). Primary pulmonary disease: bronchial asthma, lungworms, pneumonia, neoplasia, aspiration, vascular disease (heartworms). Mediastinal masses - lymphosarcoma (LSA). Pleural effusions (pyothorax, hemothorax, FIP, lymphosarcoma associated effusions, chylothorax). Trauma: diaphragmatic hernia, pulmonary hemorrhage/edema,pneumothorax.

The single most important laboratory test (following ausculation) for evaluation of dyspnea is a thoracic radiograph. One should be intimately familiar with the radiographic features of all of the previously mentioned diseases. If pleural fluid is strongly suspected based on physical examination, a thoracocentesis should be performed prior to obtaining radiographs. Cytologic examination of pleural fluid and ancillary tests (i.e. hemogram, FeLV test, etc.) will usually distinguish pleural effusions due to CM, FIP, LSA, chylothorax and pyothorax. The cat should be re-examined and the radiographs repeated following needle evacuation of the pleural fluid.

(Modifid from Dr Phil Fox with permission)

Asymptomatic But High Risk Cardiomyopathies

Certain structural and functional abnormalities associated with diastolic heart disease (HCM, RCM) may increase morbidity and mortality. Based upon studies in affected humans and experimental animals (Note- not clinical feline clinical trials), certain conditions may warrant specific therapies.

Myocardila Infarction (MI) may be suspected from echocardiography (regional LV hypokinesis/dyskinesis, or segmental LV free wall thinning). Cause(s) remain unknown. Beta-adrenergic Blockers [propranolol, 2.5 to 5mg q8 - 12h PO; atenolol 6.25 - 12.5mg q12 to 24h PO]decrease mortality in people with acute MI and cardiac arrhythmias, and reduce long term mortality in chronic MI by antiarrhythmic effects and by preventing reinfarction. Sympathetic nervous system antagonists may indirectly improve ventricular compliance by reducing heart rate and myocardial ischemia. Angiotensin-Converting Enzyme (ACE) Inhibitors (Enalapril, 0.5 mg/kg q24h PO; benazepril (0.25-0.5mg/kg q 24h PO: avoid use with hypotension) have been advocated in human post myocardial infarction trials based upon their role in reducing cardiovascular remodeling, improving hemodynamics, reducing ischemic events, and increasing survival. These agents appear to be quite safe in cats with heart disease.

Tachyarrhythmias diminish systolic and diastolic function, reduce diastolic filling (which can increase outflow gradients and reduce forward cardiac output), and thus increase myocardial oxygen utilization and ischemia. Beta-adrenergic blockers (propranolol, 5 - 10 mg q8 to 12h PO; atenolol, 6.25 - 12.5 mg q12 - 24h PO) antagonize the sympathetic nervous system, and may be useful for treating serious ventricular or supraventriculr tachycardias. While digoxin (0.031 mg [ie, 1/4 of a 0.125 mg tablet] per 4.5 kg cat q 48h PO) or diltiazem may be administered for atrial tachyarrhythmias, heart rate control often requires the addition of a beta-blocker which is titrated to effect.

Although the severity of hypertrophy is not a recognized risk factor for sudden death in human HCM, unfavorable prognosis may be associated with severe LV hypertrophy in some cats (LVd free wall or interventricular septal thickness > 8 mm). Beta-blockers may be used with the following rationale: 1) heart rate control (negative chronotropism) and associated indirect improvement of diastolic filling; 2) reduction of dynamic LV outflow tract obstruction; 3) reduction in myocardial oxygen utilization; 4) antiarrhythmic effects; 5) ability to blunt sympathetic myocardial stimulation. Clinical reduction of resting heart rate to 120-160 beats/min is usually attainable with atenolol (6.25 - 12.5 mg q 12 - 24h PO) or propranolol (5 - 10 mg q 8 to12h PO) for an average size (4.5 kg) cat. Calcium Channel blockers are often advocated based upon their action to promote positive lusiotropy (ie, to directly improve ventricular diastolic relaxation and filling). Diltiazem may slightly slow the heart rate in some cats but not in others, and heart rate reduction is much weaker compared with beta-blocker therapy. Several preparations of diltiazem are available. Diltiazem hydrochloride comes in 30 mg tablets and is dosed at 7.5 mg q 8 -12h. Cardizem CD© capsules can be compounded and dosed at 10 mg/kg q24h; Dilacor XR is dosed initially at 30 mg/cat q12-24h; some cats may tolerate 60 mg q 12-24h though anorexia and vomiting may occur. (Note: each Dilacor XR 240 mg capsule contains four controlled-released 60 mg tablets which can be broken in half to create a 30 mg dose.) ACE inhibitors may blunt neuroendocrine activation and prevent deleterious cardiovascular remodeling. ACE inhibitors have been used safely, most commonly added to other therapies (Enalapril, 0.25 to 0.5mg/kg q 24h PO).

Syncope Recurrent syncope is a risk factor for sudden death in humans with HCM. In cats, syncope can be associated with tachyarrhythmias, dynamic LV outflow obstruction (LVOTO), and ischemia (infarction). Symptoms can often be managed successfully with beta-blockers to reduce or abolish LVOTO.

Spontaneous Echo Contrast ("Smoke") and Stasis. Associated with blood stasis, spontaneous echo contrast is considered to presage thrombosis and is associated with increased thromboembolic risk. It should warrant antiplatelet drugs (aspirin, 25mg/kg q72hours) and perhaps more aggressive therapies.

"Malignant" Familial History (High Risk genotype) Pedigrees are occasionally identified with a documented heritable pattern of HCM with severe morbidity and mortality (eg, Maine coon cats, others). Early intervention with calcium channel blockers or beta-adrenergic blockers may be contemplated based on experimental considerations which hold that a pathway to the phenotypic expression of LV hypertrophy is influenced by triggers such as higher LV pressure and work load.

Myocardial Failure In some HCM cats LV contractility is mildly to moderately reduced (e.g., fractional shortening, 23-29%; LV end-systolic dimension, 12-15 mm). This can result from acute or chronic myocardial infarction, myocarditis, and other causes of LV remodeling. Oral taurine supplementation (250 mg q 12 - 24h) is initiated whenever myocardial failure is detected. ACE inhibitors may be added to counteract neurohormonal activation and reduce remodeling. Judicious beta-blocker therapy might be beneficial if myocardial infarction is suspected, or with tachyarrhythmia.

Symptomatic Cats With Diastolic Heart Failure

Acute Management of CHF
Pulmonary edema is rapidly progressive and life threatening. Initially, furosemide is administered IV (1- 2 mg/kg) every 1 to 2 hrs until the congestive state is substantially reduced. Then, the dosage frequency is reduced, typically to every 8 to 12 hours IM or SC. Peak diuresis usually occurs within 30 minutes of IV administration. Resolution of edema may be enhanced in the first 24 to 36 hours of therapy by adding the preload reducer, 2% nitroglycerin ointment (1/4 to ½ inch q 6hr cutaneously- alternate 12 hrs with and 12 hrs without nitroglycerine therapy to reduce tolerance). Supplemental oxygen (40 to 60% O2-enriched inspired gas) may improve pulmonary gas exchange. Clinical resolution is indicated by reduced respiratory rate and work of breathing, resolved lung crackles, and radiographic clearing of alveolar infiltrates (usually complete by 24 to 36 hours). The end point of diuretic therapy is relief of clinical signs or progressive increase in BUN and creatinine. Dehydration and hypokalemia can result from overzealous diuresis.

Chronic Management of CHF
There are currently no data to indicate the most effective therapies, whether combined therapy is more advantageous than monotherapy, or whether therapy is significantly better than no therapy. Drugs are administered on an empirical basis, relying on clinical experiences, biases, and theoretical benefits.

Chronic therapy is individualized to eliminate congestion; prevent arterial thromboembolism; halt, slow, or reverse myocardial dysfunction (theoretically); promote enhanced quality of life; and prolong survival. Udentifiable conditions (systemic hypertension, taurine deficiency, hyperthyroidism, anemia) are treated.

Diuretics. Furosemide is gradually decreased to the lowest effective dosage, typically, 6.25-12.5 mg q 12 - 24h). Some cats remain stable on 1- 2 mg/kg PO given every other day while in others, diuretics may be used twice weekly or even discontinued. In contrast, upward titration is may be necessary with recurrent CHF. Because diuretic resistance may occur as heart failure progresses, cats with recurrent CHF are likely to benefit acutely from intravenous furosemide which has higher bioavailability, or to administration of two diuretics. (see Recurrent and Refractory Congestive Heart Failure, below). It is prudent to assess BUN, creatinine, electrolytes and blood pressure in anorectic cats.

Beta-adrenergic Blockers. Prolonged activation of the sympathetic nervous system may lead to cardiovascular injury, disease progression, or arrhythmias. Since LV diastolic function is very sensitive to increases in sympathetic tone, by decreasing heart rate with beta-blockers, diastole is prolonged and passive ventricular filling and compliance may improve. Prolonged diastolic filling also allows more time for coronary blood flow and reduces myocardial ischemia. Beta-blockers decrease myocardial oxygen requirements by reducing cardiac sympathetic stimulation, heart rate, LV contractility, systolic myocardial wall stress, and systemic blood pressure. Dynamic LV outflow tract obstruction and related pressure gradient is often reduced or abolished with beta-blocker therapy. Propranolol (5 - 10 mg q8 - 12h PO) or atenolol (6.25-12.5 mg q12 - 24h PO) are commonly used agents. Adverse reactions are uncommon but include lethargy or hypotension.

Calcium Channel Blockers. These agents are used to enhance diastolic performance, may reduce heart rate (verapamil much more so than diltiazem) and blood pressure; exert a mild negative inotropic effect (reducing myocardial oxygen consumption); and improve rapid diastolic ventricular filling. Diltiazem is generally ineffective to resolve dynamic LV outflow obstruction. For diltiazem hydrochloride (Cardizem, 1mg/kg tid PO), the reported half life (t1/2) is 113 ± 24 minutes; peak concentration following oral administration was achieved in 45 ± 36 minutes; and bioavailability 50 to 80%. Clinically, this drug is dosed at 7.5 mg tid PO. A long-acting diltiazem formulation is Cardizem CD, 10mg/kg PO q 24h (t1/2 411 ± 59 minutes; peak concentration following oral administration achieved in 340 ± 140 minutes; bioavailability 22 to 59%). Another diltiazem preparation, Dilacor XR, is available in an extended release formulation. Each 240 mg capsules contains four controlled-released 60 mg tablets. Starting dose for a 5kg cat is 30 mg q 24h and titration to 60 mg daily is tolerated in some patients, although vomiting is a side effect.

Angiotensin Converting Enzyme (ACE) Inhibitors. Neurohormonal activation plays an important role in heart failure. Thus, disruption of neurohormonal activation represents therapeutic rationale for using ACE inhibitors. The RAS plays a prominent role in human HCM patients by influencing or regulating the expression of myocardial hypertrophy. Inhibition of RAS has a beneficial effect on extracellular remodeling in CHF, and ACE inhibitors reduce ventricular remodeling by blocking the tropic effects of angiotensin II on myocytes. There is also survival value provided by early use of ACE inhibitors in acute human myocardial infarction. Many clinicians combine an ACE inhibitor (usually enalapril) with furosemide, with or without a beta-blocker or diltiazem, particularly with recurrent heart failure. Enalapril (0.25-0.5 mg/kg q24h PO) and benazepril (0.25 - 0.5 mg/kg q24h PO) are clinically well tolerated. Optimal timing for ACE inhibitor therapy and the effects of these agents on morbidity and mortality in feline cardiomyopathy is undetermined.

Negative inotropic drugs that reduce or eliminate LVOT obstruction have been widely used in humans with the obstructive form of HCM. In cats reduction of outflow gradient is usually best accomplished with beta-blocker therapy. Stimuli that provoke or intensify LV outflow tract gradients should theoretically be avoided including positive inotropes, reduction of LV volume, or decreased afterload. The clinical importance of decreasing obstruction, particularly in asymptomatic cats, has not been established. However, beta-blockers reduce or abolish syncope associated with dynamic LVOT obstruction.

Recurrent and Refractory CHF
When pulmonary edema or biventricular failure reoccurs, emergency treatment may be required (see above- Acute Pulmonary Edema). Therapy is then modified to either 1) increase the diuretic dose, 2) increase the "primary" drug dose (i.e., beta-blocker, calcium channel blocker, or ACE inhibitor), 3) change to a different class of primary drugs, or 4) add a second or even third primary agent. When CHF recurs in spite of these manipulations, particularly with severe, chronic effusions, further upward dose titration of furosemide (e.g., 2 - 4 mg/kg q 8 - 12h PO) may be required. Probably more effective is selective nephron blockade- the addition of a second diuretic agent which acts at a different site in the nephron (and thus, act synergistically with furosemide). Hydrochlorothiazide (1-2 mg/kg PO q12 - 24h PO) and hydrochlorothiazide-spironolactone (Aldactazide, 2.2 mg/kg/day PO) have proven to be useful "second" diuretic agents. Close monitoring for dehydration, azotemia, hyponatremia, and hypokalemia is advised. Digitalization may be prescribed for unresponsive right-sided CHF, atrial fibrillation or myocardial (systolic) failure (see below). For continued refractory CHF: 1) ascertain that prescribed drugs are being administered as directed, 2) recalculate drug doses based on current body weight, 3) generate and re-evaluate a new data base (e.g., ECG, radiographs, echocardiogram, clinical pathology) to rule out systemic and metabolic disease, heartworms, neoplasia, 4) assess serum T4 concentrations (cats > 6 years old), and 5) refer to a cardiologist.

Systolic (Myocardial) Dysfunction

Initial Therapy
Treatment Goals Initial therapy is directed to reduce or eliminate pulmonary and systemic venous congestion, promote increased forward cardiac output, control serious tachyarrhythmias or bradyarrhythmias, and improve myocardial contractility. General supportive measures such as thoracocentesis, external heating to combat hypothermia, oxygen administration, and minimization of stress are important and include the following considerations:

Thoracocentesis: If breathing is compromised by severe pleural effusion (muffled heart and lung sounds, dull thoracic percussion note), thoracocentesis is advised, even before radiographs are taken.

Acute Pulmonary Edema: Life threatening pulmonary edema is uncommon with myocardial failure. When edema is severe, therapy is similar as was discussed above (see Diastolic Failure).

Inotropic Support: Synthetic sympathomimetic amines possess greater inotropic activity, provide quicker onset of action, and allow finer control than digoxin. Dobutamine (2-10 mg/kg/min constant rate infusion) is the preferred agent for hemodynamic support for severe myocardial failure. A common adverse side effect is seizures which are typically focal-facial, but occasionally become generalized. Often, they do not reoccur when the dose is reduced below 5 mg/kg/min.

Taurine Supplementation: Although taurine deficiency is now a rare cause of DCM, taurine is inexpensive and safe, and is empirically administered (250 to 500 mg q12h PO) for 8 weeks (re-evaluate by echocardiography).

Chronic Maintenance Therapy

Diuretics: When congestion is controlled, furosemide is tapered to the lowest effective dose. To manage chronic effusions, upward dose titration (2.2 to 4.2 mg/kg q8 - 12h PO) or sequential nephron blockade (additional diuretic agents such as hydrochlorothiazide and spironolactone) may be effective. Refractory cases may require periodic thoracocentesis.

ACE Inhibitors: These drugs may help blunt adverse neurohormonal alterations, limit progressive cardiac chamber remodeling (dilation), and prevent or delaying clinical deterioration. Enalapril monotherapy (0.5mg/kg PO daily) has been used to successfully manage some cases of mild idiopathic myocardial failure (%FS 23-29%; LVDs 12-14 mm). More severe systolic failure often require the addition of diuretics and digoxin.

Digitalis (Digoxin): While digitalis is the traditional agent for management of myocardial failure, there is little clinical data in cardiomyopathic cats, and digoxin's low therapeutic index makes its role controversial. Although higher plasma levels and more accurate dosing can be achieved with the elixer form, it is less palatable to cats than tablets. Renal insufficiency will reduce digoxin clearance and increase serum concentration. Digoxin can be given when a cat is hydrated and eating. Based upon a calculated dose of 0.005 to 0.01 mg/kg lean body weight and relatively normal BUN/creatinine, the following guidelines are suggested: for cats weighing 1.9 to 3.2 kg, ¼ of a 0.125-mg digoxin tablet (0.031 mg) every 2 to 3 days; for cats weighing 3.3 to 6.0 kg, ¼ tablet daily or every other day; and for cats weighing more than 6.0 kg, ¼ tablet daily (occasionally, q12h). Blood concentration should be evaluated 10 to 14 days after initiating therapy. When blood is drawn 10 to 12 hours post administration, a serum digoxin concentration of 1- 2 ng/ml is presumed to be therapeutic. Anorexia and depression are early signs of toxicity.

Arrhythmogenic Right Ventricular Cardiomyopathy (Arvc)

Right-sided CHF is treated with furosemide, digoxin, and an ACE inhibitor. For atrial fibrillation or atrial tachycardia, digoxin combined with diltiazem or atenolol is used to maintain the resting heart rate between 140 to 160 beats/min. Symptomatic ventricular tachycardia has been successfully managed acutely with lidocaine (10-40 mg/kg/min CRI), and chronically with sotalol (2-4mg/kg q12 hr PO).


More aggressive thrombolytic therapy should be considered when the thrombosis is thought to be of less than 8 hours duration. Streptokinase can be given intravenously at 90,000 IU for the fisrt hour and then 45,000 IU/hr for a total of 6-8 hours. This therapy should not be combined with heparin as excessive hemmorrhage may occur. Thrombolysis and resultant reperfusion may be associated with severe hyperkalemia and acidosis and associated rhythm abnormalities. Therefore thrombolytic therapy should not be attempted if electrocardiographic monitoring and rapid serial electrolyte/acid-base monitoring cannot be performed. Anuria is another contraindication to thrombolytic therapy usually indicating that renal infarction has occured.

The optimal therapy for prevention of initial or recurrent thromboembolic episodes is unknown. Aspirin administered at a dose of 25mg/kg PO Q3D has been the standard yet unproven recommendation. More recently clinicians have advocated the use of warfarin as the prophylactic anticoagulant of choice. Most cats are adequately anticoagulated when receiving 0.5 mg orally once daily but there is wide variation among patients requiring careful and frequent monitoring.. Recommendations for monitoring are varied. Historically the recommendation was to adjust the dose of warfarin to attain a PT of 1.3-1.6 times normal. It is now recommended that the PT=s be standardized using the international normalization ratio (INR).

INR= (patient PT ? control PT) ISI

ISI is the international sensitivity index of the thromboplastin used in the PT assay and is provided by the manufacturer for each batch produced. When using the INR the goal is to obtain Alow intensity warfarin therapy@ which translates to an INR of 2-3.

Treatment Goals: Therapy is directed toward 1) managing concomitant CHF or serious arrhythmias when present, 2) general patient support including nutritional supplementation, correction of hypothermia, and prevention of self mutilation, 3) adjunctive therapies to limit thrombus growth or formation, 4) close patient monitoring and 5) thrombus prevention. Limb and/or organ viability is enhanced by rapid resolution of arterial occlusion. Acutely affected cats are a high surgical/anesthesia risk.

Supportive Therapies: Various medical treatments have been proposed, although most are empirical and efficacy is unsubstantiated. Pain relief is most critical during the first 24-36 hours. It is also important to maintain hydration, electrolyte balance, and nutritional support. Placement of a nasoesophageal feeding tube is advocated for anorectic cats. Self mutilation is common following a saddle embolus and is characterized by excessive licking or chewing of the toes or lateral hock. Application of a loose-fitting bandage or stockinette is usually effective.

Thrombolytic Therapy: Streptokinase (loading dose [90,000 IU/cat over 20-30 minutes] followed by a constant rate infusion [45,000 IU/hr for 3 hours]) and urokinase generate the nonspecific proteolytic enzyme, plasmin, through conversion of the proen. Recombinant tissue-type plasminogen activator, t-pa (0.25 to 1.0 mg/kg/hr IV for a total dose of 1 to 10 mg/kg), has a lower affinity for circulating plasminogen and does not induce a systemic fibrinolytic state. It binds to fibrin within the thrombus and converts the entrapped plasminogen to plasmin. This initiates a local fibrinolysis with limited systemic proteolysis. Complications include bleeding and hyperkalemia (70%).

Anticoagulation Therapy: Heparin and warfarin (Coumadin©) have no effects on established thrombi. Their use has been based on the premise that by retarding clotting factor synthesis or accelerating their inactivation, thrombosis from activated blood clotting pathways can be prevented. Heparin binds to lysine sites on plasma antithrombin III, enhancing its ability to neutralize thrombin and activated factors XII, XI, X, IX; this prevents activation of the coagulation process. Efficacy in treating cats with thromboembolism has not been established and reported dosages vary widely. Low molecular weight heparins hold promise but doses have yet to be established. Warfarin impairs hepatic vitamin K metabolism, a vitamin necessary for synthesis of procoagulants (factors II or prothrombin, VII, IX, and X). Initial oral daily dosage (0.25 to 0.5 mg/cat) is adjusted to prolong the prothrombin time to twice the normal value, or it is adjusted by the international normalization ratio (INR) to maintain a value of 2.0 to 3.0. Hemorrhage is a potential complication.

Anti-Platelet Drugs: Exposure of blood to subendothelial connective tissue leads to rapid platelet activation, formation of platelet plugs and subsequent thrombus. Pharmacologic measures are directed to modify platelet aggregation. Aspirin induces a functional defect in platelets by irreversibly inactivating (through acetylation) cyclo-oxygenase. This enzyme is critical for converting arachidonic acid to thromboxane A2, which in the vascular wall is responsible for converting arachidonic acid to prostacycline. Thromboxane A2 induces platelet activation (through release of platelet adenosine diphosphate) and vasoconstriction (as does serotonin), while prostacycline inhibits platelet aggregation and induces vasodilation. In cats aspirin (25 mg/kg, or 1/4 of a 5-grain tablet q48 - 72h PO) inhibits platelet function for 3 to 5 days and is relatively safe. The optimal dose to inhibit thromboxane A2 production but spare vascular endothelial prostacyclin synthesis is unknown for cats.

Prevention/Treatment of Hypercoagulable States: Hyperhomocysteinemia occurs in some cats with thromboembolism. Supplementation with B vitamins based upon this strategy for affected people has been advocated for cats.



A "systolic dysfunction" syndrome (myocardial failure) with decreased LV ejection fraction and fractional shortening (FS%) similar to DCM in cats. There is significant decrease in myocardial inotropic state readily identified by echocardiography. Arrhythmias (especially atrial fibrillation) are common; tachycardia worsens the failure state by decreasing ventricular filling time. In atrial fibrillation, there is loss of the normal atrial "kick", which further decreases ventricular preload, especially at rapid ventricular heart rates.A-V anulus dilatation or papillary muscle atrophy often result in left or right A-V valve incompetency with MR/TR.Decreased cardiac output and renal and hormonal compensatory mechanisms lead to venous congestion causing left and/or right-sided heart failure.Acute ventricular arrhythmias may lead to syncope or sudden death and are very common in Doberman Pinscher dogs.

Clinical Syndrome

Signalment -
"Giant" breeds and other large dogs (> 15 kg). Occasionally other breeds especially Springer and Cocker Spaniels. Males > Females. Age - usually 2-5 years.

Client complaint and anamnesis
Animals are usually presented for signs referable to heart disease or CHF: Respiratory: Hyperpnea - tachypnea - dyspnea - orthopnea - coughing Weight loss - often dramatic; it can occur within the 2-4 weeks prior to admission; this cardiac cachexia is severe in some dogs like Doberman Pinschers, Weakness Lethargy - anorexia Abdominal distension (ascites) Syncope Some dogs are asymptomatic

Physical examination
Weight loss is common, weakness, depression, possibly cardiogenic shock (obtunded, hypothermic, pale), pulse abnormalities: Hypokinetic from decreased output and arrhythmias, Erratic, with pulse deficits when atrial fibrillation or VPC/ventricular tachycardia is present, abnormal jugular pulses from TR, arrhythmias, or right-sided CHF, hyperpnea and dyspnea are common due to pulmonary edema or pleural effusion, pleural fluid may be evident on percussion or auscultation, muffled breath sounds are heard if there is pleural effusion; crackles if there is pulmonary edema. Abnormal heart sounds including reduced intensity S1 (myocardial failure) with S3 or summation gallops is common (the gallop is especially loud when the dog is in sinus rhythm), left or right apical systolic murmurs (due to MR or TR) are usually soft ausculatatory evidence of cardiac arrhythmia, often atrial fibrillation (most common), slow capillary refill time; possible cyanosis from CHF, hepatomegaly with or without ascites, distended peripheral veins with right-sided CHF

Usually significant generalized cardiomegaly and CHF are evident, although LVE and LAE may be most evident in early cases. In Doberman Pinschers, marked LAE is the major finding, signs of CHF are common, including pulmonary venous congestion, pulmonary edema - often diffuse in Doberman Pinschers, pleural effusion, hepatomegaly, ascites

Tachycardia - often due to atrial fibrillation, sinus rhythm or sinus tachycardia with atrial or ventricular premature complexes, ventricular tachycardia is very common in Doberman Pinschers/Boxers, prolonged QRS (> 0.06 sec), possible increased voltages (R > 3.0 Lead II) suggesting LV dilatation, may have "sloppy" R wave descent with ST-T coving, suggesting myocardial disease; LV ischemia. may have low voltages (effusion, concurrent hypothyroidism)

Clinical Pathology -
Routine hematologic tests and urinalysis are usually normal unless altered by a) severe heart failure (e.g. pre-renal azotemia, elevated ALT, low Na, b) therapy for heart failure (e.g. hypokalemia and metabolic alkalosis from diuresis), or c) concurrent disease. Hypothyroidism may be present in some dogs as a complicating disease

Echocardiography -
Echocardiography is the "gold standard" for diagnosis. Dilated cardiomyopathy is characterized by dilation (eccentric hypertrophy) of the left and, typically the right heart chambers. Systolic wall and septal motion is poor, causing the left ventricular systolic as well as diastolic dimensions to be increased; thus, fractional shortening and other indices of myocardial function are reduced. Increased mitral valve E point to septal separation and reduced aortic root motion are common, while left ventricular freewall and septal thicknesses are normal to decreased.

Differential diagnosis is generally not difficult since giant breeds seldom develop symptomatic endocardiosis. Congenital disease can usually be eliminated by noting the lack of prior signs of congenital HD (i.e. no murmur). Heartworm disease, bacterial endocarditis, cardiac tumors, and pericardial disease should be ruled out. Some breeds develop both DCM and endocardiosis (e.g.s. Spaniels, standard Schnauzers, Afgan hounds)


Principles include:
  1. Control of arrhythmias and CHF. For atrial fibrillation, initiate long-term therapy with digitalis to increase contractility and slow ventricular rate, followed 72-96 hours later by judicious use of diltiazem (1.0-1.5 mg/kg, t.i.d.) or Beta blocker like propranolol or atenolol to further reduce the ventricular rate.
  2. Digoxin is used initially unless there are severe ventricular arrhythmias. A daily maintenance dose of .375 to .75 mg of digoxin (÷ BID) is given to most giant breed dogs. In general don't exceed .015 mg/kg/day and don't exceed .375 mg per day in Doberman
  3. Pinschers. If necessary, oral loading dose (2x maintenance dose) can be given the first 24-48 hours to dogs in atrial fibrillation. An ECG is recorded daily, and the heart rate and rhythm are noted.
  4. When there is AF, slowing of the ventricular rate response is achieved with chronic administration of digitalis and then either diltiazem or a beta-blocker (Inderal, atenolol, nadolol) until the ventricular rate is controlled at 100-150 bpm at rest.
  5. The above Rx merely controls the ventricular rate, by depressing A-V nodal conduction; it generally does not convert the rhythm from atrial fibrillation to sinus rhythm although this occasionally occurs.
  6. If ventricular arrhythmias are present then typically procainamide or sotalol is given.
  7. Signs of CHF are treated as discussed in previous chapters. Typical therapy includes: digoxin, furosemide, captopril or enalapril, and antiarrhythmic drugs as required.

If they can be stabilized, about 25-40% live for > 6 months. Our experience is most unfavorable for Doberman Pinschers. Sudden arrhythmic death is common, even when CHF is controlled.


Cause unknown, myocarditis, myocardial failure and the presence of ventricular arrhythmias are important. Dogs can be (1) asymptomatic with PVC's, (2) affected by ventricular arrhythmias, or (3) resemble dogs with CHF caused by "giant-breed" canine DCM. Keene has found carnitine deficiency in a family of Boxer dogs.

Signalment and history
6-11 year old Boxers, no sex incidence. Many signs are related to the presence of severe ventricular arrhythmias and include syncope, weakness, and collapse. Approximately 1/3 of the dogs in one study (Harpster) had heart failure, while another 1/3 were asymptomatic.

Physical examination
A small percentage have overt signs of CHF. The most common signs in many dogs are related to arrhythmias. One may auscult regular rhythms with premature beats, totally irregular rhythms, or regular sinus rhythms. 50% in Harpster's study also had mitral regurgitation murmurs.

Signs of left atrial, left ventricular and right ventricular enlargement with or without evidence of CHF may occur. Thoracic radiographs may be normal

Ventricular arrhythmias are most common. Less than 20% have normal rhythms. We have observed severe multifocal ventricular rhythms, paroxysmal and sustained ventricular tachycardias. The VPC's usually have a LBBB pattern (upright in lead II). APC's and atrial arrhythmias are less common but may also occur.


Involves management of the arrhythmias with expectations toward long-term control with quinidine, procainamide, or tocainide, (+/- a beta blocker) or sotalol (Betapace) for ventricular ectopia. Initial control may require lidocaine infusions, parenteral Pronestyl or quinidine, and hospitalization. Drug combinations and (?) prednisone (1 mg/kg/day x 2 weeks) may be needed for refractory arrhythmias.

For persistent supraventricular tachycardias, digitalis, diltiazem or propranolol are used.Medical management of CHF is indicated if signs of CHF are present as per "typical DCM". Beware using digoxin if VPC's are frequent. L-Carnitine - 2 qm t.i.d. may be given but L-Carnitine is very expensive


Almost 50% with ventricular arrhythmias (not CHF) will be alive after 1 year (Harpster). Our experience with fewer numbers is similar.


Diseases affecting primarily the pericardium account for approximately 1% of all patients with cardiovascular disease.1 Although primary pericardial disease represents a small percentage of the total number of cardiac diseases in small animals, it is an important cause of right heart failure in the dog. Pericardial disease of all types are uncommon in the cat.2,3 Several types of primary and secondary pericardial diseases occur, the most common of which are those resulting in the accumulation of pericardial effusion.

There are several congenital diseases of the pericardium recognized in small animal species. While peritoneopericardial diaphragmatic hernias (PPDH) are the most common type of congenital abnormality encountered 1, sporadic reports of partial pericardial defects 5,6 and intrapericardiac cysts 4 have been published. Congenital complete absence of the pericardium is quite rare.5

Pericardial Defects
Peritoneopericardial diaphragmatic hernias are commonly reported in dogs and cats. Peritoneoperi-cardial diaphragmatic hernias have been reported in littermates, but there is no reported evidence that the lesion is hereditary. It has been suggested that Weimaraners are predisposed to PPDH.6

A large portion (48%) of dogs and cats with PPDH are diagnosed prior to one year of age and another 36% are diagnosed between one and four years of age.6 Clinical signs are most commonly gastrointestinal (anorexia, vomiting, discomfort following a meal) or respiratory (cough, dyspnea). Signs of cardiac compromise (abdominal distention and acute collapse) may occur, but are uncommon.

Physical examination may reveal an apical impulse which is displaced or decreased in intensity. Cardiac murmurs may be detected if concurrent cardiac malformations are present. If the hernia is large and a significant amount of abdominal viscera has herniated, the abdomen may seem empty on palpation. Signs of CHF (ascites, jugular venous distension) may be present, but are uncommon. Concurrent defects (sternal malformations, cranial abdominal hernias) may be detected.

Thoracic radiographs are extremely helpful in establishing a definitive diagnosis of PPDH. Radiographic abnormalities may include: overlap of the caudal cardiac silhouette and cranial diaphragm, variable radiographic densities within the cardiac silhouette, gas-filled bowel loops crossing the diaphragm, and sternal malformations. Oral adminis-tra-tion of barium may help outline bowel loops present within the pericardial sac. Ultrasonography can readily identify the presence of abdominal viscera within the pericardial sac and help establish a definitive diagnosis

Surgical correction of the hernia with replacement of viable herniated viscera is the recommended therapy. Consideration of the severity of concurrent congenital malformations should be made prior to surgical intervention. In uncomplicated (no concurrent malformations) cases, the prognosis following surgical repair is excellent.


Pericardial Effusion
Diseases causing pericardial effusion are the most common causes of clinically significant pericardial disease in the dog.1 Idiopathic intrapericardial hemorrhage (Golden retrievers are overrepresented) with or without pericardial reaction and neoplasia of the heart, heart base, or pericardium are the most common causes of hemorrhagic effusion in dogs.1 Clinically important tumor types in dogs include hemangiosarcoma of the right atrium (especially common in German Shepherds and Golden Retrievers). Aortic body tumors (chemodectoma, nonchrom-affin paragangli-oma) with invasion of the heart base is most commonly seen in aged brachyce-phal-ic breed dogs, ectopic (heart base) thyroid carcinoma, mesothelioma of the pericardium, and metastat-ic carcinoma. - A well recognized but uncommon cause of intraperi-cardial hemorrhage in small breed dogs is left atrial tear secondary to severe chronic endocard-iosis of the mitral valve.


Special breed predilections have been noted previously. Most frequently, animals with pericardial disease are presented with vague signs. Clients will frequently describe lethargy, exercise intolerance, and anorexia. Occasionally, patients will be presented for signs of compromise of right heart function: abdominal distension, respiratory difficulty, or syncope.

Signs of elevated right heart pressures are consistently present in patients with clinically significant pericardial disease. Jugular venous distention or a positive hepato-jugular reflux are invariably present, but commonly overlooked. Heart sound intensity is frequently diminished. Lung sounds may be diminished if pleural effusion is present. Other auscultato-ry abnormalities (gallop rhythms, cardiac murmurs, arrhythmias) are uncommon. Dogs with left atrial tears secondary to chronic degenerative valvular disease will have a systolic murmur that may be decreased in intensity when compared to previous examinations. Hepatomegaly and free abdominal fluid are common findings. If the disease is chronic, significant weight loss may be observed.

Thoracic radiography usually demonstrates abnormalities when there is significant accumulation of pericardial fluid. The cardiac silhouette loses its angles and waists and becomes globe-shaped (Figure 3). Most cases are not "classic" and require integra-tion with the other data. Pulmonary vascularity is often reduced from low cardiac output in contrast to CHF from cardiomyopathy or valvular disease in which the pulmonary vascularity may be increased (especially the pulmonary veins). If CHF has developed, distension of the caudal vena cava hepatomegaly and pleural effusion are usually evident. Less commonly, distension of the pulmonary veins and increased pulmonary interstitial densities (edema) may be detected. Heart base tumors may deviate the trachea and produce a mass effect.

Although there are no pathognomonic electrocardiographic findings for pericardial disease, there are several electrocardiographic abnormalities that are commonly seen. Electrical alternans is a beat-to-beat voltage variation of the QRS or ST-T complexes. It may be recorded in as many as 50% of patients with pericardial effusion. Elevation of the ST segment is commonly recorded in patients with pericardial disease. This represents an epicardial injury current. Reductions in QRS voltage (R < 1 mV in Lead II) are commonly recorded in dogs with pericardial effusion. Low electrocardiographic QRS voltage is considered a weak predictor of the presence of pericardial effusion. In the author's experience, arrhythmias other that sinus tachycardia are uncom-mon in primary pericardial disease.

Echocardiography is the most sensitive and specific non-invasive method of detecting pericardial effusion currently available. The hemodynamic consequences of pericardial effusion depend not only on the amount of pericardial effusion present, but also on the rapidity with which the effusion has accumulated. A small or moderate amount of fluid accumulating rapidly (left atrial rupture) may produce significant hemodynamic compromise, while a large amount of effusion accumulating over months may have little hemodynamic effect. These principles should be remembered when assessing the significance of an echocardiographically-detected pericardial effusion. Echocardiography can detect as little as 15 ml of intrapericardial fluid. An anechoic space between the epicardium and pericardium is the classic echocardiographic finding in pericardial effusion. Cardiac motion is commonly abnormal often with dramatic side-to-side movement and diastolic compression. Overall cardiac chamber size is usually diminished due to impaired cardiac filling. Intrapericardiac or cardiac mass lesions may be visualized.


Pericardiocentesis is the treatment of choice for initial stabilization of dogs and cats with pericardial effusion and cardiac tamponade. When per-formed properly, pericardiocentesis is associated with minimal complications. Prior to performing pericardiocentesis, it is necessary to shave and surgically prepare a large area of the right hemithorax (sternum to mid thorax, third to eighth rib). Local anesthesia is usually adequate; however, mild sedation is sometimes necessary. It is important to insure that the pleura has been infiltrated, as pleural penetration seems to cause significant discomfort. The patient is placed in sternal or lateral recumbency, depend-ing on demeanor. Occasionally, pericardiocentesis can be accomplished in the standing animal, but adequate restraint is essential to prevent cardiac puncture or pulmonary laceration. Electrocardiographic monitoring during the procedure is helpful since epicardial contact often causes ventricular arrhythmias.

The puncture site is usually determined based on the location of the heart on thoracic radiographs. This is most commonly between the fourth and sixth rib spaces at the costo-chondral junction. Ultrasound guidance is infrequently necessary unless the volume of effusion is very small or the effusion is compartmentalized. The size of the needle or catheter used is dependent on the size of the animal. In cats, a 19 to 21 gauge butterfly catheter may be adequate, while in large dogs, a 16 gauge over-the-needle catheter (usually with additional side holes) may be needed. The needle or catheter should be attached to a 3-way stopcock, extension tubing, and a syringe, to allow constant negative pressure to be applied during insertion and drainage. Care should be taken to avoid the large vessels that run along the caudal border of the ribs. Once the catheter has been inserted through the skin, negative pressure should be applied. If pleural effusion is present, it will be obtained immediately upon entering the thoracic cavity. It is most commonly a clear to pale yellow color. As the catheter is advanced and contacts the pericardium, a scratching sensation will be noticed. Minimal advancement will result in penetration of the pericardium.

Most pericardial effusions are hemorrhagic and have a "port wine" appearance. Once effusion of this character is obtained, the catheter should be advanced over the needle, and the needle removed. The remainder of the drainage should be performed using the catheter. Advancing the needle too far will result in contact with the epicardium. This is often felt as a tapping or more intense scratching sensation and commonly results in ventricular arrhyth-mias. These arrhythmias are usually self-limiting following retraction of the needle or catheter.

Pericardial effusion can be differentiated from peripheral blood in that it rarely clots unless it is from very recent hemorrhage and the PCV is significantly lower than that of peripheral blood. Every attempt should be made to drain the pericardial space as completely as possible. Drainage of the pericardium is often associated with an increase in the complex size on the ECG, a reduction in heart rate, and an improve-ment in arterial pulse quality. Potential complications include cardiac puncture (with resultant hemorrhage or arrhythmias), coronary artery laceration, lung puncture or laceration, and dissemination of infection or neoplasia throughout the thoracic cavity. Diagnostic evaluations of fluid obtained should include PCV and cytologic evaluation. Bacterial culture and sensitivity should be performed if indicated by cytologic evaluation. Caution should be exercised when evaluating the cellular component of pericardial effusion. Clinically important neoplasia of the heart and pericardium (hemangiosarcoma, chemodecto-ma) commonly do not exfoliate, resulting in frequent false negative evaluations. Reactive mesothelial cells within the pericardial sac are commonly over interpreted as being neoplastic, causing false positive results.

The long-term prognosis for dogs with hemorrhagic effusion is dependent on the underlying etiology. With idiopathic hemorrhagic pericardial effusion, pericardiocentesis is curative in approximately 50% of the cases. In the remainder, repeat centesis is necessary to control clinical signs. Fluid may reaccumulate rapidly (within several days) or may not recur for months to years. In patients requiring more than 2 centeses, the author recommends subtotal pericardiectomy. Following the initial pericardial tap, administration of oral prednisolone (starting at a dose of 1 mg/kg orally every 12 hours, then gradually tapering off over a two to three week period) may be beneficial. Although antiinflam-matory doses of prednisolone are commonly administered to dogs with idiopathic pericardial effusion, there are no controlled studies to confirm the efficacy of this therapy. Subtotal pericardiectomy is usually curative in dogs with idiopathic pericardial effusion.

If cardiac or pericardial neoplasia is the cause of the pericardial effusion, the recommended therapy is subtotal pericardiectomy. The prognosis is again dependent on the nature of the underly-ing etiology. Aortic body tumors are commonly associated with slow growth and are late to metastasize. Subtotal pericardiectomy may afford palliation for up to three years.5 Hemangiosarcoma of the right atrium is associated with a poor long-term prognosis. Most mass lesions involving the right atrium or right ventricle are not amenable to surgical removal. The tumor has commonly spread to the lungs at the time of diagnosis and these patients may have neoplastic lesions in the spleen or liver as well. In those patients, subtotal pericardiectomy should be considered palliative.

Recent reports have suggested that both thorascopic pericardiectomy and percutaneous pericardial balloon dilation may be reasonable alternatives to subtotal pericardiectomy in both neoplastic and benign effu-sions. These techniques allow the pericardial fluid to drain into the pleural space to be reabsorbed. This may provide significant palliation for patients with pericardial effusion and the resultant cardiac tamponade without necessitating a thoracot-omy. These therapeutic modalities warrant further evaluation in canine patients.

Pericardial diseases appear to be quite uncommon in cats.2,3 Recent reports addressing the topic suggest that the most common single cause of pericardial disease in the cat is feline infectious peritonitis (FIP).2,3 FIP infection can cause massive accumulations of intrapericardial fluid and resultant cardiac compromise. Pericardial effusion is common secondary to cardiomyopathy. Echocardio-graphy can readily detect pericardial effusion and determine the nature of concurrent myocardial disease. Peritoneopericardial diaphragmatic hernias may go undiagnosed for years in cats. Sternal abnormalities are commonly observed along with PPDH. Frequently, only falciform fat and liver will be present within the pericardial sac, making barium contrast studies less informative in cats than it is in dogs.

  1. Buchanan, JW. Causes and prevalence of cardiovascular disease. In: Kirk RW,Bonagura JD, edsKirk's current veterinary therapy XI: Small animal practice, Philadelphia: Saunders,W., 1992; 647-655.
  2. Rush JE, Keene BW,Fox PR. Pericardial disease in the cat: a retrospective evaluation of 66 cases. J Am Anim Hosp Assoc 1990;26:39-46.
  3. Harpster, NK. The Cardiovascular System. In: Holzworth J, ed Diseases of the Cat. Medicine and Surgery, Philadelphia: W.B. Saunders, 1987; 820-887.
  4. Sisson D, Thomas WP, Reed J, Atkins CE,Gelberg HB. Intrapericardial cysts in the dog. J Vet Intern Med 1993;(In Press)
  5. Miller MW and Sisson DD. Pericardial Disorders. In: Ettinger SJ and Feldman EC, eds Textbook of Veterinary Internal Medicine, ed. 5th Philadelphia: W.B.Saunders, 2000; 923-937.
  6. Reed, JR. Pericardial Disease and Cardiac Tumors. In: Fox PR, Sisson DD and Moise NS eds Canine and Feline Cardiology, Philadelphia: W. B. Saunders, 1999; 679-701.

© 2003 - Matthew W. Miller, DVM, MS, DACVIM - All rights reserved