By Phillip Taylor,2014-06-26 20:21
9 views 0


     Congestive heart failure (CHF) in the dog is a clinical syndrome initiated by a cardiac lesion and characterized by hemodynamic abnormalities (limited cardiac output, increased vascular resistance, elevated venous pressures), activation of neurohormones and various cytokines, and renal retention of sodium and water. Many of the clinical signs of acute CHF stem from fluid accumulation in the lungs or pleural space. Clinical signs include tachypnea or hyperpnea often with cough exercise

    intolerance, and varying degrees of respiratory distress. Orthopnea is also a common sign. Signs related to hypotension (hypothermia, profound weakness, or depression) are variable.

     Heart failure in dogs most often develops consequent to mitral/tricuspid valvular disease, dilated cardiomyopathy, or cardiac tamponade. Bacterial endocarditis, pulmonary thromboembolism, hypertrophic cardiomyopathy, myocardial infarction, myocarditis, myocardial neoplasia, relentless tachyarrhythmias, severe

    bradyarrhythmia, dirofilariasis, and congenital heart disease are other causes of CHF in dogs. Most of these are chronic or subacute lesions; however, heart failure can become “acute” when cardiac lesions rapidly develop, or when progressive signs of

    cardiac decompensation are unrecognized or ignored. Examples of “acute” cardiac lesions in dogs include ruptured mitral valve chordae tendineae, the sudden onset of atrial fibrillation in a dogs with previously-compensated disease, acute myocardial infarction (rare), and massive pulmonary thromboembolism. Some dogs with dilated cardiomyopathy (DCM) are presented for signs of “acute” CHF, though they have been treated previously for “pneumonia.” Cardiac tamponade, a cause of both acute and

    chronic heart failure, is not treated medically.


     The diagnosis of CHF is not particularly difficult provided a complete examination can be undertaken. However, the severity of respiratory distress may preclude such evaluation, and initial treatment may be empiric based on inspection of the patient (level and type of respiratory distress), a rapid examination of pulses, precordium, mucous membranes and abdomen, and expedient auscultation and percussion of the heart and lungs. Diagnostic studies crucial in establishing the diagnosis of heart failure include 1) careful examination for gallops, murmurs, or arrhythmias; 2) detection of pulmonary edema (crackles or loud bronchial sounds + tachypnea) or pleural effusion (muffled sounds ventrally + tachypnea); 3) exclusion of primary thoracic or airway diseases (typically by thoracic radiography); and 4) echocardiography to verify the cause of heart failure. The precise staging of diagnostic examinations depends on the presentation and stability of the dog. Some patients are best treated with furosemide and supplemental oxygen (+/- nitroglycerin & sedation), with continuous observation for an hour or so. This initial stabilization often permits additional studies to be safely performed with less struggling. Other diagnostic tests may include: arterial blood pressure (ABP) measurement; thoracocentesis with fluid analysis; an electrocardiogram; a serum biochemical profile; a CBC; urinalysis; blood cultures (in suspected bacterial endocarditis); heartworm test; pulse oximetry; or arterial blood gas determinations.

     The vast majority of dogs with “acute” CHF have pulmonary edema with varying

    degrees of pleural effusion, and are affected by either advanced mitral regurgitation (MR) from endocardiosis or dilated cardiomyopathy (DCM). Since most of the compensations activated in CHF are designed to maintain ABP, most dogs have a normal systolic ABP at presentation or within an hour of initial stabilization. This is especially true in cases of MR. Dogs with DCM are more often hypotensive and more likely to require aggressive inotropic support during the first 48 hours of treatment. Occasionally, dogs with MR are overtly hypertensive (probably from concurrent renal disease), and may require aggressive treatment to reduce arterial blood pressure to an

acceptable range. The resting heart rate is also inconsistent in dogs with CHF. While

    typically regular and increased (120 180/min), the heart rate can be slower.

    Furthermore, the rhythm can be irregular from sinus arrhythmia, atrial fibrillation, or



     Goals of therapy include: increasing the pO and reducing oxygen demand; 2

    reducing venous pressure and the tendency towards edema formation; and maintaining

    cardiac output and tissue perfusion. The first goals can generally be attained by with

    supplemental oxygen therapy along with sedation (if needed). If there is a moderate to

    large pleural effusion, thoracocentesis will decrease pulmonary atelectasis. Ascites

    sufficient to impair ventilation can be reduced by about 1/3 with abdominocentesis,

    leaving the balance of the fluid (and protein) for medical management. Infrequently,

    artificial ventilation is needed. Diuresis and venodilator therapy act in concert to reduce

    venous and capillary hydrostatic pressures. Cardiac output and tissue perfusion are

    addressed by unloading the left ventricle, providing inotropic support, if needed, and

    titrating treatment to the measured ABP. When acute CHF is complicated by cardiac

    arrhythmias, additional treatments may be needed. An appropriately-equipped and

    staffed hospital should be able to perform the following procedures:

    - Conduct an efficient but careful history and physical examination

    - Safely sedate dyspneic or stressed patients

    - Obtain “non-stressed” radiographs and clinical laboratory tests

    - Recognize pleural effusion and perform thoracocentesis

    - Measure arterial blood pressure noninvasively

    - Monitor, record and interpret electrocardiogram rhythm strips

    - Administer oxygen therapy

    - Intubate, suction the airway, and mechanically ventilate the patient if required

    - Stock and effectively use cardiovascular drugs

    - Manage the transition from “acute” hospital to “chronic” home care

     Medical therapy is appropriate initial management of virtually all causes of congestive

    heart failure except when the condition is pericardial effusion with tamponade (in which case,

    the treatment is pericardiocentesis). The following caveats should be considered. First handle

    the dog gently and don’t position the patient on its back for radiographs! If you believe there is

    a large pleural effusion, perform thoracocentesis immediately. If the dog is struggling to breathe,

    appears frantic, or resists handling, sedate the patient. There is no perfect sedative for CHF.

    Morphine sulfate has theoretical benefits and is dosed at 0.05 to 0.1 mg/kg, IM or SQ (give 25%

    SQ, wait 15 minutes; then administer the balance). Beware vomiting which can precipitate

    cardiac arrest. The combination of acepromazine (0.025 mg/kg) mixed with buprenorphine

    (Buprenix 0.05 to 0.01 mg/kg) or butorphanol (0.2 - 0.4 mg/kg) can be used intramuscularly.

    Provide oxygen by face mask, cage, tent or nasal catheter if the patient will tolerate it. If not,

    direct the airflow of a fan to the face (there are receptors in the face which may be activated and

    reduce the “dyspneic” situation). Allow the dog to stabilize with continual observation. A small

    catheter line can be placed into a peripheral vein for IV treatments; however, one should avoid

    parenteral fluid therapy other than to provide a vehicle for drugs like dobutamine or sodium

    nitroprusside. Remember that most dogs will drink once they can breathe. In my opinion, a

    central venous line is neither needed nor worth the struggle in dogs with dyspnea from left-sided

    CHF. A central venous pressure does not accurately predict the pulmonary capillary wedge

    pressure in MR or DCM, and a large catheter line is unnecessary since volume replacement

    even “maintenance” fluid therapy – is the wrong initial treatment for CHF. If desired, a Swan-

    Ganz thermodilution catheter can be floated to measure occlusion (wedge) pressure, pulmonary

    artery pressures, and cardiac output. However, few practices are equipped for this

    instrumentation, and as of yet there is no compelling evidence that such monitoring improves

    the outcome in dogs. It is important to tabulate and trend important clinical signs: body

    temperature, respiratory rate and depth, breath sounds, heart rate, heart rhythm, mucous

    membrane color and refill time, pulse strength, attitude, and noninvasive arterial blood pressure,

and possibly pulse oximetry values. A number of specific treatment plans have proven useful

    for urgent management of CHF in the dog as summarized below.


     FON - Furosemide, Oxygen, and Nitroglycerine Ointment - This form of therapy is

    applicable to most cases of CHF regardless of cause, and is especially effective in mild to

    moderate pulmonary edema. Diuresis is initiated, pO is increased, and the tendency towards 2

    edema is reduced. Loop diuretics are carried by renal blood flow to the proximal nephron

    where they are actively secreted into the filtrate before passing to the loop of Henle. In severe

    CHF with impaired renal perfusion, furosemide may not be effectively delivered to the proximal

    nephron. For this reason, we often use a relatively high initial furosemide dose (4 to 5 mg/kg,

    IV) in severe cases of CHF. The dog is checked every 30 minutes for evidence of diuretic effect

    (observation for urination and palpation of the urinary bladder). Once diuresis ensues, the dose

    is reduced to 2 mg/kg q8-12h, IV or SQ. Nitroglycerine ointment (1 to 2 inches, cutaneously,

    q12h), if effective, works by pooling blood in capacitance veins. Most mild cases of CHF will

    respond to this treatment.

     FON-H - Furosemide, Oxygen, Nitroglycerine Ointment, and Oral Hydralazine - This

    form of therapy is applicable to most cases of severe left-sided CHF caused by MR, and works

    by lowering left atrial and pulmonary venous pressures. Clinical indications for this treatment

    include nasal frothing or hemoptysis, severe respiratory distress, lack of response to simple

    FON, or a “white-out” lung of fulminant pulmonary edema as seen radiographically. Most of

    these dogs have normal arterial blood pressure (especially after brief cage rest and initial FON

    treatment) and can tolerate the afterload reducing effects of hydralazine (usually 1 to 2 mg/kg,

    PO, q12h). In our experience, unloading the left ventricle with oral hydralazine is more likely

    to significantly reduce the mitral regurgitant volume acutely than is treatment with an oral ACEI.

    A more potent alternative to FON-H is to substitute the “balanced” vasodilator, sodium

    nitroprusside (Nipride, 0.5 to 5 mcg/kg/min, IV infusion; follow label directions for formulation), for the nitrate ointment and hydralazine. Frequent ABP monitoring should be

    done. We typically titrate the doses of these vasodilator drugs to a systolic ABP of 85 to 95 mm

    Hg (as well as clinical signs) and continue treatment for 24 to 72 hours. Once the situation is

    stable, we stop the nitrate/hydralazine (or taper the nitroprusside dose over about 6 hours), and

    substitute these treatments for home care (see below).

     FON - D - Furosemide, Oxygen, Nitroglycerine Ointment, and Dobutamine - This

    form of therapy is applicable to cases of cardiogenic shock (pulmonary edema or pleural

    effusion with hypotension) and other forms of CHF with low cardiac output (e.g., massive

    pulmonary embolism). Dilated cardiomyopathy dogs (often Doberman pinschers) represent the

    typical case. The administration of arterial vasodilator drugs to overtly hypotensive dogs is

    contraindicated. Dobutamine (or dopamine) can effectively increase ABP in these dogs

    primarily by a positive inotropic effect (at lower doses) or by arterial vasoconstriction or

    increased heart rate (at higher doses, generally > 5 mcg/kg/min). Neither vasoconstriction

    (afterload mismatch) nor sinus tachycardia (increased oxygen demand) represent an advantage

    to a failing left ventricle. It is preferable to increase cardiac output by stimulating myocardial

    contractility (and filling). First administer furosemide, oxygen & nitroglycerine ointment.

    Allow the patient at least 15 to 30 minutes to stabilize and while preparing the dobutamine

    solution. Place an IV in a peripheral vein. Attach ECG monitoring leads if available. Prepare

    the dobutamine solution in 500 ml of 5% dextrose in water with 8 mEq of KCl added per 500

    ml. Prepare a stock solution of dobutamine for dogs as follows: 1) Obtain crystalloid solution

    and needed infusion set(s); 2) Add KCl 8 mEq per 500 ml D5W; 3) Add 250 mg of dobutamine

    to the 500 ml of 5% dextrose solution (yielding an approximate concentration of 500 mcg

    dobutamine per ml); 4) Hang the bag of 500 ml D5W with additives, attach the appropriate

    infusion set for accurate control, and flush and prime the line with dobutamine solution. 5)

    Attach the infusion line to the infusion pump. Begin the dobutamine infusion (2.5 mcg/kg/min),

and try to increase the dose after 30 to 60 minutes (to 5 mcg/kg/min).

     Use the following guide for a 5 microgram/kg/minute infusion rate; adjust as needed

    Weight in kg Micrograms per minute mcg needed per hour ml of fluid per hour

    10 50 3000 6

    20 100 6000 12

    30 150 9000 18

    40 200 12000 24

    50 250 15000 30

    60 300 18000 36

Re-measure the clinical trend variables often (see above). Doses greater than10

    mcg/kg/min are rarely used in our hospital. Therapeutic effects of dobutamine include

    increased cardiac output, elevated ABP, increased tissue perfusion (better color and

    shorter refill time, stronger pulse), increasing body temperature, and improvement in

    attitude and strength. Adverse effects, necessitating dose reduction, include increasing

    heart rate, excessive vasoconstriction, and induction of extrasystoles. Seizure activity

    and vomiting are infrequently observed. Once the ABP is stable (systolic pressure 90

    to 120 mm Hg), other vasoactive drugs can be added to treatment. As a minimum,

    enalapril or benazepril (0.25 to 0.5 mg/kg, PO once or twice daily, depending on ABP)

    is begun since this benefits neurohormonal status, reduces aldosterone secretion, and

    reduces afterload. This seems the most practical vasodilator to add in this setting, as it

    will also constitute part of the home treatment. Alternatively, sodium nitroprusside (see

    above) can be initiated at 1 mcg/kg/min and titrated to a systolic ABP of 85 to 90 mm

    hg if there is marked pulmonary edema. After 48 hours of therapy, reduce the

    dobutamine rate by 50% every 2 4 hours until you have reached 2.5 ug/kg for 4 hours,

    then stop the infusion. If you cannot wean the patient from dobutamine (i.e. ABP is too

    low), up the infusion rate to increase ABP and either increase the enalapril (to 0.5

    mg/kg PO b.i.d.) or add hydralazine (0.5 to 1 mg/kg, PO, b.i.d.). Eventually establish

    home therapy with oral furosemide, an ACEI, and digoxin.

     Heart Failure with Arrhythmia - When CHF is complicated by atrial fibrillation, digoxin

    is also prescribed. In general, digitalis glycosides are not particularly useful in the initial therapy

    of CHF; however, in the setting of atrial fibrillation, digoxin should be initiated to slow the

    ventricular rate response. After confirming the rhythm diagnosis with an ECG, administer

    digoxin (Lanoxin, Cardoxin) using a modified loading dose (0.01 to 0.015 mg/kg bid for two

    doses), then begin, maintenance treatment (0.005 mg/kg PO q12h). After 24 to 48 hours, if there

    has been satisfactory control of CHF, add either a beta blocker (propranolol starting at 0.25

    mg/kg PO q8h) or the calcium channel antagonist, diltiazem, (starting at 0.5 mg/kg PO q8h) to

    the regimen to better control ventricular rate response. Beware the negative inotropic effects of

    these drugs. In settings of severe CHF with ventricular tachycardia, it may be worthwhile to

    consult with a cardiologist. In the interim, lidocaine (2 mg/kg IV boluses; 40 60 mcg/kg/minute, IV infusion) or procainamide (2 mg/kg IV boluses to 10 mg/kg; or 10 to 20

    mg/kg IM q6h; or 25 40 mcg/kg/min IV infusion) can be used. Procainamide is a negative

    inotropic drug and may also result in peripheral vasodilation.


     After 24 to 72 hours of hospital therapy, and following completion of the initial diagnostic workup (thoracic radiographs, serum biochemical profile, ECG, echocardiogram), oral home therapy is begun. This treatment consists of a maintenance dose of furosemide (typically 2-4 mg/kg, PO, bid), an angiotensin converting enzyme inhibitor (ACEI; i.e., enalapril, benazepril, or lisinopril), and often digoxin (0.005 mg/kg, PO, bid). Oral furosemide does not appear to be equipotent to parenteral furosemide (probably related to absorption and delivery); therefore, switching to the same oral dose is probably analogous to reducing the dose by 25 to 50%. For ACEI, we most often use enalapril starting at 0.5 mg/kg/day. It may be useful to repeat renal function tests at the time of release for future comparison and to guide medication dosages. We typically re-evaluate the patient in 7 to 14 days. At that time, an examination, ABP measurement, and serum biochemical profile are performed. Clinical signs determine if another chest x-ray or ECG is needed. A repeated echocardiogram is unnecessary and rarely guides adjustments in drug dosages. At this visit we usually increase the dose of enalapril to 0.5 mg/kg/day b.i.d if renal function and ABP are satisfactory (i.e. BUN or creatinine have not increased by > 2 times baseline and systolic ABP is >90 mm Hg). This is especially important in dogs with DCM. Diuretic and ACEI therapy is always individualized to thwart fluid retention (increasing doses for progressive edema), or to mitigate azotemia or hypotension (decreasing doses to improve renal perfusion or filtration fraction). Digoxin is prescribed for home care in advanced CHF and especially in dogs with atrial fibrillation. Relative contraindications to digitalis include complex ventricular ectopia, azotemia, sinus node dysfunction, or pre-existent atrioventricular block.


    John D. Bonagura, D.V.M., DACVIM

Introduction The pericardium functions to limit acute cardiac dilatation, maintain

    cardiac geometry and ventricular compliance, reduce friction, provide a barrier to inflammation from contiguous structures, and buttress the atria. A small amount of fluid is normally found between the epicardial (visceral pericardial) and the parietal pericardial membranes. The term pericardial effusion indicates excessive or abnormal

    accumulation of pericardial fluid has developed. Pericardial effusion or constriction (of the heart) may impair cardiac function by interfering with normal cardiac filling. When the heart is compressed, intrapericardial pressure rises, and cardiac filling is impaired, a state of cardiac tamponade is said to be present. Congenital hernias, intrapericardial

    cysts (rare), and acquired causes of pericardial effusion are the most clinically relevant disorders of the pericardium in small animal practice.

Peritoneopericardial Diaphragmatic Hernia Important congenital forms of pericardial

    disease include congenital peritoneopericardial diaphragmatic hernia and the rare congenital cysts. Hernias are common in cats and can develop in dogs (Weimaraner dogs predisposed). It is typical for the hernia to contain only fat and hepatic lobes in the cat; whereas, in the dog the hernia more often contains loops of intestine. Careful radiographic examination leads one to suspect the diagnosis. One typically observes altered radiographic density in the caudoventral portion of the pericardial space. Ventral to the caudal vena cava there may be a persistent mesothelial remnant

    indicating the dorsal border of the hernia. Often the carina is displaced cranial relative to the caudal border of the heart. Ultrasonography or a barium swallow (if intestinal loops are present) is diagnostic studies. Cardiac tamponade is an infrequent

    complication and urgent care is more likely to become necessary should there be entrapment of a loop of bowel or strangulation of the liver. The condition is treated surgically, but since the hernia is often an incidental finding in mature animals, the

situation may not warrant intervention.

Pericardial Effusion Acquired pericardial effusion, is very common in dogs and is

    observed sporadically in cats. Transudation into the pericardial space secondary to

    right-sided CHF, peritoneopericardial diaphragmatic hernia, cysts, hypoalbuminemia, or infections/toxemia (or other causes of increased vascular permeability). These accumulations tend to be necropsy or ultrasound findings and not impair heart function. There are two noteworthy clinical exceptions. Mass lesions at the heart base can obstruct lymphatic drainage leading to a large and compressive, water-like, transudative pericardial effusion. In cats with severe CHF, a very large pericardial effusion may develop which may resolve with successful therapy of heart failure. Exudation caused by infective or non-infective pericarditis is not common in small

    animals. In the dog and cat, Nocardia infection and perforating foreign bodies are potential causes. Fungal involvement of the pericardium is recognized with Coccidiomyocosis in the dog or with opportunistic fungi in immunosuppressed dogs (e.g. aspergillosis). Idiopathic, sterile (inflammatory) pericarditis can develop occasionally in the dog and may be a sequelae to some cases of recurrent, idiopathic intrapericardial hemorrhage. Pericarditis has been associated infrequently with feline cardiomyopathy. It can occur as part of the polyserositis from infection with feline infectious peritonitis virus. Intrapericardial hemorrhage (with or without secondary

    pericardial reaction) is not uncommon. The most frequent cause is idiopathic pericardial hemorrhage in dogs. This is a disorder of dogs typically less than 8 years of age. In some areas, golden retrievers are predisposed. Neoplasia of the heart, heart base, or pericardium frequently leads to a hemorrhagic effusion. Hemangiosarcoma of the right atrium (especially common in >8 year old German Shepherd dogs, golden retrievers, and Labrador retrievers), can be multicentric with splenic involvement and pulmonary metastasis. Aortic body tumors (chemodectoma) grow along the heart base (and are especially common in aged brachycephalic breed dogs). Ectopic (heart-base) thyroid carcinoma can cause a large heart base mass that can invade the myocardium. Mesothelioma of the pericardium also occurs but is often a controversial diagnosis in light of so-called pericardial fronds, which can develop in dogs with recurrent pericardial effusion. Metastatic carcinoma to the heart is not common. Lymphosarcoma of the right atrium and ventricles is the most important cardiac neoplasm in the cat, but is considered a rare cause of pericardial effusion in dogs. Uncommon causes of pericardial hemorrhage include: left atrial rupture in dogs with mitral regurgitation; blunt chest trauma; puncture of the heart (knife, bullet, and missile); coagulopathy, and complicated thoracocentesis. Chyle is a very rare fluid

    type in pericardial effusions.

Pathophysiology Cardiac tamponade refers to "the decompensated phase of cardiac

    compression resulting from an unchecked rise in the intrapericardial fluid pressure." The normally negative inspiratory pericardial pressure becomes positive. Tamponade is the mechanism by which low cardiac output and congestive heart failure (CHF) develop with pericardial effusion. Development depends on the rate of fluid accumulation, not simply the volume of pericardial fluid. With few elastic fibers in the pericardium, intrapericardial pressures can rise rapidly as the elastic limits of the membrane are exceeded. Important pathophysiologic features include: Increased (positive) intrapericardial pressure with diastolic collapse of the right atrium and right ventricle; compression of the vena cava; reduced right ventricular filling; decreased preload and cardiac output, and potential for arterial hypotension if compensatory mechanisms are insufficient. Coronary perfusion may be impeded by increased intrapericardial pressures. Syncope or sudden death may occur if the systemic hypotension is acute and severe. Given sufficient time, compensatory measures are activated to maintain arterial blood pressure. These include heightened sympathetic discharge, systemic vasoconstriction, renal retention of sodium and water, and

elevated venous pressures. Extremely high venous pressures may develop behind the

    heart. Congestive heart failure, with a predominately right-sided component (ascites, pleural effusion) is the consequence of chronic cardiac tamponade. Additional

    hemodynamic features include equilibration of diastolic pressures in the ventricles, atria and great veins, and respiratory variation in arterial blood pressure (pulsus

    paradoxicus). The latter is explained by exaggeration of the normal respiratory-induced variation that occurs in right and left-sided cardiac filling.

    Clinical Findings in Pericardial Effusion Special species and breed

    predilections have been noted above. The client complaint may be vague. Syncope and collapse are particularly common with acute cardiac tamponade (e.g., sudden hemorrhage) or after diuretic therapy and volume depletion. Overt signs of right-sided CHF may be evident. The physical examination findings of elevated jugular venous pressure, muffled heart sounds, and ascites (with or without pleural effusion) should prompt investigation of the pericardial space. If

    venous distension is missed, an erroneous diagnosis of liver disease or

    abdominal neoplasia may be entertained. Arterial hypotension or pulsus paradoxicus may be detected. The central venous pressure is generally quite

    O [normal < 5 cm]. In acute cardiac tamponade, high, often exceeding 12 cm H2

    the major clinical signs may be low blood pressure and jugular distension but without any fluid accumulation. Fever or thoracic pain may indicate infection or inflammation within the pericardial space. Cardiac auscultation is characterized by distant heart sounds. A pericardial friction rub may indicate pericarditis, but

    this is rare in dogs and cats. Breath sounds are muffled and there will be tachypnea or respiratory distress if there is pleural effusion from CHF. Evidence

    of systemic disease, such as lymphosarcoma or hemangiosarcoma of the spleen

    may be noted during a complete physical examination.

Diagnostic studies Routine diagnostic studies are helpful. An electrocardiogram may

    show any of the following: decreased amplitude QRS complexes (most common but

    variable); electrical alternans (with large effusates and swinging of the heart); ST

    segment elevation (an epicardial injury current with pericarditis). Sinus tachycardia is typical but vagal reflexes can be invoked that promote sinus arrhythmia or

    bradyarrhythmias. Atrial and ventricular arrhythmias may be observed secondary to

    myocardial involvement, ischemia, or concurrent primary heart disease. Radiography

    generally demonstrates abnormalities once there is a significant accumulation of

    pericardial fluid. The cardiac silhouette enlarges, loses its angles and waists, and

    eventually becomes globular in shape ("basketball or soccer ball heart") and sharp in

    outline (from diminished motion). Should a metallic foreign body be observed over the

    heart on two views, constrictive or constrictive-effusive disease is likely. Pulmonary vascularity is often reduced from low cardiac output (in contrast to CHF from

    cardiomyopathy or valvular disease). If CHF has developed, there may be increased

    pulmonary interstitial densities (edema), distension of the caudal vena cava,

    hepatomegaly, or pleural effusion. Heart base tumors may deviate the trachea

    (generally to the right and dorsad), producing a mass effect. Fluoroscopy may

    demonstrate reduced cardiac motion. Pneumopericardiography can identify

    intrapericardial mass lesions, but is rarely done as echocardiography is safer.

     The echocardiogram is a highly sensitive test for detecting pericardial effusion.

    Abnormal fluid accumulation is evident as a sonolucent (generally black) space

    between the epicardium and pericardium, extending from apex to base. Cardiac mass

    lesion, a mixed intrapericardial echogenic pattern (cellular exudate or recent

    hemorrhage), or pleural effusion are other potential echocardiographic findings. The

    recognition of diastolic collapse of the right atrium or right ventricular wall is supportive of increased intrapericardial pressure and corresponds to effusion with tamponade. In

    my experience, this finding usually indicates an intrapericardial pressure of >12 cm

O (where normal is subatmospheric). There are however both false positives H2

    (occasionally pleural effusion causes this in dogs) and false negatives (if there is concurrent right sided CHF with elevated CVP expanding the cardiac chambers). The distinction between idiopathic hemorrhagic pericardial effusion and bleeding from a tumor may not be possible without a high resolution, technically proficient,

    echocardiogram recorded from each side of the thorax and using multiple angled views. In some cases, exploratory surgery or advanced imaging (CT, MRI) is needed to

    exclude a mass lesion.

     The clinical laboratory evaluation is may simply reflect the consequences of

    heart failure or prior diuretic therapy. The CBC may indicate inflammation, infection, or hemorrhage. Increased numbers of circulating nucleated RBC’s are suggestive of

    hemangiosarcoma of the spleen (and heart). Analysis of pleural or peritoneal effusions generally indicates fluid of obstructive origin (transudate, modified transudate, or infrequently chyle). Bacterial cultures of the effusate, serum fungal titer

    (coccidiomycosis), or ELISA tests for FeLV or FIP (cats) may be positive when

    pericarditis is related to these infections.

     Fluid can be collected by pericardiocentesis. Measurement of "static" intrapericardial fluid pressure, prior to removing any pericardial effusion, can be accomplished by attaching one end of a saline-filled extension tube to the intrapericardial catheter and the other end to a central venous pressure manometer. Cases of tamponade

    demonstrate a high (positive) pressure, usually > 12 cm HO above the midsternal line, 2

    with the patient resting in lateral recumbency. The pressure becomes subatmospheric following pericardiocentesis and rises and falls with ventilation. With constrictive-effusive pericardial disease, pericardial effusion without tamponade, or isolated pleural effusion, the intrapericardial pressure is essentially normal (i.e. near zero cm HO). 2

    While this relatively crude method does not precisely measure intrapericardial pressure, it can offer useful clinical information. If the pH of pericardial fluid obtained is < 7.0, this finding is suggestive of pericardial inflammation or idiopathic hemorrhage, though more data are needed to precisely define the predictive value of a pH >7.0. Values of 7.4 or greater are more typical of neoplasia or recent hemorrhage. Collected fluid can be classified as a transudate, exudate, hemorrhage, or chyle (see above). Unfortunately, except in cases of lymphosarcoma or septic inflammation, cytologic examination may not be especially helpful. It can be difficult to conclusively identify neoplastic cells within pericardial effusates. The problems include poor exfoliation or overinterpretation of reactive mesothelial cells.

    Therapy of pericardial effusion/cardiac tamponade The treatment of choice for initial stabilization is pericardiocentesis using a needle, butterfly infusion needle (for cats or very small dogs), a through-the-needle catheter, an over-the-needle

    catheter, a commercial thoracocentesis trocar system, or a balloon dilation catheter (which can be used to rip the pericardium). We prefer a 14 to 16 gauge Angiocath, over-the-needle catheter. An IV should be placed for emergencies or

    for volume loading should hypotension develop. If arterial blood pressure is

    stable, mild sedation is often tolerated and improves the procedure for all (buprenorphine 0.005 mg/kg mixed with acepromazine 0.025 mg/kg, both given IV). Should hypotension develop after sedation, quickly infuse saline solution intravenously. The dog is placed in lateral recumbency and the spine elevated slightly with a radiographic foam wedge. ECG leads are attached. The needed

    depth of penetration and the ideal puncture site can be guided by

    echocardiography (to simply identify the largest effusion space); alternatively, one can note the strongest palpable cardiac impulse (both points are usually the same). Placing the patient in a slightly oblique position, and later rotating the animal as needed, facilitates fluid withdrawal and patient restraint during the procedure. After gloving for the procedure, one additional side hole is cut into the edge of the catheter and the needle is replaced. The tap can proceed from

    either the right side (cardiac notch) or left hemithorax (depending on preference, the situation, radiography, and echocardiography). We prefer the right-sided intercostal approach to avoid the largest coronary vessels. Following scrubbing

    of the skin, a local 2% lidocaine block of the skin, subcutaneous tissues, pleura, and superficial pericardium is made with a 25- or 23- gauge needle. Often the small gauge needle will transiently enter the pericardial space, providing some

    guide to the depth needed for catheter placement. Next, the catheter is

    advanced through the skin, subcutaneous tissue, intercostal space and deliberately into the pericardial space. The ECG is monitored for extrasystoles

    in case the heart is pricked with the catheter (note: dorsal approaches may cause the catheter to perforate the atrium and this will not be associated with premature ventricular beats). Once the pericardial space is entered, fluid (usually bloody) enters the catheter lumen. If intrapericardial pressure will be measured, the line connecting the CVP-manometer is immediately attached to the catheter because the intrapericardial pressure rapidly declines with aspiration of the fluid.

    After measuring intrapericardial pressure, fluid samples are collected for cytology (EDTA and plain tubes) and culture (pending cytology). The effusion is

    now drained as completely as possible. Owing to the relatively inelastic properties of the pericardium, the removal of even modest amounts of effusate

    may be very beneficial. The effects on the patient are often dramatic with a marked improvement in attitude, color, and peripheral pulse pressure. When complete, the aspirated fluid volume is quantified. Repeated intrapericardial

    pressure measurement and/or echocardiography can be used to verify the

    benefit of the procedure if desired. A sample of the effusate is evaluated by microscopy for cellular abnormalities and bacteria, and is then cultured (aerobic,

    anaerobic) if appropriate.

     Medical therapy of cases with pericardial effusion is not a prominent feature of this disorder. Intravenous saline, at shock doses, may be needed in cases of hypotension

    due to severe or sudden cardiac tamponade. Thoracocentesis is a helpful adjunct in

    large pleural effusions. Ascitic effusions need not be tapped if pericardiocentesis is performed. While furosemide and venodilators can decrease elevated venous

    pressures, they are not substitutes for pericardiocentesis in the symptomatic patient;

    furthermore, these drugs may reduce ventricular filling predisposing to hypotension. In general, diuretics are contraindicated except in recurrent, neoplastic-related right-sided CHF in which venous pressures can become exceptionally high. Following successful

    pericardiocentesis, it is appropriate to administer one mg/kg furosemide SQ for one or two doses to enhance renal excretion of sodium (and overcome the sodium-retaining

    consequences of cardiac tamponade that often persist for some time following

    pericardiocentesis or pericardiectomy). In patients with culture negative, idiopathic pericardial hemorrhage (or idiopathic pericarditis), conservative treatment with catheter drainage, may be “curative,” though diligent follow-up (for at least one year) is needed

    to assure that constrictive pericardial disease does not develop. Empirical use of

    antibiotics and of corticosteroids has offered no certain benefit. Drugs that prevent fibrosis might be considered, but these have not been suitably investigated in dogs and cats. Antineoplastic drugs have provided generally poor results in patients with cardiac tumors.

     Surgery may be necessary for successful management of pericardial diseases.

    Subtotal pericardiectomy (ventral to the phrenic nerves) may be needed in recurrent

    idiopathic hemorrhagic effusion. The treatment for infective, suppurative pericarditis is specific antibiotic therapy based on aerobic and bacterial anaerobic culture, catheter drainage of the pericardium, and subsequent surgical removal and drainage of the

    pericardial space (to prevent constriction). A foreign body should be sought in these cases. Surgery is also indicated if constrictive (effusive) pericarditis is diagnosed or highly suspected, or if there is a need to explore the pericardium to rule out or to

    attempt removal of a tumor. Palliative subtotal pericardiectomy (generally via

    pericardial window) can also be performed by thoracoscopy in some centers; however, the size of the window may limit long term success in cases of idiopathic or septic pericarditis. Nevertheless, this approach, is a very reasonable palliation for neoplasia-associated pericardial effusion and it may be a consideration for debilitated dogs with infective pericarditis (later perform pericardiectomy). Specific causes of pericardial infection - e.g. coccidiomycosis - have specific adjunctive treatments. The prognosis of pericardial disease depends on the cause, but is generally favorable with idiopathic hemorrhagic pericardial effusion, guarded with infective pericarditis, and unfavorable with cardiac or heart base neoplasia (unless there is good surgical access for removal). While a chemodectoma grows slowly, right atrial hemangiosarcoma has invariably metastasized by the time of diagnosis. Ectopic thyroid carcinomas can be particularly invasive.

Constrictive Pericardial Disease Pericardial constriction most often develops

    secondary to chronic inflammation, particularly from infective pericarditis or recurrent hemorrhage. Rarely, the pericardium may undergo calcification. With chronic inflammation, the pericardial space can become obliterated, and the heart is encased in a rigid, poorly-expansive sac. As the fluid is reabsorbed and the pericardium scars and contracts, the ventricles are constricted in their ability to expand and fill. This conditions leads to limited cardiac output and right-sided (or biventricular) CHF. The term "constrictive-effusive" pericarditis refers to a state of constrictive physiology with concurrent pericardial effusion (but without tamponade). This is particularly important in the dog. The constrictive pericardium prevents diastolic expansion of the ventricles, thereby interfering with normal cardiac filling. With constrictive pericarditis, both ventricles are affected, but again the thinner-walled right heart is most susceptible. Filling of the ventricles can only occur in early diastole (before ventricular expansion is "checked" by the pericardium. A prominent 'y' descent occurs in the venous pressure. This initial decline in ventricular diastolic pressure is quickly followed by a marked pressure increase and plateau, as the balance of ventricular filling requires very high venous/atrial/ventricular diastolic pressures. The right ventricular pressure curve typically shows an initial diastolic “dip” created by the suction of active ventricular relaxation which is quickly followed by a “plateau” in the pressure tracing (square-root

    sign). A similar finding is observed on the Doppler echocardiographic recordings of the mitral and tricuspid inflow - there is a marked early filling (E wave) with attenuated mid to late diastolic filling and may correspond to a loud pericardial “knock”(timed as an S3), a marker for abrupt restriction of ventricular filling. Disparate rates of cardiac filling are also reflected by prominent and multiple diastolic movements of the ventricular septum on 2D echocardiography and dramatic variations in transvalvular inflow related to the phase of ventilation. Overall, increases in venous pressure can be explained by the diastolic ventricular dysfunction and the usual compensatory circulatory mechanisms for decreased cardiac output. The result for the patient is (right-sided) congestive heart failure. These animals are usually presented with hepatomegaly, ascites, and even subcutaneous edema. Systemic venous distension is prominent and an important clinical finding. Pleural effusions are possible.

    The treatment of choice for constriction is surgical removal of the pericardium and possible decorticating of the epicardium. This carries a significant risk.

Report this document

For any questions or suggestions please email