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Cardiology: Making the Diagnosis

Paul D. Pion, DVM, DipACVIM (Cardiology)
Veterinary Information Network, Inc., Davis, CA
Paul@vin.com

INTRODUCTION

Many colleagues report that evaluation of suspected cardiac disease is difficult to "sell" to their clients. Reasons stated (and my interpretation/translation) include:

STATED REASON: the problems are usually not visible to my client

INTERPRETATION: this is not an important problem to my client

STATED REASON: I am not able to assess/treat the conditions presented with the tools available in private practice

INTERPRETATION: I am afraid to admit that I don't know enough cardiology

STATED REASON: appropriate evaluation may require technology that is not locally available

INTERPRETATION: I do not want to refer cases and lose clients

STATED REASON: nothing can be done to alter the course of the condition, so why bother

INTERPRETATION: since I don't know what can be done or what difference it will make I assume that my client is not interested in further evaluation.

There is some truth in all of the above statements. When combined with the frustration of feeling insecure about one's ability to diagnose/manage cardiac disease, the end result is often conscious or subconscious communication of these apprehensions to clients.

Clients are not very likely to want to pursue a diagnostic/therapeutic plan that their veterinarian does not believe will be valuable? We need to overcome these self-imposed obstacles and base recommendations made to owners of pets with suspected cardiac disease more confidently. The way to gain that confidence is to firmly understanding the diagnostic and therapeutic value of the services we offer.

As with all diagnostic decisions, a consideration of the risks, benefits, and costs of pursuing (or not pursuing) a cardiac workup must be considered.

In symptomatic patients the decision making process often appears easy. All involved realize that something must be done soon or the patient will continue to suffer or die. In some cases death is inevitable given our current abilities to reverse cardiovascular disease. The goal is to help clients to understand their options. To maximize the information gained and minimize the risks, we should avoid the urge to do every test possible; instead, the secret is to find the right mix of testing and intervention needed to develop a rational initial therapeutic plan to relieve suffering and maximize the chances for survival while not getting too aggressive, too early, and causing the premature death of a patient. Unfortunately, in symptomatic cases, the decisions made often do not avert the inevitable for long. No matter the outcome, most clients appreciate knowing why their pet is having problems -- and that everything possible was done to avert discomfort.

In asymptomatic patients with abnormal cardiac sounds the decision is not as easy. In these cases the reason for pursuing a cardiac workup again comes down to "knowing what we are dealing with". This information can be important for future decision making processes. To suspect that a patient has heart disease and not pursue the problem is akin to finding a suspicious "lump" or tumor and deciding not to biopsy the lesion because it might be "nothing significant". It might as likely be malignant and untreatable, or worse yet (in light of the decision made), malignant and treatable. Without the information that the biopsy or cardiac workup provides, it is not possible to make informed recommendations to the client regarding present and future management of the patient. It is important to remember that clients want to know what to expect. Without a diagnosis you cannot offer VALUABLE information regarding the patient's prognosis. The bottom line is that the decision whether or not to pursue the cardiac workup should rest with the client after being appropriately educated by the attending veterinarian.

CARDIOLOGY IS EASY!!

Remember this -- cardiology is easy IF you approach it systematically and apply what we will cover in our time together.

To begin, we will review basic concepts which underlie the diagnosis of cardiovascular disease in small animals and the diagnostic value of specific cardiovascular diagnostic tests. Armed with this general knowledge, it becomes easy to understand the specifics that apply to common cardiac disorders afflicting patients of any species.

Arriving at a diagnosis of cardiac disease is based upon history, physical examination, ancillary tests (electrocardiography, radiography, echocardiography including Doppler, and, in some cases, cardiac catheterization), and response to therapy.

HISTORY

A complete history (taken in conjunction with the physical examination serves to answer the most basic (and important) questions that will help guide the clinician's decision as to whether or not to pursue a diagnosis of cardiac disease in this patient:

1)  Are the signs displayed by this animal compatible with a diagnosis of cardiac disease?

2)  Is this disease significant to this patient?

3)  In the case of congenital disease, is this a potential problem for the breed?

Compared to the value of a good history in a dog with suspected cardiovascular disease, the history is often not as helpful when evaluating feline cardiac disease. It is useful to acquire information regarding the patient's overall health, but reduced exercise capacity is not a common complaint in cats with cardiac disease. In fact, one of the most common histories I receive from owners with cats with SEVERE cardiac disease, even those presented for extreme dyspnea, is that "the cat appeared normal and ate well yesterday (or this morning)".

Elucidation and evaluation of coughing as a prominent clinical signs should influence ones decision to pursue cardiac or respiratory disease. Dogs with heart disease often present with cough as a clinical sign. However, often respiratory disease (upper or lower airway) are also present and make it difficult to determine how much cardiac changes are contributing to the cough. Heartworm disease may also present with a history of coughing.

Coughing is not generally considered a common presenting sign in cats with cardiovascular disease. This latter comment should be tempered by stating that it may be that owners don't often complain about coughing in cats with heart disease. The literature, my experience, and clinical impression reported to me by many colleagues implies that vomiting is a common presenting sign in cats with cardiac disease. More and more we are recognizing that what owners are describing as "gag" or "wretching" is actually a report of coughing. Often when tracheal manipulation induces a cough in these patients, the client responds by saying, "that's what he does at home!". Looks like a gag, but it is a cough.

Cyanosis may be noted by owners. In the absence of respiratory distress or toxicosis, this should lead the clinician to suspect a lesion which results in shunting of blood from the venous to the systemic arterial circulation by a route other than the normal pulmonary circulation (table 1). This is often a young animal diagnosis but can be seen in the mature patient with an abnormal connection between the atria, ventricles, or great vessels that begins to shunt right-to-left when pulmonary vascular resistance rises as a result of primary lung disease, pulmonary thromboemboli, heartworm disease, etc. (see Table 1 below). In the absense of these types of lesions, cyanosis is not a common finding in cardiac patients though it tends to be over-reported because many clinicians believe it should be.

Table 1. Cardiac defects which result in right to left shunting and cyanosis.

- R->L patent ductus arteriosus ("selective cyanosis")

- Pulmonic stenosis or pulmonary hypertension with an atrial or ventricular septal defect (e.g.,Tetralogy of Fallot)

- Other complex defects

Reports of "epileptic-type episodes" must be carefully evaluated to differentiate between seizures and syncope. Seizures are usually preceded and followed by a pre- and post-ictal period, respectively, and commonly have tonic and/or clonic components. Syncopal episodes appear to the owner as if the previously normal animal "passed out" and then was "normal" immediately after righting (see Table 2).

Evaluation of the patient's RESPONSE TO THERAPY can provide useful information regarding the accuracy of a specific diagnosis. Response to medication should guide further adjustments to the therapeutic protocol.

Table 2. Conditions associated with cardiac syncope in dogs and cats.

-Heart block (high 2nd or 3rd degree)

-Sick sinus syndrome

-Fixed obstructive lesions (aortic or pulmonic stenosis)

-Rapid ventricular or supraventricular tachycardia

-Pulmonary hypertension

-Mitral regurgitation (rare)

PHYSICAL DIAGNOSIS

Auscultation is the most sensitive and informative screening test for cardiovascular system disease. While ausculting the thorax the following questions should be answered as you listen to all regions (i.e., left and right apexes and bases, the entire length of the sternum, and the thoracic inlet) in a systematic manner:

1.  Which sound is the first heart sound? second heart sound?

2.  Do I hear any murmurs or extra sounds between the first and second heart sounds (systole)? between the second and first heart sounds (diastole)?

3.  Where is the murmur or extra sound loudest?

4.  Is it a high or low pitched sound.

Murmurs indicate turbulence within the heart or great vessels. Unfortunately, as opposed to dogs, the identification and characterization of a murmur in cats often DOES NOT provide the clinician with a clear cut diagnostic plan to follow. Timing murmurs in the cardiac cycle (systole vs. diastole) provides important clinical information (table 3) but can be difficult to discern at higher heart rates. Cats with congenital or purely valvular disease, do often follow the rules presented in table 3, but cats with myocardial disease can have murmurs in any location -- often they are sternal.

Table 3: Basic localization and timing of cardiac murmurs

 

Systole

Diastole

Continuous

Apex

AV Regurgitation

AV Stenosis

 

Base

Semi-lunar Stenosis

Semi-lunar Regurgitation

PDA

Take time to be sure that you understand WHY these murmurs are localized to these locations and heard during that specific period of the cardiac cycle. Studying the cardiac cycle is key to understanding this table and echo/Doppler studies.

Although the localization and timing of murmurs lends itself to being laid out in chart form and logical algorithms for discriminating between the possible differential diagnoses, the clinical decision process is often thwarted by owner and clinician imposing the barrier of blindly attempting to decide when to consider a murmur significant.

I cannot provide a clear cut rule stating when a cat deserves further workup and when it does not. Many clinicians auscult murmurs in cats and do not pursue the issue further or even mention it to the owner because the cat has no clinical signs and because they have seen many cats with murmurs that proved to not have cardiac disease upon further evaluation. While this is true, there are also a large number of cats that are seen for no reason other than the presence of a murmur where significant cardiac disease is recognized upon further evaluation. I believe that EVERY cat with a murmur deserves to have it evaluated and in most cases, this means an echocardiogram.

As stated above, many cats with, or without, significant cardiac disease, present with murmurs, the origin of which is often poorly understood even when a skilled echocardiographer performs extensive echocardiographic and Doppler investigation of the heart. These murmurs are most often ausculted along the sternum, at the level of the cardiac apex. That these murmurs may be ausculted in cats with "cardiomyopathies" and in cats in which we cannot find significant cardiac disease makes it difficult for the primary clinician to feel confident about his/her ability to differentiate between "innocent" murmurs and "pathologic" murmurs. No one has completed a thorough survey to determine what percentage of these murmurs represent significant disease - and until that time we will all feel somewhat insecure about answering our clients questions as to the "CHANCES" of the murmur being insignificant.

This often makes veterinarians feel inadequate and deters them from recommending a workup. The available information -- a murmur is present -- is a valid indication for further investigation AND there is no reason why you should be able to tell your client what the murmur represents BEFORE running the test. In fact, if you could do that, there would be no reason to run the test. Presented properly, clients will appreciate, not resent a "normal" result to the echocardiogram. Doesn't it make sense that they should be wishing for a "it's normal" or "no big deal" rather than "it's real bad" result in the pet they love.

In most cases, deciding which dogs need further evaluation is simpler. It is unusual to hear significant murmurs in adult dogs that do not have cardiac disease. We do sometimes hear "innocent" or "physiologic" murmurs in young animals. Clues that a murmur falls within this category are that it is soft (I-II out of VI) murmur, short in duration (cannot be heard throughout systole), and often found to disappear before maturity is reached. Since it is impossible to absolutely decide that a murmur that does not resolve is not an indication of significant cardiac disease, a chest radiograph and echocardiogram are indicated to definitively rule out significant cardiac disease in any young animal with a persistent cardiac murmur. Any systolic murmur that is loud, or is heard throughout systole and any diastolic murmur should be considered significant.

For example, a mature dog with a soft, short-duration, systolic murmur, no clinical signs or compatible history, and normal thoracic radiographs probably does not need further evaluation to assure the owner that this is probably not currently a major risk to this animal's health. The same presentation in a breeding animal (dog or cat) should precipitate a complete workup in order to rule out any congenital (and possibly) heritable defect that represents a risk to potential offspring and therefore the breed.

Other abnormal heart sounds include an audible 3rd or 4th heart sounds (gallop), split 2nd hearts sounds and systolic clicks. Split heart sounds and clicks are uncommon in cats.

Gallop sounds are audible 3rd or 4th heart sounds. They are abnormal in dogs and cats. Gallop sounds in cats are easily recognized by most. In dogs, a gallop sound is less easily recognized. They are low frequency sounds, best heard with the bell of the stethoscope at the left apex (sternal border in many cats) in early or late diastole. These audible 3rd (early diastole) or 4th (late diastole) heart sounds may be auscultated in patients with stiff ventricular walls or with a ventricle that has a large volume of blood rapidly "dumped" into it during diastole (e.g., mitral or aortic regurgitation). Ventricular stiffening may be associated with abnormally thickened (e.g., hypertrophic cardiomyopathy), or infiltrated (e.g., restrictive cardiomyopathy) ventricles or ventricles that are unable to relax normally (e.g., hypertrophic or dilated cardiomyopathy).

Narrow splitting of the second heart sound may be detected in some normal dogs when carefully auscultated. It is normal that the pulmonic valve close slightly after than the aortic valve at the end of systole.; when the separation in timing of closing of these valves becomes long enough for human ears to "resolve" the difference we report a split second heart sound. When splitting of the second sound is prominent, it is usually abnormal and in dogs is most commonly associated with pulmonary hypertension.

Systolic clicks are high frequency sounds heard over the left apex in dog breeds susceptible to chronic valvular disease. They are believed to represent mitral valve prolapse prior to the onset of regurgitant flow. They are commonly misinterpreted as an audible S3 or S4 (gallops sound) or a split heart sound.

Many clinicians report "intermittent gallops" in cats. The significance and reality of this finding is debatable.

Palpation of the arterial pulse simultaneous with cardiac auscultation allows detection of pulse deficits associated with arrhythmias. The pulse "strength" detected by palpation is a function of the difference between the systolic and diastolic arterial pressures (pulse pressure) and the ability of the examiner to place the correct amount of pressure over the artery. A blood pressure of 220/180 cannot be differentiated from a pressure of 120/80 by palpation alone. Bounding pulses are associated with a rapid and exaggerated increase and decay of arterial pressure. The most common clinical correlates are patent ductus arteriosus (left to right shunt) and aortic insufficiency. Weak pulses may be associated with shock like conditions or conditions that impede ejection of blood from the left ventricle. Clinical correlates include shock (cardiogenic and others), pericardial tamponade and aortic stenosis.

It can be difficult to palpate the femoral arterial pulse in normal cats. It can be equally difficult to determine that there is in fact no palpable femoral arterial pulse, a common finding in cats with an aortic thromboembolus. Darkening of the color of the foot pads and nail beds can aid in the diagnosis. Sometimes it is necessary to cut a nail short or perform an angiographic procedure to confirm that a cat presenting with posterior paresis has an aortic thromboembolus and not neurologic disease. During a 1 year period when I was collecting cases for thrombolysis with tissue plasminogen activator (t-PA, Activase, Genentech, South San Francisco) I would estimate that at least 60% of the cases referred for thrombolysis had some form of neurologic or musculoskeletal disease rather than an aortic thromboembolus. In some of these cases it was necessary to perform an aortic angiogram to make a definitive decision regarding the etiology of the observed clinical signs.

Examination of the systemic veins is an important portion of the physical examination. Distension of systemic veins is associated with elevated systemic venous pressures, often as a result of right heart failure. Important differential diagnoses include venous thrombosis, intra- or extravascular masses, and congenital cor triatriatum dexter, causing obstruction to venous return. The presence of jugular pulses may indicate right heart disease (usually tricuspid insufficiency), but may also be associated with arrhythmias that result in atrioventricular dissociation in which the atria contract when the tricuspid valve is closed resulting in retrograde flow and fluid wave transmission. Pericardial tamponade should also be considered when jugular distension or pulsation is detected.

Table 4. Localization of murmurs in common cardiac lesions.

   

Left Base

Right Base

Left Apex

Right Apex

Carotid Artery

Right Sternum

REGURGITANT LESIONS

MITRAL REGURGITATION

 

 

S,PMI

S,R

 

 

TRICUSPID REGURGITATION

 

 

 

S,PMI

 

 

AORTIC REGURGITATION

D,PMI

D,+/-

D,R

 

 

 

OBSTRUCTIVE LESIONS

AORTIC STENOSIS

S,PMI

S,+/-

S,+/-

 

S,R

 

PULMONIC STENOSIS

S,PMI

 

 

 

 

 

SHUNTING LESIONS

VENTRICULAR SEPTAL DEFECT

S,+/-,*

 

 

 

 

S,PMI

ATRIAL

SEPTAL DEFECT

S,+/-,*

 

 

 

 

 

TETRALOGY

OF FALLOT

S,PMI

 

 

 

 

S,+/-

PATENT DUCTUS ARTERIOSUS (LEFT-TO-RIGHT)

C,PMI

 

S,**

 

 

 

PATENT DUCTUS ARTERIOSUS (RIGHT-TO-LEFT)

**** USUALLY NO MURMUR *****

Key to symbols in above table:

S = SYSTOLIC MURMUR

D = DIASTOLIC MURMUR

C = CONTINUOUS MURMUR

PMI = POINT OF MAXIMAL INTENSITY

+/- = HEARD IN MINORITY OF CASES

R = LOCATION MURMUR COMMONLY RADIATES TO

* = DUE TO A "RELATIVE PULMONIC STENOSIS"

** = MURMUR OF MITRAL REGURGITATION - SECONDARY LESION

Evaluation of mucous membrane color may aid in the diagnosis of cardiac disease. Cyanosis was discussed above. Pale mucous membranes may indicate anemia or poor perfusion (cardiogenic or hypovolemic shock, etc.). To attempt to maintain systemic arterial pressure in shock, diffuse peripheral vasoconstriction occurs. Injected mucous membranes are associated with peripheral vasodilation as may be seen in septic animals or after treatment with arteriolar vasodilators such as hydralazine.

ANCILLARY TESTS

The results of a general and cardiovascular physical examination will, in most cases, provide sufficient information for the clinician to generate a brief list of differential diagnoses. In many cases, the definitive diagnosis will be apparent at this point. Common ancillary tests available for confirming or ruling out diagnoses include radiography, electrocardiography, echocardiography, and Doppler echocardiography, Cardiac catheterization and angiography are available at most veterinary universities and in some larger private practices but their use is decreasing as acceptance of spectral Doppler and color flow Doppler become more common in veterinary practice.

In the ideal clinical situation each of these tests should be performed only to answer specific questions that the clinician asks prior to ordering the tests. In practice, suspecting structural cardiac disease may justify ordering a minimum database consisting of a chest radiograph, electrocardiogram and echocardiogram, if available. The clinician should be aware of the information each examination may provide and then utilize the information for answering specific questions. Table 6 illustrates the relative value of information gained from cardiac diagnostic tests employed in cats and dogs. It should never be forgotten that the physical examination is the most valuable test for evaluating most cardiac diseases, Other than a complete physical examination, the most valuable tests for evaluating acquired or congenital, structural or functional cardiac disease are radiography and echocardiography.

ELECTROCARDIOGRAPHY is a valuable clinical tool. Unfortunately veterinarians often misuse it. Electrocardiography is relatively insensitive for detecting anatomical changes (i.e., chamber enlargement). If signs of chamber enlargement are present on the electrocardiogram, they should still be confirmed by other ancillary tests. The major (and very important) utility of electrocardiography to the veterinarian is for evaluating rhythm disturbances. In this regard, appropriate therapy, if deemed necessary, can usually be chosen after assessing whether the dysrhythmia represents a bradycardia or tachycardia and whether, in the case of tachyarrhythmias, the rhythm is supraventricular or ventricular in origin. After making these relatively simple judgments, the clinician can consult a large number of veterinary references for guidance in choosing appropriate therapy.

RADIOGRAPHY is an important and useful tool in veterinary cardiology. It does, however have definite limitations, especially in the cat. The use of radiography to differentiate between right and left ventricular enlargement has been grossly overemphasized and is almost futile in the cat. Radiography is useful for detecting left atrial enlargement in some cats. Under ideal situations, radiography can provide an assessment of overall cardiac size. However this has not proven to be a very sensitive indicator of cardiac disease in cats.

Radiography is most useful for detecting sequelae to cardiac dysfunction (e.g., pulmonary venous congestion, pulmonary edema, enlarged great veins, pleural effusion, etc.). Great care must be taken not to over-interpret pulmonary vascular and parenchymal patterns, especially in radiographs of obese animals and radiographs exposed in an expiratory phase. Radiography is an excellent tool for detecting moderate to severe pulmonary edema, pleural effusions, and ascites. in a patient with tachypnea, dyspnea, or cough. It is relatively poor at detecting mild edema in many dogs.

EXTREME CAUTION SHOULD BE TAKEN BEFORE SUBJECTING A DYSPNEIC CAT TO RADIOGRAPHIC EVALUATION!!!! STRESSING DYSPNEIC CATS CAN BE FATAL!!!

The major problem with assessing overall cardiac size is the manner in which cardiac size is evaluated by many clinicians. Cardiac size evaluation is subjective and is usually done by comparing heart size to chest cavity size and configuration. Clinicians must remember and be cognizant of the fact that a heart that looks large may in fact be large or alternatively, the chest cavity surrounding it may be small. Small chest cavities are common in small and chondrodystrophic breeds, on radiographs not taken at full inspiration (>80% of all chest radiographs) and in obese dogs. It is not unusual to have a heart that appears enlarged when it is not. The opposite may also be true. In large, deep-chested dogs the heart often appears small because of the large chest cavity size surrounding it. As an example, Doberman Pinchers with dilated cardiomyopathy oftentimes do not have hearts that appear grossly enlarged on chest radiographs.

After using echocardiography side-by-side with radiography for the past 15 years, it is obvious that many veterinarians continue to over-interpret chest radiographs in dogs in dogs . Because our patients come in many shapes and sizes and do not often obey when asked to "take a deep breath and hold it", we usually find ourselves attempting to "normalize" our judgments to meet the individual situation. Because our patients come in many shapes and sizes and do not often obey when asked to "take a deep breath and hold it", we usually find ourselves attempting to "normalize" our judgments to meet the individual situation. Similar to echocardiography, radiography will always provide greater insight when combined with knowledge of the patient's physical examination. If careful attention is not paid to what can be learned in a complete physical exam, and echocardiographic backup is unavailable, accurate assessment of the cardiac silhouette is often questionable, at best.

Table 6: Relative value of information gained from common cardiac diagnostic tests regarding specific clinical questions in cats.

Note * The table is exactly the same for dogs with the exception of the first line

QUESTION TO ADDRESS

RADIOGRAPH

ECG

ECHOCARDIOGRAM

ASSESS OVERALL CARDIAC SIZE (CAT)*

++

+

+++

ASSESS OVERALL CARDIAC SIZE (DOG)*

+++

+

++

ASSESS SPECIFIC CHAMBER SIZE

++

+

++++

EVALUATE

MYOCARDIAL FUNCTION

-

-

+++

ASSESS/DETECT CHF

+++

-

+

EVALUATE

CARDIAC ANATOMY

++

-

++++

DETECT

PERICARDIAL EFFUSION

+

+

++++

EVALUATE

RHYTHM DISTURBANCE

-

++++

+

CLASSIFY PATHOPHYSIOLOGY

+

-

++++

ECHOCARDIOGRAPHY

I would not go as far as to state that cardiovascular disease in cats and dogs CANNOT be assessed and treated without echocardiography. But as the years go on, I get much closer to stating that we SHOULD NOT claim to completely assess and treat cardiac patients without ready access to echocardiography.

As an example, consider a thoracic radiograph in which you determine that the overall cardiac size is moderately enlarged with "increased sternal contact", a classical radiographic sign of right ventricular enlargement. You might suspect right heart disease. But if you know that the patient is a 12 year old poodle which has a left apical systolic murmur and no jugular venous distention or pulses, it would be inappropriate to diagnose right heart disease. This patient obviously has mitral valve disease. Echocardiographic evaluation of this patient would objectively confirm that the left and not the right ventricle is affected.

When echocardiography is available, the accuracy of the echocardiographic diagnosis in an individual patient is enhanced greatly when the clinician interpreting the study has a full and accurate assessment of the patients physical examination. Almost anyone can be taught to acquire diagnostic quality echocardiograms. However, in order to accurately interpret the data, the clinician must have a firm understanding of cardiac anatomy and pathophysiology. When utilized by persons without a firm understanding of cardiac pathophysiology many false conclusions can be reached.

CLASSIFICATION OF CARDIAC DISEASE

HEART DISEASE includes any condition in which there is a cardiac abnormality. This ranges from the patient with a murmur caused by trivial mitral regurgitation to one with a fatal congenital or acquired cardiac condition. HEART FAILURE is a clinical syndrome and should not be considered a final diagnosis. It may be divided into congestive and low output states. Congestive right heart failure results in elevated central venous pressure which may manifest as ascites (a common finding in small animals with right heart failure) and peripheral edema (not a prominent finding in small animals). Congestive left heart failure results in elevated pulmonary venous and capillary pressures that may manifest as pulmonary edema (and probably also pleural effusion in cats). Biventricular failure results in elevation of systemic and pulmonary venous pressures and may manifest as any of the above signs or pleural effusion. In this scheme, the classification of cats with pleural effusion is the most controversial. In dogs, pleural effusion may be present in animals which apparently have purely right heart disease whereas Pleural effusion may be present in cats which, when clinically evaluated, appear to have pure left heart disease.

MYOCARDIAL FAILURE means that the heart muscle is weak (i.e., myocardial contractility is decreased). It is important to realize that heart failure and myocardial failure represent heart disease (as does a heart murmur) and that heart failure, either congestive or low output, may, in some cases be a result of myocardial failure. However heart failure can, and often is, present in the absence of myocardial failure. Similarly, myocardial failure may be present in association with or in the absence of heart failure. Heart failure may be the result of valvular, systolic, or diastolic dysfunction. When the ability of the ventricle to eject blood is impaired, we speak of a SYSTOLIC DYSFUNCTION. When the ability of the ventricle to relax is impaired, we speak of a DIASTOLIC DYSFUNCTION. Palliative (i.e., diuretics, vasodilators, etc) therapy is, in many, but not all, cases the same regardless of the underlying dysfunction. However definitive therapy addressing the underlying etiology (valvular, systolic, or diastolic dysfunction) may be quite different. Echocardiography can be used to noninvasively differentiate conditions causing systolic from those causing diastolic dysfunction, helping to guide appropriate therapy. This is one piece of information, essential to appropriate management, that cannot be noninvasively confirmed without echocardiography or other technologically intensive noninvasive imaging modalities.

The heart responds to hemodynamic abnormalities in predictable ways. Classification of cardiac disease in a manner that can be evaluated by available diagnostic techniques, as described in table 4, enhances the clinicians ability to choose and interpret appropriate diagnostic tests. When the ventricle is pumping against an increased pressure load we speak of a PRESSURE OVERLOAD. When the ventricle is pumping an increased volume, we speak of a VOLUME OVERLOAD. Concentric hypertrophy (thickening of the ventricular walls with minimal or no increase in chamber diameter (and thus volume) is the means by which the heart responds to a pressure overload. Eccentric hypertrophy (dilatation of the ventricle with minimal or no increase in wall thickness) is the typical response of the heart to a volume overload. Thus, when combined with a complete physical examination, evaluation of the chest radiograph and the echocardiogram, greatly assist in differentiating conditions which result in pressure and volume overload. (Table 7)

CONCLUSION

The importance of physical diagnostic techniques and interpretation of the physical examination cannot be overemphasized. Electrocardiography is essential for accurate interpretation of cardiac rhythms but is grossly over utilized and misused in veterinary practice when applied to every case, when an arrhythmia is not suspected. The real problem is not the performing of the ECG (as it might provide some useful hint in some cases) but in the false sense of having worked up the case completely after performing an ECG or receiving a report from a transtelephonic ECG service.

Echocardiography provides invaluable information regarding cardiac anatomy and function. In recent years, an expanded number of specialists and generalists utilize echocardiography directly, via referral, and telemedicine technologies. This has greatly increased the chances for definitive diagnosis of patients with cardiovascular disease. As the number of veterinary practices utilizing echocardiography directly and indirectly, increases, it becomes increasingly important that we not minimize the learning curve which all new users must climb before appropriately applying these technologies to their patients. There exists a significant danger that marketing pressures will place more and more ultrasound units in practices that previously referred these cases to specialists. This concern increases as more telemedicine companies emerge and market telemedicine as a new profit center for practices, which may not understand the time investment required to gain proficiency in acquiring images. The need to recoup equipment investment costs may, as a result, ultimately reduce quality of care in some situations. Therefore, at this point in time, appropriate attention to referral, training, and understanding the limitations of telemedicine become increasingly important. It would be a shame if these wonderful technologies became little more than a mechanism for receiving a "pretty and saleable report" that added little true value to the diagnostic process.

Radiography above all provides information regarding the clinically significant consequences of cardiac disease (pulmonary edema, pleural effusion). Appropriate diagnosis and therapy should be achieved after properly combining the results of the aforementioned techniques.

In most cases the cause of death due to cardiac disease is either sudden death due to a fatal dysrhythmia or a relatively slow death resulting from severe congestive heart failure. Sudden death is difficult to predict and to this date probably impossible to reliably prevent. Appropriate therapy for congestive heart failure requires an accurate diagnosis, an understanding of cardiac physiology and pharmacology and clinical judgment. Many textbooks deal with the subject much better than I possibly could in this limited space. Having said that, it still remains true that no matter how technologically advanced our cardiac imaging abilities become, the chest radiograph and the patients clinical response which guide our assessment of therapy of congestive heart failure, the only cause of death among cardiac patients that we are at all effective in delaying.

WHAT DO WE DO ONCE WE MAKE A DIAGNOSIS?

We have come a long way in our ability to accurately diagnose (or at least classify) cardiac disease but we must admit that effective therapy lags far behind our diagnostic abilities. There is little doubt that we can prolong life by administering diuretics to relieve signs of congestive heart failure. Vasodilators, especially angiotensin-converting enzyme inhibitors, may also improve survival. Inotropic therapy is controversial. Antiarrhythmic drugs may improve the appearance of the electrocardiogram to the clinician and improve clinical symptoms in very rapid tachyarrhythmias but there is no evidence that we effectively delay sudden death in veterinary patients at risk (subaortic stenosis, cardiomyopathies) with available drugs.

Catheter and surgical manipulation of diseased vessels and valves is utilized in some veterinary institutions but true progress for managing patients with many conditions such as of chronic mitral valvular disease in dogs awaits significant advances in this area of veterinary cardiology. Balloon valvuloplasty and pacemaker implantation are two examples where significant advances have been made in this realm in veterinary medicine.

We should be proud of the recent advances we have made in veterinary cardiology -- primarily in the realm of diagnostics. However, the ability to diagnose the patient is only the first step. More effective therapy or prevention will hopefully be the next great advancement in veterinary cardiology.

Table 7. Classification scheme for common cardiac diseases

   

LV

RV

LVMF

LHF

RHF

   

REGURGITANT LESIONS

MITRAL REGURGITATION

V

   

+

+++

-

   

TRICUSPID REGURGITATION

   

V

-

-

+++

   

AORTIC REGURGITATION

V

   

+++

++++

-

   

OBSTRUCTIVE LESIONS

AORTIC STENOSIS

P

   

R

R

-

   

PULMONIC STENOSIS

   

P

-

-

R

   

SHUNTING LESIONS

VENTRICULAR SEPTAL DEFECT

V

   

R

+

-

   

ATRIAL

SEPTAL DEFECT

   

V

-

R

+

   

TETRALOGY

OF FALLOT

   

P

-

-

R

   

PATENT DUCTUS ARTERIOSUS (LEFT-TO-RIGHT)

V

   

+

++++

-

   

PATENT DUCTUS ARTERIOSUS (RIGHT-TO-LEFT)

   

P

-

-

R

   

ENDOCARDIAL CUSHION DEFECT

V

V,P

-

R

R

   

PRIMARY MYOCARDIAL DISEASES

   

DYSFUNCTION

DILATED CARDIOMYOPATHY

NA

NA

++++

+++

++

SYSTOLIC

HYPERTROPHIC CARDIOMYOPATHY

NA

NA

R

+++

R

DIASTOLIC

RESTRICTIVE CARDIOMYOPATHY

NA

NA

+

+++

R

DIASTOLIC

   

   

   

   

   

   

   

PERICARDIAL TAMPONADE

NA

NA

NA

+

+++

DIASTOLIC

Key to symbols in above table:

V = VOLUME OVERLOAD

P=PRESSURE OVERLOAD

R = RARE

NUMBER OF (+) INDICATES RELATIVE INCIDENCE OF CLINICAL SIGNS NOTED

NA = NOT APPLICABLE

- = NOT PRESENT

LV = LEFT VENTRICLE; RV = RIGHT VENTRICLE; LHF = LEFT HEART FAILURE; RHF = RIGHT HEART FAILURE; LVMF = LEFT VENTRICULAR MYOCARDIAL FAILURE


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