• Syncope/lethargy - due to reduced cerebral perfusion.
• Weakness/reduced stamina - due to reduced skeletal muscle perfusion.
• Dyspnea/wheeze/cough/orthopnea - Dyspnea is due to pulmonary edema or pleural effusion. Cough may occur due to pulmonary edema or due to mitral valve insufficiency with left atrial enlargement and compression of the left main-stem bronchus; this latter cause may often occur in the absence of congestive heart failure. Many dogs with heart failure may not cough, whereas dyspnea, wheezes and sometimes orthopnea (difficulty breathing when lying down) are common historical findings. Some dogs will cough with relatively mild edema and others only cough with severe pulmonary edema. It appears that the speed with which the pulmonary edema develops may play a role in determining when or if cough is to develop.
• Abdominal distention - due to ascites and/or
• Hepatomegaly or splenomegaly.

Physical examination findings may include (signs of both reduced cardiac output and elevated preload):

• slow capillary refill time (> 2 sec)
• pale or cyanosed mucous membranes
• dry or tacky mucous membranes
• cool extremities or reduced rectal temperature
• jugular venous distention or positive hepato-jugular reflux test
• dyspnea, cough, harsh lung sounds, wheezes, or crackles on auscultation
• thrill on precordial palpation
• cardiomegaly on precordial palpation
• hepatomegaly and/or splenomegaly
• abdominal effusion
• subcutaneous edema
• weak femoral arterial pulse
• pulse deficits with irregular cardiac rhythm
• muffled heart sounds, gallop rhythms, heart murmurs, or arrhythmias may be detected on cardiac auscultation

Explanation of Auscultatory findings to follow.

Pulse deficits are present when the pulse rate is less than the heart rate. This occurs because a cardiac contraction or several contractions take place prematurely not allowing enough time for ventricular filling (preload). This results in heart beats that do not eject enough blood to generate a palpable pulse.

The presence of pulse deficits should alert the diagnostician to the occurrence of premature ectopic beats. These may be either supraventricular or ventricular in origin, only the ECG can distinguish these.

This test checks for the presence of jugular distention or jugular pulsations when pressure is placed in the region of the cranial abdomen in a ventral to dorsal direction. The animal should be standing or in sternal recumbency to perform this test.

A positive test result indicates that there is elevated pressure in the right atrium or right ventricle. If one were to classify an elevated pressure in the right heart as mild, moderate or severe, venous distention at rest indicates a severe elevation in pressure, whereas a positive HJR indicates a moderate elevation in pressure. Patients with a mild elevation in pressure to the right heart cannot be identified on physical examination.

The arterial pulse may be classified as weak, normal, or strong.

The palpable strength of the pulse is determined by:

• the Pulse Width (known as Pulse Pressure) = Systolic Pressure - Diastolic Pressure
• the rate of change from systolic to diastolic pressure and back again to systolic pressure

The arterial pulse (through the effect of systolic and diastolic pressure) is affected by:

• left ventricular stroke volume
• ejection velocity
• the relative compliance and capacity of the arterial system
• the pressure waves that result from the antegrade flow of blood and reflections of the arterial pressure pulse returning from the peripheral circulation

The most exuberant arterial pulses occur with patent ductus arteriosus and aortic valve insufficiency. Strong arterial pulses occur with enhanced sympathetic tone (anemia, hyperthyroidism, and fever). Weak arterial pulses occur with reduced stroke volume or aortic stenosis.

Comment: The arterial pulse can be maintained near normal in the face of a reduced cardiac output, mainly due to the effect of the compensatory arterial vasoconstrictor mechanisms.

• palpation
• auscultation
• thoracic radiography
• electrocardiography
• blood work
• echocardiography
• other invasive, sophisticated tests

Precordial palpation is useful to: 

• detect a thrill - a thrill refers to a vibration on the chest wall due to fluid turbulence within the heart that also causes a heart murmur on auscultation. Only the very loudest heart murmurs will be accompanied by a thrill
• detect dysrhythmias
• suspicion of cardiomegaly
• location of apex beat - usually on left - some disorders will cause the apex beat to shift to the right chest wall

Auscultation remains the most useful and expedient assessment of the cardiac patient. It can frequently result in a definitive diagnosis or when combined with the signalment and history can often provide a strong differential diagnosis.

The goals of auscultation are:

1. To determine the heart rate

Bradycardia, normal, or tachycardia

2. To determine if there is a rhythm disorder

To be distinguished from a respiratory arrhythmia

3. To rule out muffled or absent heart sounds

Occur due to insulation between sound source and stethoscope as in:

• Presence of fluid in the pericardial space = pericardial effusion
• Presence of fluid in the pleural space = pleural effusion
• Mass in the pleural space or pericardial space
• Pleural tumors
• Pericardial tumors
• Diaphragmatic hernia either to the pleural or pericardial space
• Lung parenchymal disease
• Obesity

May be a normal variant in some dogs

4. To rule out extra sounds such as

Heart murmurs

Gallop sounds: S3 or S4 or summation

Systolic clicks

Split heart sounds: S1 or S2

Pericardial friction rubs - rare in small animals

Other than for detecting asystole, auscultation cannot provide definitive evidence of heart failure. Rarely, individuals may have heart failure in the face of normal heart sounds and cardiac rhythm. The finding of gallop sounds is often very strong evidence of severe myocardial dysfunction. The presence of a murmur does not equate with heart failure. In fact, most patients with a heart murmur do not have heart failure.

To hear examples of normal and abnormal heart sounds, go to this section of the notes at www.vetgo.com/cardio/sounds/hsmonth.php

1. Most of the disorders that promote abnormal heart sounds produce sounds that do not fall into the audible range. Thus, to detect those few that do fall into the audible range, careful auscultation is necessary to locate these sounds.

2. For the best sound reproduction, consider the following:

3. Only auscult a patient when in the standing or sitting position. Auscultation of the patient in lateral or dorsal recumbency can result in creating false murmur like sounds (perhaps rubbing sounds) and/or impairs our ability to localize the PMI for a "real" murmur.

S1

S2

Heart murmurs are abnormal, extra sounds that are of a relatively long duration.

Heart murmurs occur as a result of turbulence within the heart created by disturbed blood flow.

Reynolds number defines the variables that promote disturbed (non laminar) flow in a vessel or chamber. When Reynolds Number exceeds a critical value flow becomes turbulent.

Reynolds No = (Area)(Velocity)(Density) / Viscosity

Area = cross-sectional area of the chamber, orifice, or vessel; Velocity = velocity of blood flow (note that this is related to the area); Density = density of blood; Viscosity = viscosity of blood (affected mainly by the red blood cell count and protein count)

Blood flow turbulence can be created by high-velocity flow, flow from a narrow region into a larger area, or low blood viscosity.

1. Causes of turbulence:

• Valvular insufficiency
• Valvular stenosis
• Connections between the cardiac chambers (i.e. interatrial and interventricular defects (holes)
• Connections between the great vessels (i.e. PDA)

2. Not associated with organic disease:
• May be innocent / physiologic associated with low blood viscosity (anemia, hypoproteinemia)
• < grade 3
• occur in early to mid systole
• Note that if blood viscosity is increased, a murmur may be masked
• May be observed in young adults likely associated with ejection of blood into the great vessels
• < grade 3
• occur in early to mid systole
• Associated with increase in blood flow across a normal valvular orifice as with flow across the pulmonic valve in a VSD and ASD or across the aortic valve in bradycardia such as 3rd degree AV block

Anything that muffles the heart sounds can obscure a murmur such as obesity, thoracic effusions, or loud respiratory sounds.

Functional (physiologic) heart murmurs occur in the absence of cardiac disease in a variety of situations. These murmurs are most commonly identified in the growing young dog, where they are referred to as innocent murmurs. These murmurs should resolve by 6 months of age, and tend to have the following characteristics:

• soft, low intensity sounds (grade 1/6 to 2/6)
• occur early in systole
• PMI over the left base
• may vary in intensity with a change in HR or body position

It is my belief that similar innocent heart murmurs may also occur in the adult, particularly of large and giant breed dogs.

Functional (physiologic) murmurs may also occur:

• in athletes
• in pathologic states such as fever, anemia, or hypoproteinemia

These are important features to distinguish innocent murmurs from congenital heart murmurs.

A presumptive diagnosis is usually possible based primarily on the timing of the heart murmur, and the point of maximal intensity (PMI) of the murmur.

These "other features" are clearly of secondary use and less sensitive than the primary features of timing and PMI.

1. Point of Maximal Intensity (PMI):

The PMI refers to the location where the murmur is loudest.

The left chest wall is typically divided with respect to PMI into two positions.

• left heart base (includes both the pulmonic valve and aortic valve areas, and discriminating between these two is often problematic)
• left heart apex (mitral valve area)

The right chest wall is typically divided with respect to PMI into two positions.

mid heart (tricuspid valve area)

sternal border (typical of a VSD)

2. Timing:

Timing of murmurs, at the PMI, is generally divided into one of three classes:

systolic (occurring during systole)

diastolic (occurring during diastole)

continuous (present at all times)

Systolic murmurs:

• The very vast majority of murmurs are systolic
• When soft they are usually early in systole and disturb the end of S1. S1 often appears slurred in these cases as opposed to ending abruptly as is normally the case.
• The careful clinician focuses on the end of S1 for soft systolic murmurs.
• Holosystolic murmur: refers to a systolic murmur that begins during or immediately after S1 and ends with the onset of S2
• Pansystolic murmur: refers to a systolic murmur that begins during or immediately after S1 and continues into and obscures S2 (note that left ventricular pressure continues to be greater than left atrial pressure after aortic valve closure - during isovolumetric relaxation).

Download examples of systolic murmurs to your desktop (play in Meditron Player):

Example 1, Example 2, Example 3

Diastolic murmurs:

• Very rare
• Low frequency
• Rather low intensity and so are graded out of 4, not 6
• Best identified with the bell of the stethoscope

Continuous murmurs:

• Common, but less so than systolic
• Typically associated with a PDA, but also arteriovenous fistulas
• Usually vary in intensity throughout the cardiac cycle, however the murmur is detected at all times
• The continuous nature of the murmur may only be noted at the PMI, while at other locations it may only be systolic, for example.

Download examples of continuous murmurs to your desktop (play in Meditron Player):

Example 1, Example 2

To and Fro murmurs:

• The name for the situation when a systolic murmur and a diastolic murmur (due to different physiologic etiologies) coexist.

Download examples of to and fro murmurs to your desktop (play in Meditron Player):

Example 1

Using the timing and PMI of a murmur, the following algorithm may be used to arrive at a presumptive diagnosis:

Recall causes for a continuous murmur: PDA or Arteriovenous Fistula

3. Intensity:

The intensity of the murmur at its origin is related to (Blood flow velocity) x (Rate of flow). Overall, the intensity of a heart murmur is not related to the severity of the lesion; however for some diseases there is a rough correlation between the intensity of the murmur and the severity of the lesion such as:

• Mitral valve insufficiency
• Aortic / subaortic valve stenosis
• Pulmonic valve stenosis

The intensity of a murmur is graded on a scale of 1 to 6:

Grade 1 = a very soft, localized murmur detected only after several minutes of listening.

Grade 2 = a soft murmur, heard immediately but localized to a small area.

Grade 3 = a moderately intense murmur that is readily detected and detected over more than one location.

Grade 4 = a moderately intense or loud murmur, detected over several areas, usually both sides of the chest, however a precordial thrill is not detected in this case.

Grade 5 = a loud murmur accompanied by a precordial thrill over the point of maximal intensity.

Grade 6 = a very loud murmur accompanied by a precordial thrill and the murmur is detected when the stethoscope is pulled slightly off the chest wall.

1. GALLOPS:

• result in a tripling or quadrupling of the heart sounds, resembling the canter of a horse
• best heard with the bell of the stethoscope

S₃ gallop (ventricular gallop)

• Low frequency sound
• Occurs shortly after the S2 sound, at the beginning of diastole, during the rapid filling phase.
• Called a ventricular gallop
• Not normal in dogs and cats. Indicates ventricular failure. May be an early finding and the only auscultatory evidence of heart failure.
• Indicates diastolic dysfunction
• Associated with reduced compliance of the ventricle while filling under conditions of high filling pressures (stiffer ventricle).
• Caused by the sudden termination of longitudinal expansion of the ventricular wall during brisk early diastolic filling during the period of rapid ventricular filling.
• Indicates severe myocardial disease

S₄ gallop (atrial gallop)

• Low frequency sound
• Occurs shortly before the S1 sound, at the end of diastole, during atrial contraction.
• Called an atrial gallop
• Not normal in dogs and cats. Usually indicates ventricular failure. May be the only auscultatory evidence of heart failure.
• Indicates diastolic dysfunction
• Associated with the atria trying to force blood into an already over-distended ventricle or because the atria are forcing blood into a stiff ventricle. Atrial contraction is required for an audible S4 sound. Thus it does not occur in atrial fibrillation.
• Occurs in disorders with impaired relaxation of the ventricle typical of disorders of concentric hypertrophy
• May be a normal finding in older stressed cats

Summation gallop

• At fast heart rates an S3 and S4 gallop will superimpose to cause one sound called a summation gallop.

4. FRICTION RUBS:

• More common in large animals
• Scratchy sounds
• May have a:
• periodicity with the heart rhythm (then it is difficult to distinguish from a continuous murmur)
• periodicity with respiration
• caused by fibrin present on the pleural surfaces of chest wall, lungs, or pericardium

5. ARRYTHMIAS:

• Isolated premature beats or pairs or short bursts of premature beats result in disturbances to the cadence of the heart rhythm.
• Premature beats may result in only the presence of abnormally long pauses between beats. If the premature beat is extremely early (premature) no additional heart sounds will be detected, only the presence of the abnormal pause that follows. One might suspect that so-called “dropped beats” are occurring. PVCs tend to cause longer pauses than SVPCs.
• If the premature beat is slightly less premature only an S2 will be detected, so that the rhythm will sound like S1 then S2 and another S2 in rapid succession. This could be misinterpreted as a gallop. Gallops should not be intermittent like premature beats and they are not followed by an abnormal pause.
• Even less premature beats may be associated with both an early S1 and S2.
• A regular rhythm does not mean the rhythm is necessarily normal/sinus. Sustained ventricular or supraventricular tachycardia can be associated with a regular rhythm.

Radiography cannot detect a reduction in cardiac output for the needs of the tissue (heart failure) but can provide evidence of pulmonary congestion to suggest congestive heart failure (pulmonary venous engorgement, pulmonary interstitial edema, and obscuring and enlargement of the cardiac silhouette). 

Radiography provides the most readily available means to identify pulmonary edema and pulmonary venous congestion. Because the vast majority of cases of pulmonary edema are due to congestive heart failure - then the finding of pulmonary edema is strong evidence of congestive heart failure. 

Since pulmonary venous congestion (distention) will/must occur prior to the development of cardiogenic pulmonary edema, to identify the presence of pulmonary venous congestion is also strong evidence of congestive heart failure. 

*See also the Thoracic Radiographic Tutorial section of these notes.

• On the lateral view the pulmonary veins to the cranial lung lobes are greater than 75% the width of the proximal 1/3 of the fourth rib
• The pulmonary vein to the cranial lung lobe is obviously larger than its accompanying pulmonary artery (normally they are of equal width)

Pulmonary edema refers to an abnormal accumulation of fluid in the interstitium and/or the alveoli of the lungs. As fluid weeps out of the capillaries, at first it accumulates in the perivascular and peribronchial interstitial spaces (producing silhouetting of the vessels, and/or peribronchial pattern on radiographs). Continued fluid accumulation results in edema of alveolar walls and ultimately, alveolar edema (producing air-bronchograms or coalescent [so called cotton-like] pulmonary densities).

Although alveolar edema is usually preceded by interstitial edema, many clinical cases represent a mixture of interstitial and alveolar edema.

Radiographic Appearance:

• Venous engorgement - distention of the veins.
• Interstitial edema - shows a clouding (or silhouetting) of the pulmonary vasculature (perivascular pattern). The walls of the pulmonary vessels are obscured by edema fluid. A peribronchial pulmonary pattern (the most common sign of interstitial edema noted in the dog) also may occur as noted. This pattern is characterized by thickened airway walls. Normally the airway walls are not discernible radiographically after the third generation bronchi due to the lack of cartilaginous support. We typically infer the presence of a bronchus due its position between the artery and vein that lie on each side. The prominent appearance of airway walls throughout the lungs indicates a peribronchial lung pattern, which implies a cellular and/or fluid accumulation in the walls rendering them visible. On cross-section the airway walls are "donut-like", on long axis view they are "railway tracks-like."
• Alveolar edema - (flooding of air spaces) shows as coalescing fluffy densities and/or air-bronchograms.

Location of edema:

• Dog: Appears first in the central perihilar area progressing outward and caudodorsally. There is also a high incidence of edema in the anterior ventral area on the lateral view.
• Cat: Variable distribution often occurring in a patchy, irregular pattern primarily in the caudal lobes.

Schematic Of An Air Bronchogram vs A Peribronchial Pattern

Note how the lumenal wall is readily identified in both examples, but the outside wall is obscured with air-bronchograms.

Radiography can also assist in the diagnosis of: 

• chamber enlargement
• great vessel enlargement
• heartworm disease
• pericardial effusion or pleural effusion

Radiography is a simple and effective means of diagnosing cardiac chamber enlargement. In most forms of heart failure cardiac enlargement is present.

It is important to determine the cardiac structures that contribute to the silhouette of the heart on the lateral and D/V or V/D view.

Always be consistent with your lateral (R or L) and D/V or V/D views. Always obtain films at end inspiration.

Some general guidelines on cardiac size in the dog (criteria from end inspiratory films):

On the lateral view normal cardiac dimensions:

• horizontal plane:
  • < 3.5 intercostal spaces for:
    • brachiocephalic breeds
    • immature dogs
    • small breeds
  • < 3 intercostal spaces for "average dog"
  • < 2.5 intercostal spaces for deep chested breeds
    
• vertical plane:
  • the vertical distance from the cardiac apex to the carina is normally 2/3 to 3/4 the vertical distance from the cardiac apex to the vertebral column
  • as cardiac enlargement occurs in this plane the trachea tends to parallel the vertebral column and the vertical distance from the cardiac apex to the carina is increased

A schematic diagram of a lateral radiographic view of the chest. Normally A is approximately 1/3 to 1/4 of A + B, and B is approximately 2/3 to 3/4 of A + B.

On the D/V or V/D view normal cardiac dimensions:

• the greatest horizontal cardiac dimension should be < 2/3 of the chest wall to chest wall thoracic dimension at that location.

A schematic diagram of a V/D or D/V radiographic view of the chest. In normal hearts R is approximately equal to L; B is < 2/3 of A.

Significance of cardiac enlargement in the lateral view:

• In the Horizontal Plane:
  • Suggests right ventricular enlargement, however left ventricular enlargement tends to produce at least mild enlargement in this plane.
    
• In the Vertical Plane:
  • Suggests left ventricular enlargement, however right ventricular enlargement tends to produce at least mild enlargement in this plane.

Significance of cardiac enlargement in the V/D or D/V view:

• A reduced right heart to chest wall dimension suggests right ventricular enlargement.
• A reduced left heart to chest wall dimension suggests left ventricular enlargement.

Single chamber enlargement is unusual and therefore enlargement in one chamber tends to cause enlargement in other areas of the heart.

Some general guidelines on cardiac size in the cat:

• The heart is more elongated and elliptical in shape than in the dog on the lateral view.
• The ventricular area occupies about 2 to 2 1/2 intercostal spaces in the lateral view.
• In the lateral view the cat heart tends to be more horizontal; as cats age, the heart tends to horizontalize even more (called a "lazy" heart).
• In the D/V or V/D projection, the cat heart is more oval and thinner than the dog. The cardiac apex usually lies on the midline.

Vertebral Heart Size (VHS) is a technique that measures the width and breadth of the heart and compares it to the length of the vertebral bodies. It can be useful because the measurements are independent of respiration and the position of the heart within the chest. However, because of the test's low sensitivity, a normal VHS does not rule out an enlarged heart. It also does not rule out the possibility of cardiac disease that does not have an effect on heart size.

To calculate VHS, use a lateral view that clearly shows the T4-T13 vertebrae, with minimal rotation of the thorax (rib arches and costochondral junctions should be aligned).
Long axis: Measure the distance (using a ruler or piece of paper) from the carina to the apex of the heart.
Short axis: Measure the widest part of the heart on an axis perpendicular to the long axis.
Compare to vertebrae: Starting from the cranial edge of the T4 vertebral body, measure the length of the axes by the number of vertebrae. Measure to 0.1 of a vertebral body. The vertebral heart size is the sum of the length of the short and the long axes in vertebrae (VHS = long + short).

Reference intervals for VHS:

• Normal dogs: 8.5-10.7
• Boxers: 10.3-12.6
• Labrador Retrievers: 9.7-11.7
• Cavalier King Charles Spaniels: 9.9-11.7
• Cats: 6.7-8.1

Radiography is a simple means to determine changes in the great vessels.

• Distention of the aorta in the region of the aortic arch with aortic stenosis:
  • may not be apparent unless aortic stenosis (or subaortic) is severe
• Dilation of the main pulmonary artery (MPA):
  • due to pulmonic stenosis, heartworm disease, or pulmonary artery hypertension
• Pulmonary over-circulation:
  • left to right shunt
• Pulmonary under-circulation:
  • right to left shunt
  • under-perfusion/hypovolemia/dehydration
• Caudal vena caval enlargement:
  • Caudal vena cava Present if the caudal vena cava is persistently of greater diameter than the descending thoracic aorta on the lateral view (normally they are roughly equal).
  • Suggests right heart failure with elevated volumes in the caudal vena cava.

• Right ventricular enlargement
• Dilation of main pulmonary artery (MPA)
• Tortuosity of pulmonary arteries (PAs)
• Truncated PAs
• Enlargement of PAs

• Lateral
• DV

Radiography is useful to suggest a diagnosis of pericardial effusion.

• A very rounded (globose) enlarged heart is present; individual chambers cannot be visualized
• Pleural effusion is common (therefore, obscures the cardiac silhouette), ascites is common
• Pulmonary edema is usually absent, however pleural effusion obscures our ability to visualize the features of pulmonary edema.

• Lateral
• DV

No. In many cases of heart failure the ECG is normal.

A schematic diagram of the conduction system of the heart.

• Class I Animals; horses and cattle:
  • extensive arborization of the Purkinje system within the ventricular wall from endocardium to epicardium
• Class II Animals; man, dog and cat:
  • minimal branching of the Purkinje system within the ventricular wall with penetration of only the endocardium
• In all domestic animals the ECG is the diagnostic test of choice to detect and diagnose dysrhythmias (arrhythmias).
• In Class II animals - the ECG is also useful to provide clues to chamber enlargement.
• ECGs can also suggest:
  • electrolyte imbalance
  • myocardial ischemia/hypoxemia
  • drug intoxication
  • thoracic effusion
  • pericardial effusion

Please refer to the Electrocardiography section for further information about electrocardiography.

There is no blood test that can definitively determine the existence of heart failure. However, the detection of certain circulating hormones or enzymes, so-called biomarkers, may provide strong evidence in support of heart failure or even heart disease. See below.

• A number of findings can support a reduced cardiac output:
  • evidence of reduced renal perfusion (reduced GFR)
    • increase BUN/creatinine or reduced urinary output
  • depressed venous oxygen tension (venous pO₂) levels
  • elevated lactate levels
  • reduced serum sodium

• Muscle enzyme elevations (CPK, SGOT, LDH) are almost uniformly of no value in detecting heart disease of domestic animals; isoenzymes may be of more value to detect myocardial necrosis.
• Circulating cardiac troponin I (cTnI) is a general marker of cardiac myocyte injury. It is elevated in a number of canine and feline cardiac diseases, including dilated and hypertrophic cardiomyopathies, subaortic stenosis, and chronic mitral valve disease, but also in other diseases that may secondarily cause myocardial injury. In dilated cardiomyopathy, cTnI levels may relate to prognosis. Several human cTnI assays have been validated in dogs and cats.
• Plasma norepinephrine is elevated in all causes of heart failure and the level relates to prognosis.
• Plasma aldosterone and angiotensin II are elevated in heart failure.
• Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP) are elevated in humans, cats, and dogs with heart failure of various causes. For more information on BNP see the next question.
• Use of certain cardiac drugs, like digoxin, necessitates monitoring drug levels.
• Can detect electrolyte imbalances that may contribute to heart disease.
• Can detect acid-base imbalance that may contribute to heart disease.
• Can detect thyroid imbalance that may contribute to heart disease.
• Can suggest infection in cases of infective heart disease.
• Can assay serum taurine levels or carnitine levels, which may be important in dilated cardiomyopathy.
• Can assay for Lyme's Disease, which can cause myocarditis and conduction abnormalities.
• Can assay for evidence of heartworm disease

BNP, specifically NT-proBNP, has been demonstrated in human medicine to have an extremely important role in the diagnosis and management of heart disease and heart failure:

• It is used to discriminate between a primary respiratory disorder and CHF in patients with respiratory signs.
• It predicts prognosis in patients with CHF.
• It may reflect response to treatment, and so help guide therapy.
• It may be useful to identify asymptomatic (occult) cardiac disease prior to the onset of symptoms.

Review of BNP:

• Released from the heart due to:
  • Atrial or ventricular stretch/dilation
  • High hydrostatic pressure
  • Hypertrophy
  • Ischemia, neurohormones
• Effect of BNP:
  • Causes natriuresis and vasodilation
  • Counteracts the RAAS
• Metabolism of BNP:
  • Produced as a prohormone
  • Cleaved by a neutral endopeptidase into 2 moieties
    • C-BNP
      • The biologically active moiety
      • Unstable with a very short half life
    • NT-proBNP
      • Biologically inactive
      • Stable with a long half life
      • ELISA assay used to detect
• The current assay available in veterinary medicine is called Cardiopet proBNP through IDEXX labs.

  
  Use of the NT-proBNP test in Cats:

  • Why might there be a place for this test in cats?
    • Many cats with heart disease are asymptomatic
    • Radiographic findings in cats with heart disease can be variable and inconclusive
    • Heart murmurs or gallops in cats with heart disease may be intermittent, difficult to detect, or not present. Furthermore, innocent or physiologic murmurs are common in cats.
    • Although echocardiography is usually definitive, it may not be available or may be expensive
  • Role for NT-proBNP in Cats:
    • Identify heart disease in high-risk populations that are asymptomatic (to determine if they are “likely” or “unlikely” to have heart disease)
      • Older cats
      • Cats with either a heart murmur or a gallop
      • Breeds at high risk such as the Maine Coon
      • Recommendations:
        • NT-proBNP > 50 pmol/l is highly likely to indicate underlying heart disease.
    • Sensitivity and specificity are reported to be 90% and 85% respectively, however this may apply mostly to the detection of severe disease. Therefore recognize that there is the potential for false negatives, particularly in the case of mild to moderate disease. False positives are also possible.
      • For cases that are too fragile for diagnostics or that can’t afford echocardiography.
      • Radiographs are always indicated in the presence of respiratory signs, however findings can sometimes be inconclusive.
      • Recommendations:
        • NT-proBNP > 270 pmol/l is highly likely to indicate the presence of CHF
      • Cats with NT-proBNP between 50-270 pmol/l likely have heart disease but may or may not have CHF.

  
  Use of the NT-proBNP test in Dogs:

  • Where might there be a place for this test in dogs?
    • To identify dogs with asymptomatic (occult) DCM
    • To differentiate between primary respiratory disease and CHF as the cause for respiratory clinical signs
    • To assess prognosis and guide therapy
  • To identify dogs with asymptomatic heart disease:
    • Recommendations:
      • NT-proBNP > 900 pmol/l is likely to indicate the presence of heart disease
      • Recognize again that both false positives and false negatives will occur.
    • Dogs with DCM tend to have higher values than dogs with CMVI
    • The more advanced the heart disease the higher the levels of NT-proBNP
    • NT-proBNP > 680 pmol/l were associated with radiographic evidence of cardiomegaly (VHS > 11.5)
  • To differentiate between primary respiratory disease and CHF as the cause for respiratory clinical signs:
    • Recommendations:
      • NT-proBNP > 2700 pmol/l is highly likely to indicate the presence of CHF in patients with evidence of heart disease.
      • Dogs with NT-proBNP between 900-2700 pmol/l likely have heart disease but may or may not have CHF.

    
    Limitations:

    • Prerenal and renal azotemia may cause significant elevations in NT-proBNP therefore levels must be interpreted with caution in patients with elevated urea and creatinine.
    • Pulmonary artery hypertension (without left sided heart disease) also elevates NT-proBNP levels, and may be present in patients with primary respiratory disease.
    • Prolonged shipping or inappropriate storage will result in a reduction (degradation) of NT-proBNP.
    • Day to day variability likely exists. Week to week variability in normal dogs ranged between 37 to 51%.

Echocardiography (ultrasound of the heart) is the most expedient means of detecting and quantifying a weakened heart muscle (systolic dysfunction) or abnormal filling (diastolic dysfunction). It is also ideal to detect a great number of other disorders that contribute to heart disease and heart failure.

Although echocardiography cannot definitively determine if heart failure is present (that is, the adequacy of cardiac performance), it can potentially provide strong evidence to support or refute the presence of heart failure.

Echocardiography can detect:

• Changes in chamber dimensions and wall thicknesses which can suggest the etiology of congenital or acquired heart disorders
• Chronic valvular disease
• Dilated cardiomyopathy
• Hypertrophic cardiomyopathy
• Pericardial disease
• Bacterial endocarditis
• Cardiac tumours
• Doppler echocardiography can be used to detect and quantify stenotic and insufficient valvular heart disease and pulmonary artery hypertension
• Diastolic disorders of myocardial function

Doppler echocardiography allows for the detection of abnormal blood flow patterns as well as the velocity of blood cells as they move throughout the heart.

Doppler echocardiography allows for the diagnosis and quantification of the severity of:

• stenotic valvular disorders
• valvular insufficiency disorders
• septal defects
• pulmonary artery hypertension
• intracavitary stenotic disorders
• diastolic disorders
• wall motion abnormalities