Page 150 - Small Animal Internal Medicine, 6th Edition
P. 150
122 PART I Cardiovascular System Disorders
compensated heart failure occurring over months to years filling pressures. Jugular pulsations and distention are more
are also common. evident with cranial abdominal compression (positive hepa-
VetBooks.ir are more common in dogs with advanced disease. These tojugular reflux). Ascites or hepatomegaly may be evident in
Episodes of transient weakness or acute collapse (syncope)
dogs with right-sided CHF.
Concurrent diseases that could be confused with decom-
could occur from tachyarrhythmias, an acute vasovagal
response, PH, or an atrial tear. Coughing spells can precipi- pensated CHF from CMVD include tracheal collapse,
tate syncope, as can exercise or excitement. Signs of right- chronic bronchitis, bronchiectasis, pulmonary fibrosis, pul-
sided CHF usually are associated with severe TR, PH, or monary neoplasia, pneumonia, pharyngitis, heartworm
both. These include abdominal distension (ascites, hepato- disease, DCM in larger breeds, and infective endocarditis
megaly) and respiratory distress from pleural effusion. (which is rare with CMVD).
Gastrointestinal (GI) signs could accompany splanchnic
congestion. Only rarely does noticeable peripheral tissue
edema develop in dogs with CMVD. DIAGNOSIS
The typical auscultatory finding is a holosystolic murmur
heard best in the area of the left apex (left fourth to sixth CLINICOPATHOLOGIC FINDINGS
intercostal space). The murmur can radiate in any direction. Routine clinical laboratory tests often are normal or reflect
Mild regurgitation can be inaudible or cause a murmur only changes consistent with CHF or concurrent extracardiac
in early systole (protosystolic). Exercise and excitement often disease. Elevations in natriuretic peptide concentrations
increase the intensity of soft MR murmurs. Louder murmurs tend to reflect increasing disease severity. Dogs with high
have been associated with more advanced disease; in dogs levels (e.g., NT-proBNP ≥ 1500 pmol/L) are more likely to
with massive regurgitation and severe heart failure, however, have CHF (or develop it sooner) and have a worse prognosis.
the murmur can be soft or even inaudible. Occasionally, the Elevations in circulating cardiac troponin I (cTnI) also occur
murmur sounds like a musical tone or whoop. Some dogs in moderate to severe CMVD and increase with severity of
with early MVD have an audible mid- to late-systolic click, clinical signs. This could be a marker for myocardial fibrosis
with or without a soft murmur. In dogs with advanced in chronic heart disease.
disease and myocardial failure, an S 3 gallop might be audible
at the left apex. TR typically causes a holosystolic murmur RADIOGRAPHY
best heard at the right apex. Features that aid in differentiat- Thoracic radiographs are normal in dogs with early (stage
ing a TR murmur from radiation of an MR murmur to the B1) CMVD. As MR severity increases, progressive LA and
right chest wall include jugular vein pulsations, a precordial then LV enlargement develops (stage B2), usually over a
thrill over the right apex, and a different quality to the period of years (Fig. 6.1). Dorsal elevation of the carina and,
murmur heard over the tricuspid region. as LA size increases, dorsal main bronchus displacement
Pulmonary sounds can be normal or abnormal. Accentu- occur. Severe LA enlargement can cause the appearance of
ated, harsh breath sounds and end-inspiratory crackles carina and left mainstem bronchus compression (Fig. 6.1, C).
(especially in ventral lung fields) develop as pulmonary Fluoroscopy might demonstrate dynamic airway collapse (of
edema worsens. Fulminant pulmonary edema causes wide- the left main bronchus or other regions) during coughing or
spread inspiratory, as well as expiratory, crackles and wheezes. even quiet breathing because concurrent airway disease is
Some dogs with chronic MR have abnormal lung sounds common in these cases. Extreme dilation of the LA can result
caused by underlying pulmonary or airway disease rather over time, even without clinical heart failure. The vertebral
than CHF. Although not a pathognomonic finding, dogs heart score (VHS) increases with the growing volume over-
with CHF often have sinus tachycardia, whereas marked load. In coughing dogs with CMVD, a VHS ≤ 11.4 v suggests
sinus arrhythmia is common in those with chronic pulmo- a noncardiac cause; dogs with cardiac or mixed-origin cough
nary disease. Pleural effusion may cause diminished pulmo- tend to have higher VHS. The rate of change in VHS, as well
nary sounds ventrally. as the echocardiographic dimensions of LA and LV in both
Other physical examination findings may be normal or diastole and systole, becomes greatest at the onset of CHF.
noncontributory. Heart rate and rhythm generally are The increase in cardiac size occurs most rapidly within the
normal, although sinus tachycardia is more typical as CHF 12 months preceding CHF onset. Variable right heart
develops. Arrhythmias are more likely to occur with enlargement occurs in association with chronic TR, but this
advanced disease. Peripheral capillary perfusion and arterial may be masked by left heart and pulmonary changes associ-
pulse strength usually are good, although pulse deficits ated with concurrent MVD.
might be present in dogs with tachyarrhythmias. A palpable Pulmonary venous congestion can be an early sign of
precordial thrill accompanies loud (grade 5-6/6) murmurs. left-sided congestive failure. However, visibly distended pul-
Jugular vein distention and pulsations are not expected in monary veins are not always appreciable. Interstitial edema
dogs with MR alone. In animals with TR, especially PH, occurs with the onset of left-sided CHF. Radiographic find-
jugular pulses occur during ventricular systole; these are ings associated with early pulmonary edema can appear
more evident after exercise or in association with excitement. similar to those caused by chronic airway or pulmonary
Jugular venous distention results from elevated right heart disease. With CHF, progressive interstitial and alveolar