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Pulmonary Hypertension (Arterial) 839

• Weak pulse ○ Pulmonary vascular bed occlusion: ○ Qualitative confirmation of PH: char-
• Right-sided congestive heart failure (CHF) PTE; parasites (D. immitis, A. vasorum); acteristic two-dimensional (2D) and
VetBooks.ir • Split-second heart sound (pulmonic valve ○ Pulmonary parenchymal disease: inter- PH are dilation of right ventricle and Diseases and Disorders
embolism (e.g., tumor)
M-mode findings in moderate to severe
(e.g., jugular distention or jugular pulse,
ascites)
atrium, thickening of right ventricular
stitial pneumonia (A. vasorum, E. canis);
closing after aortic valve)
tening, prominent pulmonary artery, and
(p. 27)
• TR murmur (systolic, right-sided) interstitial lung disease (p. 553); ARDS wall and papillary muscles, septal flat-
• Pulmonic regurgitation murmur (rare; ○ Multiple mechanisms can occur simultane- decreased left ventricular chamber size.
diastolic, left heart base) ously (e.g., heartworm infection causing CAVEAT: 2D abnormalities are usually
• Hyperemic mucous membranes due to obstruction by intravascular parasites, prominent only if PH is severe or acute.
erythrocytosis (response to hypoxemia) vasculitis, thrombosis, hypoxic vasocon- ○ Quantitative confirmation of PH: Doppler
• Differential cyanosis in reverse PDA (often striction, and vascular remodeling) exam is the most useful noninvasive
only after exercise) clinical tool to confirm and quantitate
Group 2: PH with left-sided heart disease; same DIAGNOSIS severity of PH. Velocity of TR correlates
as PAH plus with right ventricular systolic pressure and
• Loud mitral regurgitation murmur, increased Diagnostic Overview therefore, barring pulmonic stenosis, with
lung sounds/crackles with CHF A clinical diagnosis of PH is made when pulmonary arterial systolic pressure. Vmax
• Intensity of mitral murmur may decrease high-velocity valvular regurgitation (tricuspid, > 3-3.5 m/s reflects mild, 3.5-4.5 indicates
with progression of PH; intensity of TR pulmonic, or both) is documented by Doppler moderate, and > 4.5 indicates severe PH.
murmur may increase. echocardiography in the absence of pulmonic In chronic PH, Vmax < 4.0 m/s does
Group 3: PH with respiratory disease/hypoxia; stenosis. not usually cause clinical signs due to
same as PAH plus PH. CAVEAT: loading conditions, right
• Stertor or stridor with upper respiratory Differential Diagnosis ventricular systolic function and sedation
obstruction • Right-sided heart failure may significantly affect peak velocities. For
• Abnormal lung sounds (e.g., harsh, loud, ○ Congenital cardiac disease: pulmonic Doppler quantification of pulmonary valve
wheezes, crackles) stenosis, tricuspid dysplasia, tricuspid insufficiency (PI), peak velocity correlates
• Altered pattern of respiration, if present, can stenosis, cor triatriatum dexter with mean PAP and end-diastolic velocity
aid in disease localization (p. 879). ○ Acquired cardiovascular disease: severe with diastolic PAP.
Group 4: PH due to thrombotic/embolic myxomatous/degenerative tricuspid valve • Electrocardiogram (ECG): document right
disease; same as PAH plus disease, right ventricular cardiomyopathy, ventricular hypertrophy (deep S waves in
• Hemoptysis pericardial effusion, heartworm leads I, II, III, aVF), right axis deviation,
• Increased lung sounds • Right ventricular hypertrophy and possible arrhythmias; in acute PH,
• Sometimes palpable tumor (e.g., neoplastic ○ Pulmonic stenosis, tetralogy of Fallot ECG abnormalities may not be present; in
embolism) chronic PH, PH must be marked to cause
• Exam findings suggestive of cause for PTE Initial Database abnormalities, and ECG therefore is not a
(e.g., signs of hyperadrenocorticism or • Thoracic radiographs; dorsoventral view is sensitive tool.
protein-losing nephropathy) particularly important. • Serology or other parasite testing (e.g., D.
○ Right ventricular and main pulmonary immitis or A. vasorum serology; Baermann
Etiology and Pathophysiology artery enlargement; nonspecific, reversed fecal exam)
• Regardless of cause, PH can lead to cor D, and increased sternal contact on the • Platelet count, coagulation profile, and
pulmonale (right ventricular hypertrophy lateral view are often overinterpreted in parameters associated with hypercoagulability
secondary to PH) and eventually to right- normal dogs and cats (expiratory films, (e.g., antithrombin and D-dimer) may be
sided heart failure. rotation of patient, thoracic conformation). abnormal with vasculitis and acute throm-
• In PAH, genetically mediated susceptibility ○ Tortuous/enlarged peripheral pulmonary bosis but mostly normal in chronic PTE.
to vascular injury is thought to be a final vasculature • Arterial blood gas analysis (p. 1058):
common response to inciting factors such ○ Peripheral pulmonary arterial markings hypoxemia in primary respiratory disease
as mechanical lesions (overperfusion), drugs, may abruptly stop with PTE. or right-to-left cardiovascular shunt
toxins, and infections. ○ Enlarged left atrium and congested pul- • CBC/biochemistry panel/urinalysis: abnormali-
• PH is a common complication of cardiac monary veins with underlying left atrial, ties may suggest parasitic disease (eosinophilia,
and extracardiac diseases causing increased ventricular, or mitral valve disease; left- basophilia; not commonly found with A.
left atrial pressure and increased pulmonary sided cardiac enlargement may decrease in vasorum), chronic inflammation (thrombo-
vascular resistance. chronic MMVD and associated chronic cytosis, hyperglobulinemia), and systemic
• Important causes: PH. disease predisposing to PTE (e.g., proteinuria,
○ Cardiac: pulmonary venous hypertension ○ Underlying bronchial, interstitial, or hypoalbuminemia, increased liver enzyme
due to increased left atrial pressure in alveolar pulmonary disease may be activities consistent with steroid hepatopathy)
left myocardial failure, most common in evident (e.g., classic peripheral interstitial • Natriuretic peptides may be increased in PH;
advanced MMVD and occasionally in to alveolar opacities in A. vasorum) but the combination of respiratory distress and
dilated cardiomyopathy, cor triatriatum importantly may also be unremarkable increased natriuretic peptides is not proof
sinister, and mitral stenosis in severe interstitial and thromboembolic for respiratory distress being caused by heart
○ Congenital left-to-right cardiac shunt: causes lung disease. failure.
pulmonary overcirculation and, in some ○ Noncardiogenic pulmonary edema,
individuals, pulmonary arterial remodel- responsive to sildenafil, may occur in Advanced or Confirmatory Testing
ing and constriction leading to PAH. This dogs with chronic pulmonary disease. • Contrast (microbubbles) ultrasound of the
results in right-to-left shunt in the minority • Echocardiogram heart and descending aorta can exclude
of patients (i.e., Eisenmenger physiology) ○ Identify causes of PH, including (acquired) right-to-left shunt. Shunt is also possible
○ Hypoxic vasoconstriction: chronic obstruc- left ventricular heart disease (MMVD), due to pulmonary arteriovenous anastomoses
tive lower airway disease (bronchitis, D. immitis (worms in pulmonary arter- secondary to PH; in this case, bubbles take
emphysema); chronic obstructive upper ies, right ventricle, or right atrium), and ≥ 3 cardiac cycles from appearance in the right
airway disease; high-altitude hypoxia congenital cardiovascular shunt. atrium until appearance in the left atrium.
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