Page 218 - Small Animal Internal Medicine, 6th Edition

190 PART I Cardiovascular System Disorders

CHAPTER 10
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Pulmonary Hypertension

and Heartworm Disease

PULMONARY HYPERTENSION other left-sided cardiac diseases. In such cases, pulmonary
arterial pressure increases to maintain pulmonary blood flow
Etiology and Pathophysiology in the face of resistance to pulmonary venous drainage. Typi-
In adult animals, the pulmonary circulation is a low pressure, cally, such “postcapillary” PAH is only mild to moderate,
low resistance, high capacitance system compared with the because pulmonary venous pressure can increase to only a
systemic circulation. Cardiac output from the right ventricle certain limit before pulmonary edema develops; a dispropor-
(RV) is equal to that of the left ventricle (in the absence of tionate elevation in pulmonary arterial pressure suggests an
systemic-pulmonary shunts), but pulmonary vascular resis- element of precapillary reactive vasoconstriction in addition
tance is much lower than systemic vascular resistance. As a to pulmonary venous hypertension (see Chapter 6, p. 130).
result, pulmonary arterial pressures are much lower than Group III PAH includes hypoxic pulmonary disease (such as
systemic arterial pressures (Pressure = Cardiac Output × pulmonary fibrosis or other chronic bronchopulmonary
Resistance). Normal pulmonary arterial pressures are disease) leading to reactive vasoconstriction, reduced vascu-
approximately 20 to 25 mm Hg (systolic), 15 mm Hg (mean), lar area, and vascular remodeling. Group IV PAH refers to
and 10 mm Hg (end-diastolic). pulmonary thromboembolic disease. Thrombotic vascular
Pulmonary arterial hypertension (PAH) is generally obstruction reduces total cross-sectional pulmonary vascu-
defined as systolic pulmonary arterial pressures greater than lar area by mechanically obstructing vessels and provoking
35 mm Hg or mean pulmonary arterial pressures greater local hypoxic pulmonary vasoconstriction, as well as other
than 25 mm Hg. PAH severity is graded based on pulmonary reactive changes. Underlying causes of thrombotic disease
arterial systolic pressure as follows: mild PAH (35-55 mm and hypercoagulability are discussed in Chapter 12. Heart-
Hg), moderate PAH (55-80 mm Hg), and severe PAH worm disease (HWD) is one of the most clinically important
(>80 mm Hg). PAH can occur secondary to a number of causes of PAH in dogs. The pathophysiology of PAH in
disease processes that increase pulmonary vascular resis- HWD is multifactorial, including elements of direct pulmo-
tance through various mechanisms. Common histopatho- nary arteritis, hypoxic pulmonary disease causing reactive
logic changes in affected pulmonary arteries and arterioles vasoconstriction (Group III), and pulmonary thromboem-
include medial hypertrophy, intimal proliferation and fibro- bolic disease (Group IV). HWD is therefore sometimes clas-
sis, luminal thrombosis, and eventually arterial necrosis. sified separately as a “miscellaneous” cause of PAH (Group
The World Health Organization (WHO) classifies pulmo- V). Retrospective studies report the most common causes of
nary hypertension using a five-group system that can be PAH in dogs to be pulmonary venous hypertension from
modified for application to veterinary patients. Group I PAH left-sided heart disease (Group II, ~40%) and hypoxic pul-
includes idiopathic (primary) pulmonary hypertension, con- monary disease (Group III, 20%-40%), although this distri-
genital retention of fetal pulmonary vascular resistance, and bution is heavily influenced by the incidence of HWD in the
pulmonary overcirculation from congenital left-to-right region of study.
cardiac shunts causing vascular injury and pulmonary arte- In addition to the WHO classification system, mecha-
rial remodeling. In the context of a congenital shunt, if PAH nisms of PAH can also be categorized as “precapillary” (pri-
becomes severe enough that pulmonary arterial pressure marily affecting pulmonary arteries and arterioles, before
exceeds systemic arterial pressure, shunt reversal occurs blood reaches the pulmonary capillary bed) or “postcapil-
(Eisenmenger’s physiology; see p. 114). Group II refers to lary” (primarily affecting pulmonary veins, with secondary
PAH occurring secondary to pressure buildup across the buildup of pressure across the capillary bed back to the pul-
pulmonary capillary bed due to chronically elevated pulmo- monary arterial tree). Group II PAH (pulmonary venous
nary venous pressures, as seen in mitral regurgitation and hypertension secondary to left-sided heart disease) is thus

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