Page 257 - Clinical Small Animal Internal Medicine

225

VetBooks.ir

23

Pulmonary Hypertension
Heidi B. Kellihan, DVM, DACVIM (Cardiology)

Department of Medical Sciences, University of Wisconsin, Madison, WI, USA

Etiology/Pathophysiology the nitric oxide pathway is deranged and results in
vasoconstriction, smooth muscle cell proliferation and
Pulmonary hypertension (PH) is an elevation in systolic hypertrophy, platelet aggregation, and adhesion.
pulmonary arterial pressure greater than 30 mmHgI. In addition to alterations in pulmonary vascular medi-
Typically, PH is a complication of other primary diseases ators contributing to PH, hypoxia also directly affects
and occasionally occurs as an idiopathic process. pulmonary vascular tone. Hypoxia (globally or locally)
Pulmonary arterial pressure is influenced by pulmonary results in pulmonary artery vasoconstriction, which is in
blood flow, pulmonary vascular resistance, and pulmo- contrast to the systemic vasculature which vasodilates in
nary venous pressure. Ultimately, PH can be considered response to hypoxia. Pulmonary artery vasoconstriction,
an umbrella term encompassing pulmonary arterial in response to hypoxia, is a compensatory mechanism to
hypertension (precapillary PH) and pulmonary venous divert blood away from hypoxic lung. Unfortunately, in
hypertension (postcapillary PH) (Figure 23.1). the setting of PH, hypoxia from respiratory disease and
Normally, the pulmonary vasculature is composed of left‐sided congestive heart failure will worsen preexist-
thin‐walled, low‐pressure, high‐capacitance, and low‐ ing PH severity.
resistance vessels. The pulmonary vasculature receives The vascular changes that result from the imbalance of
the complete cardiac output from the right heart with these pathways promote muscularization of normally
every contraction. Pulmonary hypertension results when nonmuscular peripheral pulmonary arteries, medial
there is an imbalance in pulmonary vascular mediators hypertrophy, loss of peripheral pulmonary arteries, inti-
favoring vasoconstriction and muscularization of pul- mal proliferation, and vascular thrombosis. Ultimately,
monary arteries. these vascular changes result in an increase in pulmo-
The three main components involved in PH develop- nary vascular resistance leading to right ventricular
ment are the endothelin pathway, the prostacyclin path- hypertrophy that can result in congestive heart failure
way, and the nitric oxide pathway. In the presence of PH, and death.
the endothelin pathway contributes to the release of the
potent vasoconstrictor, endothelin‐1 from endothelial
cells, resulting in pulmonary artery vasoconstriction, Epidemiology
smooth muscle cell proliferation, and increased collagen
synthesis. Prostacyclins, released by the pulmonary Since PH usually occurs secondary to another disease
artery endothelium, normally mediates vasodilation, yet process, the presence of PH in the population is poten-
with PH, the vasodilatory effects are negated and the tially extensive. In reports of PH in dogs, the majority of
result is pulmonary artery vasoconstriction, cellular pro- cases result from left‐sided heart disease (53%), pulmo-
liferation, and thrombosis. In the normal setting, nitric nary disease (28%), pulmonary thromboembolism (4%),
oxide release from vascular endothelium leads to an heartworm disease (4%), congenital heart disease (i.e.,
increase in vasodilatory cGMP. In the presence of PH, left‐to‐right shunts) (3%), and miscellaneous causes (7%).

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical