Canine pulmonary hypertension, Part 1: An in-depth review of its pathophysiology and classifications

This complex syndrome is not as uncommon as we once thought. Understanding its pathophysiology and classification schemes—both clinical and functional—will help you better manage this condition in your patients.

Although previously thought to be uncommon, canine pulmonary hypertension is now diagnosed with relative frequency.1 Understanding the pathophysiology of pulmonary hypertension is paramount to successful treatment. Canine pulmonary hypertension should also be recognized as a complex syndrome that is often associated with severe underlying systemic disease.

In this article, we review the anatomy of the pulmonary vascular system and discuss the regulation of pulmonary arterial pressure. We also describe the clinical and functional classifications of pulmonary hypertension.


Any elevation of pulmonary arterial pressure above normal constitutes pulmonary hypertension.2 More specifically, pulmonary hypertension can be defined as pulmonary arterial systolic pressure > 30 mm Hg, pulmonary arterial diastolic pressure > 15 mm Hg, or pulmonary arterial mean pressure > 20 mm Hg.3 Although it is possible to obtain these measurements directly through right-sided cardiac catheterization, this procedure typically requires heavy sedation or anesthesia, is considered high risk in unstable patients, and can be costly.4 Alternatively, pulmonary arterial pressures can be assessed by transthoracic echocardiography, which includes subjective assessment of cardiac changes and Doppler analysis of tricuspid valve regurgitation and pulmonary valve insufficiency.

Pulmonary arterial pressure depends on several factors, including right ventricular cardiac output (or pulmonary blood flow), pulmonary vascular resistance, and pulmonary venous pressure.3 An increase in blood flow to the pulmonary arteries, such as in congenital shunts, leads to increased pulmonary arterial pressure. Augmented activity of vascular smooth muscle, increased blood viscosity, and the presence of vascular obstruction all result in increased pulmonary vascular resistance and, thus, increased pulmonary arterial pressure. Pulmonary venous pressure, which becomes elevated in advanced left-sided heart disease, also contributes to increased pulmonary arterial pressure. Based on the variety of factors that contribute to and control pulmonary arterial pressure, it is clear that pulmonary hypertension may develop as the result of many underlying diseases.


The pulmonary vascular system is characterized as low pressure, low resistance, and high capacitance.5 Normal pulmonary arteries are elastic with distensible walls. They are composed of an inner tunica intima, middle tunica media, and outer tunica adventitia (Figure 1). The tunica intima consists of a single layer of endothelial cells, collagen, and occasional fibroblasts. The tunica media is thicker and is a combined layer consisting of elastin, collagen, and smooth muscle fibers. The tunica adventitia consists of collagen.6

Several characteristic histopathologic lesions are associated with pulmonary hypertension. These most often include concentric thickening and muscularization of the tunica intima and hypertrophy with fibrosis and proliferation of smooth muscle of the tunica media (Figure 2). In severe cases, plexiform lesions (irregularly shaped outgrowths that project from the intimal layer into the lumen of the blood vessel) may develop, and vessel wall necrosis can occur.7

1. A photograph of a cross section of a normal canine pulmonary artery. The tunica adventitia, media, and intima layers are all normal in thickness and cell structure (hematoxylin-eosin stain; 10X magnification). (Image courtesy of Pam Mouser, DVM, MS, DACVP, Angell Animal Medical Center’s Department of Pathology.)

2. A photograph of a cross section of a canine pulmonary artery in a patient with documented pulmonary hypertension. The tunica adventitia and intima layers are both thickened, supporting the clinical diagnosis of pulmonary hypertension (hematoxylin-eosin stain; 10X magnification). (Image courtesy of Pam Mouser, DVM, MS, DACVP, Angell Animal Medical Center’s Department of Pathology.)