Cassidy Sedacca, DVM, MS, DACVIM (Cardiology)
Pulmonary hypertension is a life-threatening condition widely present in veterinary medicine, yet largely underdiagnosed. Chronic upper or lower airway diseases are commonly diagnosed syndromes in dogs and cats, but few realize that long-term alveolar hypoxia created by such conditions often results in a silent transformation of pulmonary vasculature resulting in pulmonary hypertension. Left untreated, pulmonary hypertension can result in irreversible pulmonary and cardiac changes, clinical deterioration, right-sided heart failure, and death. Luckily, with the advancements of echocardiography, pulmonary hypertension is now an easily diagnosed condition. Once identified, treatments for pulmonary hypertension are also available that can provide significant improvement in patients’ quality of life and long-term prognosis.
Pulmonary hypertension is defined as an elevation of blood pressure within the arteries of the lungs (PA systolic pressure > 30 mmHg, PA diastolic pressure > 15 mmHg, or mean pressure > 20 mmHg). Pulmonary arterial pressure depends on several factors, including pulmonary blood flow (right ventricular output), pulmonary vascular resistance, and pulmonary venous pressure.
There are several causes of pulmonary hypertension, many arising from conditions seen in daily practice. Left-sided heart disease (myxomatous mitral valve disease, cardiomyopathies) may result in elevated left atrial and pulmonary venous pressure contributing to increased pulmonary arterial pressure. Long-term alveolar hypoxia from any chronic respiratory disease (collapsing trachea, brachycephalic airway disease, chronic/allergic bronchitis, asthma, pulmonary fibrosis, etc.) can cause concentric remodeling of the pulmonary vascular walls. Hypoxia induces growth factors that cause the smooth muscle and intimal layers of the arteriole to proliferate and hypertrophy causing a fixed narrowing of the vessel radius and increased capacity for vasoconstriction, both of which increase vascular resistance. The presence of vascular obstruction or occlusion (heartworm disease or pulmonary thromboembolism) can also lead to an increase in pulmonary vascular resistance and pulmonary arterial pressure. Lastly, an increase in blood flow to the pulmonary circulation, such as in congenital left-to-right cardiac shunts, leads to increased pulmonary arterial pressure.
While the above are all causes of pulmonary hypertension, severe, clinically-significant pulmonary hypertension usually only results from pulmonary vascular remodeling or pulmonary vascular occlusion/obstruction. These two conditions can lead to cor pulmonale, a term that describes alterations in the structure and function of the right side of the heart that are secondary to pulmonary hypertension. Patients with cor pulmonale commonly have exercise intolerance, exertional dyspnea, syncope, and can develop right-sided congestive heart failure.
Although it is most accurate to obtain a diagnosis of pulmonary hypertension directly through pressure measurements using right-sided cardiac catheterization, pulmonary arterial pressures can be indirectly assessed by spectral Doppler echocardiography and subjective assessment of cardiac anatomy. Once a diagnosis is made, medical management can be provided to help reduce pulmonary arterial pressure. Commonly used vasodilators to treat pulmonary hypertension include the calcium-channel blocker amlodipine and the phosphodiesterase-inhibitors sildenafil and pimobendan. Sildenafil has the beneficial property of being a highly selective arteriodilator within the pulmonary vascular bed with few systemic effects. Pimobendan is attractive because it causes pulmonary arteriodilation and increases contractility within a failing right ventricle. By screening patients that have conditions that predispose them to pulmonary hypertension, early diagnosis and treatment may provide enormous short- and long-term health benefits.
– Cassidy Sedacca, DVM, MS, DACVIM (Cardiology)