Cardiac effects of pulmonary hypertension

The right ventricle is particularly affected by pulmonary hypertension. A normal right ventricle has an output that is equivalent to that of the left ventricle; however, normal pulmonary artery pressure is much lower than the systemic blood pressure, making the design and function of the two ventricles quite different.⁶ The right ventricular free wall is thin, making it a highly compliant chamber that can easily accommodate increases in filling pressures. Systolic pressures in the right ventricle and pulmonary artery are usually less than 30 mm Hg, and the right ventricular end-diastolic pressure is usually less than 6 mm Hg. Mean pulmonary artery pressures range from 10 to 18 mm Hg. The thin-walled right ventricle is not suited to the development of high systolic pressures, and an acute increase in outflow impedance is poorly tolerated. If the pulmonary hypertension develops gradually, the right ventricle is better able to adapt to the increase in workload. In chronic cases, the right ventricle hypertrophies and becomes less compliant, and wall tension and contractility increase. These structural and functional cardiac changes secondary to respiratory disease are commonly referred to as cor pulmonale.⁶ In people, chronic cor pulmonale implies obstructive or restrictive lung disease, while acute cor pulmonale suggests acute pulmonary hypertension due to massive pulmonary embolism.⁵

The echocardiographic manifestations of pulmonary hypertension can be dramatic, and, generally, the more severe the pulmonary hypertension, the more apparent the changes. Dogs with advanced respiratory disease and hyperinflation of the lungs can be difficult to image because of imaging window reduction. The advanced cases usually demonstrate moderate to severe right ventricular free wall hypertrophy and right ventricular dilatation. Interventricular septal flattening is often easily recognized. Severe flattening is usually identified in cases in which the right ventricular pressures approximate or exceed left ventricular systolic pressures. Elevated right ventricular diastolic pressures can cause paradoxical interventricular septal motion in which the septum moves to the left during diastole as a result of increased right ventricular pressure and volume overload. The main pulmonary artery may appear enlarged and, if so, pulmonary regurgitation is often present. It is important to interrogate the right ventricular outflow tract and pulmonary valve to eliminate pulmonary stenosis as a cause of right ventricular hypertension; however, most dogs with pulmonary hypertension are middle-aged or older, which reduces the possibility of an unrecognized congenital lesion. The left ventricle may appear small when compared with the large right ventricle or may actually be small because of low cardiac output secondary to pulmonary vascular obstruction. Furosemide administration can also reduce the size of the left ventricle. With substantial tricuspid regurgitation, the right atrium may be enlarged.^1,4,7

Treating pulmonary hypertension

Therapy for primary pulmonary hypertension in people can include oxygen, digoxin, adenosine, prostacyclin infusion, nitric oxide, and high-dose calcium channel blockers.³ Treatment of secondary pulmonary hypertension in people may involve oxygen, anticholinergics, β-adrenergic agonists, theophylline, corticosteroids, digitalis, nitric oxide, and ACE inhibitors. In people with COPD, only oxygen has been shown to produce consistent pulmonary vasodilation.⁵ Oxygen relieves pulmonary vasoconstriction, which allows right ventricular stroke volume to increase, enhancing oxygen delivery to the vital organs. Sildenafil has been shown to reduce hypoxia-induced pulmonary hypertension in people and mice,^8,9 but its use in dogs has been limited.

Recommended treatment of pulmonary hypertension and associated problems in dogs includes oxygen, antibiotics, bronchodilators, calcium channel blockers, α-adrenergic blocking agents, salt restriction, ACE inhibitors, and diuretics.^4,10 The primary therapy in the two dogs in this report was supplemental oxygen. In both dogs, clinical and echocardiographic improvement in the manifestation of pulmonary hypertension was not documented except for a possible transient improvement in the echocardiographic findings in the Labrador retriever (Case 2). During this period, the animal was not receiving supplemental oxygen. In ambulatory people, long-term oxygen administration is much easier to accomplish than in dogs and has been documented to be helpful. People with COPD often need oxygen supplementation 12 or more hours a day.⁵ The heparin used in the 14-year-old mixed breed dog (Case 1) was directed at preventing and resolving any potential thromboembolic aspects of this animal's problem.