The right ventricle in pulmonary hypertension is fighting against a high pulmonary afterload, so the ideal agent must do two jobs at once: pump the heart harder and open up the pulmonary vessels. A drug that does both is termed an inodilator, and milrinone is the classic example.
Milrinone blocks phosphodiesterase-3, so cyclic AMP is not broken down. The accumulated cyclic AMP increases calcium availability in cardiac myocytes (more force) and relaxes vascular smooth muscle (less resistance). The fall in pulmonary vascular resistance directly relieves the load on the strained right ventricle, improving its output without leaning on beta receptors that may be downregulated in chronic failure.
Comparing the alternatives clarifies the choice. Dopamine tends to constrict pulmonary vessels and provoke arrhythmias at the doses needed for inotropy. Isoprenaline drives heart rate up sharply and raises myocardial oxygen demand. Halothane is a volatile anaesthetic that depresses the myocardium rather than supporting it. None of these matches the inodilator profile required for right heart failure secondary to pulmonary hypertension.
\[\boxed{\text{Milrinone}}\]