In spite of advances in our understanding of acute heart failure (AHF) and its different phenotypic expressions, AHF management is still centered on volume removal with intravenous diuretics. This narrative review describes the pathophysiology underlying hypertensive AHF and appraises therapies targeting these mechanisms. Vascular redistribution rather than volume overload may be the primary determinant of elevated cardiac filling pressures and subsequent pulmonary congestion in patients with hypertensive AHF; in these patients, vasodilators should be the predominant treatment. Additional therapy with diuretics in hypertensive AHF should be relegated to the treatment of overt volume overload or persistent congestion in spite of optimized hemodynamics. Intravenous nitroglycerin at high doses can rapidly achieve pulmonary decongestion and reduce downstream critical care needs in these patients. The therapeutic role for synthetic peptides with vasodilator properties has yet to be defined. Evidence supporting both old and new vasodilator therapies is limited by a paucity of well-designed studies and failure to demonstrate improvement in long-term outcomes. Targeted study of this phenotype of AHF is needed before vasodilator therapies become incorporated into treatment guidelines.