Hypertensive crisis can trigger the onset of an acute heart failure (AHF) episode through the steep increase in afterload that occurs as a result of the increase in blood pressure (BP) levels per se, through acute dissection of the ascending aorta, which can involve the aortic valve, leading to acute aortic regurgitation, and through an acute coronary syndrome, leading to impaired myocardial contractility with or without acute mitral regurgitation.
Besides achieving a progressive reduction and control of BP values (NOT NORMALIZATION OF BP!), treatment in this clinical setting also targets the vicious circle leading to the progression of HF: reducing the afterload with arterial and venous vasodilators, reducing the preload with diuretics, and improving systemic oxygenation.
Except for patients with acute aortic dissection (when BP should be lowered within 5–10 min to systolic BP (SBP) <120 mmHg and heart rate (HR) <60/bpm), BP values in hypertensive crisis with AHF should be lowered within the first hour by a maximum 25% of the value on admission and then gradually lowered to 160/110 mmHg in the next 2–6 h, reaching the normal BP values over the next 24–48 h.
Rapidly acting intravenous vasodilators are the first-line drugs used in this clinical setting. Loop diuretics are not recommended for immediate stabilization unless there is volume overload. β-Blockers and calcium channel blockers are contraindicated in the setting of AHF!
Overtreatment happens rather frequently when we treat patients with hypertensive crisis, showing that there is room for improvement in the management of these patients.
Cotter G, Moshkovitz Y, Milovanov O, Salah A, Blatt A, Krakover R, et al. Acute heart failure: a novel approach to its pathogenesis and treatment. Eur J Heart Fail. 2002;4(3):227–34.CrossRefGoogle Scholar
Holzer-Richling N, Holzer M, Herkner H, Riedmüller E, Havel C, Kaff A. Randomized placebo controlled trial of furosemide on subjective perception of dyspnoea in patients with pulmonary edema because of hypertensive crisis. Eur J Clin Investig. 2011;41:627–34.CrossRefGoogle Scholar
Sacetti A, Ramoska E, Moakes ME, McDermott P, Moyer V. Effect of ED management on ICU use in acute pulmonary edema. Am J Emerg Med. 1999;17(6):571–4.CrossRefGoogle Scholar
Sharon A, Shpirer I, Kaluski E. High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema. J Am Coll Cardiol. 2000;36:832–7.CrossRefGoogle Scholar
Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Bohm M, et al. 2013 ESH/ESC guidelines for the management of arterial hypertension. Eur Heart J. 2013;34:2159–219.CrossRefGoogle Scholar
Rosendorff C, Lackland DT, Allison M, Aronow WS, Black HR, Blumenthal RS, et al. Treatment of hypertension in patients with coronary artery disease: a scientific statement from the American Heart Association, American College of Cardiology, and American Society of Hypertension. J Am Coll Cardiol. 2015;65:1998–2038.CrossRefGoogle Scholar
Brooks TWA, Finch CK, Lobo BL, Deaton PR, Varner CF. Blood pressure management in acute hypertensive emergency. Am J Health Syst Pharm. 2007;64(24):2579–82.CrossRefGoogle Scholar
Friederich JA, Butterworth JF 4th. Sodium nitroprusside: twenty years and counting. Anesth Analg. 1995;81:152–62.PubMedGoogle Scholar
Robin ED, McCauley R. Nitroprusside-related cyanide poisoning. Time (long past due) for urgent, effective interventions. Chest. 1992;102:1842–5.CrossRefGoogle Scholar
Pasch T, Schulz V, Hoppelshäuser G. Nitroprusside-induced formation of cyanide and its detoxication with thiosulfate during deliberate hypotension. J Cardiovasc Pharmacol. 1983;5:77–85.CrossRefGoogle Scholar
Mann T, Cohn PF, Holman LB, Green LH, Markis JE, et al. Effect of nitroprusside on regional myocardial blood flow in coronary artery disease. Results in 25 patients and comparison with nitroglycerin. Circulation. 1992;57:732–8.CrossRefGoogle Scholar
Immink RV, van den Born BJH, van Montfrans GA, Kim YX, Hollmann MW, van Lieshout JJ. Cerebral hemodynamics during treatment with sodium nitroprusside versus labetalol in malignant hypertension. Hypertension. 2008;52:236–40.CrossRefGoogle Scholar
Varon J. Treatment of acute severe hypertension: current and newer agents. Drugs. 2008;68(3):283–97.CrossRefGoogle Scholar
Cherney D, Straus S. Management of patients with hypertensive urgencies and emergencies: a systematic review of the literature. J Gen Intern Med. 2002;17(12):937–45.CrossRefGoogle Scholar
Ayaz SI, Sharkey CM, Kwiatkowski GM, Wilson SS, John RS, Tolomello R, et al. Intravenous enalaprilat for treatment of acute hypertensive heart failure in the emergency department. Int J Emerg Med. 2016;9:28.CrossRefGoogle Scholar
Hollander JE, Carter WA, Hoffman RS. Use of phentolamine for cocaine-induced myocardial ischemia. N Engl J Med. 1992;327(5):361.PubMedGoogle Scholar
Marik PE, Varon J. Hypertensive crises: challenges and management. Chest. 2007;131(6):1949–62.CrossRefGoogle Scholar
Bodmann KF, Tröster S, Clemens R, Schuster HP. Hemodynamic profile of intravenous fenoldopam in patients with hypertensive crisis. Clin Investig. 1993;72(1):60–4.CrossRefGoogle Scholar
Erbel R, Aboyans V, Boileau C, Bossone E, Di Bartolomeo R, Eggebrech H, et al. 2014 ESC guidelines on the diagnosis and treatment of aortic diseases. Eur Heart J. 2014;35:2873–926.CrossRefGoogle Scholar
Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39:119–77.CrossRefGoogle Scholar
Roffi M, Patrono C, Collet JP, Mueller C, Valgimigli M, Andreotti F, et al. 2015 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. 2016;37:267–315.CrossRefGoogle Scholar