Hypertension following resolution of cardiac tamponade is common. The etiology can be directly related to the postcardiac tamponade state, a postprocedural complication, or from issues that are generally applicable to any postsurgical patient. In postcardiac tamponade patients, hypertension is typically due to ongoing sympathetic activation and relative baroreceptor insensitivity, although residual consequences of cardiac tamponade such as acidosis, hypervolemia or hypovolemia, and/or systemic inflammatory response can also be responsible. Serious complications that present with hypertension such as heart failure with pulmonary edema, stroke, hemorrhage, and myocardial ischemia should be ruled out. More general causes of postoperative hypertension including pain, anxiety, cold, hypoxemia, hypercarbia, and delirium should be individually addressed with specific pharmacologic and nonpharmacologic therapies.

Controlling hypertension is important not only to prevent myocardial strain and end-organ damage but also to limit direct complications including surgical bleeding and worsening reperfusion injury. The basis for maintaining MAP within 20% of baseline values comes from clinical data showing an increased risk of end-organ hyperperfusion and damage with sustained blood pressures (ie, >10 minutes) beyond this range. By targeting the patient's baseline MAP, organ perfusion pressures are maintained within the individual's autoregulatory range.

Assuming reversible causes of hypertension are corrected, the ideal antihypertensive agent for acute control should be short-acting and titratable. Clevidipine has a rapid onset-offset profile due to its metabolism by tissue and blood esterases, resulting in a half-life of approximately 1 minute and is an ideal agent for acutely controlling hypertension. Nicardipine, by contrast, has a rapid distributive α half-life of 2.7 minutes, which increases to 44.8 minutes and 14.4 hours for its intermediate β and γ half-lives, respectively. The dihydropyridine calcium channel blockers play an adjunctive role for chronic maintenance therapy in patients with ischemic heart disease and are not recommended in patients with heart failure with reduced ejection fraction.

Labetalol is a useful agent, especially in the presence of tachycardia. Given intravenously, it has an approximately 7:1 nonselective β- to α₁-antagonist effect with an onset of effect in 2 to 5 minutes. Its peak hypotensive effect occurs within 10 minutes, and its elimination half-life is 3 to 5 hours. If warranted, maintenance β-blocker therapy, with carvedilol, the nonselective β- and α₁-blocker or cardioselective agents such as metoprolol, confers additional survival benefit in this patient with ischemic heart disease and is a first-line therapy for chronic treatment.

References

• Aronson S, Dyke CM, Stierer KA, et al. The ECLIPSE trials: comparative studies of clevidipine to nitroglycerin, sodium nitroprusside, and nicardipine for acute hypertension treatment in cardiac surgery patients. Anesth Analg. 2008;107:1110-1121.
• Cheung AT. Exploring an optimum intra/postoperative management strategy for acute hypertension in the cardiac surgery patient. J Card Surg. 2006;21:S8-S14.
• Espinosa A, Ripollés-Melchor J, Casans-Francés R, et al; Evidence Anesthesia Review Group. Perioperative use of clevidipine: a systematic review and meta-analysis. PLoS One. 2016;11:e0150625.
• Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2018;71:e127-e248.