Deprescribe the redundant CCB first. Stop either the extra Cilacar (Cilnidipine) or the Nicardia Retard (Nifedipine) - continuing two dihydropyridine CCBs together adds side effects (edema, flushing, reflex tachycardia) without added antihypertensive benefit, and doesn't diversify mechanism.

Add a diuretic - this patient has ARB + CCB but no thiazide/thiazide-like agent. Adding chlorthalidone or indapamide completes standard triple therapy (ACEi/ARB + CCB + diuretic at optimized doses), which is the correct definition-of-resistance checkpoint. Only if BP remains uncontrolled after this triple combination at maximally tolerated doses is it truly "resistant hypertension."

If genuinely resistant after step 2, per PATHWAY-2 evidence and current guidance, add a mineralocorticoid receptor antagonist (spironolactone) as the 4th-line agent - shown superior to doxazosin/bisoprolol as add-on in resistant hypertension. Check potassium and renal function first, especially important post-ICH where fluid/electrolyte status may already be deranged.

Exclude pseudo-resistance and secondary causes before escalating: confirm adherence, correct cuff/technique (rule out white-coat effect with home/ambulatory BP), and screen for secondary hypertension (renal artery stenosis, primary aldosteronism, OSA) - all of which are more common in truly treatment-refractory patients.

Because this is a post-ICH patient, BP control has direct bearing on hematoma expansion risk and outcome. If this is in the acute/subacute phase and oral agents aren't achieving target fast enough, the AHA/ASA 2022 ICH guideline supports IV titratable agents (labetalol or nicardipine infusion) to reach and hold SBP in the 140-150 mmHg range with smooth, sustained control - avoiding nitroprusside (raises ICP) and avoiding overly aggressive drops below ~130 systolic, since intensive-lowering trials (ATACH-2, and recent meta-analyses) have not shown net benefit from very low targets and can risk hypoperfusion.