This handout is for primary aldosteronism (conn / bah) htn crisis (autonomous aldosterone–driven severe htn with hypokalemic alkalosis). Your care team identified this based on: severe htn + spontaneous hypokalemia (k <3.5) without diuretic — primary aldosteronism screening (funder jcem 2016 pmid 26934393).
Other reasons your team may use this plan: resistant htn (uncontrolled on ≥3 antihypertensives including diuretic) — pathway-2 pmid 26414968 demonstrated mra superiority + high prevalence of aldosteronism in this group; adrenal incidentaloma on ct/mri + htn ± hypokalemia → biochemical aldosterone screen (funder 2016); family hx primary aldosteronism, early-onset htn <30, early stroke <40 — familial hyperaldosteronism screening (fh-i glucocorticoid-remediable testable).
Take these medications exactly as prescribed. Do not stop or change a dose without talking to your provider.
| Medication | Starting dose | How | When | What it does |
|---|---|---|---|---|
| nicardipine | 5 mg/h IV titrate by 2.5 mg/h q5-15 min, max 15 mg/h | IV | continuous | ACC/AHA 2025 — predictable titration; safe in PA with renal involvement; CCB preferred acute |
| spironolactone | 25-50 mg PO daily, titrate to 100-400 mg/d | PO | daily | Endocrine Society 2016 (PMID 26934393) + PATHWAY-2 (PMID 26414968) — first-line MRA; addresses both K wasting + HTN; gynecomastia limit (10% at high dose, switch to eplerenone) |
| eplerenone | 25-50 mg PO daily, titrate to 100-200 mg/d divided BID | PO | BID | Selective MR antagonist — no androgen receptor blockade → no gynecomastia/mastalgia; less potent (1/2 of spironolactone), requires higher doses + BID dosing; preferred in young men + women of childbearing age |
| amiloride | 5-10 mg PO daily, titrate to 20 mg/d | PO | daily-BID | Endocrine Society 2016 — ENaC blocker downstream of MR; K-sparing without MR antagonism; useful add-on or alternative to MRA; less LV regression than MRA per Karagiannis JCEM |
| potassium chloride | KCl IV 10-20 mEq/h via central line if K <3 (peripheral max 10 mEq/h); KCl PO 40-80 mEq divided | IV + PO | continuous IV or QID PO | Severe hypokalemia from aldosterone-driven K wasting; replace to ≥3.5 with continuous ECG monitoring; correct K to ≥4 BEFORE drawing ARR |
| magnesium sulfate | 2-4 g IV load + 1-2 g/h infusion | IV | continuous | Mg almost always coexisting low; refractory hypokalemia without Mg correction; Torsades prophylaxis |
| amlodipine | 5-10 mg PO daily | PO | daily | CCB add-on for sustained BP control; safe during ARR washout (does not interfere with renin/aldosterone); preferred during AVS prep |
| doxazosin | 1 mg PO daily, titrate to 8 mg/d | PO | daily | Endocrine Society 2016 — α-blocker does not interfere with ARR; useful during 4-wk drug washout for ARR validity |
| verapamil | 120 mg PO daily SR, titrate to 480 mg/d | PO | daily | Endocrine Society 2016 — non-DHP CCB does not interfere with ARR; useful during washout |
| hydralazine | 10-25 mg PO TID, titrate | PO | TID-QID | Endocrine Society 2016 — direct vasodilator does not interfere with ARR; useful during washout |
| dexamethasone | 0.5-2 mg PO at bedtime, titrate to suppress ACTH | PO | daily at bedtime | FH-I (glucocorticoid-remediable aldosteronism): chimeric gene under ACTH control; low-dose glucocorticoid suppresses ACTH → suppresses ectopic aldosterone production; genetic testing confirms before lifelong glucocorticoid |
| AVOID isolated thiazide acutely | AVOID | N/A | N/A | Thiazide alone worsens hypokalemia in PA; only acceptable AFTER MRA + K replacement established + K stable ≥4 |
| AVOID isolated ACEi/ARB acutely (use after MRA + K stable) | AVOID until K stable | N/A | N/A | PA patients have suppressed RAAS so ACEi alone less effective; risk of hyperK if MRA also added abruptly; start MRA + K replacement first, then ACEi/ARB once K ≥4 stable |
| STOP MRA + ACEi/ARB + K-sparing × 4 wk before ARR | Discontinue 4 wk before ARR; use doxazosin/verapamil/hydralazine bridge | PO | discontinue | Endocrine Society 2016 PMID 26934393 — these drugs interfere with ARR (false positives or negatives); bridge with non-interfering antihypertensives during washout |
| ADRENAL VEIN SAMPLING (AVS) at high-volume center | Bilateral AVS with ACTH stim; lateralization index >4 = unilateral disease | IR | one-time procedural | Endocrine Society 2016 — AVS is gold standard for subtyping; CT alone discordant with AVS in 30-40%; AVS performed at high-volume center (>20-30 cases/y operator), success rate ≥90% with operator experience |
Plan: Primary aldosteronism HTN crisis — MRA FIRST (spironolactone or eplerenone) + K replacement + nicardipine; AVS for subtyping; APA → adrenalectomy, BAH → lifelong MRA
Contact your care team if any of the following happen:
Call 911 or go to the nearest emergency room right away if you have:
Postop: K + creatinine + aldosterone + renin at 1 wk + 6 wk; biochemical cure confirmed if aldosterone normalizes + renin recovers; HTN cure ~50% (rest have residual essential HTN — continue CCB/ACEi); BAH-medical: annual K + creatinine + BP; lifelong MRA titration; PA cardiovascular risk persists (LVH regression slow over years post-cure); annual ECG + echo for LVH; bone density q2-3 y; family screening if FH suspected (genetic counseling)
Guideline: Endocrine Society 2016 Primary Aldosteronism CPG (Funder JCEM 2016 PMID 26934393) + PATHWAY-2 (Williams Lancet 2015 PMID 26414968) + 2025 ACC/AHA HTN (Whelton)