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cardio.hypertensive-emergency.primary-aldosteronism-crisis.v1PRODUCTION
cardio.hypertensive-emergency.primary-aldosteronism-crisis.v1

Primary aldosteronism (Conn / BAH) HTN crisis (autonomous aldosterone–driven severe HTN with hypokalemic alkalosis)

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Detailed

Primary aldosteronism crisis = autonomous aldosterone secretion → mineralocorticoid receptor activation → Na+/H2O retention + K+ wasting + H+ secretion + RAAS suppression → severe HTN + hypokalemia + metabolic alkalosis. Most common curable secondary HTN (5-10% all HTN; up to 20% resistant HTN per PATHWAY-2). Pharmacology pivot: MRA FIRST (spironolactone or eplerenone) + K replacement + nicardipine acute; AVOID isolated thiazide acutely (worsens hypoK); biochemical workup requires aldosterone:renin ratio (ARR) AFTER K correction + off interfering drugs (ACEi/ARB/MRA × 4 wk; β-blocker × 2 wk acceptable bridge); confirmatory testing (saline suppression / fludrocortisone / captopril challenge / oral salt loading) before subtyping. SUBTYPING with adrenal vein sampling (AVS — gold standard for lateralization APA vs BAH) drives definitive: APA → laparoscopic unilateral adrenalectomy (curative HTN ~50%, biochemical cure ~95%); BAH → lifelong MRA (spironolactone first; eplerenone if gynecomastia). Route to parent engine for shared HTN-emergency arc; this dossier owns aldosterone-specific pharmacology + biochemical dx + AVS pathway + perioperative.

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PA phenotype identified (resistant HTN ± hypokalemia ± biochemistry positive)

Patient inputs (12)

CT adrenals 3-mm thin sections — APA typically <2 cm hypodense (<10 HU); BAH bilateral nodular thickening; carcinoma >4 cm + heterogeneous; CT often discordant with AVS in 30-40% (Funder 2016)

After ARR positive — saline suppression test (2 L NS over 4 h, aldosterone >10 ng/dL post = positive) OR fludrocortisone suppression OR captopril challenge OR oral salt loading + 24h urine aldosterone (Funder JCEM 2016 PMID 26934393)

Younger PA more often APA (Conn) — surgically curable; older with bilateral mass/hyperplasia → BAH lifelong medical

Hypokalemia (K <3.5, often <3.0) hallmark; correct K to ≥4 BEFORE drawing aldosterone:renin ratio (low K suppresses aldosterone falsely)

Metabolic alkalosis (HCO3 >28) from aldosterone-driven H+ secretion + K wasting

Measured AM after K corrected to ≥4 + off interfering meds × 4 wk; PA: aldosterone >15 ng/dL (>10 in some labs); useful as numerator of ARR

Suppressed renin <1 ng/mL/h is hallmark; numerator of ARR; off ACEi/ARB/MRA × 4 wk + K corrected

ARR >20-30 with elevated aldosterone (>15 ng/dL) — primary screening test (Funder JCEM 2016 PMID 26934393); confirmatory testing required if positive

Renal function for nicardipine, MRA, K replacement, contrast for AVS; CKD frequently coexists from chronic HTN

Defines crisis threshold; aldosterone-driven HTN often sustained, often resistant, often diastolic-prominent

Sustained DBP >100 typical in primary aldosteronism due to MR activation

Often normal; bradycardia rare; tachy suggests other etiology contribution

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Severity triggers (5)

5 need judgement
  • informationallife_threateningPA_with_severe_hypokalemia_below_2.5_with_arrhythmia
    PA crisis + K <2.5 + Torsades de pointes / VT / AF with RVR / U waves + QT prolongation — life-threatening hypokalemic arrhythmia
    Trigger could not be auto-evaluated — needs clinician judgement.
  • informationallife_threateningAVS_complications_adrenal_hemorrhage_or_thrombosis
    Adrenal vein sampling complicated by adrenal hemorrhage, vein dissection, or thrombosis — rare but serious AVS complications (~1-2% even at high-volume centers)
    Trigger could not be auto-evaluated — needs clinician judgement.
  • informationalseverepostop_APA_severe_HYPERKALEMIA
    Postop APA day 1-7 develops K >5.5 — contralateral adrenal suppression from chronic aldosterone excess → transient hypoaldosterone state
    Trigger could not be auto-evaluated — needs clinician judgement.
  • informationalseverefamilial_hyperaldosteronism_type_I_with_early_stroke_risk
    FH-I (glucocorticoid-remediable aldosteronism) with family hx of early stroke <40 — chimeric CYP11B1-CYP11B2 gene confirmed; high stroke risk if untreated
    Trigger could not be auto-evaluated — needs clinician judgement.
  • informationalmoderateBAH_with_MRA_induced_severe_gynecomastia_requiring_switch
    BAH on lifelong spironolactone develops painful gynecomastia, mastalgia, decreased libido, erectile dysfunction (men) or menstrual irregularities (women) → quality of life impact requiring switch
    Trigger could not be auto-evaluated — needs clinician judgement.

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Recommended regimen

Primary aldosteronism HTN crisis — MRA FIRST (spironolactone or eplerenone) + K replacement + nicardipine; AVS for subtyping; APA → adrenalectomy, BAH → lifelong MRA
axis: primary_aldosteronism_MRA_first_pharmacology
Selected axis "Primary aldosteronism HTN crisis — MRA FIRST (spironolactone or eplerenone) + K replacement + nicardipine; AVS for subtyping; APA → adrenalectomy, BAH → lifelong MRA" by default fallback (first axis)
  • nicardipine
    first line
    DHP_CCB
    5 mg/h IV titrate by 2.5 mg/h q5-15 min, max 15 mg/h • IV • continuous
    triggers: PA_crisis_acute_HTN
    ACC/AHA 2025 — predictable titration; safe in PA with renal involvement; CCB preferred acute
    rxcui 7396
  • spironolactone
    first line
    mineralocorticoid_receptor_antagonist
    25-50 mg PO daily, titrate to 100-400 mg/d • PO • daily
    triggers: PA_crisis_with_hypokalemia, PA_HTN_with_MR_activation, BAH_lifelong_treatment
    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)
    rxcui 9997
  • eplerenone
    first line
    mineralocorticoid_receptor_antagonist_selective
    25-50 mg PO daily, titrate to 100-200 mg/d divided BID • PO • BID
    triggers: PA_HTN_with_gynecomastia_concern, spironolactone_intolerant
    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
    rxcui 298869
  • amiloride
    second line
    ENaC_blocker
    5-10 mg PO daily, titrate to 20 mg/d • PO • daily-BID
    triggers: PA_with_MRA_intolerance, PA_with_persistent_hypokalemia_on_MRA
    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
    rxcui 644
  • potassium chloride
    first line
    electrolyte_replacement
    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
    triggers: PA_crisis_with_hypokalemia_K_below_3.5
    Severe hypokalemia from aldosterone-driven K wasting; replace to ≥3.5 with continuous ECG monitoring; correct K to ≥4 BEFORE drawing ARR
    rxcui 8591
  • magnesium sulfate
    add on
    electrolyte_replacement
    2-4 g IV load + 1-2 g/h infusion • IV • continuous
    triggers: PA_crisis_with_hypomagnesemia, arrhythmia_risk_torsades
    Mg almost always coexisting low; refractory hypokalemia without Mg correction; Torsades prophylaxis
    rxcui 6585
  • amlodipine
    second line
    DHP_CCB
    5-10 mg PO daily • PO • daily
    triggers: PA_with_persistent_HTN_on_MRA, pre_AVS_BP_control_acceptable
    CCB add-on for sustained BP control; safe during ARR washout (does not interfere with renin/aldosterone); preferred during AVS prep
    rxcui 17767
  • doxazosin
    second line
    selective_alpha1_blocker
    1 mg PO daily, titrate to 8 mg/d • PO • daily
    triggers: PA_during_ARR_washout, BP_control_when_avoiding_ACEi_ARB_BB_CCB
    Endocrine Society 2016 — α-blocker does not interfere with ARR; useful during 4-wk drug washout for ARR validity
    rxcui 49276
  • verapamil
    second line
    non_DHP_CCB
    120 mg PO daily SR, titrate to 480 mg/d • PO • daily
    triggers: PA_during_ARR_washout, BP_control_when_avoiding_DHP_CCB_effects
    Endocrine Society 2016 — non-DHP CCB does not interfere with ARR; useful during washout
    rxcui 11170
  • hydralazine
    second line
    direct_vasodilator
    10-25 mg PO TID, titrate • PO • TID-QID
    triggers: PA_during_ARR_washout, severe_HTN_with_avoidance_of_other_classes
    Endocrine Society 2016 — direct vasodilator does not interfere with ARR; useful during washout
    rxcui 5470
  • dexamethasone
    comorbidity specific
    glucocorticoid
    0.5-2 mg PO at bedtime, titrate to suppress ACTH • PO • daily at bedtime
    triggers: familial_hyperaldosteronism_type_I_glucocorticoid_remediable, CYP11B1_CYP11B2_chimeric_gene_confirmed
    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
    rxcui 3264
  • AVOID isolated thiazide acutely
    contraindication substitute
    do_not_use
    AVOID • N/A • N/A
    triggers: PA_with_K_below_3.5
    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)
    contraindication substitute
    do_not_use
    AVOID until K stable • N/A • N/A
    triggers: PA_with_borderline_K
    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
    first line
    medication_washout
    Discontinue 4 wk before ARR; use doxazosin/verapamil/hydralazine bridge • PO • discontinue
    triggers: ARR_screening_planned
    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
    first line
    diagnostic_procedure
    Bilateral AVS with ACTH stim; lateralization index >4 = unilateral disease • IR • one-time procedural
    triggers: confirmed_PA_planning_surgery
    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

outpatient playbook — drug actions (5)

  1. 1. BAH: lifelong MRA
    rxcui 9997
    Spironolactone 100-200 mg/d OR eplerenone 100-200 mg/d divided BID • PO • BID
    trigger: BAH non-surgical lifelong
    Endocrine Society 2016 PMID 26934393 + PATHWAY-2 PMID 26414968
  2. 2. APA postop: residual HTN regimen
    rxcui 17767
    Amlodipine 5-10 ± lisinopril 10-20 ± chlorthalidone 12.5 mg • PO • daily
    trigger: Residual essential HTN post-cure
    ACC/AHA 2025
  3. 3. statin for ASCVD risk reduction
    rxcui 83367
    Atorvastatin 40-80 mg PO daily • PO • daily
    trigger: Elevated ASCVD risk from chronic PA + HTN damage
    AHA/ACC 2018 lipid guideline; PA has independent CV risk per Rossi JACC 2006 PMID 17027529
  4. 4. amiloride add-on if MRA intolerant
    rxcui 643
    Amiloride 5-10 mg PO daily, max 20 mg/d • PO • daily-BID
    trigger: MRA gynecomastia/hyperK intolerant
    ENaC blocker downstream of MR
  5. 5. dexamethasone for FH-I if confirmed
    rxcui 3008
    0.5-2 mg PO at bedtime, lowest effective dose • PO • daily at bedtime
    trigger: Genetic confirmation FH-I
    FH-I glucocorticoid-remediable specific therapy

Auto-drafted A&P note

outpatient

Subjective

- Possible entry pathways: Severe HTN + spontaneous hypokalemia (K <3.5) without diuretic — primary aldosteronism screening (Funder JCEM 2016 PMID 26934393); 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).

Objective

- No vitals, labs, or imaging entered for this encounter.

Assessment

**Primary aldosteronism (Conn / BAH) HTN crisis (autonomous aldosterone–driven severe HTN with hypokalemic alkalosis)** (cardio.hypertensive-emergency.primary-aldosteronism-crisis.v1).
Scope: Primary aldosteronism crisis = autonomous aldosterone secretion → mineralocorticoid receptor activation → Na+/H2O retention + K+ wasting + H+ secretion + RAAS suppression → severe HTN + hypokalemia + metabolic alkalosis. Most common curable secondary HTN (5-10% all HTN; up to 20% resistant HTN per PATHWAY-2). Pharmacology pivot: MRA FIRST (spironolactone or eplerenone) + K replacement + nicardipine acute; AVOID isolated thiazide acutely (worsens hypoK); biochemical workup requires aldosterone:renin ratio (ARR) AFTER K correction + off interfering drugs (ACEi/ARB/MRA × 4 wk; β-blocker × 2 wk acceptable bridge); confirmatory testing (saline suppression / fludrocortisone / captopril challenge / oral salt loading) before subtyping. SUBTYPING with adrenal vein sampling (AVS — gold standard for lateralization APA vs BAH) drives definitive: APA → laparoscopic unilateral adrenalectomy (curative HTN ~50%, biochemical cure ~95%); BAH → lifelong MRA (spironolactone first; eplerenone if gynecomastia). Route to parent engine for shared HTN-emergency arc; this dossier owns aldosterone-specific pharmacology + biochemical dx + AVS pathway + perioperative.

No severity triggers fired against current inputs.

Plan

Regimen axis: **Primary aldosteronism HTN crisis — MRA FIRST (spironolactone or eplerenone) + K replacement + nicardipine; AVS for subtyping; APA → adrenalectomy, BAH → lifelong MRA**.
1. nicardipine 5 mg/h IV titrate by 2.5 mg/h q5-15 min, max 15 mg/h IV continuous (DHP_CCB, first line) — ACC/AHA 2025 — predictable titration; safe in PA with renal involvement; CCB preferred acute
2. spironolactone 25-50 mg PO daily, titrate to 100-400 mg/d PO daily (mineralocorticoid_receptor_antagonist, first line) — 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)
3. eplerenone 25-50 mg PO daily, titrate to 100-200 mg/d divided BID PO BID (mineralocorticoid_receptor_antagonist_selective, first line) — 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
4. amiloride 5-10 mg PO daily, titrate to 20 mg/d PO daily-BID (ENaC_blocker, second line) — 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
5. 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 (electrolyte_replacement, first line) — Severe hypokalemia from aldosterone-driven K wasting; replace to ≥3.5 with continuous ECG monitoring; correct K to ≥4 BEFORE drawing ARR
6. magnesium sulfate 2-4 g IV load + 1-2 g/h infusion IV continuous (electrolyte_replacement, add on) — Mg almost always coexisting low; refractory hypokalemia without Mg correction; Torsades prophylaxis
7. amlodipine 5-10 mg PO daily PO daily (DHP_CCB, second line) — CCB add-on for sustained BP control; safe during ARR washout (does not interfere with renin/aldosterone); preferred during AVS prep
8. doxazosin 1 mg PO daily, titrate to 8 mg/d PO daily (selective_alpha1_blocker, second line) — Endocrine Society 2016 — α-blocker does not interfere with ARR; useful during 4-wk drug washout for ARR validity
9. verapamil 120 mg PO daily SR, titrate to 480 mg/d PO daily (non_DHP_CCB, second line) — Endocrine Society 2016 — non-DHP CCB does not interfere with ARR; useful during washout
10. hydralazine 10-25 mg PO TID, titrate PO TID-QID (direct_vasodilator, second line) — Endocrine Society 2016 — direct vasodilator does not interfere with ARR; useful during washout
11. dexamethasone 0.5-2 mg PO at bedtime, titrate to suppress ACTH PO daily at bedtime (glucocorticoid, comorbidity specific) — 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
12. AVOID isolated thiazide acutely AVOID N/A N/A (do_not_use, contraindication substitute) — Thiazide alone worsens hypokalemia in PA; only acceptable AFTER MRA + K replacement established + K stable ≥4
13. AVOID isolated ACEi/ARB acutely (use after MRA + K stable) AVOID until K stable N/A N/A (do_not_use, contraindication substitute) — 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
14. STOP MRA + ACEi/ARB + K-sparing × 4 wk before ARR Discontinue 4 wk before ARR; use doxazosin/verapamil/hydralazine bridge PO discontinue (medication_washout, first line) — Endocrine Society 2016 PMID 26934393 — these drugs interfere with ARR (false positives or negatives); bridge with non-interfering antihypertensives during washout
15. ADRENAL VEIN SAMPLING (AVS) at high-volume center Bilateral AVS with ACTH stim; lateralization index >4 = unilateral disease IR one-time procedural (diagnostic_procedure, first line) — 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

Setting playbook (outpatient) — Lifelong endocrine surveillance — APA cured: annual BP + K + aldosterone/renin (low recurrence rate); residual HTN management; BAH: lifelong MRA + K + Cr q3-6 mo; cardiovascular risk reassessment (LVH regression slow over years); bone density q2-3 y; family screening if FH; OSA co-management
16. BAH: lifelong MRA Spironolactone 100-200 mg/d OR eplerenone 100-200 mg/d divided BID PO BID — BAH non-surgical lifelong (Endocrine Society 2016 PMID 26934393 + PATHWAY-2 PMID 26414968)
17. APA postop: residual HTN regimen Amlodipine 5-10 ± lisinopril 10-20 ± chlorthalidone 12.5 mg PO daily — Residual essential HTN post-cure (ACC/AHA 2025)
18. statin for ASCVD risk reduction Atorvastatin 40-80 mg PO daily PO daily — Elevated ASCVD risk from chronic PA + HTN damage (AHA/ACC 2018 lipid guideline; PA has independent CV risk per Rossi JACC 2006 PMID 17027529)
19. amiloride add-on if MRA intolerant Amiloride 5-10 mg PO daily, max 20 mg/d PO daily-BID — MRA gynecomastia/hyperK intolerant (ENaC blocker downstream of MR)
20. dexamethasone for FH-I if confirmed 0.5-2 mg PO at bedtime, lowest effective dose PO daily at bedtime — Genetic confirmation FH-I (FH-I glucocorticoid-remediable specific therapy)

Non-pharmacologic actions:
- Annual endocrine visit
- Cardiology if LVH or persistent HTN
- OSA management ongoing
- Genetics if young/syndromic (FH-I/II/III/IV)
- Family screening if syndromic
- Patient education on K + dietary Na
- Bone health: vitamin D + calcium

AVOID / contraindication checks:
- Spironolactone_avoid_eGFR_below_30_or_K_above_5 (KDIGO 2024)
- Eplerenone_avoid_eGFR_below_30_or_K_above_5_or_severe_hepatic
- Isolated_thiazide_AVOID_in_PA_until_K_stable (worsens hypoK)
- ARR_invalid_if_K_below_3.5 (correct K to ≥4 first)
- ARR_invalid_on_MRA_ACEi_ARB_K_sparing (washout 4 wk)
- K_replacement_via_central_line_if_above_10_mEq_per_hour_peripheral_max
- Contrast_for_AVS_contraindicated_eGFR_below_30_pretreat_with_NaHCO3_or_NS
- Postop_APA_HYPERKALEMIA_RISK_discontinue_MRA_K_supplements_ACEi_ARB
- BAH_lifelong_MRA_with_K_creatinine_q3 6mo

Monitoring

Regimen monitoring:
- continuous ECG during acute crisis and K replacement (Torsades risk)
- q4-6h K Mg glucose during acute crisis (hourly during IV K replacement)
- q12-24h BMP during oral titration
- daily weight BP during admission
- echo for LVH baseline and annually (PA causes 2-4× LVH vs essential HTN per Rossi JACC 2006 PMID 17027529)
- aldosterone renin ARR at 6 wk postop APA (cure marker — aldosterone normalizes, renin recovers)
- POSTOP K q1-2 DAYS for HYPERKALEMIA RISK (contralateral adrenal suppression → transient hypoaldosterone)
- BAH long term K creatinine q3-6 mo
- annual ECG echo for LVH regression (slow regression years)
- family genetic testing if FH suspected (KCNJ5 most common APA-associated)
- OSA screening co management (30-40% PA patients have OSA)

Setting (outpatient) monitoring:
- Annual BP + K + Cr + aldosterone/renin
- BAH: K + Cr q3-6 mo on MRA
- Annual ECG + echo for LVH regression
- DEXA q2-3 y

Follow-up plan: 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)
- Close-out criterion: biochemical cure (APA) or stable medical regimen (BAH) + lifelong endocrine surveillance booked + family screening if syndromic

Monitoring phase: Continuous ECG (hypokalemia Torsades risk); q4-6h K, Mg, glucose during acute crisis; daily K once on PO MRA (gynecomastia / hyperK risk); daily BP + weight; postop monitoring for HYPERKALEMIA (contralateral adrenal suppression → temporary hypoaldosterone state with hyperK risk especially with ongoing ACEi/MRA — typically discontinue these post-cure); aldosterone + ARR repeat at 6 wk (cure marker); annual cardiovascular risk reassessment + LVH regression on echo; bone density (chronic K wasting + secondary effects)

Disposition

Current setting: outpatient — Lifelong endocrine surveillance — APA cured: annual BP + K + aldosterone/renin (low recurrence rate); residual HTN management; BAH: lifelong MRA + K + Cr q3-6 mo; cardiovascular risk reassessment (LVH regression slow over years); bone density q2-3 y; family screening if FH; OSA co-management

Disposition criteria:
- Long-term continuation; cross-link to cardio.htn.core.v1 if persistent essential HTN; cross-link to endo.osteoporosis if bone disease; cross-link to pulm.osa if OSA dominant

Escalation triggers (move to higher acuity):
- BP rebound → re-eval medical regimen
- Hyperkalemia on MRA → reduce dose or switch to amiloride
- New symptoms (palpitations, weakness, cramps) → check K + Mg + repeat ARR
- Recurrent APA symptoms → repeat aldosterone + imaging (rare recurrence)

Earlier-Return Triggers

Return-precaution thresholds (watch for):
- [LIFE_THREATENING] PA crisis + K <2.5 + Torsades de pointes / VT / AF with RVR / U waves + QT prolongation — life-threatening hypokalemic arrhythmia
- [LIFE_THREATENING] Adrenal vein sampling complicated by adrenal hemorrhage, vein dissection, or thrombosis — rare but serious AVS complications (~1-2% even at high-volume centers)
- [SEVERE] Postop APA day 1-7 develops K >5.5 — contralateral adrenal suppression from chronic aldosterone excess → transient hypoaldosterone state

Citations

- Endocrine Society 2016 Primary Aldosteronism CPG (Funder JCEM 2016 PMID 26934393) + PATHWAY-2 (Williams Lancet 2015 PMID 26414968) + 2025 ACC/AHA HTN (Whelton) [PMID:26934393](https://pubmed.ncbi.nlm.nih.gov/26934393/)
- Cited evidence (PMID 26414968) [PMID:26414968](https://pubmed.ncbi.nlm.nih.gov/26414968/)
- Cited evidence (PMID 19726771) [PMID:19726771](https://pubmed.ncbi.nlm.nih.gov/19726771/)
- Cited evidence (PMID 14764777) [PMID:14764777](https://pubmed.ncbi.nlm.nih.gov/14764777/)
- Cited evidence (PMID 17027529) [PMID:17027529](https://pubmed.ncbi.nlm.nih.gov/17027529/)

Last reconciled with current guidelines: 2026-05-15.
References
  • Endocrine Society 2016 Primary Aldosteronism CPG (Funder JCEM 2016 PMID 26934393) + PATHWAY-2 (Williams Lancet 2015 PMID 26414968) + 2025 ACC/AHA HTN (Whelton) — PMID:26934393
  • Cited evidence (PMID 26414968) — PMID:26414968
  • Cited evidence (PMID 19726771) — PMID:19726771
  • Cited evidence (PMID 14764777) — PMID:14764777
  • Cited evidence (PMID 17027529) — PMID:17027529