Microvascular Dysfunction — Clinical Workflow Pack

Section 01

Auto-Scoring System

Mark each symptom present (1 point each). Enter lab values where available (+2 points each). Total each step column. Highest total = Dominant Step. Ties → treat the lower-numbered step first.

Symptom / Marker	Step 1 🟢 Endothelium	Step 2 🟠 Platelets	Step 3 🔵 Fibrin	Step 4 🔴 Fibrinolysis
Diffuse head pressure	☐ +1
Light sensitivity (non-migraine)	☐ +1
Orthostatic dizziness / heat intolerance	☐ +1
Air hunger / BP or pulse fluctuation	☐ +1
Pressure behind one eye / temple		☐ +1
Visual brightness / contrast distortion		☐ +1
Sound sensitivity / derealization		☐ +1
Tingling or buzzing sensations		☐ +1
Brain fog / word-finding difficulty			☐ +1
Mental fatigue disproportionate to effort			☐ +1
Exercise intolerance / post-exertional malaise			☐ +1
"Low oxygen" feeling without hypoxia			☐ +1
Plateaued recovery despite effort				☐ +1
Waxing/waning without clear triggers				☐ +1
Cold extremities / poor peripheral circulation				☐ +1
Symptoms don't clear with rest				☐ +1
LAB: vWF antigen/activity ↑	+2
LAB: ADAMTS13 low-normal	+2
LAB: MPV elevated		+2
LAB: Fibrinogen ↑			+2
LAB: α2-antiplasmin ↑				+2
LAB: PAI-1 ↑				+2
TOTAL SCORE →	____	____	____	____

Dominant Step Action Guide

Step 1 Highest

Endothelium / NO

Start: NO + endothelial support

Step 2 Highest

Platelet Stabilization

Add: omega-3, magnesium

Step 3 Highest

Anti-inflammatory

Consider anticoagulation eval

Step 4 Highest

Specialist Escalation

Fibrinolysis evaluation

Section 02

4-Step Mechanism Map

The microvascular dysfunction cascade. Treat upstream first — do NOT jump to Step 3/4 without addressing Step 1/2.

Step 1Endothelium / NO

Step 2Platelets / PMPs

Step 3Fibrin Structure

Step 4Fibrinolysis

1

Endothelium / NO

vWF Release & Nitric Oxide

Mechanism

↓ Nitric oxide (NO) → endothelial dysfunction
↑ vWF secretion from stressed endothelial cells
Platelet inhibition reduced (NO deficit)
Autonomic rebound → vasoconstriction
Sources: SSRI withdrawal, viral injury, oxidative stress

Lab Signals

vWF antigen/activity >150% of normal
CRP >3 mg/L
ADAMTS13 low-normal (<60% activity)

2

Platelet Amplification

PMP Release & vWF Interaction

Mechanism

Dysregulated platelets from SSRI-depleted serotonin
Platelets bind ultra-large vWF (UL-vWF) strings
Platelet microparticles (PMPs) shed — mobile clotting platforms
PMPs bind vWF → seed dense micro-aggregation scaffolds
Gas6 (vitamin K-dependent) signaling disrupted

Lab Signals

MPV elevated (>11 fL)
Platelet count normal (distinguishes from TTP)
vWF still elevated

3

Fibrin Structure

Dense Clot Formation

Mechanism

Thrombin generation ↑ (from PMP phosphatidylserine)
Fibrin polymerization altered → denser, tighter networks
Amyloid-like fibrin in severe/prolonged states (Long COVID)
Capillary flow limited → oxygen delivery uneven
Post-exertional worsening pattern emerges

Lab Signals

Fibrinogen >4.0 g/L
D-dimer normal or mildly elevated (<1 mg/L FEU)
CRP often still elevated

4

Fibrinolysis Shutdown

α2-Antiplasmin / PAI-1 Lock

Mechanism

α2-antiplasmin cross-linked into fibrin by Factor XIII
PAI-1 ↑ → plasminogen activator inhibited → no plasmin
Microclots become plasmin-resistant → persist in capillaries
Fluctuating symptoms: partial obstruction → brief relief cycles
Self-sustaining loop unless upstream drivers addressed

Lab Signals

α2-antiplasmin >120% activity
PAI-1 >50 ng/mL
D-dimer LOW despite persistent symptoms

Section 03

Lab Panel & Thresholds

LifeLabs (Canada) and Labcorp (US) codes with clinical action thresholds.

⚠️ Key Insight: PT/INR/aPTT are often NORMAL in this pattern. These tests measure bulk coagulation cascades, not platelet–vWF dynamics, fibrin architecture, or fibrinolysis resistance. A normal clotting panel does not rule out microvascular dysfunction.

Core Panel — Order First

Test	LifeLabs	Labcorp #	Action Threshold	Interpretation
vWF Antigen	vWF Antigen	086280	>150% of normal	Endothelial activation; key Step 1 marker
vWF Activity (Ristocetin)	vWF Activity	086264	>150% activity	Functional vWF; compare to antigen ratio
ADAMTS13 Activity	Send-out (spec. coag)	117913	<60% activity	Low relative to vWF = critical imbalance
D-Dimer	D-Dimer	115188	>0.5 mg/L FEU	Active clot turnover; normal ≠ rules out microclots
Fibrinogen (Clauss)	Fibrinogen	001610	>4.0 g/L	Dense clot tendency; Step 3 marker
CBC + MPV	CBC w/ diff	005009	MPV >11 fL	Reactive platelets; count usually normal
hs-CRP	hs-CRP	120766	>3 mg/L	Inflammatory driver of Steps 1–3

Extended Panel — Add if Core Abnormal

Test	LifeLabs	Labcorp #	Action Threshold	Interpretation
α2-Antiplasmin activity	Specialty coag (send)	500540	>120% activity	Fibrinolysis inhibition; Step 4 marker
PAI-1	Limited availability	500512	>50 ng/mL	Blocks plasmin generation; Step 4 marker
Plasminogen Activity	Send-out	500538	<70% activity	Reduced fibrinolytic capacity

Contextual / Viral — Order if Clinically Indicated

Test	LifeLabs	Labcorp #	Threshold	Interpretation
EBV (VCA IgM/IgG, EBNA)	EBV serology	—	Active IgM or ↑ IgG	Herpesvirus reactivation → ↑ vWF, ↓ ADAMTS13
CMV IgM/IgG	CMV serology	—	Active IgM	Same mechanism as EBV
Ferritin	Ferritin	004828	>300 µg/L	Hyperferritinemia = systemic inflammation
LDH	LDH	004549	>250 U/L	Tissue/endothelial injury marker

Section 04

SSRI Withdrawal Protocol

Typically Steps 1–2 dominant. Microvascular dysfunction is functional (not structural) and resolves as the nervous system recalibrates. Most cases stabilize at Steps 1–2 without escalation.

Step Priority — SSRI Withdrawal

Step	Focus	Priority	Typical Timeline	Notes
Step 1 — Endothelium/NO	vWF, NO, endothelial stabilization	⭐⭐⭐ PRIMARY	Days 1–14	Address first. Often sufficient.
Step 2 — Platelets/PMP	Platelet reactivity, PMP shedding	⭐⭐⭐ CO-PRIMARY	Days 3–21	Main source of sensory symptoms.
Step 3 — Fibrin Structure	Dense clot tendency, fibrinogen	⭐ RARE	Only if persistent (>4 weeks)	Escalate only if labs support.
Step 4 — Fibrinolysis	α2-antiplasmin, PAI-1	⭐ VERY RARE	Exceptional cases only	Specialist evaluation required.

Phase 1 — Immediate (Days 0–7): Stabilize NO / Endothelium

Hydration: 2–3 L/day + electrolytes (sodium, potassium, magnesium)
Sleep: consistent schedule — key NO/endothelial regulator
Pacing: avoid exertion spikes; gentle walking if tolerated
Vitamin K2 (MK-4): endothelial + Gas6 platelet signaling support
Omega-3 fatty acids: endothelial + platelet stabilization
Reduce sympathetic load: minimize caffeine; breathwork; cool environment
If hyperadrenergic: consider clonidine (clinician-guided)

Phase 2 — Early Stabilization (Days 7–21): Platelet Stabilization

Omega-3 (higher dose range — clinician-guided)
Magnesium glycinate or malate (stabilizes platelet + vascular tone)
Polyphenols: quercetin-type compounds (anti-platelet + anti-inflammatory)
If Step 2 dominant: confirm with MPV, vWF activity
Consider low-dose antiplatelet only with clinician decision — weigh bleeding risk if still on SSRI

Phase 3 — Escalation (>4 Weeks, Persistent): Only if labs support

Re-evaluate SSRI taper strategy — slower taper may reduce microvascular burden
Anti-inflammatory focus: address sleep, gut inflammation, metabolic stress
Consider statin (clinician-guided): pleiotropic endothelial + anti-inflammatory effects
Anticoagulation only if fibrinogen clearly elevated AND symptoms persistent

⚠️ Safety Note — SSRI + Antiplatelet Bleeding Risk SSRIs already deplete platelet serotonin. Combining with antiplatelet agents significantly increases bleeding risk. Any antiplatelet or anticoagulant decision requires clinician assessment. Gastric protection (PPI) is mandatory if antiplatelets are added.

Section 05

Long COVID / Post-Viral Protocol

Often progresses to Steps 3–4. Involves structural changes (amyloid-like fibrin microclots, sustained endothelial injury, possible viral persistence). Multi-layered, longer-duration treatment is typical.

Step Priority — Long COVID

Step	Focus	Priority	Typical Timeline	Notes
Step 1 — Endothelium/NO	vWF, NO, endothelial stabilization	⭐⭐⭐ REQUIRED	Weeks 1–ongoing	Necessary but rarely sufficient alone.
Step 2 — Platelets/PMP	Platelet reactivity, PMP shedding	⭐⭐ IMPORTANT	Weeks 1–ongoing	Usually added early alongside Step 1.
Step 3 — Fibrin Structure	Dense/amyloid fibrin, fibrinogen	⭐⭐⭐ CORE	Weeks 2–6+	Anticoagulation often indicated here.
Step 4 — Fibrinolysis	α2-antiplasmin, PAI-1, tPA pathway	⭐⭐⭐ OFTEN LIMITING	Months 1–6+	Often the key barrier to recovery.

Layer 1 + 2 — Foundation (Start Immediately)

Endothelial stabilization: vitamin K2, omega-3, polyphenols
NO support: L-citrulline or beetroot-derived nitrates (clinician-guided)
Platelet stabilization: omega-3 (higher dose), magnesium, quercetin
Pacing strategy (CRITICAL): avoid post-exertional malaise (PEM) crashes — graded exercise therapy is contraindicated
Statins (clinician-guided): anti-inflammatory + endothelial + anti-platelet effects
Address sleep, metabolic health, viral triggers (EBV/CMV reactivation)

Layer 3 — Anticoagulation (Add when fibrinogen ↑ or symptoms persist at 2–4 weeks)

DOACs: Apixaban or Rivaroxaban (physician-prescribed, individualized dosing)
Alternative: low-molecular-weight heparin (Enoxaparin) in selected cases
Monitor: fibrinogen, D-dimer, vWF activity every 4–6 weeks
Duration: typically months — not short courses
Antiplatelet + anticoagulant combined: additive bleeding risk — specialist supervision required

Layer 4 — Fibrinolysis Restoration (Add when α2-AP/PAI-1 ↑ and plateau persists)

Specialist-guided evaluation: obtain α2-antiplasmin and PAI-1 levels
Address PAI-1 drivers: metabolic syndrome, cortisol dysregulation, inflammation
Advanced fibrinolytic approaches (hospital/specialist): tPA (Alteplase) in selected severe cases only
D-dimer may transiently rise as fibrinolysis resumes — interpret in clinical context
Reassess herpesvirus status: active EBV/CMV reactivation can suppress ADAMTS13 and perpetuate loop

Long COVID — Specific Considerations

Factors unique to Long COVID (not SSRI withdrawal): Spike protein directly alters fibrin structure toward amyloid-like conformation. Persistent viral reservoir may continuously drive endothelial activation. Autoimmune component possible (ADAMTS13 autoantibodies). Mast cell activation syndrome (MCAS) overlap may amplify vWF release. Expected recovery trajectory: months to 1–2 years.

Section 06

Escalation Rules

Built-in decision logic: "If X doesn't improve → do Y."

🟢 Step 1 Escalation Rules

If: vWF remains ↑ after 2 weeks of endothelial support

Then: Add omega-3 + magnesium (Step 2 support). Re-check vWF at 4 weeks.

SSRI: common. LC: expected — broaden to Step 2 immediately.

If: CRP ↑ and not resolving

Then: Investigate inflammatory drivers: sleep, gut health, viral reactivation, metabolic factors. Consider statin (clinician).

Statin: pleiotropic anti-inflammatory + eNOS upregulation.

If: Orthostatic symptoms dominant + not improving

Then: Evaluate for POTS/dysautonomia overlap. Consider clonidine if hyperadrenergic (clinician).

SSRI: autonomic rebound common. LC: dysautonomia often co-exists.

If: NO support interventions insufficient

Then: Consider ACE inhibitor/ARB or PDE5 inhibitor (Sildenafil) — clinician decision only.

Sildenafil: amplifies NO via cGMP — useful in microvascular flow impairment.

🟠 Step 2 Escalation Rules

If: MPV stays elevated + sensory symptoms persist after 3 weeks

Then: Consider low-dose antiplatelet (ASA 81mg). Weigh bleeding risk carefully.

SSRI: elevated bleeding risk. LC: more commonly indicated.

If: Steps 1 + 2 addressed and symptoms plateau

Then: Check fibrinogen. If ↑, escalate to Step 3. This is the key decision gate before adding anticoagulation.

If: PMP-driven amplification suspected (focal/asymmetric sensory)

Then: Confirm: MPV ↑, vWF ↑, platelet count normal. Consider clopidogrel if ASA inadequate.

Combining antiplatelet + anticoagulant requires specialist oversight.

🔵 Step 3 Escalation Rules

If: Fibrinogen ↑ and symptoms persist >4 weeks despite Steps 1+2

Then: Add anticoagulation: DOAC (Apixaban/Rivaroxaban) — physician-prescribed.

SSRI: rare. LC: commonly required, often for months.

If: Fibrinogen ↓ but symptoms remain

Then: Advance to Step 4 evaluation (α2-antiplasmin, PAI-1).

Fibrin structure may have normalized but fibrinolysis still impaired.

If: D-dimer rises during anticoagulation

Then: May indicate improved clot breakdown — interpret alongside symptoms. Do NOT automatically increase anticoagulation.

Rising D-dimer + improving symptoms = positive signal.

🔴 Step 4 Escalation Rules

If: α2-antiplasmin and/or PAI-1 elevated + recovery plateau

Then: Specialist referral required. Advanced fibrinolytic evaluation.

tPA (Alteplase) used in selected LC cases — hospital-level decision only.

If: PAI-1 ↑ driven by metabolic syndrome

Then: Address insulin resistance, weight, cortisol. GLP-1 agonists may reduce PAI-1 (emerging evidence).

If: Persistent despite all steps

Then: Reassess for: herpesvirus reactivation (EBV/CMV), autoimmune ADAMTS13 antibodies, MCAS overlap.

These are upstream perpetuating factors preventing full resolution.

Section 07

Drug Algorithm

FDA-approved agents mapped to each mechanism step. Sequencing matters: address Steps 1–2 before escalating. All medications require prescriber decision.

Step 1 — Endothelium / NO

Goal: ↑ NO bioavailability · ↓ vWF release · ↓ endothelial activation

Drug	Class	Mechanism	Dosing	SSRI Use	LC Use
Lisinopril / Enalapril	ACE inhibitor	↑ NO, ↓ endothelial activation, ↓ vWF	Oral daily	✓ Applicable	✓✓ Recommended
Losartan / Valsartan	ARB	Endothelial protection, ↑ NO	Oral daily	✓ Applicable	✓✓ Recommended
Atorvastatin / Rosuvastatin	Statin	↓ CRP, ↓ vWF, ↑ eNOS activity, pleiotropic	Oral daily	✓ Applicable	✓✓✓ Core
Sildenafil	PDE5 inhibitor	Amplifies NO via cGMP → microvascular flow	Oral PRN/daily	✓✓ Applicable	✓✓ Applicable
Clonidine	Alpha-2 agonist	↓ Sympathetic tone → ↓ vasoconstriction	Oral low-dose	✓✓ Hyperadrener.	✓ Dysautonomia

Step 2 — Platelets / PMPs

Goal: ↓ platelet activation · ↓ PMP shedding · ↓ platelet–vWF binding

Drug	Class	Mechanism	Dosing	SSRI Use	LC Use
Aspirin 81 mg	Antiplatelet (COX-1)	↓ Thromboxane A2 → ↓ platelet activation	Oral daily	⚠️ Bleeding risk	✓✓ Applicable
Clopidogrel	Antiplatelet (P2Y12)	↓ ADP-mediated platelet activation	Oral daily	⚠️ Bleeding risk	✓ With ASA
Statin (dual role)	Pleiotropic	Also reduces platelet reactivity	See Step 1	✓ Applicable	✓✓ Recommended

Step 3 — Fibrin Structure

Goal: ↓ thrombin → less dense fibrin networks

Drug	Class	Mechanism	Dosing	SSRI Use	LC Use
Apixaban	DOAC (Xa inhibitor)	↓ Thrombin → less dense fibrin networks	Oral BID	Rare	✓✓✓ Core
Rivaroxaban	DOAC (Xa inhibitor)	↓ Thrombin generation	Oral daily/BID	Rare	✓✓✓ Core
Enoxaparin	LMWH	↓ Thrombin, anti-Xa; preferred in hospital	SC injection	Rare	✓✓ Applicable

Step 4 — Fibrinolysis Shutdown

Goal: restore controlled fibrinolysis — requires specialist guidance

Drug	Class	Mechanism	Dosing	Notes
Alteplase (tPA)	Fibrinolytic	Converts plasminogen → plasmin → breaks fibrin	IV (hospital only)	SSRI: very rare. LC: specialist decision. Hospital-level only.
GLP-1 agonists	Metabolic (emerging)	May reduce PAI-1; address insulin resistance	Individualized	Both conditions — emerging evidence for PAI-1 reduction.

⚠️ Safety Flags for Drug Combinations (1) SSRIs deplete platelet serotonin → additive bleeding risk with any antiplatelet. (2) Antiplatelet + anticoagulant combined requires specialist supervision. (3) tPA is hospital/specialist use only — not outpatient. (4) PDE5 inhibitors contraindicated with nitrates.

Section 08

Symptom → Step Mapper

Bedside rapid identification: find dominant symptom cluster → identify step → initiate protocol.

1

Endothelium / NO — Flow Instability

Think: vasoconstriction / NO deficit · vWF ↑ · CRP ↑

Diffuse head pressure (often back of head)

Light sensitivity (not true migraine aura)

Orthostatic lightheadedness

Heat intolerance · air hunger

Fluctuating BP / pulse · global, not focal

First Actions

NO support: hydration, pacing, sleep

Vitamin K2, Omega-3, reduce sympathetic load

Clinician: consider ACE/ARB, statin

2

Platelet Amplification — Microvascular Hotspots

Think: platelet clustering · MPV ↑ · focal pattern

Pressure behind one eye / temple (asymmetric)

Visual brightness / contrast exaggeration ("HD")

Sound sensitivity / distortion

Derealization / "split perception"

Tingling or buzzing sensations

First Actions

Omega-3 + Magnesium

Polyphenols (quercetin)

Clinician: ASA 81mg (weigh risk carefully)

3

Fibrin / Microflow Limitation

Think: capillary obstruction · fibrinogen ↑ · PEM pattern

Brain fog / word-finding difficulty

Mental fatigue disproportionate to effort

Exercise intolerance / post-exertional malaise

"Low oxygen" feeling without hypoxia

Delayed recovery hours/days after exertion

First Actions

Pacing — CRITICAL, avoid PEM crashes

Anti-inflammatory focus (diet, sleep, metabolic)

Clinician: DOAC if labs support and persistent

4

Fibrinolysis Shutdown — Stuck State

Think: α2-AP ↑ · PAI-1 ↑ · D-dimer paradoxically low

Plateaued recovery despite partial improvement

Waxing/waning without clear triggers

Cold extremities / poor peripheral circulation

Symptoms don't clear with rest

Morning heaviness / "stuck" sensation

First Actions

Evaluate α2-antiplasmin, PAI-1

Address metabolic drivers (insulin resistance)

Specialist referral + rule out viral reactivation

⚡ Ultra-Fast Bedside Shortcut

Symptom Pattern	Dominant Step	First Move
Global pressure + light sensitivity	→ Step 1	NO + endothelial support
Focal pressure + sensory overload	→ Step 2	Omega-3 + Magnesium
Fatigue + brain fog + PEM	→ Step 3	Pacing + anti-inflammatory
Plateau + stuck / persistent	→ Step 4	Specialist + fibrinolysis eval
Mixed presentation	→ Score all	Treat highest-scoring step first

SSRI Withdrawal vs. Long COVID — Side-by-Side

Feature	SSRI Withdrawal	Long COVID
Fibrin structure	Likely normal; functional	Amyloid-like; protease-resistant
Platelets	Dysregulated / unstable	Hyperactivated (structural)
NO signaling	Fluctuating / reduced	Persistently reduced
Endothelium	Transiently stressed	Damaged / inflamed
Microcirculation	Intermittently impaired	Persistently impaired
Step 1 priority	⭐⭐⭐ Primary	⭐⭐⭐ Required
Step 2 priority	⭐⭐⭐ Co-primary	⭐⭐ Important
Step 3 priority	⭐ Rare	⭐⭐⭐ Core
Step 4 priority	⭐ Very rare	⭐⭐⭐ Often limiting

Section 09

Treatment Monitoring — 8-Week Tracker

Markers normalize in a predictable sequence. Patients often feel better before late markers normalize. Track this order: Endothelium → Platelets → Fibrin → Fibrinolysis.

Earliest Response
Days to ~1 week

↓vWF activity falls

↓CRP decreases

↓Symptoms less severe

↓MPV begins to normalize

Intermediate
Weeks 1–4

↓Fibrinogen decreases

↑vWF:ADAMTS13 ratio improving

↓Symptom consistency improves

↓MPV normalized

Late Resolution
Weeks 4–12+

↓α2-antiplasmin normalizes

↓PAI-1 falls

~D-dimer may transiently ↑

✓Full symptom resolution

⚠️ D-Dimer Rising During Treatment If D-dimer rises during anticoagulant treatment, this may indicate improved clot breakdown — a therapeutic signal, not a complication. Interpret alongside symptom trajectory. Do NOT automatically increase anticoagulation based on D-dimer alone.

8-Week Tracking Table

Marker (units)	Step	Baseline	Week 2	Week 4	Week 6	Week 8
vWF Activity (%)
ADAMTS13 Activity (%)
hs-CRP (mg/L)
MPV (fL)
Platelet Count (×10⁹/L)
Fibrinogen (g/L)
D-Dimer (mg/L FEU)
α2-Antiplasmin (%)
PAI-1 (ng/mL)
Symptom Score (0–10)	—

Monitoring Cadence: Every 4–6 weeks initially · Space to every 8–12 weeks once stable · Long COVID: extend tracking to 6–12 months · Add α2-antiplasmin and PAI-1 only if plateau persists.

Section 10

Patient Assessment Form

Complete at each visit. Use the scoring system (Section 1) to assign the dominant step.

Patient Information

Patient Name

Date of Birth

Visit Date

Clinician

Referring Diagnosis

Condition Pattern

SSRI Withdrawal Long COVID / Post-viral Other post-viral Unknown / Mixed

Symptom Checklist

Check all symptoms present. Count totals per step for scoring.

Auto-Score Result

Step 1 Score

Step 2 Score

Step 3 Score

Step 4 Score

Dominant Step

Lab Results

Test	Value	Threshold	Flag ↑/↓/N
vWF Antigen (%)		>150%
vWF Activity (%)		>150%
ADAMTS13 (%)		<60%
D-Dimer (mg/L)		>0.5
Fibrinogen (g/L)		>4.0
MPV (fL)		>11
hs-CRP (mg/L)		>3
α2-Antiplasmin (%)		>120%
PAI-1 (ng/mL)		>50
Platelet Count (×10⁹/L)		Normal
LDH (U/L)		>250

Clinical Plan

Current step(s) being treated

Escalation trigger (if met)

Medications initiated / adjusted

Follow-up / next labs

Next visit date

Notes

Quick Safety Flags

Currently on SSRI → caution with any antiplatelet (bleeding risk) Antiplatelet + anticoagulant combination → specialist supervision required Rapid worsening or focal neurological deficit → urgent evaluation On nitrates → contraindicated with PDE5 inhibitors (Sildenafil)

Microvascular DysfunctionClinical Workflow Pack

Auto-Scoring System

Dominant Step Action Guide

4-Step Mechanism Map

Mechanism

Lab Signals

Mechanism

Lab Signals

Mechanism

Lab Signals

Mechanism

Lab Signals

Lab Panel & Thresholds

Core Panel — Order First

Extended Panel — Add if Core Abnormal

Contextual / Viral — Order if Clinically Indicated

SSRI Withdrawal Protocol

Step Priority — SSRI Withdrawal

Long COVID / Post-Viral Protocol

Step Priority — Long COVID

Long COVID — Specific Considerations

Escalation Rules

🟢 Step 1 Escalation Rules

🟠 Step 2 Escalation Rules

🔵 Step 3 Escalation Rules

🔴 Step 4 Escalation Rules

Drug Algorithm

Step 1 — Endothelium / NO

Step 2 — Platelets / PMPs

Step 3 — Fibrin Structure

Step 4 — Fibrinolysis Shutdown

Symptom → Step Mapper

⚡ Ultra-Fast Bedside Shortcut

SSRI Withdrawal vs. Long COVID — Side-by-Side

Treatment Monitoring — 8-Week Tracker

8-Week Tracking Table

Patient Assessment Form

Patient Information

Condition Pattern

Symptom Checklist

Auto-Score Result

Lab Results

Clinical Plan

Quick Safety Flags

Microvascular Dysfunction
Clinical Workflow Pack