MICRO CIRCULATORY MONITORING

1. INTRODUCTION & CONCEPTUAL FRAMEWORK

What is the Microcirculation?

The microcirculation comprises:

• Arterioles (<100 μm)
• Capillaries (5–10 μm)
• Venules (<100 μm)

Its primary function is:

• Oxygen delivery
• Nutrient exchange
• Removal of metabolic waste
• Immune cell trafficking
• Endothelial signaling

Key concept:
Restoration of macrocirculation (MAP, CO) does NOT guarantee restoration of microcirculation.

This phenomenon is called hemodynamic incoherence.

2. PHYSIOLOGY OF MICROCIRCULATION

Determinants of Microcirculatory Flow

Functional Capillary Density (FCD)

• Number of perfused capillaries per tissue area
• Strongest determinant of tissue oxygenation

Loss of FCD → tissue hypoxia despite normal DO₂

Oxygen Transport at Microcirculatory Level

• Governed by Krogh cylinder model
• Oxygen extraction depends on:
• Capillary spacing
• Transit time heterogeneity
• RBC velocity

3. PATHOPHYSIOLOGY: MICROCIRCULATORY FAILURE

Mechanisms

1. Endothelial Dysfunction

• NO dysregulation
• Increased permeability
• Leukocyte adhesion

2. Glycocalyx Shedding

• Seen in:
• Sepsis
• Trauma
• Ischemia-reperfusion
• Leads to:
• Capillary leak
• Loss of mechanotransduction

3. Flow Heterogeneity

• Patchy perfusion
• Shunting
• Areas of no-flow adjacent to normal flow

4. Microthrombosis

• Sepsis-associated DIC
• COVID-19
• TTP/HUS

5. RBC Dysfunction

• Reduced deformability
• Sludging
• Altered oxygen off-loading

4. HEMODYNAMIC INCOHERENCE

Definition

A state where:

Macro-hemodynamic variables normalize but microcirculation remains impaired

Seen in:

• Septic shock
• Post-cardiac surgery
• Trauma resuscitation
• VA-ECMO
• Advanced heart failure

Clinical implication:

Raising MAP from 65 → 75 mmHg may not improve tissue perfusion

5. WHY MONITOR MICROCIRCULATION?

Limitations of Conventional Monitoring

Microcirculation = Final Common Pathway of Shock

“Cells die not from hypotension, but from hypoxia.”

6. METHODS OF MICROCIRCULATORY MONITORING

A. DIRECT VISUALIZATION TECHNIQUES (GOLD STANDARD)

1. Handheld Vital Microscopy (HVM)

Evolution

• OPS – Orthogonal Polarization Spectral Imaging
• SDF – Sidestream Dark Field Imaging
• IDF – Incident Dark Field Imaging (latest)

Incident Dark Field (IDF) Imaging

Principle

• Green light (530 nm)
• Absorbed by hemoglobin
• RBCs appear dark against bright background

Site

• Sublingual microcirculation
• Thin mucosa
• Easy access
• Correlates with splanchnic perfusion

Parameters Assessed

Normal Values (Adult)

Clinical Utility

• Septic shock prognosis
• Fluid responsiveness at micro level
• Vasopressor titration
• Transfusion decision-making

Limitations

• Operator dependent
• Offline analysis
• Cost
• Not continuous
• Not bedside routine yet

B. INDIRECT MICROCIRCULATORY MONITORING

1. Near-Infrared Spectroscopy (NIRS)

Principle

• Measures tissue oxygen saturation (StO₂)
• Reflects balance of oxygen delivery & consumption

Sites

• Thenar eminence
• Forearm
• Cerebral cortex

Vascular Occlusion Test (VOT)

• Inflate cuff > systolic pressure
• Measure:
• Deoxygenation slope → oxygen consumption
• Reoxygenation slope → microvascular recruitment

Interpretation

Limitations

• Measures mixed arterial-venous signal
• Influenced by edema, skin pigmentation
• Not organ-specific

2. Peripheral Perfusion Indices

a. Capillary Refill Time (CRT)

• Strong prognostic value (ANDROMEDA-SHOCK trial)
• Target-guided resuscitation superior to lactate-guided

b. Skin Mottling Score

• Reflects cutaneous hypoperfusion
• Associated with mortality in septic shock

c. Temperature Gradient

• Core-to-toe temperature difference

3. Venous-Arterial CO₂ Gap (P(v-a)CO₂)

• Reflects microcirculatory flow adequacy
• High gap (>6 mmHg):
• Low flow states
• Microvascular shunting

4. Lactate Kinetics

• Surrogate of cellular hypoxia
• Clearance >10% in 2–6 hours favorable

C. ORGAN-SPECIFIC MICROCIRCULATION

7. MICROCIRCULATION IN SHOCK STATES

Septic Shock

• ↓ Capillary density
• ↑ Flow heterogeneity
• Endothelial & glycocalyx damage

Microcirculatory failure may persist even after lactate normalization

Hemorrhagic Shock

• Capillary derecruitment
• Improved rapidly with volume & transfusion

Cardiogenic Shock

• Low driving pressure
• High venous pressure impairs capillary flow

Obstructive Shock

• Venous congestion → impaired microflow

8. THERAPEUTIC IMPLICATIONS

Fluids

• Improve microcirculation only if recruitable
• Excess fluids → glycocalyx damage

Vasopressors

• Norepinephrine:
• May improve microcirculation if MAP low
• Excess → vasoconstriction

Inotropes

• Dobutamine may improve microflow independent of CO

RBC Transfusion

• May improve microcirculation if baseline impaired
• No benefit if normal microflow

Steroids

• Improve endothelial responsiveness

9. FUTURE DIRECTIONS

• AI-based automated microcirculatory analysis
• Continuous bedside IDF devices
• Microcirculation-guided resuscitation protocols
• Integration with ECMO and shock platforms

10. KEY TAKEAWAYS 

• Microcirculation is the final determinant of tissue oxygenation
• Hemodynamic coherence is not guaranteed
• Sublingual IDF imaging is gold standard
• CRT-guided resuscitation has outcome benefit
• Normal MAP does not exclude tissue hypoxia