Use lactate, capillary refill time and the venous-arterial CO2 gap together to judge tissue perfusion and guide resuscitation.
At the bedside
- 1
Measure lactate early and repeat
Measure within 1 h of suspected sepsis/shock; repeat every 2-4 h if raised. SSC 2026 suggests serial lactate to guide resuscitation, but individualise fluid after the first bolus rather than chase a normal value.
- 2
Check capillary refill time
Press the index finger pulp with a glass slide for 10 s, release, time to return of colour: normal ≤ 3 s. Repeat every 30 min during resuscitation.
- 3
Calculate CO2 gap
Paired central venous (SVC) and arterial gas drawn together: Pcv-aCO2 > 6 mmHg = low flow relative to CO2 production → look for low CO (fluids if responsive, inotrope).
- 4
Combine with ScvO2
Low ScvO2 + high CO2 gap: low DO2/flow. Normal/high ScvO2 + high CO2 gap: flow still inadequate (microcirculatory). Normal CO2 gap + high lactate: consider non-hypoxic causes.
- 5
Consider non-perfusion causes of high lactate
Adrenaline (beta-2), salbutamol, metformin, liver failure, seizures, thiamine deficiency, malignancy, mesenteric ischaemia, cyanide, methanol, propofol infusion syndrome, linezolid.
- 6
Avoid over-resuscitation
Lactate clears slowly (hours); do not give repeated fluid boluses solely to 'normalise lactate' if the patient is not fluid responsive. CRT normalises faster.
Causes of hyperlactataemia
| Type A (hypoperfusion/hypoxia) | Type B (other) |
|---|---|
| Shock of any type | Adrenaline/salbutamol (beta-2 agonists) |
| Severe hypoxaemia | Liver failure (reduced clearance) |
| Severe anaemia | Metformin, linezolid, propofol infusion syndrome, NRTIs |
| Regional ischaemia (mesenteric, limb) | Thiamine deficiency (beri-beri, alcohol) |
| CO / cyanide poisoning | Seizures, malignancy, toxic alcohols, DKA (D-lactate rarely) |
Persistent hypoperfusion after initial resuscitation
Step 1 of ~3
Decision: Non-hypoxic cause likely (adrenaline, liver failure, metformin)?
Based on Mallat J, Lemyze M, Tronchon L, Vallet B, Thevenin D; Hernandez G, Ospina-Tascon GA, Damiani LP, et al. Educational use; follow local protocol.
Pathophysiology
Lactate is produced by glycolysis and is a marker of stress metabolism (beta-2 adrenergic stimulation of Na-K ATPase) as much as of anaerobic metabolism; clearance is mainly hepatic. CO2 gap rises when flow is too low to wash out tissue CO2 (stagnation), so it is a marker of flow adequacy rather than of hypoxia.
Evidence
- ANDROMEDA-SHOCK (424 patients): CRT-targeted resuscitation vs lactate-targeted: 28-day mortality 34.9% vs 43.4% (not significant), less organ dysfunction at 72 h [Hernandez 2019].
- SSC 2026 suggests serial lactate to guide resuscitation and capillary refill time as an adjunct (both conditional, low certainty) [SSC 2026].
- CO2 gap > 6 mmHg is associated with higher mortality and identifies patients with inadequate CO despite normal ScvO2 [Mallat 2016].
Controversies
- Optimal target and frequency of lactate measurement; whether pushing CO to normalise CO2 gap improves outcome.
🇮🇳 India notes
- Lactate is available on most Indian blood gas analysers; CRT is free and can be measured by nurses every 30 min.
- In tropical infections (malaria, dengue, leptospirosis) high lactate often reflects severity; thiamine deficiency is relevant in alcohol use and malnutrition.
References
Test yourself
Module quiz · score 70% to complete the module
Educational reference for trained clinicians. Check doses against your hospital protocol and the patient in front of you.

