blood

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Blood

Hemorrhage, coagulation cascade (intrinsic and extrinsic pathways), blood volume tracking, and systemic effects on perfusion and oxygen delivery. Disabled by default; activated for hemorrhagic or surgical wound studies.

Biology

Wound healing begins with hemostasis, the arrest of bleeding. When a vessel is injured, two coagulation pathways activate in parallel: the intrinsic pathway (contact activation of factor XII by exposed subendothelial collagen) and the extrinsic pathway (tissue factor exposure from damaged cells). Both converge on thrombin generation, which converts fibrinogen to fibrin and amplifies platelet aggregation to form a stable clot (Versteeg et al. 2013).

Platelets aggregating at the wound site release growth factors (PDGF, TGF-beta) from their alpha-granules, initiating the inflammatory cascade that recruits neutrophils and macrophages (Singer and Clark 1999). The provisional fibrin clot matures over approximately 4 hours and begins fibrinolytic remodeling after about 48 hours.

Significant blood loss reduces circulating volume and hemoglobin, impairing tissue perfusion and oxygen delivery to the wound bed. Below the hemorrhagic shock threshold (approximately 40% volume loss), perfusion drops sharply and wound healing is severely compromised (Guo and DiPietro 2010). Tissue oxygen tension is a direct predictor of wound infection risk (Hopf et al. 1997).

Clinical modifiers include anticoagulant therapy (which slows clotting but increases bleeding) and thrombocytopenia (low platelet count impairing clot formation).

Model

Three coupled subsystems:

1. Hemorrhage
   bleed_rate * (1 - barrier) * vascularity * anticoagulant_boost
   -> reduces blood_volume over time
   -> volume_recovery partially compensates

2. Coagulation Cascade
   (intrinsic_rate + extrinsic_rate) * anticoag_penalty * platelet_factor
   -> coag_state (0 to 1, activation level)
   -> thrombin generation from converged pathways
   -> thrombin enhances fibrin deposition (hemostasis module coupling)
   -> platelet cytokine release (PDGF, TGF-beta) to inflammation

3. Blood Volume and Systemic Effects
   blood_volume tracks cumulative hemorrhage vs recovery
   Below shock_threshold: perfusion * shock_perfusion_penalty
   Below anemia_threshold: O2 delivery * anemia_o2_penalty

Hemorrhagic shock: When blood volume drops below shock_threshold (default 0.6), perfusion is progressively penalized down to shock_perfusion_penalty (0.3x), modeling circulatory failure.

Anemia: When hemoglobin drops below anemia_threshold (default 0.7), oxygen delivery is reduced by anemia_o2_penalty, impairing aerobic wound healing.

Anticoagulant therapy: Therapeutic anticoagulation (warfarin, heparin) reduces coagulation rates by anticoag_coag_penalty while increasing bleeding by anticoag_bleed_boost.

Thrombocytopenia: Platelet counts below thrombocytopenia_threshold proportionally reduce coagulation cascade activation.

Parameters

From modules/blood/config.toml:

Parameter	Default	Units	Description	Source
enabled	false	bool	Master switch (opt-in)	Convention
bleed_rate	0.02	normalized	Baseline blood loss rate from wound	Calibrated
depth_bleed_factor	1.5	multiplier	Deeper wounds bleed more	Calibrated
vascularity_coupling	true	bool	Bleed rate scales with local perfusion	Convention
intrinsic_rate	0.01	per step	Contact activation (factor XII)	Versteeg et al. 2013 (DOI)
extrinsic_rate	0.05	per step	Tissue factor exposure from injury	Versteeg et al. 2013 (DOI)
thrombin_rate	0.03	per step	Thrombin generation from converged pathways	Versteeg et al. 2013 (DOI)
thrombin_fibrin_coupling	0.02	per step	Thrombin to fibrin conversion	Versteeg et al. 2013 (DOI)
platelet_aggregation_rate	0.04	per step	Platelet aggregation at wound site	Singer and Clark 1999 (DOI)
platelet_cytokine_coupling	0.001	per step	PDGF/TGF-beta release to inflammation	Singer and Clark 1999 (DOI)
clot_maturation_h	4.0	hours	Clot stabilization time	Calibrated
fibrinolysis_delay_h	48.0	hours	Fibrinolysis onset delay after clot formation	Calibrated
initial_volume	1.0	normalized	Normal blood volume	Convention
volume_loss_rate	0.01	per hour	Volume loss fraction at bleed_rate=1.0	Calibrated
volume_recovery_rate	0.005	per hour	Physiological compensation and resuscitation	Guo and DiPietro 2010 (DOI)
shock_threshold	0.6	fraction	Below this: hemorrhagic shock	Guo and DiPietro 2010 (DOI)
shock_perfusion_penalty	0.3	multiplier	Perfusion reduction in shock	Guo and DiPietro 2010 (DOI)
hemoglobin	1.0	normalized	Hemoglobin level (1.0 = 14 g/dL)	Convention
anemia_threshold	0.7	fraction	Below this: impaired O2 delivery	Hopf et al. 1997 (DOI)
anemia_o2_penalty	0.5	multiplier	O2 delivery reduction factor	Hopf et al. 1997 (DOI)
anticoagulant_level	0.0	0 to 1	Anticoagulant therapy level (0 = none, 1 = therapeutic)	Convention
anticoag_coag_penalty	0.4	multiplier	Coagulation rate reduction from therapy	Calibrated
anticoag_bleed_boost	1.8	multiplier	Bleed rate increase from therapy	Calibrated
platelet_count	1.0	normalized	Platelet count (1.0 = 250k/uL)	Convention
thrombocytopenia_threshold	0.4	fraction	Below this: impaired clotting	Calibrated

Coupling

Reads

Field	Source module	How used
Vascular (perfusion)	angiogenesis	Vascularity coupling for hemorrhage rate; perfusion modification target
Oxygen	oxygen	Anemia penalty applied to O2 delivery
Barrier	epithelial	Gates hemorrhage (open wound = bleeding)

Writes

Field	Consumer modules	What is written
Vascular (perfusion)	angiogenesis, oxygen	Reduced by hemorrhagic shock
Oxygen	metabolism	Reduced by anemia
Fibrin	hemostasis	Enhanced by thrombin generation
Inflammation	immune	Platelet cytokine release (PDGF, TGF-beta)

Source files

File	Purpose
source_hook.h	Hemorrhage, coagulation cascade, blood volume tracking, systemic perfusion and O2 effects
params.h	Parameter struct (BloodParams)
config.toml	Module configuration