Example of Systemic Dysfunction
Hypothesis

HIGH BLOOD PRESSURE

Blood flow through the vascular system depends on a pressure gradient. When blood encounters increased resistance, maintaining adequate flow requires a greater pressure difference. To generate this higher pressure, the heart must work harder and contract with greater force to push blood through the high-resistance vascular network. If this increased workload persists, the heart can undergo structural adaptation. The left ventricular muscle may thicken, increasing cardiac workload further and eventually contributing to heart failure.

High blood pressure is commonly explained through established mechanisms including increased peripheral vascular resistance, arterial stiffness, increased circulating volume, sympathetic activation, kidney-related regulation, and metabolic factors. In many patients with primary hypertension, however, no single physical obstruction responsible for the elevated pressure is identified.

Carbon Monoxide–Driven Fibrin Amyloid Microvascular Obstruction as a Cause of High Blood Pressure

​THE CARCO STRESS MODEL: Microvascular Hypertension

Carbon Monoxide Exposure → Fibrin Amyloid Formation → Persistent Partial Obstruction Within Microvessels → Increased Resistance to Blood Flow → Greater Pressure Gradient Required Across the Obstructed Microvascular Network → Increased Upstream Arterial Pressure

Mechanistic Explanation

Carbon Monoxide Exposure Creates the Upstream Microvascular Burden

Within the CARCO Stress Model, repeated carbon monoxide exposure promotes continued fibrin amyloid formation. As these abnormal fibrin structures persist in the circulation, they can progressively obstruct a greater number of capillaries and other microvessels.

The resulting vascular disturbance is therefore not limited to a transient effect of carbon monoxide in the bloodstream. Continued exposure can create a growing physical fibrin amyloid burden within the microcirculation, allowing the consequences of exposure to persist through the structural obstruction itself.

Partial Microvascular Obstruction Increases Resistance

Fibrin amyloid microclots can become positioned within capillaries and other microvessels, creating partial obstructions along the normal path of blood flow. Blood continues through these vessels, but when it reaches an obstructed segment it encounters greater resistance.

Maintaining flow across the affected region therefore requires a greater pressure gradient. As carbon monoxide–driven fibrin amyloid obstructions become distributed across larger portions of the microvascular network, total resistance to tissue perfusion increases and greater upstream pressure is required to continue driving blood through the affected microvascular pathways.

The central physical sequence is:

Partial Microvascular Obstruction → Increased Resistance → Greater Pressure Gradient Required to Maintain Flow

High Blood Pressure as a Compensatory Response

Under this hypothesis, elevated arterial pressure helps preserve tissue perfusion despite increased physical resistance within the microcirculation.

High blood pressure can therefore develop downstream of carbon monoxide exposure through a structural pathway:

Carbon Monoxide Exposure → Fibrin Amyloid Burden → Microvascular Resistance → Increased Arterial Pressure

The increased pressure can represent a compensatory response required to move blood across partially obstructed regions. High blood pressure may consequently become one of the first clearly measurable abnormalities while the underlying carbon monoxide–related fibrin amyloid obstruction remains undetected.

Why the Underlying Mechanism May Be Missed

Routine evaluation of hypertension does not normally establish whether widespread microscopic fibrin amyloid obstructions are present throughout the capillary network or whether repeated environmental carbon monoxide exposure contributed to their formation.

If these obstructions are not identified, elevated blood pressure is treated through established hypertension mechanisms while the physical source of increased microvascular resistance remains unchanged.

Under this hypothesis, this distinction can help explain variation in treatment response. Treatment may modify conventional contributors to blood pressure while leaving the carbon monoxide–driven fibrin amyloid burden and the resulting physical resistance to microvascular blood flow untouched.

Why Lifestyle Changes May Have Little Effect

Dietary and lifestyle changes can lower blood pressure when elevated pressure is being driven by mechanisms that those interventions modify.

However, dietary changes do not remove persistent fibrin amyloid microclots or eliminate the physical resistance created by carbon monoxide–driven partial microvascular obstruction.

When persistent fibrin amyloid microvascular obstruction is the primary driver of elevated blood pressure, and no significant parallel blood-pressure mechanisms are present, dietary modification is unlikely to have a meaningful effect because it does not remove the underlying physical resistance to blood flow.

If carbon monoxide exposure also continues, additional fibrin amyloid formation may further increase the microvascular burden while lifestyle interventions leave the upstream exposure and physical obstruction unresolved.

Blood-Pressure Reduction and Tissue Perfusion

If elevated arterial pressure is compensating for increased resistance within an obstructed microvascular network, lowering systemic pressure does not remove the fibrin amyloid obstruction produced downstream of carbon monoxide exposure.

Under this hypothesis, sufficiently reducing upstream pressure could reduce the pressure gradient available to move blood through partially obstructed microvessels. Tissue perfusion and oxygen delivery could therefore decline while the underlying physical resistance remains unchanged.

This creates an important distinction between reducing the measured blood pressure and removing the mechanism that created the increased pressure requirement.

Blood pressure Medication can worsen tissue perfusion

Blood-pressure medication lowers arterial pressure by reducing cardiac output, circulating volume, vascular tone, or a combination of these. However, if the elevated pressure is driven by permanent physical obstructions within the microvasculature, lowering systemic pressure does not remove the underlying resistance. It may instead reduce the pressure gradient available to drive blood through the remaining open microvascular pathways, potentially further limiting tissue perfusion. This means that even less oxygen may reach the tissues for cellular energy production.

Sources