Organ perfusion is dependent on arterial pressure, determined by the product of cardiac output and vascular resistance.

Inadequate organ perfusion is dependent on cardiac output and correct blood distribution.

Within an organ, adequate perfusion will depend on microvascular patency, tone, and blood flow distribution.

Tissue perfusion depends on four factors:

• Cardiac

• Vascular

• Microcirculatory

• Humoral

Cardiac output is dependent upon heart rate and stroke volume.

Stroke volume will be influenced by preload (filling pressure), afterload (systolic resistance), and contractility (force of contraction).

Heart rate is dependent on sympathetic and parasympathetic balance.

Vascular resistance depends on vessel length, blood viscosity and is inversely proportional to the fourth power of the vessel radius.

Therefore, the cross-sectional vessel area is the most signficant factor in blood flow resistance.

Arteriolar vessel determines resistance to flow and vessel cross-sectional area is determined by vascular tone.

Neuronal, humoral and local factors regulate vascular smooth muscle tone.

Sympathetic, tonic vasoconstricting tone predominates in vascular smooth muscle.

Level of sympathetic tone is reflexly determined by arterial and cardiopulmonary baroreceptors.

Tone is affected by circulating levels of epinephrine and norepinephrine released by the adrenal medulla.

Local metabolic factors also promote vascular smooth muscle changes.

• These vasodilatory changes due to increased metabolic activity are mediated primarily by adenosine and prostaglandins.

Other local factors that promote vasodilation include low PO₂ (causing prostaglandin release) and endothelial relaxing factor (nitric oxide, NO).

Factors that cause vasoconstriction: endothelin I, angiotensin II

Microcirculatory failure is the most critical failure in shock.

Pathological factors such as leukocyte/platelet adhesion and coagulation can result in microvessel occlusion.

Microvascular flow is affected by the balance between colloid forces (tending to retain intravascular fluid volume) and capillary hydrostatic pressure (tending to force fluid into extravacular space)

Vasoconstriction of precapillary resistance vessels reduce capillary hydrostatic pressure and vasoconstiction of postcapillary venules tend to increase hydrostatic pressure gradients.

• In hypoxic states, arteriolar metabolic effects may dominate causing precapillary vasodilation and with vasoconstriction of postcapillary venules, movement of fluid into extravascular spaces is favored.

• Tissue edema may be further worsened by circulating toxins which enhances capillary permeability.

• Intravascular plasma protein loss decreases oncotic (colloid) forces which causes additional intravascular fluid loss.