• 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

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• 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.

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• 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

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•  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.

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• CNS, cellular and immunological responses to shock cause an increase in levels of epinephrine and other catecholamines, renin, vasopressin, prostaglandins,and ANF.

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