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Nursing Pharmacology Chapter 5: Blood Pressure Control

Table of Contents


  • 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


Tissue Perfusion: Cardiac

  • 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.


Tissue Perfusion: Vascular Resistance

  • 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 Factors

  • 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.


Humoral Factors

  • 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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Hollenberg, S.M. and Parrillo, J.E., Shock, In Harrison's Principles of Internal Medicine 14th edition, (Isselbacher, K.J., Braunwald, E., Wilson, J.D., Martin, J.B., Fauci, A.S. and Kasper, D.L., eds) McGraw-Hill, Inc (Health Professions Division), 1998, p. 215-222