Page 81 - Cardiac Nursing

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C HAPTER 2 / Systemic and Pulmonary Circulation and Oxygen Delivery 57
J
(J
/
/
concentration gradient and blood flow (through the delivery or across a short segment of exchange vessel (J v /A) having a curvilin-
(
J
removal of the substance). The rate of diffusion ( J s J ) is described ear relationship to the net pressure difference (i.e., limited fluid
P
as flow-limited. movement at low P c P ) across the vessel wall. 145 In Starling’s initial
˙
J s J J (C a C C i C )Q conceptualization, the net pressure difference reflected the alge-
C
C
braic sum of four pressures: intravascular (capillary) pressure (P c P ),
P
C
where C a C is the concentration of the substance in the arterial interstitial fluid pressure (P i P ), plasma oncotic pressure ( c ), and
P
C
blood, C i C is the concentration of the substance in the interstitium, interstitial oncotic pressure ( i ). The true pressure opposing fil-
˙
and Q is the rate of blood flow. Flow-limited diffusion has po- tration (P o P ) is not simply plasma oncotic pressure, but rather on-
P
tentially important implications for oxygen delivery in the setting cotic plasma pressure minus interstitial oncotic pressure plus in-
of decreased oxygen delivery (e.g., cardiogenic shock or during se- terstitial hydrostatic pressure and the reflection coefficient:
vere exercise when flow rates are so high that diffusion is limited).
P
However, most substances have intermediate endothelial perme- P o P P ( p i )
P i P
ability, and the rate of diffusion depends on endothelial perme- However, the effective oncotic force that opposes fluid filtration
ability and flow. 13 across the microvessel wall is the local oncotic pressure difference
Most solutes, including small lipophilic and hydrophilic mole- across the endothelial surface glycocalyx (the structure that covers
cules and macromolecules, move through membranes of exchange the entire capillary endothelium and is the primary filter for pro-
vessels by diffusion. The route of diffusion depends on the type teins) and not the global difference between the oncotic pressure
of membrane (continuous, fenestrated, discontinuous, and tight- in the plasma and tissue. 148 Models of this new conceptualization
junction) and the characteristics of the substance (e.g., lipid soluble, suggest that the oncotic pressure opposing filtration is greater than
ionic, large macromolecule). Water diffuses through the endothe- estimated from blood–tissue protein concentration differences,
lium primarily through intercellular clefts. 140,141 Lipid-soluble sub- and transcapillary fluid flux is smaller than predicted from the
stances, such as O 2 , CO 2 , and anesthetic gases, which pass easily original Starling equation. Therefore, in the Starling equation,
through the lipid bilayer of the microvascular wall, diffuse relatively the pressures P i P and i are the local hydrostatic pressure behind the
P
rapidly through the endothelium. Small hydrophilic solutes, such as glycocalyx and oncotic pressure on the tissue side of the matrix
ions and simple sugars, pass primarily through fenestrae, junctions layer, respectively, and not the values from the tissue space. 148,149
between cells, or intracellular clefts. The primary mode of macro- Capillary pressure (P c P ) is the primary force behind filtration.
P
molecular transport is through vesicles or possibly large pores. 141 Mean capillary pressure (P c P ) is determined by the arterial and ve-
P
The transport or movement of the macromolecules into the inter- nous pressures and the ratio of postcapillary resistance (R v R ) to pre-
R
stitium contributes to interstitial oncotic pressure. capillary resistance (R a R ), as described by the following equation: 150
R
Ultrafiltration P c P P (P v P
P a P ) R v R R
P
P
Starling’s hypothesis of microvascular fluid exchange is described R a R R
by the following equation 142–145 : where P v P is venous pressure, P a P is arterial pressure, R v R is postcapil-
R
P
P
R
J v J J lary midpoint resistance, and R a R is precapillary midpoint resist-
P
P
L p ([P c P P i P ] s[p c p i ])
P
R
R
R R
P
A ance (where R v R
R a R R Total ). An increase in either P a P or P v P re-
sults in an increase in P c P , unless counteracted by a decrease in the
P
/
/
J v J J /A fluid filtration across the capillary wall per unit area R v R R /R a R ratio. The lower the R v R /R a R ratio (i.e., increased precapillary
R
R
R
L p hydraulic permeability of the capillary wall resistance or decreased postcapillary resistance) the lower the cap-
P c P P global value for capillary pressure illary pressure. It is the adjustment in R v R /R a ratio, primarily
R
P i P P global value for interstitial pressure through regulation of precapillary resistance (R a R ) in the skeletal
R
osmotic reflection coefficient muscle and skin, that constitutes the primary effector mechanism
c global value for capillary oncotic pressure for the central nervous system-mediated control of plasma vol-
i global value for interstitial oncotic pressure 151,152
ume. However, the centrally mediated decrease in mean
In Starling’s initial conceptualization of ultrafiltration, it was capillary pressure occurs only to the extent allowed by local auto-
thought that at the arterial end of the capillary, the net forces fa- regulatory adjustments.
vored the movement of fluid out of the vessel (filtration). Some- In response to hypovolemic hypotension, compensatory pre-
P
where in the middle of the vessel, an equilibrium point was capillary vasoconstriction (increased R a R ) decreases the mean P c P ,
reached at which there was neither a gain nor a loss of fluid. Fi- and the net pressure in the downstream (venous) segment of the
nally, on the venous end of the exchange vessel, the net forces fa- exchange vessel favors transient reabsorption. This autotransfu-
vored reabsorption. Although the validity of Starling’s equation sion is the result of a change in the ratio of the postcapillary to
has been repeatedly confirmed, the conceptualization of upstream precapillary resistance on mean capillary pressure. 153 Of note, this
filtration and downstream reabsorption has been questioned. 145 response is decreased in older individuals, which may impair their
In general, the forces opposing filtration do not exceed capillary response to orthostasis or hemorrhage. 154
pressure, and filtration occurs along the entire length of the ex- In addition to the hydrostatic and oncotic forces, two other
change vessel. 146 The net filtration is necessary to wash out the factors affect fluid movement across the exchange vessel: the hy-
proteins that are continuously diffusing out of the vessels into draulic conductivity of the wall (L p ) and the reflection coefficient
the interstitium. 146,147 The ultrafiltrate and proteins that cross the ( ). Hydraulic conductivity is a measure of the permeability of
vessel wall into the interstitial fluid are subsequently removed by the exchange vessel to fluid, with the highest L p values for fenes-
the lymphatic system. trated endothelia and lowest for tight-junction endothelia. 13 Hy-
The primary direction of ultrafiltration is out of the vessel (fil- draulic conductivity is difficult to measure and is estimated by the
tration versus reabsorption), with the rate of fluid movement capillary filtration coefficient. The capillary filtration coefficient,