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CHAPTER 31: The Pathophysiology of the Circulation in Critical Illness 241
Cardiovascular management of cardiogenic and noncardiogenic management of fluid therapy. There were no differences in com-
40
edema aims to reduce edema formation and accumulation without plications between the two groups and no further beneficial effects
inducing inadequate Q ˙ t or D (see Table 31-3), thereby decreasing the were observed after 5 days. These results favoring conservative fluid
O 2
duration and complications of intensive care. Cardiogenic edema is management likely underestimated the observed outcome, as random
88
caused by high Pmv, often related to acute or acute-on-chronic LV dys- assignment to treatment groups did not start until 43 hours after admis-
function that increases LVEDP. Reducing the central blood volume by sion to the ICU. Support for underestimation comes from several case
venodilating agents (eg, morphine, furosemide, or nitroglycerin) reduces reports demonstrating improvement with Ppw reduction within the
LVEDP and edemagenesis, but excess preload reduction will adversely first 24 hours after ICU admission. 30,31,37-39,88 These considerations
reduce Q ˙ t from a poorly functioning ventricle that often requires a encourage early and aggressive reduction of circulating volume and
higher LVEDP (16-30 mm Hg) than normal (8-12 mm Hg). Where Ppw with care to avoid hypoperfusion (ie, patients in shock are not
indicated, vasoactive drugs to enhance systolic function (eg, dobuta mine, eligible for this strategy). This approach constantly seeks the least Ppw
milrinone, nitroglycerin) or reduce afterload (eg, fenoldopam, nicar- associated with an adequate Q ˙ t and D during the early stage of edema
O 2
dipine, or nitroprusside) and measures to correct diastolic dysfunction formation in ARDS. Of course, this is only symptomatic treatment; as
(eg, prolong filling time, maintain coordinated atrial contraction, or yet there are no specific therapies for the acute lung injury that correct
correct myocardial hypoxia and ischemia) act to reduce the LVEDP an increased K and a reduced σ. The aim is to minimize the edema con-
f
required for adequate Q ˙ t and thus reduce cardiogenic edema formation sequences of vascular injury and thereby shorten duration of ventilation
by the Starling equation. Increasing π by colloid infusion also reduces and care in the intensive care unit. 37-39
mv
edema formation, provided Pmv is not increased; an albumin infusion
that raises π from 15 to 20 mm Hg and Pmv from 25 to 30 mm Hg causes
mv
more Q ˙ e because σ = 0.7. Colloid infusion is even less helpful in reduc-
ing noncardiogenic edema, where σ is much reduced. In one study of oleic KEY REFERENCES
acid–induced noncardiogenic edema in dogs, raising π by 5 mm Hg had • De Backer D, Biston P, Devriendt J. Comparison of dopamine
mv
no effect on edema when Pmv was not allowed to change. 78 and norepinephrine in the treatment of shock. N Engl J Med.
The management of acute lung injury in canine models parallels the 2010;362(9):779-789.
treatment of cardiogenic pulmonary edema (Fig. 31-13). Reducing Ppw
by 5 mm Hg 1 hour after lung injury stopped edema accumulation and • Fessler HE, Brower RG, Wise RA, Permutt S. Effects of positive
end-expiratory pressure on the gradient for venous return. Am
Q ˙ t was maintained by infusion of dopamine or nitroprussside. 87,92,93
Many intensivists used this approach in treating ARDS, while others Rev Respir Dis. 1991;19:143.
maintained or increased Ppw to avoid hyperperfusion. 35,36 A compari- • Funk DJ, Jacobsohn E, Kumar A. The role of venous return in
son of conservative versus liberal fluid management based on the out- critical illness and shock—Part I: Physiology. Crit Care Med.
comes of 1000 patients with ARDS demonstrated that 255/500 subjects 2013;41:255-262.
resumed spontaneous breathing after 5 days of conservative fluid man- • Kramer A, Zygun D, Hawes H, Easton P, Ferland A. Pulse pres-
agement while 200/500 were breathing spontaneously after liberal sure variation predicts fluid responsiveness following coronary
artery bypass surgery. Chest. 2004;126:1563-1568.
• Magder S, Point: the classical Guyton view that mean sys-
A
600 Ppw = 11 temic pressure, right atrial pressure, and venous resistance
govern venous return is/is not correct. J Appl Physiol. 2006;101:
1523-1525.
400 • Malo J, Goldberg H, Graham R, et al. Effect of hypoxic hypoxia on
EVLL mL PI (Ppw = 6) systemic vasculature. J Appl Physiol. 1984;1403-1410.
PI + Dop (Ppw = 6) • Manthous CA, Schumacker PT, Pohlman A, et al. Absence of
200 NP (Ppw = 6)
supply dependence of oxygen consumption in patients with septic
shock. J Crit Care. 1993;8:203.
• The National Heart Lung and Blood Institute Acute Respiratory
B
8 Ppw = 11 Distress Syndrome (ARDS) Clinical Trials Network. Comparison
PI + Dop (Ppw = 6) of two fluid management strategies in acute lung injury. N Engl J
6 NP (Ppw = 6) Med. 2006;354:2564-2575.
QT (L/min) • Richard C, Warszawski J, Anguel N, et al. Early use of the pul-
. 4 PI (Ppw = 6) monary artery catheter and outcomes in patients with shock and
2 acute respiratory distress syndrome: a randomized controlled
trial. JAMA. 2003;290:2713.
• Schmidt GA. Cardiopulmonary interactions in acute lung injury.
0 1 1½ 3 5
Curr Opin Crit Care. 2013;19:51-56.
FIGURE 31-13. Schematic diagram illustrating the effects of reducing pulmonary wedge • Walley KR, Becker CJ, Hogan RA, et al. Progressive hypoxemia
pressure (Ppw) 1 hour after hydrochloric acid or kerosene aspiration at time 0 hour (abscissa) limits left ventricular oxygen consumption and contractility. Circ
˙
on extravascular lung liquid (EVLL by thermal dilution; A), and cardiac output Qt; B. Data Res. 1988;63:849.
are compiled from six studies by the same group with similar experimental protocols. 85,89,90 • Wood LDH, Hall JB. A mechanistic approach to providing ade-
A. Edema increases linearly with time after injury in the control group (Ppw = 11 mm Hg, quate oxygenation in acute hypoxemic respiratory failure. Respir
continuous line), but reduction of Ppw to 6 mm Hg at 1 hour by plasmapheresis (Pl) or sodium Care. 1993;38:784.
nitroprusside (NP) stops edema accumulation (interrupted line) such that EVLL is less than half
that in the control group by 5 hours; all EVLL values were confirmed by gravimetric edema
measures in the lungs excised at 5 hours. B. Qt did not change with time when Ppw was
˙
˙
maintained in the control group; when Ppw was reduced by plasmapheresis, Qt decreased to REFERENCES
˙
half its control value but Qt could be maintained at reduced Ppw by infusion of dopamine or
NP (continuous line). Plasmapheresis alone reduced Qt by decreasing Ppw (interrupted line). Complete references available online at www.mhprofessional.com/hall
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