-
Acute renal failure (ARF)is a common compli-cation in critically
illpatients. In a 5-yearanalysis of incidence
and mortality published in 2002,Pruchnicki and Dasta1
estimatedthat it occurs in up to 25% of allpatients admitted to the
hospitalwith a critical illness. In a more recentmulticenter,
multinational analysis2
of almost 30000 intensive care unit(ICU) admissions in 54 study
cen-ters in 23 countries, ARF developedduring the hospital stay in
5.7% ofall the patients. Of those patients,approximately 60% died,
with ahigher prevalence among patientsreceiving renal replacement
therapy.
Acute Renal Failure andMechanical Ventilation:Reality or
Myth?
This article has been designated for CE credit. Aclosed-book,
multiple-choice examination fol-lows this article, which tests your
knowledge ofthe following objectives:
1. Understand the pathophysiology of acuterenal failure
2. Describe the systemic effects of mechanicalventilation
3. Recognize how mechanical ventilation maycontribute to the
pathogenesis of acute renalfailure
CEContinuing Education
62 CRITICALCARENURSE Vol 29, No. 2, APRIL 2009
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Although dialysis techniques havemarkedly improved since the
1980s,resulting in improved outcomes,ARF remains an independent
pre-dictor of hospital mortality in criti-cally ill patients.2,3 In
fact, the processof or the comorbid conditions asso-ciated with the
development of ARFappear to contribute to overall mor-tality. Thus,
patients admitted tothe ICU who subsequently haverenal failure seem
to have worseoutcomes than do patients admittedwith preexisting
acute renal failure.4
Development of ARF in patientswho are not critically ill is
associatedwith significant increases in mortal-ity and in hospital
costs due to longerlengths of stay and treatmentsrelated to ARF.
When ARF developsin patients with critical illness, thecosts and
adverse outcomes increaseeven more dramatically.5-7 Liangoset al6
used data from the 2001National Hospital Discharge Surveyto explore
the relationship betweenARF and hospital length of stay
andmortality. Patients with ARF had a2-day increase in length of
stay, ahigher mortality rate, and an adjustedodds ratio of 2.0 for
discharge toshort- or long-term care facilities. In
Caroline C. Broden, RN, MSN, ACNP, CCNS, CCRN
Clinical Article
PRIME POINTS
What changes associ-ated with mechanical ven-tilation can acute
renalfailure be linked to?
How does pulmonaryinflammation and/or rup-ture of alveoli affect
renalfunction?
Research is needed onlung-protective ventilationstrategies,
including judi-cious use of PEEP, optimalfraction of inspired
oxy-gen, tidal volume control,airway pressure releaseventilation,
high-frequencyoscillatory ventilation, andtraditional
mechanicalventilation.
2009 American Association of Critical-Care Nurses doi:
10.4037/ccn2009267
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63
a smaller study, Vieira et al8 found alink between acute kidney
injury andunsuccessful weaning from mechani-cal ventilation
resulting in increasesin duration of mechanical ventilation,lengths
of stay, and ICU mortality.
Although common, perhaps ARFis not inevitable. Evidence suggests
alink between positive-pressure ventila-tion and ARF.9 In this
article, I brieflyreview renal anatomy and physiology,acute renal
failure, the systemic effectsof mechanical ventilation, and
howattempts to salvage respiratory func-tion may actually
compromise otherend-organ function.
Renal Anatomy and Physiology
Although their primary function isto filter and excrete wastes
and toxins,the kidneys also regulate fluids, elec-trolytes, and
acid-base balance. Theyreceive 20% to 25% of the entire car-diac
output. More than half of theblood flow through the kidney
consistsof plasma. Of the renal plasma flow,approximately 20% is
filtered throughthe glomeruli (the glomerular filtra-tion rate
[GFR] is an estimate of theamount of blood that passes througheach
minute). The remaining plasmaflows through efferent
arterioles.10,11
The amount that flows through thesearterioles depends directly
on renalblood flow (RBF), and any alterationsin blood flow will
alter the GFR.
Each kidney receives its bloodsupply through a single renal
artery
that divides into different branches,which divide even further
to pro-vide blood to all of the nephrons.The nephrons are unique
becausethey have 2 capillary systems: thehigh-pressure glomeruli
and thelow-pressure reabsorptive peritubu-lar capillary network.
Each glomeru-lus is flanked by afferent and efferentarterioles
(Figures 1 and 2), whichselectively constrict or dilate to regulate
the pressure within theglomeruli.11 Blood passes through
the glomerulus and into structurescalled Bowmans capsules
(Figure 2).
The glomerular capillary mem-brane has 3 layers: the inner
capil-lary endothelium, the basementmembrane, and the outer
capillaryepithelium10,11 (Figure 2). The glomeru-lar filtrate
passes through all 3 lay-ers, through the nephrons, and intothe
proximal tubule. From there,the filtrate continues to travel
throughthe loops of Henle and into distaltubules before passing on
to thecollecting ducts (Figure 1). At eachstep, fluids, ions, and
electrolytesare exchanged.
Of note, nephrons are the func-tional units of the kidney and
con-sist of the cortical nephrons (85%)and juxtamedullary
nephrons(15%).13 The primary functions of
CPT Caroline Broden is an acute care nurse practitioner in the
US Army Nurse Corps atWilliam Beaumont Army Medical Center, El
Paso, Texas.
Corresponding author: CPT Caroline Broden, RN, MSN, ACNP, CCNS,
CCRN, Department of Nursing, William BeaumontArmy Medical Center,
5005 N. Piedras Ave., El Paso, TX 79920 (e-mail:
[email protected]).
To purchase electronic or print reprints, contact The InnoVision
Group, 101 Columbia, Aliso Viejo, CA 92656.Phone, (800) 899-1712 or
(949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail,
[email protected].
Author
Figure 1 The nephron.Reprinted from Gray.12
Duct of Bellini
Ascending limb
Spiral tubuleInterlobular artery
Intertubular capillaries
Efferent vesselAfferent vessel
1st convoluted tubuleNeck
Irregulartub.
2nd convoltub.
Cortical substance
Boundary zone
Medullarysubstance
Collectingtub.
Junctional tub.
Glomerular capsule
Interlobular vein
{Henlesloop Descending limb
Venous archArterial arch
Arteria recta
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cortical nephrons are excretory andregulatory, whereas the
primaryfunction of juxtamedullary nephronsis urine concentration
and dilutionthrough a countercurrent mecha-nism as the urine
travels throughthe long loops of Henle.13 Althoughthe cortical
nephrons have loops ofHenle, the loops are of various lengthsand do
not include the thin ascend-ing loop that is present in the
jux-tamedullary nephrons. The long,ascending loops and the vasa
rectaare responsible for urine concentra-tion and dilution.13 (The
vasa rectaare vessels that closely follow theloops of Henle and
with them,through a countercurrent mecha-nism, play an important
role inurine concentration and dilution.13)
Autoregulation maintains thepressure within Bowmans capsulesat a
reasonably constant rate of 80to 180 mm Hg.10 At higher
pressures,the afferent arterioles constrict, pre-venting increased
glomerular bloodflow. At lower pressures, the arteri-oles dilate,
increasing glomerular
blood flow. This process maintainsa fairly constant filtration
and excre-tion of fluids and solutes.10 The reflex-ive relationship
between RBF andarterial pressure is maintained byneural regulation.
With decreasedsystemic arterialpressures, sympa-thetic nerve
activ-ity signals thebaroreceptors inthe aortic arch.Decreased
pres-sures cause renalarteriolar vaso-constriction, whichdecreases
filtrationand excretion.This mechanismincreases intravas-cular
volume andthus increasesblood pressure.Conversely,increased
sys-temic arterialpressure leads torenal arteriolar
vasodilatation and increased filtra-tion and excretion of
fluids.10,11
Acute Renal FailureARF is defined as a sudden
reduction (from hours to days) inGFR14 and is associated with
anaccumulation of nitrogenous wastesand alterations in fluid,
electrolyte,and acid-base balance.15-17 ARF maybe associated with
decreased urineoutput and is often manifested byan output of less
than 30 mL/h orless than 400 mL/d.15 Fortunately,ARF can usually be
reversed ifdetected early.17 ARF is classified asprerenal,
intrarenal, or postrenal(Table 1). It has many causes, whichcan
include conditions inherent to apatients disease process, such
asinfections, vascular obstructions,and severe hypotension. The
causecan also be iatrogenic, such asadministration of contrast
mediumor medications.15,16
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Figure 2 Bowmans capsule and glomerular apparatus.Adapted from
Huether,10 2002, with permission from Elsevier.
Distal convoluted tubule
Juxtaglomerular cells
Podocytes(visceral cells)
Maculadensa
Afferentarteriole
Efferentarteriole
Pores in endothelium
Parietalepithelial cell Mesangial cell Mesangial
matrix
Visceralepithelium
(podocytes)Capillarylumen
BasementmembranePodocyte
(cell body)Pedical
(cell process)Capsular slits
(filtration)Capillary
endothelium
Pseudofenestrationswith central knobsBowman
capsule
Parietalepithelial
cellProximal
convolutedtubule
Glomerulus
Table 1 Major causes of acute renal
failureaCauses/characteristics
HypovolemiaLow cardiac outputRenal hypoperfusion due to
impaired
autoregulationIatrogenic renal hypoperfusionAltered renal
systemic vascular resistance ratio
(ie, relationship between systemic vasodilatationand renal
vasoconstriction)
Renovascular obstructionDisease of glomeruli or renal
microvasculatureAcute tubular necrosisInterstitial nephritisToxic
agents
Endogenous: myoglobin (as in rhabdomyolysis)Exogenous: chemicals
(eg, organic solvents orheavy metals), medications (eg,
aminoglyco-sides), other materials (eg, contrast media)
Obstruction of all urine flow caused by tumors orstrictures of
the ureters, bladder neck (mostcommon, can completely block flow
from bothkidneys), or urethra
Type
Prerenal
Intrarenal
Postrenal
a Derived from data in Brady and Brenner,14 Huether,15
Gallagher-Lepak,16 andPorth.17
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Prerenal failure, the most com-mon cause of ARF,14 is caused by
amild to moderate decrease in RBF,14
which decreases glomerular filtra-tion.15 Hypovolemia, whether
rela-tive (eg, through third spacing) orabsolute (eg, through blood
loss), orlow cardiac output decreases renalperfusion. The renal
vasoconstrictioncaused by decreased cardiac outputultimately causes
renal hypoperfu-sion with a general impairment of therenal
regulatory response.15,16,18 How-ever, renal damage generally does
notoccur, and if it does, it can usually bequickly reversed if
treated promptly.14
Intrarenal failure is categorizedaccording to the location where
itoccurs, such as tubular, interstitial,or glomerular.16 It is
often caused bythe same processes that cause prere-
nal failure, such as ischemia, whichmay be caused by severe
hypoten-sion due to hypovolemia, or nephro-toxins.9,14,15 Acute
tubular necrosis iscommon and often occurs after sur-gery.
Different parts of the kidneyare more sensitive to the effects
ofischemic injury than are others. Forexample, the proximal tubules
dependon mitochondrial respiration forenergy,9 and any interruption
inperfusion decreases oxygen delivery.Intrarenal ischemia generates
releaseof oxygen free radicals and inflam-matory mediators, such as
tumornecrosis factor (TNF-), whichcause marked tissue injury.9
Therenal medulla is more susceptiblebecause it becomes more
hypoxicthan the renal cortex does withdecreased blood flow.9,15
Although generally rare, postrenalfailure is generally
characterized byblockage of all urine flow by obstruc-tion of the
ureters, bladder neck, orurethra.14,16 The obstruction leads to
aretrograde urinary flow into the renalstructures because urine
cannot beexpelled. Over hours to days, renalstructures gradually
distend, leadingto a decrease in the overall GFR.14
Systemic Effects of Mechanical Ventilation
Recent evidence suggests thatmechanical ventilation may
contributeto the pathogenesis of ARF, and sev-eral mechanisms have
been proposedto explain the association9,19 (Figure3). One possible
mechanism is com-promise of RBF by permissive hyper-capnia or
permissive hypoxemia.
Figure 3 Mechanisms associated with mechanical ventilation that
may lead to acute renal failure.Based on data from Kuiper et al9
and Lee and Slutsky.19
Positive-pressuremechanicalventilation
PaCO2 PaO2
Renal blood flow
Renalvasoconstriction
Renalvasoconstriction?
Proinflammatorycytokine release
Nephrotoxicmediators
Bacterialtranslocation
Ischemia
Acute renal failure
Renal blood flow
Cardiacoutput
Urine outputCreatinine clearanceFraction of sodium
absorption
Tidalvolume
Ventilation/oxygenation
Positive end-expiratory pressure
Biophysical injuryShear
StretchAlveolar-capillary permeability
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Another possibility is a pulmonaryinflammatory reaction in
responseto biotrauma, with the release ofinflammatory mediators and
theinduction of a systemic inflamma-tory reaction.9,20
Hypercapnia and HypoxemiaMechanical ventilation, through
the manipulation of PaCO2 andPaO2, may affect vascular
dynamicsvia activation or inactivation ofvasoactive factors such as
nitricoxide, angiotensin II, endothelin,and bradykinin.9
Hypercapnia isinversely correlated with RBF andcauses renal
constriction by directand indirect mechanisms.9
The direct mechanisms includeactivation of the sympathetic
nervous
system by release of norepineph-rine. The increased
sympatheticactivity reduces RBF and GFR andcontributes to a
nonosmotic releaseof vasopressin.9
The indirect mechanism is adecrease in systemic vascular
resist-ance due to systemic vasodilatation.The decrease leads to
further releaseof norepinephrine and stimulationof the
renin-angiotensin-aldosteronesystem, causing decreased RBF21
(Figure 4). These hypercapniceffects occur independently of
PaO2and determine the renovascularresponse to changes in
arterialblood gas parameters.9
Severe hypoxemia (PaO2
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67
affect cardiac function, even inpatients not receiving
mechanicalventilation.22 In healthy individuals,cardiovascular
effects appear to bedirectly related to the amount ofpressure
change within the thorax.22
Positive-pressure mechanical venti-lation markedly affects
cardiac per-formance by acting on preload andcardiac output.23,24
Intrathoracicpressures influence the epicardiumand affect the
function and volumeof both ventricles. Decreased intra -thoracic
pressures usually causedecreased transmural pressures(difference
between intraventricularand pleural pressures25,26), and
thedecreases in transmural pressureassist in ventricular filling.22
Thus,if positive pressure increases pleuralpressure, transmural
pressure andafterload are decreased.22,26 Positiveintrathoracic
pressure impairs venousreturn, decreases ventricular
disten-sibility,24 and causes decreased ven-tricular filling. The
decreased venousreturn leads to a decrease in rightventricular
preload, which throughsustained pressure changes in
thecardiopulmonary vasculature leadsto a sustained, decreased left
ven-tricular afterload.22,27 Ultimately,decreased left ventricular
preloaddecreases left ventricular afterload.These changes reduce
cardiac out-put because although left ventricularafterload is
reduced, the decreasedleft ventricular filling has a greatereffect
on cardiac output.28 In patientswith pulmonary disease, this effect
isexacerbated. For example, in patientswith reduced lung volumes,
as mightoccur in obstructive disorders ordecreased functional
residual capac-ity (eg, supine positioning, anesthe-sia),
resistance in the extra-alveolarpulmonary vessels can occur.22
Positive end-expiratory pressure(PEEP) may reduce cardiac
outputby causing a further increase inintrathoracic pressures,
which com-presses the pulmonary vasculature.29
This change increases right ventric-ular afterload, leading to a
decreasein emptying and ultimately a decreasein left ventricular
preload.29-32 Left ven-tricular distensibility also decreases,with
an associated decrease in leftventricular function, especially
withPEEP greater than 15 cm H2O. Thedecrease in left ventricular
functioncauses a decrease in venous returnto the right side of the
heart and anincrease in pulmonary artery pres-sures.30-32 In
studies in animals, theeffects of PEEP on hemodynamicparameters
have varied. In one study,PEEP up to 14 cm H2O did notadversely
affect ejection fraction orleft ventricular end-diastolic volumebut
at levels greater than 21 cmH2O had marked effects on these
2parameters.33 However, in otherstudies, PEEP at 10 to 14 cm
H2O,markedly affected cardiac index.33
Harmful effects of PEEP may be moreimportant with patients with
addi-tional comorbid conditions such asmay be found in a systemic
inflam-matory response. However, euvolemicpatients without
additional comor-bid conditions are considered to beat less risk34
because blood vessels inpatients with adequate volume areless
likely to collapse.26
Because the kidneys receive20% to 25% of cardiac output,
anydecrease in cardiac output causedby PEEP affects RBF.9 RBF is
prima-rily affected by PEEP because ofsympathetic activation
related toincreased plasma renin activity.29
Results of other studies9,35 have alsosuggested that although
total RBF
is relatively unchanged, blood flowis redistributed from the
cortical tothe juxta medullary nephrons. Thisredistribution would
be associatedwith decreased urine output,decreased creatinine
clearance, andan increased fractional resorptionof sodium35 (Figure
4).
PEEP further affects the hormonaland sympathetic pathways.
Theeffect is due to an increase in sym-pathetic tone, which is
caused byincreased plasma renin activity anddecreases GFR because
of decreasedblood flow. PEEP has a transienteffect on aortic blood
pressure, andthis effect reflexively activates thesympathetic
nervous system throughaortic and (sino)carotid barorecep-tors.
Changing renal function thenslowly affects intravascular
volume.9
Ventilator-Induced Lung Injuryand Cytokine Response
In addition to altering RBF,mechanical ventilation alters
renalfunction through the release ofproinflammatory
cytokines.Researchers20,36-38 have shown a linkbetween mechanical
forces in dis-eased lungs and the resultinginflammation and/or
rupture ofalveoli, which leads to the release ofproinflammatory
cytokines. Diseasedlungs such as those that occur invarious
respiratory disease syndromeshave smaller capacities than dohealthy
lungs, a characteristic thatcan make the diseased organs
moresusceptible to mechanical injurythrough mechanical
ventilation.39
As alveoli repeatedly open and close,more injury occurs through
shearstresses.40 This situation can lead toregional lung injuries,
a processcalled recruitment/derecruitment.41
Because of the collapsed areas (as
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may occur in atelectasis), smallerareas are available for
mechanicalventilation. This decrease leads toexcessive dilatation
of the remainingareas of normally aerated lung tissuethat are
naturally more compliant(nonatelectatic).41,42 In fact, the
ini-tial trigger of ventilator-induced lunginjury (VILI) is
mechanical injury,not inflammation.43 Therefore, ifmechanical
injury is reduced, therisk for VILI is reduced.
Mechanical forces affect fibers ofthe extracellular matrix and
alveolarcells, producing alveolar cell strain.39
The fibers of the extracellular matrixsystem contain collagen
and elastinthat connect the endothelium andepithelium. The elastin
is springlikeand allows the lungs to return totheir resting state
during exhalation.If the extracellular matrix fiber sys-tem is
overdistended through high-volume or high-pressure ventilation,the
fibers stretch and cannot recoilfully. The collagen is fairly
nonelasticand acts as a stop-length fiber.39 Itsability to distend
is finite, and ifoverdistended, it can rupture, just asa rubber
band does that is stretchedtoo far (Figure 5).
Three-quarters of all lung cells(by volume) are located in
gas-exchange regions. Type II epithelialcells (surfactant) are
located in alve-olar corners. Type I epithelial cells,which account
for approximately90% of the alveolar surface, are flatand wide. A
single type I epithelialcell may have up to 4 endothelialcells
embedded in it, in a sandwich-like manner.39 In most alveolar
struc-tures, type I epithelial cells share acommon basal membrane
withendothelial cells (Figures 6 and 7).This characteristic
suggests that thecells are mechanically coupled.
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Figure 5 Stretch and rupture of fibers in the extracellular
matrix.Based on data in Gattioni et al.39
Epithelium
Epithelium
Alve
olus
Flui
d
Bacterialcytokines
Endothelium
Endothelium
Figure 6 Air-blood barrier.Reprinted from Weaver,44 with
permission.
Alveolus
Type I epithelial cell
Type II epithelial cell
Endothelial cell
Red blood cell
Type 1 epithelial cell
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With its associated fibroblasts, thefiber system and myosin and
actinfilaments contribute to mechanicalsupport and are located in
the basalmembrane (extracellular matrix).The epithelial and
endothelial cellsare anchored to the basal membranevia
integrins.39
All of the anchored cells accom-modate as stretch and strain
areapplied, but only to a point.39 Thecells react to strain-induced
defor-mation by recruiting intracellularlipids to the cell surface
to reinforceor seal the plasma membranes.39
This process causes an upregulationof inflammatory cytokines. As
thealveolar cell surfaces increase because
of the addi-tional stretch,the progressivestrain
causesmacrophages toproduce inter-leukin 8 (IL-8),43
which recruitsneutrophils tothe site, andmetallopro-teins,
whichremodel theextracellularmatrix.39 In ananimal model,a 50%
surfacestrain wasequivalent to atotal volumechange greaterthan
total lungcapacity, and70% of the cells died.39
Ultimately, neu-trophil recruit-ment leads toinflammation
in proportion to strain.39 Damage isincreased by the duration of
theinjury, the amplitude of the pres-sures, and frequency of the
injury.
As strain increases in the pul-monary capillaries, the
capillarymeshwork begins to flatten, whereasthe corner vessels
maintain orincrease patency.39 The increasedresistance to blood
flow causes anincrease in pulmonary artery pres-sures and an
increase in filtrationrate in excess of the increased lymphflow;
the result is accumulation offluid in the interstitial spaces.
Pul-monary edema impairs gas exchangeand promotes formation of
hyalinemembranes and infiltration of neu-
trophils. Furthermore, the increasedpermeability of the
capillary networkcauses increased hydrostatic pres-sure, and
possibly an increase inneutrophil-induced inflammation.
The increased strain inducesbacterial translocation within
thealveolar system46 (Figure 5). Repeatedopening and closing of
distal alveolimay cause shearing of epithelial lay-ers, which are
extremely thin44,45
(Figures 6 and 7). With high-volumeventilation, surfactant is
then inac-tivated, primarily because of atelec-tasis. Subsequently,
epithelialdesquamation may cause easierbacterial access to the
bloodstream.The effect of higher peak inspiratorypressure without
PEEP may causeintra-alveolar edema as alveolarseptal walls thicken,
proteinaceousfluid accumulates, and neutrophilsinfiltrate.43
Studies38,43 in animal models inrecent years also showed that
high-tidal-volume ventilation coupledwith low PEEP created a
higherpropensity for bacterial translocationinto the bloodstream.
However, PEEPcan stabilize alveoli and seems toreduce the risk of
microatelectasis.43
The ultrastructural changes tolung parenchyma include damageto
endothelial and epithelial cells.46,47
Damaged endothelium then releasesinflammatory mediators. The
medi-ators amplify endothelial injurydirectly or indirectly by
recruitinginflammatory cells into the vascular,interstitial, and
alveolar spaces. Themediators released, such as TNF-and -thrombin,
activate proteinkinase Cdependent signaling path-ways. This
activation of proteinkinase C isoforms causes endothe-lial
cytoskeletal elements to contract,enhancing barrier
dysfunction.
Figure 7 Alveolar cell walls. Only 2 thin cells, the
alveolarepithelial cell and the capillary endothelial cell,
separate thealveolar airspace from fluid in the
capillary.Abbreviation: RBC, red blood cell.Reprinted from
Bender,45 with permission.
Alveolar airspace
Capillaryendothelium
Basementmembrane
Epithelialcell
RBC
Alveolar airspace
Interstitium
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Some of the cytokines (eg, angio -tensins, bradykinin,
-thrombin,thromboxane, prostacyclin, andendothelin) have important
vaso-motor effects48-53 (Table 2). Metabo-lism may be impaired
by
endothelial cell damage, which maylead to adverse effects on
interstitialfluid fluctuations.47 These alteredlevels of
endothelium-derivedvasoactive mediators contribute
tomicrocirculatory dysfunction,
including release of reactive nitro-gen and oxygen species, and
post-capillary resistance may be increasedthrough microcirculatory
dysfunc-tion. As the capillary pressuresincrease, pulmonary edema
worsens,
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Table 2 Effects of cytokines and mediatorsCytokine or
mediator
Angiotensin50
Bradykinin49,53
-Thrombin53Thromboxane48
Endothelin51
Fas9,55
Soluble Fas ligand (FasL)9,54,55
Serotonin52
Tumor necrosis factor (TNF-)9,54
Interleukin 69,54
Interleukin 810,55
Effects/comments
Is a vasoconstrictor approximately 40 times stronger than
noradrenalineCauses primarily arteriolar vasoconstriction
(splanchnic, renal, and cutaneous vessels) Also causes venous
vasoconstriction, leading to reduced blood volumeIn the kidney,
causes vasoconstriction of efferent glomerular arterioles,
maintaining arterial pres-
sure sufficient for glomerular filtrationStimulates secretion of
aldosterone
Is a powerful vasodilator, especially in capillariesIncreases
capillary permeability, inducing edemaStimulates release of
antidiuretic hormoneCauses bronchoconstrictionIs an endogenous
mediator released during inflammation
Is an endogenous mediator released during inflammation
Is produced by plateletsCauses vasoconstrictionIs a potent
hypertensive agentFacilitates platelet aggregation
Causes strong, long-lasting vasconstriction
Reflects renal dysfunction and mediates apoptosis
Causes apoptosis of renal epithelial cellsIncreases levels of
biochemical markers that reflect renal dysfunctionIn combination
with Fas induces apoptosis of glomerular cells
Has cardiovascular effects dependent on dose, species,
condition, and vascular stateCauses either vasoconstriction
(especially in renal vessels) or vasodilatation depending on
vessel
tone and on normal or disease state (vasodilatation if normal;
vasoconstriction if diseased)Causes venous constrictionProbably
causes venous thrombosesPromotes platelet aggregationIncreases
capillary permeabilityMay cause hypertension or hypotension or have
no effectCauses bronchoconstriction
Is the principal cytokine that mediates acute
inflammationStimulates the coagulation pathwayActivates
neutrophilsPromotes extracellular killing by neutrophilsUpregulates
Fas on renal cells, stimulating production of more TNF-,
interleukin 6, and interleukin 8Causes sequestration of glomerular
and tubulointerstitial neutrophilsUpregulates leukocyte adhesion
moleculesAlters vascular tone, causing decreased filtration
fractionIncreases in pulmonary, hepatic, and renal systems when
high tidal volumes occurCorrelates with development of acute renal
failure
Is a proinflammatory cytokine secreted by T cells and
macrophagesStimulates the liver to produce acute-phase
proteinsIncreases production of neutrophils
Is a cytokine produced by macrophages and other cell typesIs
produced by macrophages within alveoliAttracts neutrophils to site
of inflammation
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impairing the bactericidal activityof alveolar
macrophages.38,46,47
Lung injury caused by releaseof inflammatory mediators
furtherreduces the caliber of small airways.The associated increase
in circulat-ing levels of thromboxane A2 andserotonin are linked to
increases inpulmonary artery pressure. Thecellular particulate
material anddebris and the accumulatingperivascular edema cause
additionalobstruction that impairs cardiacoutput. These alterations
in thepulmonary circuit also alter thecompensatory mechanism of
pul-monary hypoxic vasoconstriction.42
Mechanical ventilation has amajor effect on inflammatory
cellsand soluble mediators in lungs.36
Several primary cytokines are releasedthrough the injury and
inflammatoryprocess. They include IL-8,9 IL-6,54,55
and TNF-.9,54 These promoteglomerular and
tubulointerstitialsequestration of neutrophils, upreg-ulation of
leukocyte adhesion mole-cules, and a decrease in filtrationfraction
associated with alterationsin vascular tone9,54 (Table 2).
Increases in tidal volume areassociated with increases in
pul-monary, hepatic, and renal levels ofIL-6, which correlate with
develop-ment of ARF.9 In addition, releaseof soluble Fas ligand
(sFasL), theligand for the receptor Fas, causesapoptosis
(programmed cell death)of renal epithelial cells and leads
toincreased levels of biochemicalmarkers indicative of renal
dysfunc-tion. The Fas-FasL system inducesapoptosis of glomerular
cells.9
Apoptosis in ARF is due to receptor-mediated activators such as
TNFand the Fas-FasL system.9 Cytotoxicevents, such as ischemia,
hypoxia,
and anoxia, as well as oxidant injuriesand nitric oxide, also
lead to apop-tosis.56 Tremblay and Slutsky38
reported a relationship betweenvarious ventilatory modes and
sub-sequent effects on end organs thatincluded increased apoptosis
ofcells in the kidney and small intes-tine and changes in host
immunityand susceptibility to infection.
Areas for Further EvaluationLung-protective mechanical
ventilation techniques are still underinvestigation. These
investigationsshould include determining theoptimal combination of
PEEP andtidal volume. Other areas to exam-ine are different types
of ventilation,such as airway pressure release ven-tilation (APRV)
and high-frequencyoscillatory ventilation (HFOV). Inaddition,
conventional ventilationtechniques should be
reevaluated.Furthermore, nurses should considerthe consequences of
temporary ces-sation of ventilatory support and howcessation may or
may not cause lunginjury. Another area of interest is hownutrition
can affect the inflamma-tory process in critically ill
patientsreceiving mechanical ventilation.All of these areas are
importantbecause potentially preventable lunginjury caused by
mechanical ventila-tion may have deleterious effects onrenal
function.
Lung-Protective VentilationEfforts to decrease the risk of
renal failure induced by mechanicalventilation must include
furtherresearch in lung-protective ventila-tion strategies,
including judiciousapplication of PEEP,57 which in ratmodels can
delay VILI. Because PEEPreduces the pressures required to
ventilate lungs, it may be moreimportant than tidal volume in
pre-venting lung injury. The reductionin pressure delays
overdistention ofthe lungs, reduces the mechanicalenergy load, and
ultimately stabi-lizes damaged alveoli.47 Althoughmuch research in
this area has beendone, information is still needed onwhat
constitutes optimal PEEP.
Optimizing Fraction of Inspired Oxygen
Another way to decrease lunginjury is to reduce pulmonary
inflam-mation. Maintaining the fraction ofinspired oxygen at less
than 0.60may reduce injury caused by oxygenbecause a high fraction
of inspiredoxygen causes formation of cytotoxicoxygen free
radicals.24,54 Of equal inter-est is the phenomenon of
absorptionatelectasis, in which well-ventilatedalveoli empty their
oxygen acrossthe concentration gradient andincrease the possibility
of their col-lapse.24,58 The process is exacerbatedby nitrogen
washout. Breathed air isa combination of multiple gases, ofwhich
nitrogen is the major compo-nent. The combination of gases
isinhaled into the alveoli, where thegases either are absorbed into
theplasma or remain in the alveoli.Nitrogen is not particularly
solublein the plasma; therefore, larger con-centrations remain in
the alveoli,helping the alveoli maintain theirstructure. If the
nitrogen in the alve-oli is replaced by other gases, suchas excess
amounts of highly diffusibleoxygen, the alveoli lose much of
theirability to retain their open structure.59
Tidal Volume ControlOptimizing tidal volume reduces
the risk of lung overinflation. The
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Acute Respiratory Distress SyndromeNetwork60 recommends
maintain-ing a tidal volume of 6 mL/kg, andplateau pressures less
than 30 cmH2O reduce barotrauma and decreasethe release of
inflammatory media-tors. However, additional research43
has suggested that compared withlow tidal volumes coupled with
highPEEP, which decrease alveolar insta-
bility, low tidal volumes coupledwith low PEEP may actually be
inju-rious, causing increased release ofIL-8. Although mechanical
injurymay be reduced, optimal tidal vol-umes have not yet been
determined.
Airway Pressure Release Ventilation
APRV does not add tidal volumeventilation to baseline airway
pres-sures.61 Instead it decreases airwaypressure to less than
baseline pres-sure to augment ventilation.34 Thisaugmentation
allows patients tobreathe spontaneously and releasesairway pressure
from an elevatedbaseline value to stimulate expira-tion. This
elevated baseline improvesoxygenation while timed airwaypressure
release aids in carbon diox-ide removal. The advantages of
thisventilation mode include decreasedlung injuries because of
lower peakpressures. Pressure limits also elimi-nate or reduce
alveolar overdisten-tion and high-volume lung injury.Maintaining
low airway pressurelimits lung injury by decreasing rep-
etitious alveolar opening. BecauseAPRV does not increase
intrathoracicpressures, venous return is not com-promised. This
situation leads to animproved cardiac output because aspatients
breathe spontaneously,associated decreases in
intrathoracicpressures facilitate venous return.34
Disadvantages of APRV include per-missive hypercapnia,61 which
can be
inversely correlated with RBF andcan cause renal
constriction.9
High-Frequency Oscillatory Ventilation
Use of HFOV has been tradition-ally reserved for neonates and
chil-dren.40,62 In studies in animals,tracheal aspirates had lower
levelsof IL-6, IL-8, TNF-, and othermediators with HFOV than
withstandard positive-pressure ventila-tion strategies. HFOV is
also beingevaluated as a treatment for adultswith lung injuries.63
Studies41,64 haveshown that HFOV can provide ade-quate gas exchange
with small tidalvolumes and high end-expiratorypressures without
producing alveo-lar overdistention. Decreased alve-olar distention
should result indecreased VILI, which in turn maylead to further
reduction in alveolarinflammatory processes due tomechanical
injury. However, poten-tial complications associated withHFOV could
outweigh the benefits.In a study of adults with acute respi-ratory
distress syndrome, Chan et al64
found that central venous pressureand pulmonary artery
occlusionpressures increased, and clinicallyinsignificant decreases
in cardiacoutput and some decreases in strokevolume index and
end-systolic anddiastolic area indexes occurred. In astudy in pigs
with normal lungs,Roosens et al65 found that HFOV wassafe and
effective but did not improve
mortality rates and in fact greatlyelevated intrathoracic
pressures.Although this method of ventilationprovides valuable lung
protectionand may prevent VILI, more researchis needed to discover
how significantthe changed hemodynamic parame-ters affect renal
function.
Traditional Mechanical VentilationSome of the more
traditional
strategies to reduce the impact ofmechanical ventilation on
cardiacoutput in patients with reducedlung volume include assisted,
non-invasive ventilation modes such ascontinuous positive airway
pressure,bilevel positive airway pressure, andpressure-support
ventilation. Theseventilation methods help recruitalveoli while
reducing adverse car-diovascular effects, although moreresearch is
needed in this area.22
Suctioning TechniquesSuctioning in patients receiving
mechanical ventilation needs to befurther examined. PEEP can
impairsuctioning because of the pressure
72 CRITICALCARENURSE Vol 29, No. 2, APRIL 2009
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Nurses who care for patients receiving mechanicalventilation
must recognize the possible renal conse-quences of this pulmonary
intervention.
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73
gradients between the suctioncatheter tip, the end of the
endotra-cheal tube, and the alveoli. The pos-itive pressure that is
blown throughthe end of the endotracheal tubemaintains PEEP within
the alveolidespite the negative pressure in thesuction catheter
created duringclosed-system suctioning. This posi-tive pressure
forces the secretions toflow distally, away from the
suctioncatheter66 and has the effect of lay-ering the secretions
around thealveolar walls. In the past, nursesattempted to overcome
the layeringeffect by instilling normal salineinto the endotracheal
tube, a prac-tice that is now considered unhelp-ful and possibly
harmful.67,68 Withopen-system suctioning methods,such as stopping
positive-pressureventilation during the suctioning,the pressure
gradient is zero and thecatheters can easily remove
availablesecretions.66,69 However, stoppingPEEP, for even short
periods, facili-tates rapid alveolar derecruitment39
and requires higher pressures afterthe intervention to recruit
lost alve-oli. These higher pressures increasethe risk of creating
higher intrapul-monary stresses and often lead toadditional
stress-induced lung injury.It may take several hours before
thecollapsed alveoli are recruited again.47
NutritionNew enteral nutrition formulas
can lead to improved mortality andmorbidity in critically ill
patients
receiving mechanical ventilation.70,71
These low-carbohydrate, high-fatformulations are enriched in
antiox-idants, eicosapentaenoic acid, and-linolenic acid. They can
control thedevelopment of proinflammatorymediators.20,70,71
Interestingly, com-pared with patients who received tra-ditional
enteral feedings, patients whoreceived these special
formulationshad lower total neutrophil counts,had decreased
alveolar levels of IL-6and IL-8, were weaned from mechani-cal
ventilation at a much higher rate,and had less end-organ
failure.20,70
ConclusionNo consensus exists that positive-
pressure ventilation impairs renalfunction, although evidence
that itdoes is mounting. Nurses who carefor patients receiving
mechanicalventilation must recognize the pos-sible renal
consequences of this pul-monary intervention. Astute
nursingassessments of pulmonary and renalfunction are required.
Additional nursing research isneeded to examine the effects
ofdifferent suctioning techniques onpulmonary function. What is
theimpact of intermittent cessation ofpositive pressure on overall
out-comes? In addition, could the valueof being able to transport
patientsfor diagnostic purposes be balanced,or overshadowed, by the
possibleharm of cessation of positive-pressureventilation to some
patients fragilepulmonary condition? What couldbe considered
optimal combinationsof PEEP and tidal volume for differ-ent
conditions? A particularly inter-esting topic for further research
isthe potentially adverse renal effectsof treating patients with
vasopressinand norepinephrine for hypotension.
Are the effects of treatment the sameas those of the endogenous
releaseof those substances? Could thistreatment lead to activation
of thesympathetic nervous system, thusdecreasing RBF and GFR?
Healthcare providers should be aware thattreatments that benefit
one organsystem may adversely affect another.Patients are not
exclusively a respira-tory system, or a renal system, or ahepatic
system, or any other specificorgan system. They are an integra-tive
whole and must be treated asthat whole, with the realization
thatany intervention that affects onepart of a patient may cause
unex-pectedand unwelcomeresultsin another body system.27 CCN
AcknowledgmentsThanks to Mark Yerrington, visual
informationspecialist at William Beaumont Army MedicalCenter, for
his creative assistance with the figures.The opinions or assertions
contained herein arethe private views of the author and should
notbe construed as official or as reflecting theviews of the US
Army Medical Department,Department of the Army, or the Departmentof
Defense. Citations of commercial organiza-tions and trade names in
this report do notconstitute an official Department of the Armyor
Department of Defense endorsement orapproval of such products or
services of theseorganizations.
Financial DisclosuresNone reported.
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CE Test Test ID C0922: Acute Renal Failure and Mechanical
Ventilation: Reality or Myth?Learning objectives: 1. Understand the
pathophysiology of acute renal failure 2. Describe the systemic
effects of mechanical ventilation 3. Recognize howmechanical
ventilation may contribute to the pathogenesis of acute renal
failure
Program evaluationYes No
Objective 1 was met Objective 2 was met Objective 3 was met
Content was relevant to my
nursing practice My expectations were met This method of CE is
effective
for this content The level of difficulty of this test was: easy
medium difficult
To complete this program, it took me hours/minutes.
Test answers: Mark only one box for your answer to each
question. You may photocopy this form.
1. Where does urine concentration and dilution occur?a. Proximal
tubules c. Distal tubulesb. Loops of Henle d. Collecting duct
2. What is a result of decreased systemic arterial pressure?a.
Increased filtrationb. Increased excretionc. Renal arterial
arteriolar vasoconstrictiond. Increased renal blood flow
3. What is a result of increased systemic arterial pressure?a.
Increased excretionb. Renal arteriolar vasoconstrictionc. Decreased
filtrationd.Increased intravascular volume
4. What is the most common form of acute renal failure (ARF)?a.
Prerenal c. Intrarenalb. Intrinsic d. Postrenal
5. What is a cause of postrenal ARF?a. Acute tubular necrosisb.
Interstitial nephritisc. Glomerulonephritisd.Bilateral ureteral
obstructions
6.Hypovolemia causes which form of ARF?a. Prerenal c.
Intrarenalb. Intrinsic d. Postrenal
7. Hypercapnia causes renal constriction by which direct
mechanism?a. Decreased systemic vascular resistanceb. Sympathetic
nervous system activationc. Renin-angiotensin-aldosterone system
stimulationd.Systemic vasodilatation
8.Which PaO2 will cause renal vasoconstriction and increased
renalvascular resistance?a. 38 mm Hg c. 68 mm Hgb. 58 mm Hg d. 88
mm Hg
9. What do positive intrathoracic pressures cause?a. Augmented
venous returnb. Increased right ventricular preloadc. Increased
left ventricular preloadd.Decreased left ventricular afterload
10. What is associated with the redistribution of blood flow
from thecortical to the juxtamedullary nephrons?a. Polyuriab.
Increased creatinine clearancec. Increased glomerular filtration
rated.Increased fractional resorption of sodium
11. What is the principal cytokine that mediates acute
inflammation?a. Tumor necrosis factor- c. Bradykininb. Angiotensin
d. Interleukin 8
12. What is the effect of positive end-expiratory pressure on
suctioning?a. No effect on suctioningb. Easier suctioning through
the inverse pressures generated by positive
end-expiratory pressure and tidal volume settingsc. More
difficult suctioning because positive pressure ventilation can
layer
secretions around alveolar wallsd.More tenacious secretions,
requiring instillation of normal saline into
the endotracheal tube
13. What is associated with special enteral formulations?a.
Higher neutrophil countsb. Increased alveolar interleukin 6
levelsc. Less end-organ failured.Higher failure-to-wean rates
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Caroline C. BrodenAcute Renal Failure and Mechanical
Ventilation: Reality or Myth?
Published online http://www.cconline.org 2009 American
Association of Critical-Care Nurses
2009, 29:62-75. doi: 10.4037/ccn2009267Crit Care Nurse
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byAmerican Association ofCritical-Care Nurses, published
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