crit care nurse-2009-broden-62-75.pdf

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 www.ccnonline.org

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

by guest on March 2, 2015http://ccn.aacnjournals.org/Downloaded from

www.ccnonline.org CRITICALCARENURSE Vol 29, No. 2, APRIL 2009 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


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


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



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


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


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


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.


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



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


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,


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



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


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


Nurses who care for patients receiving mechanicalventilation must recognize the possible renal conse-quences of this pulmonary intervention.



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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eLettersNow that youve read the article, create or contributeto an online discussion about this topic using eLetters.Just visit www.ccnonline.org and click Respond toThis Article in either the full-text or PDF view ofthe article.


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29. Lefrant J-Y, Juan J-M, Bruelle P, et al.Regional blood flows are affected differentlyby PEEP when the abdomen is open orclosed: an experimental rabbit model. CanJ Anesth. 2002;49(3):302-308.

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34. Frawley PM, Habashi N. Airway pressurerelease ventilation and pediatrics: theoryand practice. Crit Care Nurs Clin North Am.2004;16:337-348.

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37. Slutsky AS. Lung injury caused by mechan-ical ventilation. Chest. 1999;116(1 suppl):9S-15S.

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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

For faster processing, takethis CE test online atwww.ccnonline.org

(CE Articles in this issue)or mail this entire page to:

AACN, 101 Columbia Aliso Viejo, CA 92656.

Test ID: C0922 Form expires: April 1, 2011 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 10 correct (77%) Category: CERP A Synergy CERP ATest writer: Denise Hayes, RN, MSN, CRNP

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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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