Clinical Article

Acute Renal Failure and

Mechanical Ventilation:
Reality or Myth?
Caroline C. Broden, RN, MSN, ACNP, CCNS, CCRN

PRIME POINTS

What changes associ-

ated with mechanical ventilation can acute renal

failure be linked to?

How does pulmonary

inflammation and/or rupture of alveoli affect renal

function?

Research is needed on

lung-protective ventilation
strategies, including judicious use of PEEP, optimal
fraction of inspired oxygen, tidal volume control,
airway pressure release
ventilation, high-frequency
oscillatory ventilation, and
traditional mechanical
ventilation.

cute renal failure (ARF)

is a common complication in critically ill
patients. In a 5-year
analysis of incidence
and mortality published in 2002,
Pruchnicki and Dasta1 estimated
that it occurs in up to 25% of all
patients admitted to the hospital
with a critical illness. In a more recent
multicenter, multinational analysis2
of almost 30000 intensive care unit
(ICU) admissions in 54 study centers in 23 countries, ARF developed
during the hospital stay in 5.7% of
all the patients. Of those patients,
approximately 60% died, with a
higher prevalence among patients
receiving renal replacement therapy.

CEContinuing Education
This article has been designated for CE credit. A
closed-book, multiple-choice examination follows this article, which tests your knowledge of
the following objectives:
1. Understand the pathophysiology of acute
renal failure
2. Describe the systemic effects of mechanical
ventilation
3. Recognize how mechanical ventilation may
contribute to the pathogenesis of acute renal
failure
2009 American Association of CriticalCare Nurses doi: 10.4037/ccn2009267

Although dialysis techniques have

markedly improved since the 1980s,
resulting in improved outcomes,
ARF remains an independent predictor of hospital mortality in critically ill patients.2,3 In fact, the process
of or the comorbid conditions associated with the development of ARF
appear to contribute to overall mortality. Thus, patients admitted to
the ICU who subsequently have
renal failure seem to have worse
outcomes than do patients admitted
with preexisting acute renal failure.4
Development of ARF in patients
who are not critically ill is associated
with significant increases in mortality and in hospital costs due to longer
lengths of stay and treatments
related to ARF. When ARF develops
in patients with critical illness, the
costs and adverse outcomes increase
even more dramatically.5-7 Liangos
et al6 used data from the 2001
National Hospital Discharge Survey
to explore the relationship between
ARF and hospital length of stay and
mortality. Patients with ARF had a
2-day increase in length of stay, a
higher mortality rate, and an adjusted
odds ratio of 2.0 for discharge to
short- or long-term care facilities. In

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a smaller study, Vieira et al8 found a

link between acute kidney injury and
unsuccessful weaning from mechanical ventilation resulting in increases
in duration of mechanical ventilation,
lengths of stay, and ICU mortality.
Although common, perhaps ARF
is not inevitable. Evidence suggests a
link between positive-pressure ventilation and ARF.9 In this article, I briefly
review renal anatomy and physiology,
acute renal failure, the systemic effects
of mechanical ventilation, and how
attempts to salvage respiratory function may actually compromise other
end-organ function.

Glomerular capsule Neck

Afferent vessel
Efferent vessel
Intertubular capillaries
Interlobular vein
Interlobular artery
Spiral tubule

Although their primary function is

to filter and excrete wastes and toxins,
the kidneys also regulate fluids, electrolytes, and acid-base balance. They
receive 20% to 25% of the entire cardiac output. More than half of the
blood flow through the kidney consists
of plasma. Of the renal plasma flow,
approximately 20% is filtered through
the glomeruli (the glomerular filtration rate [GFR] is an estimate of the
amount of blood that passes through
each minute). The remaining plasma
flows through efferent arterioles.10,11
The amount that flows through these
arterioles depends directly on renal
blood flow (RBF), and any alterations
in blood flow will alter the GFR.
Each kidney receives its blood
supply through a single renal artery

2nd convol
tub.
Cortical substance

Henles Ascending limb

loop Descending limb

Boundary zone
Collecting
tub.

Arterial arch
Venous arch

Medullary
substance

Duct of Bellini

Figure 1 The nephron.

Reprinted from Gray.12

that divides into different branches,

which divide even further to provide blood to all of the nephrons.
The nephrons are unique because
they have 2 capillary systems: the
high-pressure glomeruli and the
low-pressure reabsorptive peritubular capillary network. Each glomerulus is flanked by afferent and efferent
arterioles (Figures 1 and 2), which
selectively constrict or dilate to
regulate the pressure within the
glomeruli.11 Blood passes through

Author
CPT Caroline Broden is an acute care nurse practitioner in the US Army Nurse Corps at
William Beaumont Army Medical Center, El Paso, Texas.
Corresponding author: CPT Caroline Broden, RN, MSN, ACNP, CCNS, CCRN, Department of Nursing, William Beaumont
Army Medical Center, 5005 N. Piedras Ave., El Paso, TX 79920 (e-mail: ctbroden@msn.com).
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, reprints@aacn.org.

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Irregular
tub.

Junctional tub.

Arteria recta

Renal Anatomy and

Physiology

1st convoluted tubule

the glomerulus and into structures

called Bowmans capsules (Figure 2).
The glomerular capillary membrane has 3 layers: the inner capillary endothelium, the basement
membrane, and the outer capillary
epithelium10,11 (Figure 2). The glomerular filtrate passes through all 3 layers, through the nephrons, and into
the proximal tubule. From there,
the filtrate continues to travel through
the loops of Henle and into distal
tubules before passing on to the
collecting ducts (Figure 1). At each
step, fluids, ions, and electrolytes
are exchanged.
Of note, nephrons are the functional units of the kidney and consist of the cortical nephrons (85%)
and juxtamedullary nephrons
(15%).13 The primary functions of

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Parietal
Pores in epithelial cell
endothelium

Distal convoluted tubule

Macula
densa

Afferent
arteriole

Mesangial
cell

Mesangial
matrix

Acute Renal Failure

Juxtaglomerular cells
Efferent
arteriole

Glomerulus
Visceral
epithelium
(podocytes)
Bowman
capsule
Parietal
epithelial
cell
Proximal
convoluted
tubule

Podocytes
(visceral cells)

Capillary
lumen

Pseudofenestrations
with central knobs

Basement
membrane
Podocyte
(cell body)
Pedical
(cell process)
Capsular slits
(filtration)

Capillary
endothelium

Figure 2 Bowmans capsule and glomerular apparatus.

Adapted from Huether,10 2002, with permission from Elsevier.

cortical nephrons are excretory and

regulatory, whereas the primary
function of juxtamedullary nephrons
is urine concentration and dilution
through a countercurrent mechanism as the urine travels through
the long loops of Henle.13 Although
the cortical nephrons have loops of
Henle, the loops are of various lengths
and do not include the thin ascending loop that is present in the juxtamedullary nephrons. The long,
ascending loops and the vasa recta
are responsible for urine concentration and dilution.13 (The vasa recta
are vessels that closely follow the
loops of Henle and with them,
through a countercurrent mechanism, play an important role in
urine concentration and dilution.13)
Autoregulation maintains the
pressure within Bowmans capsules
at a reasonably constant rate of 80
to 180 mm Hg.10 At higher pressures,
the afferent arterioles constrict, preventing increased glomerular blood
flow. At lower pressures, the arterioles dilate, increasing glomerular

vasodilatation and increased filtration and excretion of fluids.10,11

ARF is defined as a sudden

reduction (from hours to days) in
GFR14 and is associated with an
accumulation of nitrogenous wastes
and alterations in fluid, electrolyte,
and acid-base balance.15-17 ARF may
be associated with decreased urine
output and is often manifested by
an output of less than 30 mL/h or
less than 400 mL/d.15 Fortunately,
ARF can usually be reversed if
detected early.17 ARF is classified as
prerenal, intrarenal, or postrenal
(Table 1). It has many causes, which
can include conditions inherent to a
patients disease process, such as
infections, vascular obstructions,
and severe hypotension. The cause
can also be iatrogenic, such as
administration of contrast medium
or medications.15,16

blood flow. This process maintains

a fairly constant filtration and excretion of fluids and solutes.10 The reflexive relationship between RBF and
arterial pressure is maintained by
neural regulation. With decreased
systemic arterial
pressures, sympa- Table 1 Major causes of acute renal failurea
thetic nerve activType
Causes/characteristics
ity signals the
Prerenal
Hypovolemia
baroreceptors in
Low cardiac output
the aortic arch.
Renal hypoperfusion due to impaired
autoregulation
Decreased presIatrogenic renal hypoperfusion
sures cause renal
Altered renal systemic vascular resistance ratio
(ie, relationship between systemic vasodilatation
arteriolar vasoand renal vasoconstriction)
constriction, which
Intrarenal Renovascular obstruction
decreases filtration
Disease of glomeruli or renal microvasculature
and excretion.
Acute tubular necrosis
Interstitial nephritis
This mechanism
Toxic agents
increases intravasEndogenous: myoglobin (as in rhabdomyolysis)
cular volume and
Exogenous: chemicals (eg, organic solvents or
heavy metals), medications (eg, aminoglycothus increases
sides), other materials (eg, contrast media)
blood pressure.
Postrenal
Obstruction of all urine flow caused by tumors or
Conversely,
strictures of the ureters, bladder neck (most
common, can completely block flow from both
increased syskidneys), or urethra
temic arterial
a Derived from data in Brady and Brenner, Huether, Gallagher-Lepak, and
pressure leads to
Porth.
renal arteriolar
14

15

16

17

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Positive-pressure
mechanical
ventilation
Positive endexpiratory pressure

Ventilation/
oxygenation

PaCO2

PaO2

Cardiac
output

Renal blood flow

Renal
vasoconstriction?

Renal blood flow

Tidal
volume

Biophysical injury
Shear
Stretch
Alveolar-capillary permeability

Proinflammatory
cytokine release

Urine output
Creatinine clearance
Fraction of sodium
absorption

Renal
vasoconstriction

Bacterial
translocation

Nephrotoxic
mediators

Ischemia
Acute renal failure

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

Prerenal failure, the most common cause of ARF,14 is caused by a

mild to moderate decrease in RBF,14
which decreases glomerular filtration.15 Hypovolemia, whether relative (eg, through third spacing) or
absolute (eg, through blood loss), or
low cardiac output decreases renal
perfusion. The renal vasoconstriction
caused by decreased cardiac output
ultimately causes renal hypoperfusion with a general impairment of the
renal regulatory response.15,16,18 However, renal damage generally does not
occur, and if it does, it can usually be
quickly reversed if treated promptly.14
Intrarenal failure is categorized
according to the location where it
occurs, such as tubular, interstitial,
or glomerular.16 It is often caused by
the same processes that cause prere-

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nal failure, such as ischemia, which

may be caused by severe hypotension due to hypovolemia, or nephrotoxins.9,14,15 Acute tubular necrosis is
common and often occurs after surgery. Different parts of the kidney
are more sensitive to the effects of
ischemic injury than are others. For
example, the proximal tubules depend
on mitochondrial respiration for
energy,9 and any interruption in
perfusion decreases oxygen delivery.
Intrarenal ischemia generates release
of oxygen free radicals and inflammatory mediators, such as tumor
necrosis factor (TNF-), which
cause marked tissue injury.9 The
renal medulla is more susceptible
because it becomes more hypoxic
than the renal cortex does with
decreased blood flow.9,15

Although generally rare, postrenal

failure is generally characterized by
blockage of all urine flow by obstruction of the ureters, bladder neck, or
urethra.14,16 The obstruction leads to a
retrograde urinary flow into the renal
structures because urine cannot be
expelled. Over hours to days, renal
structures gradually distend, leading
to a decrease in the overall GFR.14

Systemic Effects of
Mechanical Ventilation
Recent evidence suggests that
mechanical ventilation may contribute
to the pathogenesis of ARF, and several mechanisms have been proposed
to explain the association9,19 (Figure
3). One possible mechanism is compromise of RBF by permissive hypercapnia or permissive hypoxemia.

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Legend

Sympathetic
activity

Kidney

Lungs
Liver

Surface of pulmonary
and renal endothelium:

ACE

Secretion from
an organ

Na+
K+
Tubular Na+ CI+
CIreabsorption and K
excretion. H2O retention H O
2

Stimulatory
signal
Inhibitory signal
Reaction
Active transport
Passive transport

Angiotensinogen

Decrease in
renal perfusion
(juxtaglomerular
apparatus)

Angiotensin I

Angiotensin II

Adrenal gland
cortex
Aldosterone
secretion

Water and salt

retention. Effective
circulating volume
increases. Perfusion
of the juxtaglomerular
apparatus increases.

Renin
Arteriolar
vasoconstriction.
Increase in blood
pressure

Arteriole

Kidney
ADH secretion
Pituitary gland:
posterior lobe

Collecting duct:
H2O absorption

H2O

Figure 4 Renin-angiotensin-aldosterone system.

Abbreviations: ACE, angiotensin-converting enzyme; ADH, antidiuretic hormone.
Reprinted from Rad,21 with permission.

Another possibility is a pulmonary

inflammatory reaction in response
to biotrauma, with the release of
inflammatory mediators and the
induction of a systemic inflammatory reaction.9,20
Hypercapnia and Hypoxemia

Mechanical ventilation, through

the manipulation of PaCO2 and
PaO2, may affect vascular dynamics
via activation or inactivation of
vasoactive factors such as nitric
oxide, angiotensin II, endothelin,
and bradykinin.9 Hypercapnia is
inversely correlated with RBF and
causes renal constriction by direct
and indirect mechanisms.9
The direct mechanisms include
activation of the sympathetic nervous

system by release of norepinephrine. The increased sympathetic

activity reduces RBF and GFR and
contributes to a nonosmotic release
of vasopressin.9
The indirect mechanism is a
decrease in systemic vascular resistance due to systemic vasodilatation.
The decrease leads to further release
of norepinephrine and stimulation
of the renin-angiotensin-aldosterone
system, causing decreased RBF21
(Figure 4). These hypercapnic
effects occur independently of PaO2
and determine the renovascular
response to changes in arterial
blood gas parameters.9
Severe hypoxemia (PaO2 <40 mm
Hg) causes renal vasoconstriction
and increased renal vascular resist-

ance, which leads to renal hypoperfusion, decreased GFR, and functional renal insufficiency. The effects
of moderate hypoxemia on renal
hemodynamics are less understood.
One suggestion is that mild hypoxemia, without simultaneous hypercapnia, may not markedly affect
renal hemodynamics.9 Another suggestion is that acute normocapnic
hypoxemia increases renal vascular
resistance, leading to renal hypoperfusion and decreased GFR.9
Cardiopulmonary Dynamics

The proximity of the pulmonary

and cardiac vasculature within the
thorax and the dynamic mechanical
pressure functions ensure that any
changes in intrathoracic pressures

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affect cardiac function, even in

patients not receiving mechanical
ventilation.22 In healthy individuals,
cardiovascular effects appear to be
directly related to the amount of
pressure change within the thorax.22
Positive-pressure mechanical ventilation markedly affects cardiac performance by acting on preload and
cardiac output.23,24 Intrathoracic
pressures influence the epicardium
and affect the function and volume
of both ventricles. Decreased intrathoracic pressures usually cause
decreased transmural pressures
(difference between intraventricular
and pleural pressures25,26), and the
decreases in transmural pressure
assist in ventricular filling.22 Thus,
if positive pressure increases pleural
pressure, transmural pressure and
afterload are decreased.22,26 Positive
intrathoracic pressure impairs venous
return, decreases ventricular distensibility,24 and causes decreased ventricular filling. The decreased venous
return leads to a decrease in right
ventricular preload, which through
sustained pressure changes in the
cardiopulmonary vasculature leads
to a sustained, decreased left ventricular afterload.22,27 Ultimately,
decreased left ventricular preload
decreases left ventricular afterload.
These changes reduce cardiac output because although left ventricular
afterload is reduced, the decreased
left ventricular filling has a greater
effect on cardiac output.28 In patients
with pulmonary disease, this effect is
exacerbated. For example, in patients
with reduced lung volumes, as might
occur in obstructive disorders or
decreased functional residual capacity (eg, supine positioning, anesthesia), resistance in the extra-alveolar
pulmonary vessels can occur.22

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Positive end-expiratory pressure

(PEEP) may reduce cardiac output
by causing a further increase in
intrathoracic pressures, which compresses the pulmonary vasculature.29
This change increases right ventricular afterload, leading to a decrease
in emptying and ultimately a decrease
in left ventricular preload.29-32 Left ventricular distensibility also decreases,
with an associated decrease in left
ventricular function, especially with
PEEP greater than 15 cm H2O. The
decrease in left ventricular function
causes a decrease in venous return
to the right side of the heart and an
increase in pulmonary artery pressures.30-32 In studies in animals, the
effects of PEEP on hemodynamic
parameters have varied. In one study,
PEEP up to 14 cm H2O did not
adversely affect ejection fraction or
left ventricular end-diastolic volume
but at levels greater than 21 cm
H2O had marked effects on these 2
parameters.33 However, in other
studies, PEEP at 10 to 14 cm H2O,
markedly affected cardiac index.33
Harmful effects of PEEP may be more
important with patients with additional comorbid conditions such as
may be found in a systemic inflammatory response. However, euvolemic
patients without additional comorbid conditions are considered to be
at less risk34 because blood vessels in
patients with adequate volume are
less likely to collapse.26
Because the kidneys receive
20% to 25% of cardiac output, any
decrease in cardiac output caused
by PEEP affects RBF.9 RBF is primarily affected by PEEP because of
sympathetic activation related to
increased plasma renin activity.29
Results of other studies9,35 have also
suggested that although total RBF

is relatively unchanged, blood flow

is redistributed from the cortical to
the juxtamedullary nephrons. This
redistribution would be associated
with decreased urine output,
decreased creatinine clearance, and
an increased fractional resorption
of sodium35 (Figure 4).
PEEP further affects the hormonal
and sympathetic pathways. The
effect is due to an increase in sympathetic tone, which is caused by
increased plasma renin activity and
decreases GFR because of decreased
blood flow. PEEP has a transient
effect on aortic blood pressure, and
this effect reflexively activates the
sympathetic nervous system through
aortic and (sino)carotid baroreceptors. Changing renal function then
slowly affects intravascular volume.9
Ventilator-Induced Lung Injury
and Cytokine Response

In addition to altering RBF,

mechanical ventilation alters renal
function through the release of
proinflammatory cytokines.
Researchers20,36-38 have shown a link
between mechanical forces in diseased lungs and the resulting
inflammation and/or rupture of
alveoli, which leads to the release of
proinflammatory cytokines. Diseased
lungs such as those that occur in
various respiratory disease syndromes
have smaller capacities than do
healthy lungs, a characteristic that
can make the diseased organs more
susceptible to mechanical injury
through mechanical ventilation.39
As alveoli repeatedly open and close,
more injury occurs through shear
stresses.40 This situation can lead to
regional lung injuries, a process
called recruitment/derecruitment.41
Because of the collapsed areas (as

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Epithelium
Alveolus

Endothelium

Epithelium

Endothelium

Fluid

Bacterial
cytokines

may occur in atelectasis), smaller

areas are available for mechanical
ventilation. This decrease leads to
excessive dilatation of the remaining
areas of normally aerated lung tissue
that are naturally more compliant
(nonatelectatic).41,42 In fact, the initial trigger of ventilator-induced lung
injury (VILI) is mechanical injury,
not inflammation.43 Therefore, if
mechanical injury is reduced, the
risk for VILI is reduced.
Mechanical forces affect fibers of
the extracellular matrix and alveolar
cells, producing alveolar cell strain.39
The fibers of the extracellular matrix
system contain collagen and elastin
that connect the endothelium and
epithelium. The elastin is springlike
and allows the lungs to return to
their resting state during exhalation.
If the extracellular matrix fiber system is overdistended through highvolume or high-pressure ventilation,
the fibers stretch and cannot recoil
fully. The collagen is fairly nonelastic
and acts as a stop-length fiber.39 Its
ability to distend is finite, and if
overdistended, it can rupture, just as
a rubber band does that is stretched
too far (Figure 5).
Three-quarters of all lung cells
(by volume) are located in gasexchange regions. Type II epithelial
cells (surfactant) are located in alveolar corners. Type I epithelial cells,
which account for approximately
90% of the alveolar surface, are flat
and wide. A single type I epithelial
cell may have up to 4 endothelial
cells embedded in it, in a sandwichlike manner.39 In most alveolar structures, type I epithelial cells share a
common basal membrane with
endothelial cells (Figures 6 and 7).
This characteristic suggests that the
cells are mechanically coupled.

Figure 5 Stretch and rupture of fibers in the extracellular matrix.

Based on data in Gattioni et al.39

Alveolus

Type I epithelial cell

Type II epithelial cell
Endothelial cell
Red blood cell
Type 1 epithelial cell

Figure 6 Air-blood barrier.

Reprinted from Weaver,44 with permission.

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of the additional stretch,

Alveolar
airspace
the progressive
strain causes
macrophages to
Interstitium
RBC
produce interleukin 8 (IL-8),43
which recruits
neutrophils to
the site, and
metalloproteins, which
remodel the
extracellular
matrix.39 In an
animal model,
Capillary
a 50% surface
Alveolar
endothelium
airspace
strain was
Basement
equivalent to a
membrane
total volume
Epithelial
cell
change greater
than total lung
capacity, and
70% of the
Figure 7 Alveolar cell walls. Only 2 thin cells, the alveolar
cells died.39
epithelial cell and the capillary endothelial cell, separate the
Ultimately, neualveolar airspace from fluid in the capillary.
Abbreviation: RBC, red blood cell.
trophil recruitReprinted from Bender, with permission.
ment leads to
inflammation
in proportion to strain.39 Damage is
With its associated fibroblasts, the
fiber system and myosin and actin
increased by the duration of the
filaments contribute to mechanical
injury, the amplitude of the pressupport and are located in the basal
sures, and frequency of the injury.
membrane (extracellular matrix).
As strain increases in the pulThe epithelial and endothelial cells
monary capillaries, the capillary
are anchored to the basal membrane
meshwork begins to flatten, whereas
via integrins.39
the corner vessels maintain or
increase patency.39 The increased
All of the anchored cells accommodate as stretch and strain are
resistance to blood flow causes an
39
applied, but only to a point. The
increase in pulmonary artery pressures and an increase in filtration
cells react to strain-induced deforrate in excess of the increased lymph
mation by recruiting intracellular
flow; the result is accumulation of
lipids to the cell surface to reinforce
39
fluid in the interstitial spaces. Pulor seal the plasma membranes.
monary edema impairs gas exchange
This process causes an upregulation
and promotes formation of hyaline
of inflammatory cytokines. As the
membranes and infiltration of neualveolar cell surfaces increase because
45

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trophils. Furthermore, the increased

permeability of the capillary network
causes increased hydrostatic pressure, and possibly an increase in
neutrophil-induced inflammation.
The increased strain induces
bacterial translocation within the
alveolar system46 (Figure 5). Repeated
opening and closing of distal alveoli
may cause shearing of epithelial layers, which are extremely thin44,45
(Figures 6 and 7). With high-volume
ventilation, surfactant is then inactivated, primarily because of atelectasis. Subsequently, epithelial
desquamation may cause easier
bacterial access to the bloodstream.
The effect of higher peak inspiratory
pressure without PEEP may cause
intra-alveolar edema as alveolar
septal walls thicken, proteinaceous
fluid accumulates, and neutrophils
infiltrate.43
Studies38,43 in animal models in
recent years also showed that hightidal-volume ventilation coupled
with low PEEP created a higher
propensity for bacterial translocation
into the bloodstream. However, PEEP
can stabilize alveoli and seems to
reduce the risk of microatelectasis.43
The ultrastructural changes to
lung parenchyma include damage
to endothelial and epithelial cells.46,47
Damaged endothelium then releases
inflammatory mediators. The mediators amplify endothelial injury
directly or indirectly by recruiting
inflammatory cells into the vascular,
interstitial, and alveolar spaces. The
mediators released, such as TNF-
and -thrombin, activate protein
kinase Cdependent signaling pathways. This activation of protein
kinase C isoforms causes endothelial cytoskeletal elements to contract,
enhancing barrier dysfunction.

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Table 2

Effects of cytokines and mediators

Cytokine or mediator

Effects/comments

Angiotensin

Is a vasoconstrictor approximately 40 times stronger than noradrenaline

Causes primarily arteriolar vasoconstriction (splanchnic, renal, and cutaneous vessels)
Also causes venous vasoconstriction, leading to reduced blood volume
In the kidney, causes vasoconstriction of efferent glomerular arterioles, maintaining arterial pressure sufficient for glomerular filtration
Stimulates secretion of aldosterone

Bradykinin49,53

Is a powerful vasodilator, especially in capillaries

Increases capillary permeability, inducing edema
Stimulates release of antidiuretic hormone
Causes bronchoconstriction
Is an endogenous mediator released during inflammation

-Thrombin53

Is an endogenous mediator released during inflammation

Thromboxane48

Is produced by platelets
Causes vasoconstriction
Is a potent hypertensive agent
Facilitates platelet aggregation

Endothelin51

Causes strong, long-lasting vasconstriction

50

Fas9,55

Reflects renal dysfunction and mediates apoptosis

9,54,55

Soluble Fas ligand (FasL)

Causes apoptosis of renal epithelial cells

Increases levels of biochemical markers that reflect renal dysfunction
In combination with Fas induces apoptosis of glomerular cells

Serotonin52

Has cardiovascular effects dependent on dose, species, condition, and vascular state
Causes 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 constriction
Probably causes venous thromboses
Promotes platelet aggregation
Increases capillary permeability
May cause hypertension or hypotension or have no effect
Causes bronchoconstriction

Tumor necrosis factor (TNF-)9,54

Is the principal cytokine that mediates acute inflammation

Stimulates the coagulation pathway
Activates neutrophils
Promotes extracellular killing by neutrophils
Upregulates Fas on renal cells, stimulating production of more TNF-, interleukin 6, and interleukin 8
Causes sequestration of glomerular and tubulointerstitial neutrophils
Upregulates leukocyte adhesion molecules
Alters vascular tone, causing decreased filtration fraction
Increases in pulmonary, hepatic, and renal systems when high tidal volumes occur
Correlates with development of acute renal failure

Interleukin 69,54

Is a proinflammatory cytokine secreted by T cells and macrophages

Stimulates the liver to produce acute-phase proteins
Increases production of neutrophils

Interleukin 810,55

Is a cytokine produced by macrophages and other cell types

Is produced by macrophages within alveoli
Attracts neutrophils to site of inflammation

Some of the cytokines (eg, angiotensins, bradykinin, -thrombin,

thromboxane, prostacyclin, and
endothelin) have important vasomotor effects48-53 (Table 2). Metabolism may be impaired by

endothelial cell damage, which may

lead to adverse effects on interstitial
fluid fluctuations.47 These altered
levels of endothelium-derived
vasoactive mediators contribute to
microcirculatory dysfunction,

including release of reactive nitrogen and oxygen species, and postcapillary resistance may be increased
through microcirculatory dysfunction. As the capillary pressures
increase, pulmonary edema worsens,

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impairing the bactericidal activity

of alveolar macrophages.38,46,47
Lung injury caused by release
of inflammatory mediators further
reduces the caliber of small airways.
The associated increase in circulating levels of thromboxane A2 and
serotonin are linked to increases in
pulmonary artery pressure. The
cellular particulate material and
debris and the accumulating
perivascular edema cause additional
obstruction that impairs cardiac
output. These alterations in the
pulmonary circuit also alter the
compensatory mechanism of pulmonary hypoxic vasoconstriction.42
Mechanical ventilation has a
major effect on inflammatory cells
and soluble mediators in lungs.36
Several primary cytokines are released
through the injury and inflammatory
process. They include IL-8,9 IL-6,54,55
and TNF-.9,54 These promote
glomerular and tubulointerstitial
sequestration of neutrophils, upregulation of leukocyte adhesion molecules, and a decrease in filtration
fraction associated with alterations
in vascular tone9,54 (Table 2).
Increases in tidal volume are
associated with increases in pulmonary, hepatic, and renal levels of
IL-6, which correlate with development of ARF.9 In addition, release
of soluble Fas ligand (sFasL), the
ligand for the receptor Fas, causes
apoptosis (programmed cell death)
of renal epithelial cells and leads to
increased levels of biochemical
markers indicative of renal dysfunction. The Fas-FasL system induces
apoptosis of glomerular cells.9
Apoptosis in ARF is due to receptormediated activators such as TNF
and the Fas-FasL system.9 Cytotoxic
events, such as ischemia, hypoxia,

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and anoxia, as well as oxidant injuries

and nitric oxide, also lead to apoptosis.56 Tremblay and Slutsky38
reported a relationship between
various ventilatory modes and subsequent effects on end organs that
included increased apoptosis of
cells in the kidney and small intestine and changes in host immunity
and susceptibility to infection.

ventilate lungs, it may be more

important than tidal volume in preventing lung injury. The reduction
in pressure delays overdistention of
the lungs, reduces the mechanical
energy load, and ultimately stabilizes damaged alveoli.47 Although
much research in this area has been
done, information is still needed on
what constitutes optimal PEEP.

Areas for Further Evaluation

Optimizing Fraction of
Inspired Oxygen

Lung-protective mechanical
ventilation techniques are still under
investigation. These investigations
should include determining the
optimal combination of PEEP and
tidal volume. Other areas to examine are different types of ventilation,
such as airway pressure release ventilation (APRV) and high-frequency
oscillatory ventilation (HFOV). In
addition, conventional ventilation
techniques should be reevaluated.
Furthermore, nurses should consider
the consequences of temporary cessation of ventilatory support and how
cessation may or may not cause lung
injury. Another area of interest is how
nutrition can affect the inflammatory process in critically ill patients
receiving mechanical ventilation.
All of these areas are important
because potentially preventable lung
injury caused by mechanical ventilation may have deleterious effects on
renal function.
Lung-Protective Ventilation

Efforts to decrease the risk of

renal failure induced by mechanical
ventilation must include further
research in lung-protective ventilation strategies, including judicious
application of PEEP,57 which in rat
models can delay VILI. Because PEEP
reduces the pressures required to

Another way to decrease lung

injury is to reduce pulmonary inflammation. Maintaining the fraction of
inspired oxygen at less than 0.60
may reduce injury caused by oxygen
because a high fraction of inspired
oxygen causes formation of cytotoxic
oxygen free radicals.24,54 Of equal interest is the phenomenon of absorption
atelectasis, in which well-ventilated
alveoli empty their oxygen across
the concentration gradient and
increase the possibility of their collapse.24,58 The process is exacerbated
by nitrogen washout. Breathed air is
a combination of multiple gases, of
which nitrogen is the major component. The combination of gases is
inhaled into the alveoli, where the
gases either are absorbed into the
plasma or remain in the alveoli.
Nitrogen is not particularly soluble
in the plasma; therefore, larger concentrations remain in the alveoli,
helping the alveoli maintain their
structure. If the nitrogen in the alveoli is replaced by other gases, such
as excess amounts of highly diffusible
oxygen, the alveoli lose much of their
ability to retain their open structure.59
Tidal Volume Control

Optimizing tidal volume reduces

the risk of lung overinflation. The

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Acute Respiratory Distress Syndrome

Network60 recommends maintaining a tidal volume of 6 mL/kg, and
plateau pressures less than 30 cm
H2O reduce barotrauma and decrease
the release of inflammatory mediators. However, additional research43
has suggested that compared with
low tidal volumes coupled with high
PEEP, which decrease alveolar insta-

etitious alveolar opening. Because

APRV does not increase intrathoracic
pressures, venous return is not compromised. This situation leads to an
improved cardiac output because as
patients breathe spontaneously,
associated decreases in intrathoracic
pressures facilitate venous return.34
Disadvantages of APRV include permissive hypercapnia,61 which can be

found that central venous pressure

and pulmonary artery occlusion
pressures increased, and clinically
insignificant decreases in cardiac
output and some decreases in stroke
volume index and end-systolic and
diastolic area indexes occurred. In a
study in pigs with normal lungs,
Roosens et al65 found that HFOV was
safe and effective but did not improve

Nurses who care for patients receiving mechanical

ventilation must recognize the possible renal consequences of this pulmonary intervention.
bility, low tidal volumes coupled
with low PEEP may actually be injurious, causing increased release of
IL-8. Although mechanical injury
may be reduced, optimal tidal volumes have not yet been determined.
Airway Pressure Release
Ventilation

APRV does not add tidal volume

ventilation to baseline airway pressures.61 Instead it decreases airway
pressure to less than baseline pressure to augment ventilation.34 This
augmentation allows patients to
breathe spontaneously and releases
airway pressure from an elevated
baseline value to stimulate expiration. This elevated baseline improves
oxygenation while timed airway
pressure release aids in carbon dioxide removal. The advantages of this
ventilation mode include decreased
lung injuries because of lower peak
pressures. Pressure limits also eliminate or reduce alveolar overdistention and high-volume lung injury.
Maintaining low airway pressure
limits lung injury by decreasing rep-

inversely correlated with RBF and

can cause renal constriction.9
High-Frequency Oscillatory
Ventilation

Use of HFOV has been traditionally reserved for neonates and children.40,62 In studies in animals,
tracheal aspirates had lower levels
of IL-6, IL-8, TNF-, and other
mediators with HFOV than with
standard positive-pressure ventilation strategies. HFOV is also being
evaluated as a treatment for adults
with lung injuries.63 Studies41,64 have
shown that HFOV can provide adequate gas exchange with small tidal
volumes and high end-expiratory
pressures without producing alveolar overdistention. Decreased alveolar distention should result in
decreased VILI, which in turn may
lead to further reduction in alveolar
inflammatory processes due to
mechanical injury. However, potential complications associated with
HFOV could outweigh the benefits.
In a study of adults with acute respiratory distress syndrome, Chan et al64

mortality rates and in fact greatly

elevated intrathoracic pressures.
Although this method of ventilation
provides valuable lung protection
and may prevent VILI, more research
is needed to discover how significant
the changed hemodynamic parameters affect renal function.
Traditional Mechanical Ventilation

Some of the more traditional

strategies to reduce the impact of
mechanical ventilation on cardiac
output in patients with reduced
lung volume include assisted, noninvasive ventilation modes such as
continuous positive airway pressure,
bilevel positive airway pressure, and
pressure-support ventilation. These
ventilation methods help recruit
alveoli while reducing adverse cardiovascular effects, although more
research is needed in this area.22
Suctioning Techniques

Suctioning in patients receiving

mechanical ventilation needs to be
further examined. PEEP can impair
suctioning because of the pressure

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gradients between the suction

catheter tip, the end of the endotracheal tube, and the alveoli. The positive pressure that is blown through
the end of the endotracheal tube
maintains PEEP within the alveoli
despite the negative pressure in the
suction catheter created during
closed-system suctioning. This positive pressure forces the secretions to
flow distally, away from the suction
catheter66 and has the effect of layering the secretions around the
alveolar walls. In the past, nurses
attempted to overcome the layering
effect by instilling normal saline
into the endotracheal tube, a practice that is now considered unhelpful and possibly harmful.67,68 With
open-system suctioning methods,
such as stopping positive-pressure
ventilation during the suctioning,
the pressure gradient is zero and the
catheters can easily remove available
secretions.66,69 However, stopping
PEEP, for even short periods, facilitates rapid alveolar derecruitment39
and requires higher pressures after
the intervention to recruit lost alveoli. These higher pressures increase
the risk of creating higher intrapulmonary stresses and often lead to
additional stress-induced lung injury.
It may take several hours before the
collapsed alveoli are recruited again.47
Nutrition

New enteral nutrition formulas

can lead to improved mortality and
morbidity in critically ill patients

d tmore
To learn more about renal failure, read
Successful Management of Respiratory
Failure Can Improve Renal Function by
Amir Kazory and Didier Ducloux in the
American Journal of Critical Care, 2009;18:
10-11. Available at www.ajcconline.org.

www.ccnonline.org

receiving mechanical ventilation.70,71

These low-carbohydrate, high-fat
formulations are enriched in antioxidants, eicosapentaenoic acid, and
-linolenic acid. They can control the
development of proinflammatory
mediators.20,70,71 Interestingly, compared with patients who received traditional enteral feedings, patients who
received these special formulations
had lower total neutrophil counts,
had decreased alveolar levels of IL-6
and IL-8, were weaned from mechanical ventilation at a much higher rate,
and had less end-organ failure.20,70

Conclusion
No consensus exists that positivepressure ventilation impairs renal
function, although evidence that it
does is mounting. Nurses who care
for patients receiving mechanical
ventilation must recognize the possible renal consequences of this pulmonary intervention. Astute nursing
assessments of pulmonary and renal
function are required.
Additional nursing research is
needed to examine the effects of
different suctioning techniques on
pulmonary function. What is the
impact of intermittent cessation of
positive pressure on overall outcomes? In addition, could the value
of being able to transport patients
for diagnostic purposes be balanced,
or overshadowed, by the possible
harm of cessation of positive-pressure
ventilation to some patients fragile
pulmonary condition? What could
be considered optimal combinations
of PEEP and tidal volume for different conditions? A particularly interesting topic for further research is
the potentially adverse renal effects
of treating patients with vasopressin
and norepinephrine for hypotension.

Are the effects of treatment the same

as those of the endogenous release
of those substances? Could this
treatment lead to activation of the
sympathetic nervous system, thus
decreasing RBF and GFR? Health
care providers should be aware that
treatments that benefit one organ
system may adversely affect another.
Patients are not exclusively a respiratory system, or a renal system, or a
hepatic system, or any other specific
organ system. They are an integrative whole and must be treated as
that whole, with the realization that
any intervention that affects one
part of a patient may cause unexpectedand unwelcomeresults
in another body system.27 CCN
eLetters
Now that youve read the article, create or contribute
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Just visit www.ccnonline.org and click Respond to
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the article.

Acknowledgments
Thanks to Mark Yerrington, visual information
specialist at William Beaumont Army Medical
Center, for his creative assistance with the figures.
The opinions or assertions contained herein are
the private views of the author and should not
be construed as official or as reflecting the
views of the US Army Medical Department,
Department of the Army, or the Department
of Defense. Citations of commercial organizations and trade names in this report do not
constitute an official Department of the Army
or Department of Defense endorsement or
approval of such products or services of these
organizations.

Financial Disclosures
None reported.

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Crit Care Med. 2006;34(4):1033-1038.

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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 how
mechanical ventilation may contribute to the pathogenesis of acute renal failure
1. Where does urine concentration and dilution occur?
a. Proximal tubules
c. Distal tubules
b.Loops of Henle
d. Collecting duct

8.Which PaO2 will cause renal vasoconstriction and increased renal

vascular resistance?
a. 38 mm Hg
c. 68 mm Hg
b.58 mm Hg
d. 88 mm Hg

2. What is a result of decreased systemic arterial pressure?

a. Increased filtration
b. Increased excretion
c. Renal arterial arteriolar vasoconstriction
d. Increased renal blood flow

9. What do positive intrathoracic pressures cause?

a. Augmented venous return
b.Increased right ventricular preload
c. Increased left ventricular preload
d.Decreased left ventricular afterload

3. What is a result of increased systemic arterial pressure?

a. Increased excretion
b.Renal arteriolar vasoconstriction
c. Decreased filtration
d.Increased intravascular volume

10. What is associated with the redistribution of blood flow from the
cortical to the juxtamedullary nephrons?
a. Polyuria
b.Increased creatinine clearance
c. Increased glomerular filtration rate
4. What is the most common form of acute renal failure (ARF)? d.Increased fractional resorption of sodium
a. Prerenal
c. Intrarenal
11. What is the principal cytokine that mediates acute inflammation?
b.Intrinsic
d. Postrenal
a. Tumor necrosis factor-
c. Bradykinin
b.Angiotensin
d.
Interleukin 8
5. What is a cause of postrenal ARF?
a. Acute tubular necrosis
12. What is the effect of positive end-expiratory pressure on suctioning?
b.Interstitial nephritis
a. No effect on suctioning
c. Glomerulonephritis
b.Easier suctioning through the inverse pressures generated by positive
d.Bilateral ureteral obstructions
end-expiratory pressure and tidal volume settings
c.
More
difficult suctioning because positive pressure ventilation can layer
6.Hypovolemia causes which form of ARF?
secretions
around alveolar walls
a. Prerenal
c. Intrarenal
d.More
tenacious
secretions, requiring instillation of normal saline into
b.Intrinsic
d. Postrenal
the endotracheal tube
7. Hypercapnia causes renal constriction by which direct
mechanism?
a. Decreased systemic vascular resistance
b.Sympathetic nervous system activation
c. Renin-angiotensin-aldosterone system stimulation
d.Systemic vasodilatation

13. What is associated with special enteral formulations?

a. Higher neutrophil counts
b.Increased alveolar interleukin 6 levels
c. Less end-organ failure
d.Higher failure-to-wean rates

Test answers: Mark only one box for your answer to each question. You may photocopy this form.

1. K a
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2. K a
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3. K a
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4. K a
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5. K a
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6. K a
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7. K a
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8. K a
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9. K a
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11. K a
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10. K a
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12. K a
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13. K a
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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 A

Test writer: Denise Hayes, RN, MSN, CRNP

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The American Association of Critical-Care Nurses is accredited as a provider of continuing nursing education by the American Nurses Credentialing Centers Commission on Accreditation.
AACN has been approved as a provider of continuing education in nursing by the State Boards of Nursing of Alabama (#ABNP0062), California (#01036), and Louisiana (#ABN12). AACN
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Acute Renal Failure and Mechanical Ventilation: Reality or Myth?

Caroline C. Broden
Crit Care Nurse 2009, 29:62-75. doi: 10.4037/ccn2009267
2009 American Association of Critical-Care Nurses
Published online http://www.cconline.org

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