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Crit Care Nurse-2009-Broden-62-75 PDF
Crit Care Nurse-2009-Broden-62-75 PDF
Crit Care Nurse-2009-Broden-62-75 PDF
PRIME POINTS
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.
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
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2nd convol
tub.
Cortical substance
Boundary zone
Collecting
tub.
Arterial arch
Venous arch
Medullary
substance
Duct of Bellini
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).
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Irregular
tub.
Junctional tub.
Arteria recta
Parietal
Pores in epithelial cell
endothelium
Afferent
arteriole
Mesangial
cell
Mesangial
matrix
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
15
16
17
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Positive-pressure
mechanical
ventilation
Positive endexpiratory pressure
Ventilation/
oxygenation
PaCO2
PaO2
Cardiac
output
Renal
vasoconstriction?
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
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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.
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
Renin
Arteriolar
vasoconstriction.
Increase in blood
pressure
Arteriole
Kidney
ADH secretion
Pituitary gland:
posterior lobe
Collecting duct:
H2O absorption
H2O
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
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Epithelium
Alveolus
Endothelium
Epithelium
Endothelium
Fluid
Bacterial
cytokines
Alveolus
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Table 2
Cytokine or mediator
Effects/comments
Angiotensin
Bradykinin49,53
-Thrombin53
Thromboxane48
Is produced by platelets
Causes vasoconstriction
Is a potent hypertensive agent
Facilitates platelet aggregation
Endothelin51
50
Fas9,55
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
Interleukin 69,54
Interleukin 810,55
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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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
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
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
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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.
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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.
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.
References
1. Pruchnicki MC, Dasta JF. Acute renal failure in hospitalized patients: part I. Ann
Pharmacother. 2002;36(7-8):1261-1267.
2. Uchino S, Kellum JA, Bellomo R, et al;
Beginning and Ending Supportive Therapy
for the Kidney (BEST Kidney) Investigators.
Acute renal failure in critically ill patients: a
multinational, multicenter study. JAMA.
2005;294(7):813-818.
3. Metnitz P, Krenn C, Steltzer H, et al. Effect
of acute renal failure requiring renal
replacement therapy on outcome in critically ill patients. Crit Care Med. 2002;30(9):
2051-2058.
4. Clermont G, Acker CG, Angus DC, Sirio CA,
Pinsky MR, Johnson JP. Renal failure in the
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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
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
Test answers: Mark only one box for your answer to each question. You may photocopy this form.
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10. 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
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