Continuing Nursing
Education
Carol M. Headley
Barry M. Wall
lash pulmonary edema and
acute pulmonary edema are
terms used to define the sudden
development of respiratory distress related to the rapid accumulation of fluid within the lung interstitium secondary to elevated cardiac
filling pressures (Little, & Braunwald,
1997). For the purposes of this review,
flash pulmonary edema will be the
term used. One of the first studies to
describe its occurrence linked its
development to individuals with preexisting coronary artery disease and
hypertension (Lee, Cabin, & Francis,
1988). The connection between flash
pulmonary edema and kidney disease
was initially described in individuals
with bilateral renal artery stenosis
(Pickering et al., 1988). This association has been so well characterized
that the recommendation has been
made that anyone presenting with
flash pulmonary edema be considered for evaluation for renal artery
stenosis
(Missouris,
Belli,
&
MacGregor, 2000).
The risk for flash pulmonary
edema in individuals with chronic
kidney disease (CKD), primarily end
stage renal disease (ESRD), has been
under emphasized in the literature.
There are several possible explanations for the lack of reports describing
an association between flash pulmonary edema and CKD, especially
in patients with CKD receiving main-
Flash pulmonary edema, also termed acute onset pulmonary edema, is characterized by the
sudden onset of respiratory distress related to accumulation of fluid in the lung interstitium
over a matter of minutes or hours. Chronic kidney disease is often associated with predisposing cardiac risk factors that make patients susceptible to development of flash pulmonary
edema. This article highlights the connection between cardiac pathologies found in chronic
kidney disease and development of flash pulmonary edema. Nephrology nurses may be instrumental in reducing the risk of flash pulmonary edema by recognizing symptoms of heart failure and need for treatment of acute elevations in blood pressure.
Goal
Recognize the risk for development of flash pulmonary edema in patients with
chronic kidney disease and ESRD.
Objectives
1. Identify causes of flash pulmonary edema that may occur in conjunction
with chronic kidney disease and ESRD
2. Recognize signs and symptoms of flash pulmonary edema.
3. Describe nursing measures that may avert development of flash pulmonary
edema in individuals with advanced chronic kidney disease.
This offering for 1.5 contact hours is being provided by the American Nephrology Nurses
Association (ANNA).
ANNA is accredited as a provider of continuing nursing education (CNE) by the American Nurses
Credentialing Centers Commission on Accreditation.
ANNA is a provider approved by the California Board of Registered Nursing, provider number CEP
00910.
The Nephrology Nursing Certification Commission (NNCC) requires 60 contact hours for each
recertification period for all nephrology nurses. Forty-five of these 60 hours must be specific to nephrology
nursing practice. This CNE article may be applied to the 45 required contact hours in nephrology nursing.
15
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease
Figure 1
Starling Equation
Q = K[(Pmv-Ppmv)-(mv-pmv)]
Q net transvascular flow of fluid
K membrane permeability
Pmv hydraulic pressure in the microvessels
Ppmv hydrostatic pressure in the perimicrovascular interstitium
mv plasma protein osmotic pressure in the circulation
pmv protein osmotic pressure in the perimicrovascular interstitium
Note: From Staub, N.C.(1974). Pulmonary edema. Physiology Review, 54(3), page 680.
Pathogenesis of Pulmonary
Edema
Edema has been described as
increased volume within several
spaces of the body including the
blood vessels (increase in blood volume), the lungs (pulmonary interstitium and alveoli), the trunk and lower
extremities (peripheral edema), as
well as cavities within the abdomen
and lungs (i.e., pleural effusions and
ascites). Peripheral edema is most evident in the lower extremities because
of the effect of gravity. The occurrence of peripheral edema in patients
with CKD may be attributed to either
heavy proteinuria (over 3.5 grams
termed nephrotic syndrome) or
advanced deterioration in kidney
function (Bickley, Hoekelman, &
Bates, 1999). Pulmonary edema
results from fluid accumulation in the
lungs at a higher rate than can be
removed. The type of abnormality
expressed in the Starling equation
(Figure 1) differentiates the type of
pulmonary edema.. It can predict the
net flow of fluid across a membrane
based upon permeability, surface
area, and hydraulic pressures (Hanley
& Welsh, 2004).
Pulmonary edema has been classified into two categories dependent
upon the underlying cause: cardiogenic and non-cardiogenic (Hanley &
Welsh, 2004). Starling forces identified in the equation affect the fluid
balance between the interstitium and
the vascular bed within the lungs
(capillary permeability, capillary surface area, capillary and interstitial
fluid hydraulic pressures, capillary
16
Figure 2
Neurohormonal Responses in Heart Failure
Impairment
in Left
Ventricular
Function
Reduction
in Cardiac
Output
Sympathetic
Nervous
System
Increased
Oxygen
Demands
RAAS
Vasoconstriction
and
Salt & Water
Retention
Chronic
Neurohormonal
Activation
Increased
Preload &
Afterload
Natriuretic
Peptides
Natriuresis &
Vasodilatation.
Cardiac Remodeling
Further Heart
Failure
Myocyte Apoptosis,
Hypertrophy, Focal
Myocardial Necrosis
logic data has determined that 40% 50% of patients presenting with congestive heart failure have diastolic
dysfunction as the predominant etiology. The diagnosis of diastolic heart
failure is made based upon the existence of heart failure in patients with
normal systolic function (left ventricular ejection fraction of 50% or greater)
and no evidence of valvular or pericardial disease (Vasan, Benjamin, &
Levy 1995). Some individuals will
have evidence of both systolic and
diastolic heart failure contributing to
development of flash pulmonary
17
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease
18
phy using color Doppler imaging during the acute phase of pulmonary
edema with a follow up exam performed 2-3 days later. The left ventricular ejection fraction during the
acute episode was similar to the measurement obtained 2- 3 days after presentation (N = 30). Thus, a normal
left ventricular ejection fraction in a
patient with co-existing hypertension
and flash pulmonary edema suggests
that the pulmonary edema is due to
diastolic dysfunction. Transient systolic dysfunction and severe mitral
regurgitation were found to be infrequent causes for development of flash
pulmonary edema (Gandhi et al.,
2001)
Other clinical conditions that have
been identified as contributing to the
development of flash pulmonary
edema include: a) myocardial
ischemia, b) acute aortic insufficiency,
c) acute mitral regurgitation, d) mitral
stenosis, and e) renovascular hypertension (Walker, Walker, & Nielsen,
2001), but this paper will primarily
focus on diastolic heart failure as it
relates to development of flash pulmonary edema because diastolic
heart failure has received less attention and yet is believed to be highly
prevalent.
Cardiac Disease
Flash pulmonary edema occurs as
a consequence of a disruption in the
normal pressure-volume relationship
during the cardiac cycle. Ischemic
heart disease/coronary artery disease
has been linked with development of
flash pulmonary edema. Acute
myocardial ischemia has been shown
to cause systolic and diastolic dysfunction. Cocaine abuse has been
associated with development of flash
pulmonary edema for multiple reasons including its precipitation of
myocardial ischemia (coronary artery
vasoconstriction), acute rise in blood
pressure (peripheral vasoconstriction), and development of systolic as
well as diastolic dysfunction (Lange &
Hillis, 2001).
The existence of coronary artery
disease can cause intermittent
Table 1
Prevalence of Risk Factors: Diastolic Heart Failure in CKD
Risk
Prevalence
References
Hypertension
50% - 75%
NKF, 2005
LVH
Levin, 2003
Age
USRDS, 2005
35% - CKD
40% - Beginning dialysis
Levin, 2003
Heart failure
37%
19
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease
Figure 3
Pathogenesis of Diastolic Heart Failure in CKD
Decreased
Glomerular
Filtration Rate
Increased
Extracellular
Fluid Volume
Hypertension
Cardiac
Remodeling:
LVH
Diastolic
Dysfunction
Increased Cardiac
Filling Pressures
Flash Pulmonary
Edema
20
Figure 4
Transmitral Pressures used in Diagnosis of Diastolic Dysfunction
Normal E: A Ratio and Deceleration Time
E Early passive
ventricular filling
A Ventricular
filling produced by
atrial contraction
D
T
Deceleration Time
Restrictive E:A Ratio and Deceleration Time
E Early passive
ventricular filling
A Ventricular
filling produced by
atrial contraction
D
T
Deceleration Time
Normal: 0.75 greater than E:A greater than 0.75, but less than 1.5 with DT 200
32 ms
Mild Diastolic Dysfunction: E:A greater than or equal to 0.75 with DT greater
than or equal to 230 ms
Moderate Diastolic Dysfunction ("Pseudonormal"): E:A greater than 0.75 but
less than 1.5 with DT greater than 140 ms
Severe Diastolic Dysfunction: E:A greater than 1.5 with DT less than 160 ms
Adapted from: Haney, Sur, & Xu (2005). Diatsolic heart failure: A Review and
Primary care perspective. Journal of the American Board of Family Practitioners,
18(3), 189-198.
21
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease
22
Figure 5
Standing Chest Radiograph AP Prior to
Undergoing Catheter Replacement
Figure 6
Portable Chest PA Radiograph 5 Hours Later
23
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease
Nursing Implications
Pulmonary edema is a common
complication of patients with ESRD
(Evans, Reddan, & Szczech, 2004;
Shapiro, Deshetler, & Stockard,
1994). Fluid and salt abuse has been
reported to be the most common
cause of pulmonary edema in patients
receiving renal replacement therapy.
How does one differentiate between
pulmonary edema that is associated
with excessive fluid intake and cardiogenic mediated flash (acute) pulmonary edema? Pulmonary edema
that occurs without significant interdialytic weight gain or evidence of
peripheral edema on physical examination, particularly in association with
an elevation in blood pressure,
strongly supports the diagnosis of
flash pulmonary edema.
A history of ischemic heart disease, poorly controlled hypertension,
and identification of left ventricular
hypertrophy by Doppler echocardiography may signify an increased risk
for development of flash pulmonary
edema. Anemia and hypertension
have been primarily associated with
the development of left ventricular
hypertrophy and are found in the
majority of patients beginning dialysis. Poorly controlled hypertension in
the presence of a remodeled heart
(i.e., LVH) may result in diastolic dysfunction which predisposes to the
development of pulmonary edema
24
Conclusion
Patients with CKD are at risk for
developing flash pulmonary edema.
Cardiovascular disease is highly
prevalent in the kidney disease population. Diastolic heart failure is often
unsuspected without clinical suspi-
25
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease
26
Safian, R.D., & Textor, S.C. (2001). Renalartery stenosis. New England Journal of
Medicine, 344(6), 431-442.
Shapiro, R.S., Deshetler, N., & Stockard,
H. E.(1994). Fluid overload again: A
technique to enhance fluid compliance. Dialysis & Transplantation, 23(6),
303-306.
Silver, M. A., Maisel, A., Yancy, C.W.,
McCullough, P.A., Burnett, J.C. Jr.,
Francis, G. et al., (2004). BNP
Consensus Panel 2004: A clinical
approach for the diagnostic, prognostic, screening, treatment monitoring,
and therapeutic roles of natriuretic
peptides in cardiovascular diseases.
Congestive Heart Failure, 10(5 Suppl.
3), 1-30.
Staub, N.C.(1974). Pulmonary edema.
Physiology Review, 54(3), 678-811.
Sulkova, S. & Valek, A. (1988). Role of
antihypertensive drugs in the therapy
of patients on regular dialysis treatment. Kidney International, 35, S198200.
Torre-Amione, G. (2005). Immune activation in chronic heart failure. American
Journal of Cardiology, 95(11A), 3C-8C.
Tozawa, M. Iseki, K., Iseki, C., &
Takishita, S. (2002). Pulse pressure
and risk of total mortality and cardiovascular events in patients on chronic hemodialysis. Kidney International,
61(2), 717-726.
United States Renal Data System.
(USRDS 2005), USRDS 2005 annual data report Atlas of end-stage renal
disease in the United States.
Bethesda, MD: National Institute of
Diabetes and Digestive and Kidney
Diseases.
Vasan, R.S., Benjamin, E J., & Levy, D.
(1995). Prevalence, clinical features
and prognosis of diastolic heart failure: An epidemiologic perspective.
Journal of the American College of
Cardiology, 26(7), 1565-1574.
Vasan, R.S., & Levy, D. (1996). The role
of hypertension in the pathogenesis
of heart disease: A clinical mechanistic overview. Archives of Internal
Medicine, 156(16), 1789-1796.
Walker, F. Walker, D.A., & Nielsen, M.
(2001). Flash pulmonary edema,
Lancet, 358(9281), 1646-1647.
Ware, L.B., & Matthay, M.A. (2005).
Acute pulmonary edema. New
England Journal of Medicine, 353(26),
2788-2796.
37
6.
3.
4.
5.
8.
What statement is true about neurohormonal changes in congestive heart failure (CHF)?
A. Initial neurohormonal changes are
deleterious and lead to pulmonary
edema.
B. Initially stimulation of the sympathetic
nervous system decreases cardiac output.
C. Stimulation of the RAAS causes salt
and water excretion by the kidneys.
D. Long-term stimulation leads to myocyte
apoptosis, hypertrophy, and myocardial
necrosis.
hypertension
left ventricular hypertrophy
anemia
volume overload
10.
Your patient has a brain natriuretic peptide (BNP) level 700 pg/ml. What would
your next action be?
A.
B.
C.
D.
12.
13.
9.
11.
14.
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Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease
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