Flash Pulmonary Edema in Patients
with Chronic Kidney Disease and
End Stage Renal Disease
Carol M. Headley
Barry M. Wall
lash pulmonary edema and
F acute pulmonary edema are
terms used to define the sudden
development of respiratory dis-
tress related to the rapid accumula-
tion of fluid within the lung intersti-
tium 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 pre-
existing 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 associa-
tion has been so well characterized
that the recommendation has been
made that anyone presenting with
flash pulmonary edema be consid-
ered 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 explana-
tions for the lack of reports describing
an association between flash pul-
monary edema and CKD, especially
in patients with CKD receiving main-
Carol M. Headley, DNSc, RN, CNN, is
Nephrology Advanced Practice Nurse at The VA
Medical Center, Memphis, TN. She is ANNAs
National Program chairperson and a member of
ANNAs Memphis Blues Chapter.
Barry M. Wall, MD, is Professor of Medicine at
The University of Tennessee Health Science Center,
Memphis, TN, and Nephrology, Associate Chief at
The VA Medical Center, Memphis, TN.
Note: The authors reported no actual or potential
conflict of interest in relation to this continuing
nursing education article.
NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1
Continuing Nursing
Education
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 predis-
posing 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 instru-
mental in reducing the risk of flash pulmonary edema by recognizing symptoms of heart fail-
ure 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.
tenance dialysis. The sudden onset of the past decade (Foley, Parfrey, &
pulmonary edema may be assumed Samak, 1998). Kidney disease is now
to be from excessive interdialytic known to be an independent risk fac-
weight gain, inaccurate dry weight tor for cardiovascular morbidity and
prescription, or weight scale malfunc- mortality (Levey et al., 1998; Sarnak
tions rather than from a cardiogenic et al., 2003). This article will define
origin. Furthermore, treatment is flash pulmonary edema and factors
often readily available and imple- for its development, emphasizing the
mented (ultrafiltration), thus the prob- relationship between cardiovascular
lem is promptly treated. disease and chronic kidney disease.
The strong association between Lastly, a case study of a patient on
cardiovascular disease and kidney hemodialysis that developed flash
disease has been emphasized during pulmonary edema will be presented.
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 increased left atrial filling pressure

Starling Equation (Hanley & Welsh, 2004). In this type
of pulmonary edema, the rate of
Q = K[(Pmv-Ppmv)-(mv-pmv)] fluid accumulation within the lungs
is mainly dependent upon the func-
Q net transvascular flow of fluid tional capacity of the lymphatic sys-
K membrane permeability tem of the lungs to remove fluid
Pmv hydraulic pressure in the microvessels from the interstitium and alveoli
Ppmv hydrostatic pressure in the perimicrovascular interstitium
mv plasma protein osmotic pressure in the circulation
(Mason et al., 2005). As left atrial
pmv protein osmotic pressure in the perimicrovascular interstitium pressure rises, pulmonary capillary
pressures increase resulting in pro-
Note: From Staub, N.C.(1974). Pulmonary edema. Physiology Review, 54(3), page 680. tein poor fluid (edema) being forced
into the lung interstitium and alveoli.
Consequently, there is a progressive
deterioration in alveolar gas
Pathogenesis of Pulmonary and interstitial fluid oncotic pressures, exchange resulting in hypoxemia
Edema and the pressure differential across and symptoms of respiratory dis-
the capillary wall). Normally, the tress. Compensatory changes may
Edema has been described as alveolar bed within the lung serves to occur in individuals with chronically
increased volume within several protect the lung from fluid accumula- elevated left atrial pressures and per-
spaces of the body including the tion. Alveoli have very low perme- sistently elevated pulmonary capil-
blood vessels (increase in blood vol- ability for fluid and protein. Any fluid lary wedge pressures (greater than 18
ume), the lungs (pulmonary intersti- filtered into the alveoli is continuous- mmHg). In this circumstance, the
tium and alveoli), the trunk and lower ly absorbed back into the interstitium lymphatic system of the lungs
extremities (peripheral edema), as by the alveolar epithelial cells and becomes more efficient at removing
well as cavities within the abdomen drained away from the pulmonary fluid, thus reducing the likelihood for
and lungs (i.e., pleural effusions and interstitium by lymphatic vessels development of edema. It is the sud-
ascites). Peripheral edema is most evi- (Gluecker et al., 1999). den or acute elevations in left atrial
dent in the lower extremities because Non-cardiogenic pulmonary edema pressures that are more likely to
of the effect of gravity. The occur- occurs as a result of fluid accumula- result in acute pulmonary edema
rence of peripheral edema in patients tion in the alveoli resulting from a (Fraser, Mller, Colman, & Par,
with CKD may be attributed to either disruption in Starlings forces sec- 1999; Little, & Braunwald, 1997).
heavy proteinuria (over 3.5 grams ondary to increased capillary perme- It may be difficult to differentiate
termed nephrotic syndrome) or ability. The most common cause of between flash pulmonary edema and
advanced deterioration in kidney non-cardiogenic pulmonary edema is non-cardiogenic pulmonary edema
function (Bickley, Hoekelman, & acute lung injury (ALI) or acute res- since the presenting symptoms are
Bates, 1999). Pulmonary edema piratory distress syndrome (ARDS) often the same (Hanley & Welsh,
results from fluid accumulation in the associated with increased pulmonary 2004). Symptoms typically consist of
lungs at a higher rate than can be capillary permeability. Most often, dyspnea, tachypnea, and cough with
removed. The type of abnormality the concentration of protein within possible expectoration of frothy
expressed in the Starling equation the pulmonary interstitium exceeds edema fluid. The patient history and
(Figure 1) differentiates the type of 60% of the plasma protein value as determination of the factors that led
pulmonary edema.. It can predict the compared to less than 45% in cardio- to the development of the pul-
net flow of fluid across a membrane genic pulmonary edema (Hanley & monary edema becomes a priority
based upon permeability, surface Welsh, 2004). Non-cardiogenic pul- for diagnosis. Non-cardiogenic pul-
area, and hydraulic pressures (Hanley monary edema is diagnosed when monary edema is less common and
& Welsh, 2004). there is radiographic evidence of is primarily seen in individuals that
Pulmonary edema has been classi- alveolar fluid accumulation without have had recent pneumonia, sepsis,
fied into two categories dependent an elevation in the pulmonary wedge tumor, pulmonary fibrosis, trauma
upon the underlying cause: cardio- pressure greater than 18 mmHg or with multiple blood transfusions, fol-
genic and non-cardiogenic (Hanley & evidence of congestive heart failure lowing lung transplantation or resul-
Welsh, 2004). Starling forces identi- (CHF) on physical examination tant from aspiration of gastric con-
fied in the equation affect the fluid (Mason, Broaddus, Murray, & Nadel, tents.
balance between the interstitium and 2005).
the vascular bed within the lungs Cardiogenic pulmonary edema is
(capillary permeability, capillary sur- the most common type of pul-
Flash Pulmonary Edema
face area, capillary and interstitial monary edema and results from Flash pulmonary edema can origi-
fluid hydraulic pressures, capillary

16 NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1

nate from cardiogenic (i.e., cardiac Figure 2
dysfunction) and non-cardiogrenic Neurohormonal Responses in Heart Failure
causes (i.e., neurogenic pulmonary
edema) and occurs suddenly over a
period of minutes to hours (Lee, et al.,
1988). The syndrome of congestive Impairment
heart failure is the most common eti- in Left
Ventricular
ology for the development of flash Function
pulmonary edema. Traditionally, the
diagnosis of congestive heart failure
has been attributed to the presence of
myocardial systolic dysfunction, Reduction
defined as a disorder of myocardial in Cardiac
contractility leading to a reduced ejec- Output
tion fraction. Chronic systolic dys-
function results in a systemic process, Sympathetic
not solely confined to the heart Nervous
(Torre-Amione, 2005). Congestive System
heart failure is a multisystem disorder Increased
Oxygen
affecting the heart, skeletal muscle, Demands
kidneys, and nervous system pat- Chronic
Neurohormonal Natriuretic
terned by a complex neurohormonal Activation Peptides
process. Figure 2 depicts a simplified Increased Natriuresis &
version of the process. Neuro- RAAS Preload & Vasodilatation.
hormonal activation is key to the pro- Vasoconstriction Afterload
gressive nature of chronic heart fail- and
ure whereas flash pulmonary edema Salt & Water
occurs quickly and is primarily Retention
dependent upon a pre-existing condi-
tion (i.e., diastolic dysfunction) cou-
pled with an acute stressor (i.e., rise in Cardiac Remodeling
blood pressure). Further Heart
Chronic heart failure has been a Failure
challenge to treat because of its com- Myocyte Apoptosis,
plexity and its insidious character. Hypertrophy, Focal
Initially, neurohormonal changes pre- Myocardial Necrosis
sent in chronic heart failure are com-
pensatory and temporarily improve
cardiac output. These however, even-
tually become deleterious. Stimu-
lation of the sympathetic nervous sys-
tem is one of the earliest neurohor-
monal responses and initially pro- nervous systems becomes maladap- logic data has determined that 40% -
vides improved inotropic support to tive by contributing to cardiac 50% of patients presenting with con-
increase cardiac output. Stimulation myocyte apoptosis (programmed cell gestive heart failure have diastolic
of the renin-angiotensin-aldosterone death), hypertrophy, and focal dysfunction as the predominant etiol-
system (RAAS) causes release of myocardial necrosis ( Jackson et al., ogy. The diagnosis of diastolic heart
renin, plasma angiotensin II, and 2000). failure is made based upon the exis-
aldosterone. Angiotensin II causes Diastolic dysfunction, defined as a tence of heart failure in patients with
vasoconstriction of the efferent arteri- disorder of myocardial relaxation normal systolic function (left ventricu-
oles and the systemic circulation and resulting in impaired ventricular fill- lar ejection fraction of 50% or greater)
increased adrenal secretion of aldos- ing, may also result in the syndrome and no evidence of valvular or peri-
terone that results in sodium and of congestive heart failure. Diastolic cardial disease (Vasan, Benjamin, &
water retention by the kidneys heart failure is diagnosed when ele- Levy 1995). Some individuals will
( Jackson, Gibbs, Davies, & Lip, vated filling pressures are necessary have evidence of both systolic and
2000). However, long-term stimula- to achieve normal ventricular filling diastolic heart failure contributing to
tion of the RAAS and sympathetic (Grossman 2000). Recent epidemio- development of flash pulmonary

NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1 17

Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease
edema. However, diastolic heart fail-
ure occurs more frequently in patients
with preserved systolic function, thus
it has been attributed primarily to the
disorder of diastolic dysfunction
(Gandhi et al., 2001).
Although diastole involves the
process of cardiac relaxation, active
energy requiring processes occur dur-
ing this phase. The changes in cardiac
pressure that occur during diastole
are the result of isovolumetric relax-
ation from the time of the aortic valve
closure to mitral valve opening; early
rapid filling after mitral valve open-
ing; and low blood flow during mid-
diastole; and lastly late filling (high
blood flow) from atrial contraction. In
diastolic heart failure, the left ventri-
cle is stiff (reduced elastic recoil) with
impaired relaxation causing a reduc-
tion in filling. Higher diastolic pres-
sures are required to maintain ade-
quate ventricular filling (Redfield,
2004).
The literature has shown a strong
association between hypertension
and development of diastolic heart
failure, as well as a strong association
with development of flash pulmonary
edema. One study described the pres-
ence of systolic hypertension (systolic
arterial blood pressure greater than
160 mmHg) in 85% of patients pre-
senting to hospital emergency rooms
with flash pulmonary edema
(Kramer, Kirkman, Kitzman, & Little,
2000). Studies that performed
Doppler echocardiography after the
acute episode found preserved sys-
tolic function (left ventricular ejection
fraction of 50% or greater) in the
majority of patients presenting with
flash pulmonary edema. Even though
systolic function was assessed as nor-
mal, the evaluation was obtained after
treatment of the hypertensive episode
and resolution of the pulmonary
edema, thus the presence of transient
systolic dysfunction as a precipitating
cause could not be excluded
(Mansoor, Shah, & Scoble, 2001). The
primary cause for flash pulmonary
edema, systolic versus diastolic heart
failure, was addressed in a study that
examined patients with two-dimen-
sional transthoracic echocardiogra-
18
phy using color Doppler imaging dur-
ing the acute phase of pulmonary
edema with a follow up exam per-
formed 2-3 days later. The left ven-
tricular ejection fraction during the
acute episode was similar to the mea-
surement obtained 2- 3 days after pre-
sentation (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 sys-
tolic dysfunction and severe mitral
regurgitation were found to be infre-
quent 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 hyper-
tension (Walker, Walker, & Nielsen,
2001), but this paper will primarily
focus on diastolic heart failure as it
relates to development of flash pul-
monary edema because diastolic
heart failure has received less atten-
tion 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 dys-
function. Cocaine abuse has been
associated with development of flash
pulmonary edema for multiple rea-
sons including its precipitation of
myocardial ischemia (coronary artery
vasoconstriction), acute rise in blood
pressure (peripheral vasoconstric-
tion), and development of systolic as
well as diastolic dysfunction (Lange &
Hillis, 2001).
The existence of coronary artery
disease can cause intermittent
NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1
episodes of diastolic dysfunction and
systolic dysfunction (Mansoor et al.,
2001). Systolic dysfunction occurs
when there is less forward movement
of blood from the heart prompting an
increase in diastolic volume and dias-
tolic pressure precipitating pul-
monary vascular congestion leading
to pulmonary edema. In diastolic
heart failure, the myocardium is less
compliant, such that the left ventricle
is unable to accept an adequate vol-
ume of blood from the venous system
and to fill at normal low pressures
(Beattie, 2000). The net result is a rise
in diastolic pressures in order to pro-
vide adequate ventricular filling.
Heart failure resulting from diastolic
dysfunction occurs when elevated fill-
ing pressures are necessary to achieve
normal ventricular filling (Grossman,
2000). The increased resistance to
diastolic ventricular filling is most
commonly due to myocardial abnor-
malities (myocardial hypertrophy,
fibrosis, ischemia, or cardiomyopa-
thy), and less commonly to mechani-
cal abnormalities like mitral stenosis
or constrictive pericarditis (Hanley &
Welsh, 2004).
Hypertension is frequently pre-
sent in patients presenting with flash
pulmonary edema. Chronic hyper-
tension that is poorly controlled can
result in development of systolic and
diastolic dysfunction that may predis-
pose patients to the development of
flash pulmonary edema (Mansoor et
al., 2001). Even labile elevations in
blood pressures of patients with bilat-
eral renal artery stenosis have been
shown to be associated with an
increased risk for development of
flash pulmonary edema (Bloch, Trost,
Pickering, & Sos, 1999). As noted by
Vasan & Levy (1996) long standing
hypertension is a primary predeces-
sor to development of left ventricular
hypertrophy (LVH). Hypertension
leads to remodeling and augmenta-
tion of the left ventricular mass that
can result in diastolic dysfunction,
systolic dysfunction, or both.
However, it is important to realize
that not everyone with LVH will
develop heart failure. Athletes some-
times acquire what is called physio-
logic hypertrophy of the left ventricle
and maintain near or near-normal
exercise tolerance. Therefore, LVH
by itself does not constitute cardiac
dysfunction (Lorell & Carabello,
2000).
Renal Artery Stenosis and Flash
Pulmonary Edema
Renal artery stenosis (RAS) may
be identified in individuals with
apparent normal kidney function as
well as those with a diagnosis of acute
or chronic kidney disease (Missouris,
Belli, & MacGregor, 2000). Renal
artery stenosis (narrowing of the renal
artery) is most often a result of ather-
osclerosis. Fibromuscular dysplasia, is
a rare idiopathic condition in which
there is an increase in the number of
cells in the renal artery cell wall
resulting in arterial narrowing.
Atherosclerotic lesions result from the
deposition of plaque within the renal
artery and are most often seen in indi-
viduals over the age of 55, while
fibromuscular dysplasia is usually
seen in young women. Women with
fibromuscular dysplasia associated
RAS almost invariably have hyper-
tension. Lesions associated with fibro-
muscular dysplasia tend to show a
much more favorable response to
percutaneous transluminal angioplas-
ty (PTA), stent or surgery than athero-
sclerotic lesions (Olin, 2004).
The most common type of RAS
involves atherosclerotic deposition in
the artery lumen that disrupts blood
flow to the kidney parenchyma caus-
ing ischemia. The kidney responds by
secreting renin into the bloodstream,
leading to the production of
angiotensin II, which is both a potent
vasoconstrictor and a major stimulus
for adrenal secretion of aldosterone
(Safian & Textor, 2001). Hypertension
resulting from activation of the RAAS
is referred to as renovascular hyper-
tension. Mild to moderate hyperten-
sion is not commonly associated with
RAS; however, malignant and drug
resistant hypertension carries a high
degree of suspicion for RAS, having
been diagnosed in up to a third of
patients having difficult to control or
NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1
Table 1
Prevalence of Risk Factors: Diastolic Heart Failure in CKD
Risk Prevalence References
Hypertension 50% - 75% NKF, 2005
LVH 75% - Beginning dialysis Levin, 2003
Age Average age of dialysis USRDS, 2005
patient 63 years
Ischemic heart disease 35% - CKD Levin, 2003
40% - Beginning dialysis
Heart failure 37% Foley et al., 1994
malignant hypertension (Harding et has been associated with the develop-
al., 1992). Renovascular hypertension ment of flash pulmonary edema
related to bilateral renal artery steno- (Ware & Matthay, 2005). This discus-
sis is strongly associated with the sion will primarily highlight the
development of flash pulmonary pathology of diastolic heart failure. A
edema. The combination of hyper- relationship between the risk for dias-
tension and volume retention, occur- tolic heart failure in the presence of
ring as a consequence of altered kidney disease can be established by
intrarenal hemodynamics and aldos- examining the contributing factors
terone-mediated salt and water reten- that precede there development
tion are the major contributing factos (Figure 3). Diastolic heart failure can
to the development of flash pul- be caused by ischemia, left ventricu-
monary edema with bilateral renal lar hypertrophy (LVH), increased fill-
artery stenosis. In contrast pulmonary ing pressures related to chronically
edema is relatively uncommon with elevated blood pressures, infiltrative
unilateral renal artery stenosis cardiomyopathies, ischemic heart dis-
(Basaria & Fred, 2002; Jaff, 2001). ease, pericarditis, the normal aging
Unilateral renal artery stenosis leads processes, chemotherapy and genetic
to renin dependent hypertension, but anomalies (Beattie, 2000; Kramer et
not to volume expansion, since the al., 2000; Zile & Simsic, 2000). In the
non-affected kidney undergoes a general population, 50% of people
pressure natriuresis/diuresis, which over the age of 70 with a diagnosis of
prevents volume expansion making congestive heart failure will have pre-
pulmonary edema less likely to occur served systolic function and classified
(Missouris et al., 2000). as having diastolic heart failure. For
those 10 years younger (60 years of
Flash Pulmonary Edema and age) with congestive heart failure
symptoms, only 15% will have dias-
Kidney Disease tolic heart failure. Age also con-
Many of the precipitating factors tributes to mortality risk. Overall,
associated with development of flash prognosis is better for diastolic heart
pulmonary edema are frequently pre- failure (average mortality rate 5 % -
sent in patients with advanced stages 8%) than for systolic heart failure
of CKD (Table 1). Cardiovascular dis- (average mortality rate 10% - 15%),
ease and CKD are strongly linked. but diastolic heart failure in patients
Recent findings indicate that patients over 70 years has a 50% 5-year mor-
with CKD are in the highest risk tality rate (Zile & Simsic, 2000). These
group for cardiovascular disease and changes are similar to disease report-
that patients with CKD are more like- ed in the elderly, but they occur 15-20
ly to die of cardiovascular disease years earlier in kidney disease
than ESRD (Levin, 2003). (Tozawa, Iseki, Iseki, & Takishita,
Systolic and diastolic heart failure 2002; Churchill et al., 1992). Systolic
19
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease

Figure 3 and diastolic heart failure are highly

Pathogenesis of Diastolic Heart Failure in CKD prevalent in patients with advanced
CKD (Foley et al., 1994).
Increasing emphasis has been
placed on the need to control blood
Decreased pressures in all stages of CKD. Since
Glomerular hypertension is both a cause and a
complication of CKD, prevalence
Filtration Rate rates are high. Elevated blood pres-
sure is a primary contributing factor
to development of LVH and heart
failure (both systolic and diastolic).
Lucas and colleagues (2003) found
Increased that systolic hypertension and
Extracellular increased pulse pressures are com-
mon at the time of dialysis initiation.
Fluid Volume All cause mortality was significantly
higher, 14.1 deaths per 100 patient-
years for patients with uncontrolled
hypertension (BP greater than 140/90
mmHg) compared to those that were
Hypertension normotensive, 7.9 deaths per 100
patient years (RR = 1.79, P = 0.01,
95% CI = 1.152.8.). Blood pressure
control remains poor even after
beginning renal replacement therapy.
Cardiac Reports indicate that blood pressure
Remodeling: control in patients receiving dialysis is
low with 40% 90% having blood
LVH pressures higher than the National
Kidney Foundations K-DOQI rec-
ommended goal of 140/90 pre-dialy-
sis (Chalmers et al., 1999; Dhakal,
Diastolic Sloand, & Schiff, 2000; Salem, 1995).
Coronary artery disease has also
Dysfunction been recognized as a contributing fac-
tor to development of flash pul-
monary edema. Chronically elevated
blood pressure results in stiff arteries
that have diffuse arteriosclerosis.
Acute Rise in Blood Pressure Murphy (2003) reports a coronary
artery disease prevalence rate of 40%
in patients beginning dialysis, 22%
have stable angina and 8% have his-
Increased Cardiac torical documentation of a previous
myocardial infarction.
Filling Pressures The diagnosis of flash pulmonary
edema is made using a compilation of
clinical findings (Mansoor, et al.,
2001). Initial evaluation should
Flash Pulmonary include a chest x-ray and Doppler
echocardiogram. Chest radiographs
Edema characteristically demonstrate enlarge-
ment of the peribronchovascular
spaces, prominent septal lines as well
as acinar areas of increased opacity
that coalesce into frank consolidations

20 NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1

(Ware & Matthay, 2005). It is often
difficult to differentiate between sys-
tolic and diastolic heart failure based
upon patient history, physical exam,
chest radiograph, and EKG. Doppler
echocardiography is the most com-
monly utilized technique to assess
both systolic and diastolic ventricular
function. Diastolic function involves
both active and passive components.
The active phase involves energy
dependent relaxation while the pas-
sive phase predominantly reflects the
viscoelastic properties of the heart tis-
sue.
Doppler echocardiography assess-
es both of these phases by examining
pressure changes during transmitral
flow (Figure 4) in diastole. Early dias-
tolic flow occurs when the mitral
valve initially opens at the onset of
diastole. The E wave determined by
Doppler echocardiography serves as
an index of left ventricular relaxation,
compliance, and atrial pressure. Early
passive ventricular filling is followed
by the ventricular filling produced by
atrial contraction (A wave). Deceler-
ation time (DT) is a measurement of
the time it takes for passive filling.
Deceleration time will shorten when
there is a decrease in left ventricular
compliance however deceleration
times are also affected by other
pathologies that increase the left atrial
pressure and shorten DT. DT values
over 240 ms indicate impaired relax-
ation, and under 150 ms indicate a
restrictive pattern (Gilbert, Connelly,
Kelly, Pollock, & Krum, 2006).
Interpretation of E:A ratios becomes
more difficult when there are com-
bined pathologies of impaired relax-
ation and restriction, then both left
atrial and ventricular pressures
increase leading to an increase in the
magnitude of the E wave resulting in
a normal E:A ratio (pseudonormal
pattern) which can be unmasked by
maneuvers that alter cardiac preload
such as the Valsalva maneuver or
administration of nitroprusside
(Angeja & Grossman, 2003). Even
though there are problems with inter-
pretation of E:A ratios, transmitral
inflow patterns obtained with
Doppler echocardiography are non-
NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1
Figure 4
Transmitral Pressures used in Diagnosis of Diastolic Dysfunction
Normal E: A Ratio and Deceleration Time
A Ventricular
E Early passive D filling produced by
ventricular filling T atrial contraction
Deceleration Time
Restrictive E:A Ratio and Deceleration Time
A Ventricular
E Early passive filling produced by
ventricular filling D atrial contraction
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.
invasive and can offer further support morphology. The radio isotope (tech-
in determining the existence of dias- netium) is injected into a vein and
tolic heart failure, especially when absorbed immediately by healthy tis-
there is isolated maladaptive relax- sue. A gamma scintillation camera
ation of the ventricles. detects the gamma rays emitted by
If the Doppler echocardiogram is the radio isotope. If the patients heart
non-conclusive or technically inade- is normal, the technetium will be
quate due to a poor acoustic window, readily and evenly distributed in the
as often occurs in patients with an cardiac images. An uneven distribu-
abnormal body habitus, then a multi- tion of technetium in the heart may
ple-gated acquisition (MUGA) scan be indicative of coronary artery dis-
otherwise known as a cardiac blood ease, cardiomyopathy, or blood
pool scan may be required. This scan shunting within the heart. Use of the
uses a radioactive isotope to evaluate gamma scintillation camera exposes
ventricular function and detect abnor- the patient to about the same amount
malities in the heart wall (Logeart et of radiation as a chest x-ray
al., 2002). The MUGA is more accu- (Youngerman-Cole, 2005).
rate at calculating ejection fraction, Even though rarely done, the gold
but less efficient at identifying valve standard for the diagnosis of diastolic
21
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease
heart failure continues to be cardiac
catheterization allowing direct mea-
surement of volumes and pressures,
but at significantly higher cost and
risk (Gutierrex & Blanchard, 2004). It
is usually not necessary to determine
the etiology for the heart failure since
Doppler echocardiogram or MUGA
usually provide adequate diagnostic
criteria. Pulmonary artery catheteriza-
tion can also be done and has an
adverse event rate of 4.5% - 9.5%, but
it is much more precise in defining
the presence of diastolic heart failure
than MUGA or Doppler echocardio-
gram alone. If the pulmonary artery
occlusion pressure is greater than 18
mm Hg then cardiogenic pulmonary
edema exists (Harvey et al., 2005).
Laboratory testing in flash pul-
monary edema typically may include
measurement of plasma levels of tro-
ponins and brain natriuretic peptide
(BNP). Troponin I elevation in the
presence of kidney failure has
demonstrated high prognostic value
for acute coronary syndrome
(myocardial ischemia). Troponin T
elevation has not been recommended
for detecting acute myocardial
ischemia, but has been associated
with increased mortality risk (Freda,
Tang, Van Lente, Peacock, & Francis,
2002). In a recent study of 258
hemodialysis patients, elevations in
Troponin T (0.10 ng/mL or greater)
correlated significantly with the pres-
ence of left ventricular hypertrophy
(Iliou et al., 2001). The rise and fall of
Troponin I (trend) may be required to
make a definitive diagnosis of acute
coronary syndrome since 1% -6%
have been shown to have elevations
without symptoms (Freda et al.,
2002).
Elevations in brain natriuretic pep-
tide (BNP) have been routinely used
in the diagnosis of heart failure. When
the ventricular wall stretches or there
is increased ventricular pressure, BNP
is secreted. A recent consensus panel
concluded that BNP levels below 100
pg/mL indicate that heart failure is
unlikely (negative predictive value,
greater than 90%); while a BNP level
greater than 500 pg/ml indicates that
heart failure is likely (positive predic-
22
tive value, greater than 90%) (Silver et
al., 2004). Intermediate levels of BNP,
between 100 and 500 pg /mL had less
diagnostic discrimination. BNP levels
may be elevated in critically ill
patients, even in the absence of heart
failure; however, BNP levels less
than100 pg/ml continue to be useful
in excluding heart failure in these
patients. BNP levels are also elevated
in patients with chronic kidney dis-
ease, such that a cut off level below
200 pg/mL has been suggested to
exclude heart failure when the esti-
mated glomerular filtration rate is
below 60 mL per minute. Chronic ele-
vations in BNP may also be a hall-
mark of patients with or at risk for
diastolic heart failure among subjects
with preserved systolic function, inde-
pendent of the degree of left ventricu-
lar hypertrophy (Yamaguchi et al.,
2004).
Symptoms of Flash Pulmonary
Edema
Complaints of severe cough and
dyspnea are usually the primary
symptoms on presentation of flash
pulmonary edema with or without
chest discomfort. Common findings
on physical examination include:
Tachypnea with use of acces-
sory muscles of breathing.
Lung fields auscultation of
crackles in bases and scattered
throughout the lung fields,
rales or even decreased breath
sounds.
Cardiac exam possible pres-
ence of an S3 indicating an
increase in left ventricular end
diastolic volume or an S4 gal-
lop coinciding with an increase
in left atrial pressure, and a
new or changed murmur.
Jugular venous distension indi-
cating increased filling pres-
sures.
Systolic Blood pressure may
be markedly elevated. Hypo-
tension suggests left ventricular
systolic dysfunction and
impending cardiogenic shock.
Peripheral edema usually
without signs of edema, if pre-
NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1
sent, then associated with long-
standing volume expansion
(Mason, Broaddus, Murray, &
Nadel, 2005).
Flash Pulmonary Edema: A Case
Presentation
A 54-year-old male presented to
the dialysis unit of an acute care hos-
pital due to inadvertent dislodgement
of his tunneled venous catheter. He
had been receiving chronic hemodial-
ysis for 3 years at the time of presen-
tation and was oliguric. Arrange-
ments were made with the interven-
tional radiology department to have
this catheter removed and a new
catheter placed. He had undergone
hemodialysis at the community dialy-
sis center 48 hours prior to his pre-
sentation.
There was no evidence of car-
diopulmonary compromise on admis-
sion and he was able to ambulate to
the unit without difficulty. His blood
pressure was noticeably elevated and
he reported holding his antihyperten-
sives that day in anticipation of
undergoing hemodialysis. Holding
his antihypertensives on the day of
dialysis was a common practice. A
chest radiograph was obtained prior
to sending the patient to intervention-
al radiology to evaluate for any evi-
dence of volume expansion since he
would most likely miss his dialysis
treatment that day (see Figure 5).
Physical examination on presenta-
tion:
Temperature: 97.8 F;
Weight: 71 Kg (less than 2 kg
above present dry weight esti-
mate);
Blood pressure: 165/116 HR
89 (sitting); blood pressure
151/88 HR 86 (standing);
No evidence of jugular venous
distension;
Cardiovascular exam: Regular
rhythm, rate 89/minute, I/VI
systolic murmur, - no pericar-
dial rub, no gallops;
Lungs: Respirations were regu-
lar and unlabored, no tachyp-
nea noted, few scattered crack-
les in lung bases, otherwise
 Figure 5
Standing Chest Radiograph AP Prior to
Undergoing Catheter Replacement
clear to auscultation; and
No peripheral edema present.
Past medical history was signifi-
cant for:
Coronary artery disease and
myocardial infarction with
coronary artery stent place-
ment 8 months prior,
Long-standing hypertension,
and
Hyperlipidemia.
A 2-D Echocardiogram obtained 3
months earlier demonstrated:
Diffuse hypokinesia of the left
ventricle, with an approximate
ejection fraction of 29%;
Left ventricular diastolic dys-
function;
Mild eccentric left ventricular
hypertrophy;
Trace tricuspid regurgitation;
and
No pericardial effusion.
The patient returned from the
interventional radiology department
following catheter removal and place-
ment of a new cuffed hemodialysis
catheter on a stretcher. He was noted
to be in acute respiratory distress with
the head of the stretcher at 90.
NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1
Portable Chest PA Radiograph 5 Hours Later
The following findings were noted
upon his return to the dialysis unit.
Temperature: 97.6 F;
Blood pressure: 247/142 HR
127 (sitting);
Pulse oxygenation: 67 78%
(room air);
Respiratory rate: 30/minute
with use of accessory muscles;
Productive cough of frothy
white sputum;
Jugular venous distention was
present;
Cardiovascular exam- tachy-
cardia, II/VI systolic murmur,
loud S2, positive gallop
rhythm , no pericardial rub;
Lungs - decreased breath sounds
in lung bases;
No peripheral edema noted;
12 Lead EKG Sinus tachy-
cardia with rate 127/minute,
occasional premature ventricu-
lar complexes, left atrial
enlargement, left ventricular
hypertrophy and non-specific
ST segment changes;
Portable chest x-ray demon-
strated a new dialysis catheter
in place in the left internal
Figure 6
jugular vein with the tip in the
superior vena cava. The previ-
ously placed catheter had been
removed. There was diffuse
bilateral pulmonary interstitial
edema (see Figure 6);
Serial Troponin I: 0.0 1.0
ng/mL over 24 hours (Range:
0 0.6 no cardiac damage,
0.7 1.5 non-diagnostic,
greater than 1.5 Evidence of a
myocardial infarction)
Other lab results included:
Platelets: 374 K/uL
Na: 140 meq/dL
Potassium: 4.4 meq/dL
HCO3: 39 meq/L
BUN: 40 mg/dL
Creatinine: 9.8 mg/dL
Glucose: 84 mg/dL
Calcium: 10.8 mg/dL
The treatment included:
Oxygen by non-rebreather
facemask at 60%;
Nitroglycerin paste: 1 to
chest;
Labetalol: 20 mg IV over 2
minutes; and
Acute hemodialysis with vol-
ume removal.
23
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease
Hemodialysis was initiated with
ultrafiltration of 3.5 liters over a 4-
hour period. The patients blood pres-
sure improved, and he did not require
endotrachial intubation. The oxygen
by non-rebreather facemask was
slowly weaned during dialysis to a
nasal cannula oxygen by the end of
the dialysis treatment. He was admit-
ted for observation and serial tro-
ponins to rule out myocardial infarc-
tion, all of which were negative. He
returned home after 24 hours with
instructions to take his antihyperten-
sive medications the night before dial-
ysis to avoid the surge in blood pres-
sure the morning prior to his
hemodialysis treatments.
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 car-
diogenic mediated flash (acute) pul-
monary edema? Pulmonary edema
that occurs without significant interdi-
alytic weight gain or evidence of
peripheral edema on physical exami-
nation, particularly in association with
an elevation in blood pressure,
strongly supports the diagnosis of
flash pulmonary edema.
A history of ischemic heart dis-
ease, poorly controlled hypertension,
and identification of left ventricular
hypertrophy by Doppler echocardio-
graphy 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 dialy-
sis. Poorly controlled hypertension in
the presence of a remodeled heart
(i.e., LVH) may result in diastolic dys-
function which predisposes to the
development of pulmonary edema
24
during episodes of volume expansion.
The routine practice of holding anti-
hypertensives prior to undergoing
hemodialysis in certain circumstances
may need to be reconsidered. The
practice of holding antihypertensives
is to avoid low blood pressures at the
end of dialysis following volume
removal (Coomer, Schulman, Breyer,
& Shyr 1997). Blood pressures tend to
normalize with the removal of
intravascular volume during the ultra-
filtration process. It may be better to
reduce rather than hold antihyperten-
sives prior to dialysis to avoid such
extremes in blood pressure (Sulkova
& Valek, 1988).
The immediate treatment of
patients with flash pulmonary edema
is essentially the same as with any
other type of pulmonary edema.
Initial assessment should include
monitoring of hemodynamic parame-
ters and pulse oxymetry or arterial
blood gases. Patients should be given
oxygen. This oxygen support should
be provided by a non-rebreather face-
mask or by positive pressure ventila-
tion. If the work of breathing (respira-
tory rate greater than 30) and hypox-
ia is excessive (PaO2:FiO2 less than
200) endotrachial intubation may be
required (Antonelli et al., 2001).
When hypertension is felt to be con-
tributory, obtaining immediate reduc-
tion in blood pressure is paramount.
Arrangement for acute dialysis with
ultrafiltration if the patient has
already been receiving dialysis is
most beneficial.
Medications commonly used in
the treatment of flash pulmonary
edema include a) nitroglycerin, b)
furosemide, and c) morphine sulfate.
Nitroglycerin is a potent vasodilating
drug which increases cardiac output
while decreasing preload and after-
load. Nitroglycerin reduces pul-
monary edema mainly through
venous dilatation. Patients receiving
dialysis who are oliguric or anuric
may have a mild venodilatory
response to furosemide, but will not
have an effective diuresis. The benefit
of morphine in treatment of pul-
monary edema has remained contro-
versial. Morphine will reduce blood
NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1
pressure and pulmonary edema
through venous dilatation, but mor-
phine may also cause respiratory
depression (Beattie, 2000). Lowering
the blood pressure is a priority with
severely elevated blood pressures.
Labetalol is an effective antihyperten-
sive to use in hypertensive crisis since
it can be given intravenously without
renal adjustment (NHLBI, 2003). It
can be given as a slow intravenous
push starting at 20 mg over 2 min-
utes: additional 2 mg dosages can be
given every minute up to 300 mg
maximum dose to obtain a gradual
reduction in blood pressure (NKF,
2005). Lowering of the blood pres-
sure reduces cardiac filling pressures
and allows cardiac output to improve,
thus reducing fluid accumulation in
the lungs. Additionally slowing of the
heart rate will improve diastolic fill-
ing, thus improving stroke volume
and cardiac output.
Treatment of flash pulmonary
edema is aimed at resolving the
immediate threat of respiratory dis-
tress and hypoxemia and eliminat-
ing/treating the underlying cause (i.e.,
hypertensive crisis). Nurses assess
patients blood pressures pre-dialysis
and post-dialysis, thus they are the
first to note changes that may place
that patient at risk. If blood pressures
are assessed as above the recom-
mended pre-dialysis reading of
140/90, then changes in the treatment
regimen can be instituted. It may be
necessary to reduce the estimated dry
weight to achieve a normalized pre-
dialysis pressure or additional antihy-
pertensives may be required. When
hemodialysis is postponed or can-
celed, then nurses need to remind
patients to resume their antihyperten-
sives in order to avoid blood pressure
extremes and risk of flash pulmonary
edema.
Conclusion
Patients with CKD are at risk for
developing flash pulmonary edema.
Cardiovascular disease is highly
prevalent in the kidney disease popu-
lation. Diastolic heart failure is often
unsuspected without clinical suspi-
cion since the presentation is similar
to that seen with systolic heart failure.
The prevalence of LVH at the time
patients begin dialysis increases the
likelihood of patients developing both
systolic and diastolic dysfunction
which can lead to development of
flash pulmonary edema. The
National Kidney Foundation K-
DOQI guidelines for cardiovascular
disease recommends that echocardio-
grams be performed on all patients at
the initiation of dialysis and again
after achievement of prescribed dry
weight and at 3 year intervals there-
after (NKF, 2005). Nurses should
acknowledge and recommend treat-
ment of blood pressures that are
assessed to be elevated beyond the
current pre-dialysis blood pressure
recommendation of 140/90 pre-dialy-
sis and 130/80 in the CKD popula-
tion (NKF, 2005). Nurses are often
the first to assess blood pressures in
patients on dialysis and evaluate
response to changes in therapy.
Patients may institute better compli-
ance and demonstrate improvements
in blood pressure regulation with a
greater understanding of the inherent
risk. With the high preponderance of
patients beginning dialysis with car-
diovascular disease, it is imperative
that clinicians make a more concerted
effort in treating the risks for cardio-
vascular disease.
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NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1 37

 Flash Pulmonary Edema in Patients with Chronic Kidney Disease and
End Stage Renal Disease
Carol Headley, DNSc, RN, CNN and Barry M. Wall MD
(See posttest instructions on the answer form, on page 28.)
1. What statement is true about the fluid
balance between the interstitium and
the vascular bed within the lungs?
A. Alveoli have high permeability for pro-
tein and fluid.
B. Alveoli epithelial cells drain the pul-
monary interstitium.
C. The alveolar bed within the lungs serve
to protect the lung from fluid accumula-
tion.
D. The lymphatic vessels continuously
absorb fluid from the alveoli.
2. The most common cause of non-cardio-
genic pulmonary edema is
A. renal artery stenosis.
B. malignant hypertension.
C. acute lung injury.
D. aspiration of gastric contents.
3. What changes likely result in acute car-
diogenic pulmonary edema?
A. The lymphatic system becomes less
efficient in removing fluid and there is
increased likelihood for development of
edema.
B. Acute elevations in left atrial pressure
result in pulmonary capillary pressure
increases and fluid is forced into the
interstitium and alveoli.
C. Elevated pulmonary capillary wedge
pressure overwhelms the lymphatic
system and edema results.
D. Increased pulse pressure and systolic
hypertension leads to decrease cardiac
output and fluid leaks into the alveoli.
4. Congestive heart failure (CHF) is a dis-
order that affects the
A. heart only.
B. heart and kidneys only.
C. heart, kidneys, and skeletal muscle
only.
D. heart, kidneys, skeletal muscle and
nervous system.
5. What statement is true about neurohor-
monal changes in congestive heart fail-
ure (CHF)?
A. Initial neurohormonal changes are
deleterious and lead to pulmonary
edema.
B. Initially stimulation of the sympathetic
nervous system decreases cardiac out-
put.
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.
NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1
Posttest 1.5 Contact Hours
Posttest Questions
6. Diastolic dysfunction refers to a disor-
der
A. of myocardial relaxation resulting in
impaired ventricular filling.
B. of myocardial stiffness that results in
delayed ventricular emptying.
C. associated with left ventricular hyper-
trophy and abnormal filling.
D. that occurs as a result of pressure
changes related to malfunctioning
valves.
7. There is a strong association between
- and the development of dias-
tolic dysfunction and flash pulmonary
edema.
A. hypertension
B. left ventricular hypertrophy
C. anemia
D. volume overload
8. The increased resistance to diastolic
ventricular filling in diastolic heart dis-
ease is commonly due to
A. myocardial hypertrophy only.
B. myocardial hypertrophy and ischemia
only.
C. myocardial hypertrophy, ischemia, and
mitral stenosis only.
D. myocardial hypertrophy, ischemia,
mitral stenosis and pericarditis.
9. Which statement is true about the
prevalence of diastolic heart failure?
A. 50% of persons greater than age 60
with CHF will have diastolic failure.
B. Prognosis for systolic heart failure is
better than diastolic heart failure.
C. Patients over 70 years old with diastolic
failure have a 30% 5-year mortality.
D. Kidney disease contributes to the
development of diastolic heart failure at
earlier ages.
10. What statement is true about renal
artery stenosis (RAS)?
A. Chronic mild to moderate hypertension
is associated with RAS.
B. It is seen in older women with fibro-
muscular dysplasia.
C. It commonly involves atherosclerotic
plague deposition in the renal artery.
D. It is always associated with a decrease
in kidney function.
11. Your patient has a brain natriuretic pep-
tide (BNP) level 700 pg/ml. What would
your next action be?
A. CT scan of the brain
B. X-ray of the chest
C. Administer hypertensive medications
D. Complete a physical assessment
12. Common finding(s) on physical exami-
nation of a patient with flash pulmonary
edema is (are)
A. tachypnea only.
B. tachypnea and decreased breath
sounds only.
C. tachypnea, decreased breath sounds,
and new murmur only.
D. tachypnea, decreased breath sounds,
new murmur, and hypotension.
13. What common practice in dialysis units
may contribute to flash pulmonary
edema?
A. Holding BP medications pre-dialysis
B. Inaccurate dry weight assessment
C. Use of non-tunneled catheters for dial-
ysis
D. Eating on dialysis
14. Your patient arrives for dialysis with
tachypnea, hypertension, and crackles
in the bases of the lungs. You feel the
patient has cardiogenic mediated flash
pulmonary edema. Why?
A. Insignificant intradialytic weight gain
only
B. Insignificant intradialytic weight gain
and absence of edema only
C. Insignificant intradialytic weight gain,
absence of edema, and hypertension
only
D. Insignificant intradialytic weight gain,
absence of edema, and hypertension
and no history of ischemic heart dis-
ease
27
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease

ANNJ701 ANSWER/EVALUATION FORM

Flash Pulmonary Edema in Patients with Chronic Kidney Disease and
End Stage Renal Disease
Carol M. Headley, DNSc, RN, and Barry M. Wall MD
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Posttest Answer Grid (Please circle your answer choice):
1. a b c d 4. a b c d 7. a b c d 10. a b c d 13. a b c d
2. a b c d 5. a b c d 8. a b c d 11. a b c d 14. a b c d
3. a b c d 6. a b c d 9. a b c d 12. a b c d

Strongly Strongly Recognize the risk for development of flash

Evaluation disagree agree pulmonary edema in patients with chronic
1. The objectives were related to the goal. 1 2 3 4 5 kidney disease and ESRD
2. Objectives were met
a. Identify causes of flash pulmonary edema that may 1 2 3 4 5 I verify that I have completed this activity:
occur in conjunction with chronic kidney disease
and ESRD. _____________________________________________
b. Recognize signs and symptoms of flash pulmonary 1 2 3 4 5 (Signature)
edema.
c. Describe nursing measures that may avert devel- 1 2 3 4 5 Comments _____________________________________
opment of flash pulmonary edema in individuals with _____________________________________________
advanced chronic kidney disease.
3. The content was current and relevant. 1 2 3 4 5 _____________________________________________
4. This was an effective method to learn this content. 1 2 3 4 5
Suggested topics for future articles?_________________
5. Time required to complete reading assignment: _________ minutes.
_____________________________________________
_____________________________________________

28 NEPHROLOGY NURSING JOURNAL January-February 2007 Vol. 34, No. 1