F Flash Pulmonary Edema in Patients with Chronic Kidney Disease and

Transcription

Flash Pulmonary Edema in Patients
with Chronic Kidney Disease and
End Stage Renal Disease
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-
F
Carol M. Headley, DNSc, RN, CNN, is
Nephrology Advanced Practice Nurse at The VA
Medical Center, Memphis, TN. She is ANNA’s
National Program chairperson and a member of
ANNA’s 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.
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.
tenance dialysis. The sudden onset of
pulmonary edema may be assumed
to be from excessive interdialytic
weight gain, inaccurate dry weight
prescription, or weight scale malfunctions rather than from a cardiogenic
origin. Furthermore, treatment is
often readily available and implemented (ultrafiltration), thus the problem is promptly treated.
The strong association between
cardiovascular disease and kidney
disease has been emphasized during
the past decade (Foley, Parfrey, &
Samak, 1998). Kidney disease is now
known to be an independent risk factor for cardiovascular morbidity and
mortality (Levey et al., 1998; Sarnak
et al., 2003). This article will define
flash pulmonary edema and factors
for its development, emphasizing the
relationship between cardiovascular
disease and chronic kidney disease.
Lastly, a case study of a patient on
hemodialysis that developed flash
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 Center’s 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.
NEPHROLOGY NURSING JOURNAL ■ January-February 2007 ■ Vol. 34, No. 1
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
πmv – plasma protein osmotic pressure in the circulation
πpmv – 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
and interstitial fluid oncotic pressures,
and the pressure differential across
the capillary wall). Normally, the
alveolar bed within the lung serves to
protect the lung from fluid accumulation. Alveoli have very low permeability for fluid and protein. Any fluid
filtered into the alveoli is continuously absorbed back into the interstitium
by the alveolar epithelial cells and
drained away from the pulmonary
interstitium by lymphatic vessels
(Gluecker et al., 1999).
Non-cardiogenic pulmonary edema
occurs as a result of fluid accumulation in the alveoli resulting from a
disruption in Starling’s forces secondary to increased capillary permeability. The most common cause of
non-cardiogenic pulmonary edema is
acute lung injury (ALI) or acute respiratory distress syndrome (ARDS)
associated with increased pulmonary
capillary permeability. Most often,
the concentration of protein within
the pulmonary interstitium exceeds
60% of the plasma protein value as
compared to less than 45% in cardiogenic pulmonary edema (Hanley &
Welsh, 2004). Non-cardiogenic pulmonary edema is diagnosed when
there is radiographic evidence of
alveolar fluid accumulation without
an elevation in the pulmonary wedge
pressure greater than 18 mmHg or
evidence of congestive heart failure
(CHF) on physical examination
(Mason, Broaddus, Murray, & Nadel,
2005).
Cardiogenic pulmonary edema is
the most common type of pulmonary edema and results from
increased left atrial filling pressure
(Hanley & Welsh, 2004). In this type
of pulmonary edema, the rate of
fluid accumulation within the lungs
is mainly dependent upon the functional capacity of the lymphatic system of the lungs to remove fluid
from the interstitium and alveoli
(Mason et al., 2005). As left atrial
pressure rises, pulmonary capillary
pressures increase resulting in protein poor fluid (edema) being forced
into the lung interstitium and alveoli.
Consequently, there is a progressive
deterioration in alveolar gas
exchange resulting in hypoxemia
and symptoms of respiratory distress. Compensatory changes may
occur in individuals with chronically
elevated left atrial pressures and persistently elevated pulmonary capillary wedge pressures (greater than 18
mmHg). In this circumstance, the
lymphatic system of the lungs
becomes more efficient at removing
fluid, thus reducing the likelihood for
development of edema. It is the sudden or acute elevations in left atrial
pressures that are more likely to
result in acute pulmonary edema
(Fraser, Müller, Colman, & Paré,
1999; Little, & Braunwald, 1997).
It may be difficult to differentiate
between flash pulmonary edema and
non-cardiogenic pulmonary edema
since the presenting symptoms are
often the same (Hanley & Welsh,
2004). Symptoms typically consist of
dyspnea, tachypnea, and cough with
possible expectoration of frothy
edema fluid. The patient history and
determination of the factors that led
to the development of the pulmonary edema becomes a priority
for diagnosis. Non-cardiogenic pulmonary edema is less common and
is primarily seen in individuals that
have had recent pneumonia, sepsis,
tumor, pulmonary fibrosis, trauma
with multiple blood transfusions, following lung transplantation or resultant from aspiration of gastric contents.
Flash Pulmonary Edema
Flash pulmonary edema can origi-
nate from cardiogenic (i.e., cardiac
dysfunction) and non-cardiogrenic
causes (i.e., neurogenic pulmonary
edema) and occurs suddenly over a
period of minutes to hours (Lee, et al.,
1988). The syndrome of congestive
heart failure is the most common etiology for the development of flash
pulmonary edema. Traditionally, the
diagnosis of congestive heart failure
has been attributed to the presence of
myocardial systolic dysfunction,
defined as a disorder of myocardial
contractility leading to a reduced ejection fraction. Chronic systolic dysfunction results in a systemic process,
not solely confined to the heart
(Torre-Amione, 2005). Congestive
heart failure is a multisystem disorder
affecting the heart, skeletal muscle,
kidneys, and nervous system patterned by a complex neurohormonal
process. Figure 2 depicts a simplified
version of the process. Neurohormonal activation is key to the progressive nature of chronic heart failure whereas flash pulmonary edema
occurs quickly and is primarily
dependent upon a pre-existing condition (i.e., diastolic dysfunction) coupled with an acute stressor (i.e., rise in
blood pressure).
Chronic heart failure has been a
challenge to treat because of its complexity and its insidious character.
Initially, neurohormonal changes present in chronic heart failure are compensatory and temporarily improve
cardiac output. These however, eventually become deleterious. Stimulation of the sympathetic nervous system is one of the earliest neurohormonal responses and initially provides improved inotropic support to
increase cardiac output. Stimulation
of the renin-angiotensin-aldosterone
system (RAAS) causes release of
renin, plasma angiotensin II, and
aldosterone. Angiotensin II causes
vasoconstriction of the efferent arterioles and the systemic circulation and
increased adrenal secretion of aldosterone that results in sodium and
water retention by the kidneys
( Jackson, Gibbs, Davies, & Lip,
2000). However, long-term stimulation of the RAAS and sympathetic
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
nervous systems becomes maladaptive by contributing to cardiac
myocyte apoptosis (programmed cell
death), hypertrophy, and focal
myocardial necrosis ( Jackson et al.,
2000).
Diastolic dysfunction, defined as a
disorder of myocardial relaxation
resulting in impaired ventricular filling, may also result in the syndrome
of congestive heart failure. Diastolic
heart failure is diagnosed when elevated filling pressures are necessary
to achieve normal ventricular filling
(Grossman 2000). Recent epidemio-
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
edema. However, diastolic heart failure 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 during this phase. The changes in cardiac
pressure that occur during diastole
are the result of isovolumetric relaxation from the time of the aortic valve
closure to mitral valve opening; early
rapid filling after mitral valve opening; and low blood flow during middiastole; and lastly late filling (high
blood flow) from atrial contraction. In
diastolic heart failure, the left ventricle is stiff (reduced elastic recoil) with
impaired relaxation causing a reduction in filling. Higher diastolic pressures are required to maintain adequate 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 presence of systolic hypertension (systolic
arterial blood pressure greater than
160 mmHg) in 85% of patients presenting to hospital emergency rooms
with flash pulmonary edema
(Kramer, Kirkman, Kitzman, & Little,
2000). Studies that performed
Doppler echocardiography after the
acute episode found preserved systolic 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 normal, 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-dimensional transthoracic echocardiogra-
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
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
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 diastolic pressure precipitating pulmonary 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 volume 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 provide adequate ventricular filling.
Heart failure resulting from diastolic
dysfunction occurs when elevated filling pressures are necessary to achieve
normal ventricular filling (Grossman,
2000). The increased resistance to
diastolic ventricular filling is most
commonly due to myocardial abnormalities (myocardial hypertrophy,
fibrosis, ischemia, or cardiomyopathy), and less commonly to mechanical abnormalities like mitral stenosis
or constrictive pericarditis (Hanley &
Welsh, 2004).
Hypertension is frequently present in patients presenting with flash
pulmonary edema. Chronic hypertension that is poorly controlled can
result in development of systolic and
diastolic dysfunction that may predispose patients to the development of
flash pulmonary edema (Mansoor et
al., 2001). Even labile elevations in
blood pressures of patients with bilateral 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 predecessor to development of left ventricular
hypertrophy (LVH). Hypertension
leads to remodeling and augmentation 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 sometimes 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 atherosclerosis. 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 individuals over the age of 55, while
fibromuscular dysplasia is usually
seen in young women. Women with
fibromuscular dysplasia associated
RAS almost invariably have hypertension. Lesions associated with fibromuscular dysplasia tend to show a
much more favorable response to
percutaneous transluminal angioplasty (PTA), stent or surgery than atherosclerotic lesions (Olin, 2004).
The most common type of RAS
involves atherosclerotic deposition in
the artery lumen that disrupts blood
flow to the kidney parenchyma causing 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 hypertension. Mild to moderate hypertension 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
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
patient – 63 years
USRDS, 2005
Ischemic heart disease
35% - CKD
40% - Beginning dialysis
Levin, 2003
Heart failure
37%
Foley et al., 1994
malignant hypertension (Harding et
al., 1992). Renovascular hypertension
related to bilateral renal artery stenosis is strongly associated with the
edema. The combination of hypertension and volume retention, occurring as a consequence of altered
intrarenal hemodynamics and aldosterone-mediated salt and water retention are the major contributing factos
to the development of flash pulmonary edema with bilateral renal
artery stenosis. In contrast pulmonary
edema is relatively uncommon with
unilateral renal artery stenosis
(Basaria & Fred, 2002; Jaff, 2001).
Unilateral renal artery stenosis leads
to renin dependent hypertension, but
not to volume expansion, since the
non-affected kidney undergoes a
pressure natriuresis/diuresis, which
prevents volume expansion making
pulmonary edema less likely to occur
(Missouris et al., 2000).
Flash Pulmonary Edema and
Kidney Disease
Many of the precipitating factors
associated with development of flash
pulmonary edema are frequently present in patients with advanced stages
of CKD (Table 1). Cardiovascular disease and CKD are strongly linked.
Recent findings indicate that patients
with CKD are in the highest risk
group for cardiovascular disease and
that patients with CKD are more likely to die of cardiovascular disease
than ESRD (Levin, 2003).
Systolic and diastolic heart failure
has been associated with the development of flash pulmonary edema
(Ware & Matthay, 2005). This discussion will primarily highlight the
pathology of diastolic heart failure. A
relationship between the risk for diastolic heart failure in the presence of
kidney disease can be established by
examining the contributing factors
that precede there development
(Figure 3). Diastolic heart failure can
be caused by ischemia, left ventricular hypertrophy (LVH), increased filling pressures related to chronically
elevated blood pressures, infiltrative
cardiomyopathies, ischemic heart disease, pericarditis, the normal aging
processes, chemotherapy and genetic
anomalies (Beattie, 2000; Kramer et
al., 2000; Zile & Simsic, 2000). In the
general population, 50% of people
over the age of 70 with a diagnosis of
congestive heart failure will have preserved systolic function and classified
as having diastolic heart failure. For
those 10 years younger (60 years of
age) with congestive heart failure
symptoms, only 15% will have diastolic heart failure. Age also contributes to mortality risk. Overall,
prognosis is better for diastolic heart
failure (average mortality rate 5 % 8%) than for systolic heart failure
(average mortality rate 10% - 15%),
but diastolic heart failure in patients
over 70 years has a 50% 5-year mortality rate (Zile & Simsic, 2000). These
changes are similar to disease reported in the elderly, but they occur 15-20
years earlier in kidney disease
(Tozawa, Iseki, Iseki, & Takishita,
2002; Churchill et al., 1992). Systolic
19
Figure 3
Pathogenesis of Diastolic Heart Failure in CKD
Decreased
Glomerular
Filtration Rate
Increased
Extracellular
Fluid Volume
Hypertension
Cardiac
Remodeling:
LVH
Diastolic
Dysfunction
Acute Rise in Blood Pressure
Increased Cardiac
Filling Pressures
Flash Pulmonary
Edema
20
and diastolic heart failure are highly
prevalent in patients with advanced
CKD (Foley et al., 1994).
Increasing emphasis has been
placed on the need to control blood
pressures in all stages of CKD. Since
hypertension is both a cause and a
complication of CKD, prevalence
rates are high. Elevated blood pressure is a primary contributing factor
to development of LVH and heart
failure (both systolic and diastolic).
Lucas and colleagues (2003) found
that systolic hypertension and
increased pulse pressures are common at the time of dialysis initiation.
All cause mortality was significantly
higher, 14.1 deaths per 100 patientyears for patients with uncontrolled
hypertension (BP greater than 140/90
mmHg) compared to those that were
normotensive, 7.9 deaths per 100
patient years (RR = 1.79, P = 0.01,
95% CI = 1.15–2.8.). Blood pressure
control remains poor even after
beginning renal replacement therapy.
Reports indicate that blood pressure
control in patients receiving dialysis is
low with 40% – 90% having blood
pressures higher than the National
Kidney Foundations K-DOQI recommended goal of 140/90 pre-dialysis (Chalmers et al., 1999; Dhakal,
Sloand, & Schiff, 2000; Salem, 1995).
Coronary artery disease has also
been recognized as a contributing factor to development of flash pulmonary edema. Chronically elevated
blood pressure results in stiff arteries
that have diffuse arteriosclerosis.
Murphy (2003) reports a coronary
artery disease prevalence rate of 40%
in patients beginning dialysis, 22%
have stable angina and 8% have historical documentation of a previous
myocardial infarction.
The diagnosis of flash pulmonary
edema is made using a compilation of
clinical findings (Mansoor, et al.,
2001). Initial evaluation should
include a chest x-ray and Doppler
echocardiogram. Chest radiographs
characteristically demonstrate enlargement of the peribronchovascular
spaces, prominent septal lines as well
as acinar areas of increased opacity
that coalesce into frank consolidations
(Ware & Matthay, 2005). It is often
difficult to differentiate between systolic and diastolic heart failure based
upon patient history, physical exam,
chest radiograph, and EKG. Doppler
echocardiography is the most commonly 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 passive phase predominantly reflects the
viscoelastic properties of the heart tissue.
Doppler echocardiography assesses both of these phases by examining
pressure changes during transmitral
flow (Figure 4) in diastole. Early diastolic 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). Deceleration 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 relaxation, 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 combined pathologies of impaired relaxation 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 interpretation of E:A ratios, transmitral
inflow patterns obtained with
Doppler echocardiography are non-
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.
invasive and can offer further support
in determining the existence of diastolic heart failure, especially when
there is isolated maladaptive relaxation of the ventricles.
If the Doppler echocardiogram is
non-conclusive or technically inadequate due to a poor acoustic window,
as often occurs in patients with an
abnormal body habitus, then a multiple-gated acquisition (MUGA) scan
otherwise known as a cardiac blood
pool scan may be required. This scan
uses a radioactive isotope to evaluate
ventricular function and detect abnormalities in the heart wall (Logeart et
al., 2002). The MUGA is more accurate at calculating ejection fraction,
but less efficient at identifying valve
morphology. The radio isotope (technetium) is injected into a vein and
absorbed immediately by healthy tissue. A gamma scintillation camera
detects the gamma rays emitted by
the radio isotope. If the patient’s heart
is normal, the technetium will be
readily and evenly distributed in the
cardiac images. An uneven distribution of technetium in the heart may
be indicative of coronary artery disease, cardiomyopathy, or blood
shunting within the heart. Use of the
gamma scintillation camera exposes
the patient to about the same amount
of radiation as a chest x-ray
(Youngerman-Cole, 2005).
Even though rarely done, the gold
standard for the diagnosis of diastolic
21
heart failure continues to be cardiac
catheterization allowing direct measurement 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 catheterization 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 echocardiogram 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 pulmonary edema typically may include
measurement of plasma levels of troponins 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 presence 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 peptide (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 disease, such that a cut off level below
200 pg/mL has been suggested to
exclude heart failure when the estimated glomerular filtration rate is
below 60 mL per minute. Chronic elevations in BNP may also be a hallmark of patients with or at risk for
diastolic heart failure among subjects
with preserved systolic function, independent of the degree of left ventricular 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 accessory 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 presence of an S3 indicating an
increase in left ventricular end
diastolic volume or an S4 gallop coinciding with an increase
in left atrial pressure, and a
new or changed murmur.
• Jugular venous distension indicating increased filling pressures.
• Systolic Blood pressure – may
be markedly elevated. Hypotension suggests left ventricular
systolic
dysfunction
and
impending cardiogenic shock.
• Peripheral edema – usually
without signs of edema, if pre-
sent, then associated with longstanding 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 hospital due to inadvertent dislodgement
of his tunneled venous catheter. He
had been receiving chronic hemodialysis for 3 years at the time of presentation and was oliguric. Arrangements were made with the interventional radiology department to have
this catheter removed and a new
catheter placed. He had undergone
hemodialysis at the community dialysis center 48 hours prior to his presentation.
There was no evidence of cardiopulmonary compromise on admission and he was able to ambulate to
the unit without difficulty. His blood
pressure was noticeably elevated and
he reported holding his antihypertensives 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 interventional radiology to evaluate for any evidence of volume expansion since he
would most likely miss his dialysis
treatment that day (see Figure 5).
Physical examination on presentation:
• Temperature: 97.8º F;
• Weight: 71 Kg (less than 2 kg
above present dry weight estimate);
• 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 pericardial rub, no gallops;
• Lungs: Respirations were regular and unlabored, no tachypnea noted, few scattered crackles 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 significant for:
• Coronary artery disease and
myocardial infarction – with
coronary artery stent placement 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 dysfunction;
• Mild eccentric left ventricular
hypertrophy;
• Trace tricuspid regurgitation;
and
• No pericardial effusion.
The patient returned from the
interventional radiology department
following catheter removal and placement 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 90º.
Figure 6
Portable Chest PA Radiograph 5 Hours Later
The following findings were noted
upon his return to the dialysis unit.
• Temperature: 97.6º 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- tachycardia, 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 tachycardia with rate 127/minute,
occasional premature ventricular complexes, left atrial
enlargement, left ventricular
hypertrophy and non-specific
ST segment changes;
• Portable chest x-ray demonstrated a new dialysis catheter
in place in the left internal
jugular vein with the tip in the
superior vena cava. The previously 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 volume removal.
23
Hemodialysis was initiated with
ultrafiltration of 3.5 liters over a 4hour period. The patient’s blood pressure 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 admitted for observation and serial troponins to rule out myocardial infarction, all of which were negative. He
returned home after 24 hours with
instructions to take his antihypertensive medications the night before dialysis to avoid the surge in blood pressure 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 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
during episodes of volume expansion.
The routine practice of holding antihypertensives 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 ultrafiltration process. It may be better to
reduce rather than hold antihypertensives 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 parameters and pulse oxymetry or arterial
blood gases. Patients should be given
oxygen. This oxygen support should
be provided by a non-rebreather facemask or by positive pressure ventilation. If the work of breathing (respiratory rate greater than 30) and hypoxia is excessive (PaO2:FiO2 less than
200) endotrachial intubation may be
required (Antonelli et al., 2001).
When hypertension is felt to be contributory, obtaining immediate reduction 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 afterload. Nitroglycerin reduces pulmonary 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 pulmonary edema has remained controversial. Morphine will reduce blood
pressure and pulmonary edema
through venous dilatation, but morphine may also cause respiratory
depression (Beattie, 2000). Lowering
the blood pressure is a priority with
severely elevated blood pressures.
Labetalol is an effective antihypertensive 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 minutes: 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 pressure 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 filling, thus improving stroke volume
and cardiac output.
Treatment of flash pulmonary
edema is aimed at resolving the
immediate threat of respiratory distress and hypoxemia and eliminating/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 recommended 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 predialysis pressure or additional antihypertensives may be required. When
hemodialysis is postponed or canceled, then nurses need to remind
patients to resume their antihypertensives 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 population. 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 KDOQI guidelines for cardiovascular
disease recommends that echocardiograms be performed on all patients at
the initiation of dialysis and again
after achievement of prescribed dry
weight and at 3 year intervals thereafter (NKF, 2005). Nurses should
acknowledge and recommend treatment of blood pressures that are
assessed to be elevated beyond the
current pre-dialysis blood pressure
recommendation of 140/90 pre-dialysis and 130/80 in the CKD population (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 compliance and demonstrate improvements
in blood pressure regulation with a
greater understanding of the inherent
risk. With the high preponderance of
patients beginning dialysis with cardiovascular disease, it is imperative
that clinicians make a more concerted
effort in treating the risks for cardiovascular disease.
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37
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and
Carol Headley, DNSc, RN, CNN and Barry M. Wall MD
Posttest — 1.5 Contact Hours
Posttest Questions
(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?
6.
A. of myocardial relaxation resulting in
impaired ventricular filling.
B. of myocardial stiffness that results in
delayed ventricular emptying.
C. associated with left ventricular hypertrophy and abnormal filling.
D. that occurs as a result of pressure
changes related to malfunctioning
valves.
A. Alveoli have high permeability for protein and fluid.
B. Alveoli epithelial cells drain the pulmonary interstitium.
C. The alveolar bed within the lungs serve
to protect the lung from fluid accumulation.
D. The lymphatic vessels continuously
absorb fluid from the alveoli.
7.
2.
The most common cause of non-cardiogenic pulmonary edema is
A.
B.
C.
D.
3.
renal artery stenosis.
malignant hypertension.
acute lung injury.
aspiration of gastric contents.
What changes likely result in acute cardiogenic 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.
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
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.
Your patient has a brain natriuretic peptide (BNP) level 700 pg/ml. What would
your next action be?
A.
B.
C.
D.
12.
CT scan of the brain
X-ray of the chest
Administer hypertensive medications
Complete a physical assessment
Common finding(s) on physical examination 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.
The increased resistance to diastolic
ventricular filling in diastolic heart disease 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.
11.
There is a strong association between
———- and the development of diastolic dysfunction and flash pulmonary
edema.
A.
B.
C.
D.
Congestive heart failure (CHF) is a disorder 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.
Diastolic dysfunction refers to a disorder
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 dialysis
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 disease
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 fibromuscular dysplasia.
C. It commonly involves atherosclerotic
plague deposition in the renal artery.
D. It is always associated with a decrease
in kidney function.
27
ANSWER/EVALUATION FORM
ANNJ701
Flash Pulmonary Edema in Patients with Chronic Kidney Disease and
Carol M. Headley, DNSc, RN, and Barry M. Wall MD
Posttest Instructions
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Posttest Answer Grid (Please circle your answer choice):
1.
2.
3.
a
a
a
b
b
b
Evaluation
c
c
c
d
d
d
4.
5.
6.
a
a
a
b
b
b
c
c
c
d
d
d
7.
8.
9.
a
a
a
b
b
b
c
c
c
Strongly
disagree
1. The objectives were related to the goal.
1
2. Objectives were met
a. Identify causes of flash pulmonary edema that may 1
occur in conjunction with chronic kidney disease
and ESRD.
b. Recognize signs and symptoms of flash pulmonary 1
edema.
c. Describe nursing measures that may avert devel1
opment of flash pulmonary edema in individuals with
advanced chronic kidney disease.
3. The content was current and relevant.
1
4. This was an effective method to learn this content.
1
5. Time required to complete reading assignment: _________
d
d
d
10. a
11. a
12. a
Strongly
agree
b
b
b
c
c
c
d
d
d
13. a
14. a
b
b
c
c
d
d
Recognize the risk for development of flash
pulmonary edema in patients with chronic
kidney disease and ESRD
2
3
4
5
2
3
4
5
2
3
4
5
_____________________________________________
(Signature)
2
3
4
5
Comments _____________________________________
I verify that I have completed this activity:
_____________________________________________
2
3
2
3
minutes.
4
4
5
5
_____________________________________________
Suggested topics for future articles?_________________
_____________________________________________
_____________________________________________
28

F Flash Pulmonary Edema in Patients with Chronic Kidney Disease and

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